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Acute heart failure: heart failure surgery and transplantation 

Acute heart failure: heart failure surgery and transplantation
Chapter:
Acute heart failure: heart failure surgery and transplantation
Author(s):

Aikaterini N Visouli

and Antonis A Pitsis

DOI:
10.1093/med/9780199687039.003.0054_update_002

Update:

Major updates made to topics on ST-segment elevation acute myocardial infarction (STEMI), role of coronary artery bypass grafting in cardiogenic shock, ventricular septal rupture after myocardial infarction, and role of surgery in acute heart failure due to valvular disease

5 new references added

Updated on 22 February 2018. The previous version of this content can be found here.
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date: 15 October 2019

Summary

Cardiac surgery should be considered in all cases of heart failure (HF) attributed to surgically correctable causes. Surgical revascularization, repair of mechanical complications of myocardial infarction (MI), valve repair or replacement (of native or prosthetic heart valves, in the absence or presence of endocarditis), repair of acute aortic dissection, treatment of acute pericardial syndromes, surgical embolectomy in high-risk acute pulmonary embolism, mechanical circulatory support (MCS), and heart transplantation (HTx) represent the main surgical interventions that may be offered in the setting of AHF or ADCHF. Transcatheter aortic valve implantation (TAVI) for severe aortic stenosis and other transcatheter valve interventions are increasingly applied, gaining upgraded or new guideline-driven recommendations. With the exception of emergent status requiring immediate intervention, the concept of multidisciplinary approach in complicated heart disease amenable to surgery has been generally accepted.

Introduction

Cardiac surgery mechanically intervenes to restore the functional abnormality caused by coronary anatomical lesions, and to repair or replace abnormal anatomical structures that cause significant functional cardiac compromise, the most severe form of which is HF. In the presence of HF all potentially surgical correctable conditions should be identified and, if indicated, surgically corrected. With the advent of MCS and HTx, surgery offers temporary or long-term, and partial or total ventricular support of one or both failing ventricle(s), but also biological or mechanical replacement of the heart itself, when all other means have failed. Cardiac surgery in AHF is usually required in life-threatening situations that cannot be addressed otherwise; therefore, it is associated with increased mortality; nevertheless, it can be lifesaving [18].

Role of cardiac surgery in acute heart failure due to acute coronary syndromes

AHF may complicate acute coronary syndromes (ACS) that include the continuum of unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). [18]. Among unselected patients presenting to the emergency department with acute chest pain due to cardiac disease, the observed disease prevalence is 20% UA, 30%-40% NSTEMI, 10%-20% STEMI, and 30% other cardiac conditions [5]. The continuum of UA and NSTEMI is currently described as non-ST-elevation acute coronary syndromes (NSTE-ACS), which affect approximately 75% of all ACS patients [4]. Ischaemic cardiogenic shock (CS) may complicate STEMI but also NSTE-ACS [47].

Coexistence of AHF and ACS always identifies a very-high-risk group of patients, requiring immediate invasive strategy (angiography in view of revascularization) irrespective of ECG or biomarker findings [8].

When mechanical revascularization is required in ACS patients, the choice between PCI and CABG should be based on evaluation of clinical severity and acuity, coronary anatomy, comorbidities, estimated risks and benefits, expected completeness of revascularization, need for concomitant cardiac surgery, presence of previous revascularization(s), local conditions, and, in non-catastrophic situations, the patient’s preference. Generally, unstable clinical status favors PCI, offering faster revascularization, while complex coronary anatomy (severity, distribution, lesion characteristics) favors CABG, offering more complete revascularization [110].

Acute coronary syndromes without persistent ST-segment elevation (NSTE-ACS)

An urgent/immediate invasive strategy (< 2h), involving coronary angiography with intend to perform revascularization, is indicated in NSTE-ACS patients in the presence of AHF, CS, haemodynamic instability, refractory or recurrent angina, cardiac arrest, life threatening arrhythmias, mechanical complications of MI, or other very-high-risk criteria [1, 4, 5, 8]. Patients with NSTE-ACS and at least one very-high-risk criterion have poor short and long-term prognosis if left untreated, and should be managed as STEMI patients [5, 8]. In stabilized patients with NSTE-ACS and indication for early revascularization, the choice between PCI and CABG can be made as in stable coronary artery disease (CAD) [1, 4, 5], with a stronger impetus for revascularization [4].

Revascularization in NSTE-ACS patients with single vessel disease

Patients with NSTE-ACS and single-vessel disease represent approximately one third of NSTE-ACS patients undergoing angiography and are usually treated with ad hoc PCI, which is the first choice [1, 5].

Revascularization in NSTE-ACS patients with multivessel disease

The decision is more complex in patients with multivessel CAD, which represent approximately 50% of NSTE-ACS patients undergoing angiography [4] and 40–80% of NSTE-ACS patients with angiographically obstructive CAD [5]. The treatment options include culprit lesion PCI, multivessel PCI, CABG [1, 5] (or hybrid approach [1]).

In the presence of clinical or angiographic indications for urgent revascularization in NSTE-ACS patients with multivessel CAD, culprit lesion PCI does not necessitate a multidisciplinary approach [1, 5]. Thus, in continuing or recurrent ischaemia, haemodynamic instability, pulmonary oedema, recurrent ventricular arrhythmias, or total occlusion of a culprit coronary artery requiring urgent revascularization, ad hoc PCI is indicated [5]. Risk stratification (EuroSCORE, STS, SYNTAX, etc.), clinical judgment, and multidisciplinary discussion is advised [1].

In stabilized NSTE-ACS patients with multivessel CAD and SYNTAX score > 22, urgent CABG should be preferred over PCI, particularly when there is no clearly identifiable culprit lesion [1]. In up to 40% of NSTEMI-ACS patients with obstructive CAD, angiography reveals multiple complex plaques fulfilling the culprit lesion criteria [5].

Approximately 20–30% of NSTE-ACS patients have diagnosed diabetes mellitus, and at least as many have impaired glucose tolerance or undiagnosed diabetes [1]. In diabetic patients with stabilized NSTE-ACS, multivessel disease and acceptable surgical risk, CABG is recommended over PCI (I A) [1,5,12], while PCI should be considered for diabetic patients with SYNTAX score ≤22 (IIa B) [5]. When CABG is performed, bilateral internal mammary artery (IMA) grafting should be considered (IIa B); when bilateral IMAs are harvested, skeletonized IMA dissection is recommended (I B) [1].

CABG should be considered over PCI for stabilized NSTE-ACS patients with moderate or severe chronic kidney disease (CKD), multivessel CAD and symptoms/evidence of ischaemia if they have an acceptable surgical risk and life expectancy >year (IIa B), PCI should be considered over CABG if they have a high surgical risk or life expectancy <1 year (IIa B) [1, 5]. Delay of CABG after angiography (to allow amelioration of contrast media effect on renal function) should be considered (IIa C), while off-pump CABG may be considered (IIb C) [1].

Revascularization in early and late graft failure and in stent thrombosis or restenosis

Bypass graft failure may be the underlying condition in 5% of patients presenting with NSTE-ACS [5]. In patients with previous CABG, native disease progression and/or late graft failure causing severe symptoms or significant ischaemia despite optimal medical treatment (OMT), repeat revascularization is indicated if technically feasible (I B) [1]. PCI (preferably of the bypassed native artery) is the first choice (if technically feasible) (IIa C), particularly in the presence of a patent IMA [1]. Redo CABG (with IMA if available) should be considered in stable patients without a patent IMA to the LAD (IIa B), and may be considered in patients with anatomy unsuitable for PCI (IIb C) [1]. In early ischaemia after CABG, ad hoc Heart Team consultation is recommended (I C); PCI (of native vessels or IMA grafts rather than vein grafts) should be preferred over redo CABG if technically feasible (IIa C) [1]. Emergency PCI is recommended in stent thrombosis (I C), and repeat PCI (if feasible) is recommended for stent restenosis (I C) [1].

Revascularization in patients with NSTE-ACS in clinical practice

CABG is performed during the index hospitalization in approximately 10% [5] (7% - 13% [4]) of all patients with NSTE-ACS [4,5]. Almost all single-vessel disease patients are treated with ad hoc PCI, while more than 20% of multivessel disease patients are treated with CABG [4]. Data from the ACUITY trial [13], in which the decision between PCI and CABG was left to the discretion of the investigators, showed that among moderate and high-risk ACS patients with multivessel disease (n= 5,627) approximately 78% were treated with PCI and the remainder 22% with CABG. Propensity-matched comparison, showed comparable 1-month and 1-year mortality in patients treated with CABG or PCI (1-month mortality CABG 2.5% vs. PCI 2.1%, p = 0.69; 1-year mortality CABG 4.4% vs. PCI 5.7%, p = 0.58). The rates of peri-procedural stroke, MI, major bleeding, and renal injury were higher in the CABG group. The rate of recurrent ischemia requiring unplanned repeat revascularization was higher in the PCI group [13].

Optimal timing for non-emergent CABG in NSTE-ACS

The optimal timing for non-emergent CABG in NSTE-ACS patients should be determined individually [5]. Bleeding and ischaemic risks should be estimated by the Heart Team (I C) [5]. Clopidogrel and ticagrelor should be discontinued at least 24 hours pre-operatively in patients referred for urgent CABG, to reduce the risk of major bleeding (I B) [4]. When indicated, CABG should be offered without delay to patients with haemodynamic instability, ongoing myocardial ischaemia, or very-high-risk coronary anatomy, regardless of the antiplatelet treatment (I C) [5].

ST-segment elevation acute myocardial infarction (STEMI)

The importance of early reperfusion in STEMI cannot be overemphasized. The earliest the reperfusion of the infarct-related artery (IRA) the greatest the benefit of treatment. Primary PCI of the IRA is strongly indicated (I A). The maximum delay from STEMI diagnosis to PCI (wire crossing) should be ≤ 120 min to choose primary PCI over fibrinolysis. IRA stenting with drug eluting stents (DES) preferably through radial access is recommended (I A). In STEMI patients with multivessel disease routine revascularization of non-IRA should be considered before hospital discharge (IIa A), while in the presence of cardiogenic shock, non-IRA PCI should be considered during the index procedure (IIa C) [6]. Primary PCI is offered in the vast majority of STEMI patients who are mechanically revascularized.

CABG has a limited role in the acute phase of STEMI, being reserved for highly selected patients [1, 6, 7] . According to the 2013 ACCF/AHA STEMI guideline [7], urgent CABG is indicated in STEMI patients with coronary anatomy not amenable to PCI and ongoing or recurrent ischemia, severe HF, CS, or other high-risk features, and at the time of surgical repair of mechanical defects (I B) [7].

According to the 2017 ESC STEMI guidelines “CABG should be considered in patients with ongoing ischaemia and large areas of jeopardized myocardium if PCI of the IRA cannot be performed” (IIa C) [6]. Emergent CABG should be considered for STEMI patients with a patent IRA (providing time for surgical revascularization [1]), anatomy unsuitable for PCI, and either a large area of myocardium at risk of necrosis or cardiogenic shock [6]. CABG is also recommended at the time of repair of mechanical complications of MI (if revascularization is required) [1,6]. CABG is infrequently applied in STEMI patients after failed PCI or in coronary occlusion not amenable to PCI; the delay to surgical reperfusion is long, the expected benefit is uncertain, and the surgical risks are increased [1, 6].

Timing of CABG in STEMI

In the absence of robust evidence, the timing of CABG in the setting of STEMI is not well defined. There have been concerns about hemorrhagic transformation and infarct expansion related to the systemic inflammatory response, triggered by the cardiopulmonary bypass and the effects of cardioplegic arrest when CABG is performed early after STEMI [7]. The optimal timing for nonemergent CABG in patients stabilized after STEMI should be determined individually. Patients with haemodynamic compromise or at high risk of recurrent ischaemic events (mainly patients with critical stenoses affecting a large myocardial area) should be operated as soon as possible, without delay for complete recovery of platelet function. When possible, in the absence of angina or haemodynamic deterioration, waiting for 3–7 days after the acute episode appears the best compromise [1]. In haemodynamically stabilized patients without ongoing or recurrent ischaemia, the suggested waiting times after discontinuation of antiplatelet treatment are at least 3 days for ticagrelor, 5 days for clopidogrel, and 7 days for prasugrel. Aspirin should be discontinued and restarted within 6 to 24 hours postoperatively if there is no bleeding [6].

Technical aspects of CABG in ACS

The use of left IMA for bypassing the LAD is highly desirable, while bilateral IMAs may be beneficial, regarding the long-term results [1, 2] (see Acute heart failure: heart failure surgery and transplantationFigure 54.1). Avoidance of aortic manipulation is desirable. Off-pump or on-pump beating heart techniques, with or without MCS, performed by highly experienced teams may lead to improved results of CABG [1] performed in the acute phase of ACS [7].

Figure 54.1 Revascularization with bilateral internal thoracic arteries (ITAs) (yellow arrow, left internal thoracic artery (LITA) anastomosed to the LAD artery; blue arrow, right internal thoracic artery (RITA) anastomosed to the obtuse marginal branch of the circumflex artery) can offer exemplary long-term results, with very low reintervention rates.

Figure 54.1
Revascularization with bilateral internal thoracic arteries (ITAs) (yellow arrow, left internal thoracic artery (LITA) anastomosed to the LAD artery; blue arrow, right internal thoracic artery (RITA) anastomosed to the obtuse marginal branch of the circumflex artery) can offer exemplary long-term results, with very low reintervention rates.

With kind permission from Elsevier: Pitsis AA, Kelpis TG, Visouli AN, et al. Left ventricular assist device as a bridge to surgery in postinfarction ventricular septal defect. J Thorac Cardiovasc Surg 2008; 135 :951–52.

Evidence on revascularization in cardiogenic shock

The multicentre randomized SHOCK trial (n = 302, 1993–1998) showed that, in patients with CS after an AMI, emergent mechanical revascularization resulted in a significant survival benefit at 6 months (50% vs 37%, P = 0.027) and at 1 year (47% vs 34%, P = 0.025), in comparison to initial medical stabilization [14].

The choice of the revascularization strategy was based on anatomical and clinical criteria being individualized for each patient. Comparisons between PCI and CABG are observational [1417]. Revascularization was more complete after CABG. Although there was a greater prevalence of multivessel disease and diabetes in the CABG group, the survival was similar between the groups [15]. Among PCI-treated patients, multivessel PCI was significantly and independently correlated with mortality (P = 0.040) [16]. Multivessel disease was associated with more severe mitral regurgitation (MR) (P = 0.005) [18]. PCI-treated patients with severe MR experienced high mortality (67%) [16]. Results from the SHOCK registry showed that, among patients with multivessel disease, PCI-treated patients had significantly higher in-hospital mortality than CABG-treated patients [19]. Among patients of the SHOCK trial and registry with CS and left main (LM) disease (CABG, n = 79; PCI, n = 85), the prevalence of three-vessel disease was higher in the CABG group. PCI was offered earlier (mean time: PCI 7.4 hours, CABG 24.3 hours). The 30-day survival was significantly higher in the CABG group (54% vs 14%, P ≤0.001). When LM was the infarct-related artery, the 30-day survival was 40% after CABG and 16% after PCI (P = 0.03). CABG was independently associated with 30-day survival [17].

The IABP-SHOCK II randomized 600 patients with CS complicating AMI (STEMI 68.6%, NSTEMI 29.5%) and planned early revascularization, to intra-aortic balloon pumping (IABP) or no IABP. The revascularization modality (infarct-related PCI, immediate or staged multivessel PCI, or CABG) was left to the discretion of the operator. CABG was applied in 4.2% of patients. IABP did not significantly reduce the 30-day mortality (IABP 39.7% vs control 41.3%), the 6-month or 12-month mortality (IABP 52% vs control 51%). The adverse event rates were similar [20, 21].

In a large-scale observational study (STS National Cardiac Database, 2002–2005, n = 708 593) [22], the incidence of preoperative CS among CABG-treated patients was 2.1%; the overall mortality was 22% (isolated CABG: 20%; CABG plus valve surgery: 33%; CABG plus ventricular septal repair: 58%). Very few patients with CS and multivessel disease were referred for surgery (3.2–8.8%), perhaps the younger and less sick patients. The favourable results cannot be directly compared with those of PCI, due to potential selection bias favouring CABG [22].

In a large-scale observational study (National Registry of Myocardial Infarction, 775 US hospitals, 1995–2004, n=293,633) [23], the total rate of CS in STEMI patients was 8.6%. During a 10-year period, the mortality of CS decreased from 60.3% to 47.9%, in parallel with a significant increase in the primary PCI rate (from 27.4% to 54.4%), while the immediate CABG rate was not significantly changed (from 2.1% to 3.2%). [23].

Role of coronary artery bypass grafting in cardiogenic shock

CS may complicate any ACS, but it is more frequently encountered in STEMI. [6]. The more common form is pump failure, accounting for 80% of cases [5, 6, 7].

Revascularization, with PCI in amenable anatomy or CABG in anatomy not amenable to PCI (I B) [1, 5, 6], is the cornerstone of treatment of CS secondary to ACS [1]. Multidisciplinary decision making is not mandatory in the acute phase. Non-culprit lesions are treated according to the institutional protocol or the Heart Team decision. [1]

CS may develop in up to 3% of patients with NSTE-ACS and is the most common cause of death during hospitalization in this setting [5]. CS may occur in up to 4.6% of NSTEMI patients who, compared with STEMI patients, may develop CS later, have more recurrent ischaemia and re-infarction before CS, and more extensive CAD [4]. More than two thirds of patients have 3-vessel disease [5]. Immediate coronary angiography (I B), followed by immediate PCI in suitable coronary anatomy (I B), or emergency CABG in non-amenable to PCI anatomy (I B) are recommended in CS complicating NSTE-ACS [5]. PCI is most frequently applied [5]. The 30-day mortality has progressively improved, ranging currently from approximately 40% in milder forms of CS to more than 45% in severe CS [4].

CS develops is 6–10% of STEMI patients and is the leading cause of death in this setting, having a hospital mortality approaching 50% [6]. According to the 2017 ESC STEMI guidelines immediate PCI is recommended for patients with CS if the coronary anatomy is suitable. Emergency CABG is recommended if the coronary anatomy is not suitable for PCI or after failed PCI (I B). “Complete revascularization during the index procedure should be considered” (IIa C). Mechanical complications should be treated as soon as possible after discussion by the Heart Team (I C), while insertion of an Intra-Aortic Balloon Pump (IABP) should be considered (IIa C).

Routine use of an IABP is not indicated (III B). The conventional indications for IABP in cardiac surgery include its application in the perioperative period of CABG and/or repair of mechanical complications of MI (i.e. severe mitral insufficiency or ventricular septal defect [6]) in the presence of HF/CS [1, 5, 7, 8]. IABP is usually applied in these conditions if there are no contraindications, such as aortic regurgitation, aortic dissection, stents or major surgery of the aorta, abdominal aortic aneurysm, and severe peripheral vascular disease.

Short-term MCS may be considered in CS complicating NSTE-ACS (IIb C) [5] and in refractory CS complicating STEMI (IIb C) [6, 7], (according to the Heart Team protocol [1], dependent on age, comorbidities, and neurological function [8]). Short-term MCS is applied as rescue therapy (stabilization and preservation of end-organ function) and as a bridge to recovery. If myocardial recovery is not achieved, short term MCS may be used as a bridge to transplantation or to long-term MCS. Decision making is based on multidisciplinary and individualized approach [6].

Surgery in mechanical complications of acute myocardial infarction

Mechanical complications of acute MI including papillary muscle rupture with severe MR, ventricular septal rupture, or free wall rupture may occur, [although their incidence has significantly decreased in the era of primary PCI [6]. Immediate echocardiography is indicated (I C) [6], immediate Heart Team discussion is required (I C) [1, 5], emergency surgery is indicated in case of haemodynamic instability (I C) [1], prompt surgical repair with or without CABG is indicated in most cases [7]. IABP should be considered in haemodynamic instability/CS due to mechanical complications of MI (IIa C) [1, 5, 6] to provide temporary circulatory support [7, 8].

Free wall rupture after myocardial infarction

Free wall rupture (FWR) may occur within the first week following transmural MI in <1% of patients [6]. Old age, lack of reperfusion or late fibrinolysis have been associated with FWR [6,24]. Acute FWR causes cardiovascular collapse, with electromechanical dissociation, being usually fatal within a few minutes. It does not respond to standard cardio-pulmonary resuscitation and very rarely is there time to bring the patient to surgery [6,7]. Subacute FWR (“serpiginous” rupture through the different layers of the ventricular wall, sealed by thrombus, pericardium or adhesions [6], also described as pseudoaneurysm formation with contained rupture [7]) can mimic reinfarction but more frequently presents with sudden haemodynamic deterioration and signs of cardiac tamponade [6, 7]. A sealed subacute rupture, if recognized, may provide time for pericardiocentesis for haemodynamic stabilization and immediate surgery [6].

Of the 1048 patients studied from the SHOCK registry, 28 (2.7%) had a FWR or tamponade. Most patients underwent surgery and/or pericardiocentesis (27/28), with in-hospital survival similar to that of the overall group (39.3%) [25].

Ventricular repair with pericardial patch or other materials is recommended, having mortality rates fluctuating between 20 and 75%, depending on patient’s condition, extend and morphology of the rupture [6]. Direct closure infarctectomy and prosthetic patch closure, and infarct exclusion patch closure are performed on pump in the ‘blowout’ type of FWR. In patients with less catastrophic anatomy, a simpler sutureless technique to avoid suturing of friable necrotic tissue, performed off pump (with or without IABP or MCS), yielded good results (n = 32, early survival 84.4%, 5-year survival 75%). There is risk for re-rupture in the acute phase. Later pseudoaneurysm formation can be treated by surgical resection [26].

Ventricular septal rupture after myocardial infarction

Lack of consensus about the optimal timing of VSR repair after STEMI (2017 ESC STEMI guidelines, 2013 ACC/AHA STEMI guidelines)

Surgical repair is indicated in ventricular septal rupture (VSR) post MI, but there is no consensus regarding the optimal timing of VSR repair. Early surgery is associated with high mortality and high risk or recurrent rupture, due to suturing on friable, ischaemic and oedematous tissue surrounding the necrotic tissue [6]. On the other hand, delayed surgery allows safer repair on stronger scar tissue, but carries the risk of abrupt rupture expansion while waiting for surgery, resulting in sudden hemodynamic collapse and even death of previously stable patients [6, 7]. According to the 2017 ESC STEMI guidelines (web agenda), early surgery is recommended for patients with VSR and HF refractory to aggressive therapy, while delayed repair may be considered in patients responding well to aggressive HF treatment. In the 2013 ACC/AHASTEMI guidelines, emergency surgery has been recommended even for stabilized patients [7]. CABG should be performed during surgical repair, as required. IABP may be needed during preparation of surgery [7]. Short-term left ventricular assist devices (LVADs), preferably with left atrial cannulation, may be used to bridge patients to surgery, supporting end-organ function and providing time for maturation of oedematous and haemorrhagic tissue [27] (see Figure 54.2). Percutaneous VSR repair (reducing rather than eliminating the left-to-right shunt) may be considered after Heart Team discussion (IIb C) as an alternative to surgery, in selected patients and centers with appropriate experience [1]. Percutaneous closure “with appropriately designed devices may soon become an alternative to surgery” [6].

Figure 54.2 LVAD as a bridge to surgery in post-infarction VSD. Echocardiograms: (A) Preoperative four-chamber mid-oesophageal TOE, demonstrating significant left-to-right shunt. (B) Preoperative mid-oesophageal TOE, showing the tip of the inflow cannula (arrow) of the LVAD into the LA. (C) One-year follow-up echocardiogram: long-axis 3D echocardiogram, demonstrating the LV reconstruction using the bovine pericardial patch (arrow). Intraoperative photos: (D) Extensive haematoma of the LV and RV during the first operation. (E) Bovine pericardial patch of the post-infarction VSD repair in the second operation, with arrow showing a dissector with the tip inserted through the post-infarction ventricular septal defect (VSD). IC, inflow cannula; IVS, interventricular septum; LA, left atrium; LV, left ventricle; OC, outflow cannula; PVSD, post-infarction ventricular septal defect; RA, right atrium; RV, right ventricle; VC, venous cannula.

Figure 54.2
LVAD as a bridge to surgery in post-infarction VSD. Echocardiograms: (A) Preoperative four-chamber mid-oesophageal TOE, demonstrating significant left-to-right shunt. (B) Preoperative mid-oesophageal TOE, showing the tip of the inflow cannula (arrow) of the LVAD into the LA. (C) One-year follow-up echocardiogram: long-axis 3D echocardiogram, demonstrating the LV reconstruction using the bovine pericardial patch (arrow). Intraoperative photos: (D) Extensive haematoma of the LV and RV during the first operation. (E) Bovine pericardial patch of the post-infarction VSD repair in the second operation, with arrow showing a dissector with the tip inserted through the post-infarction ventricular septal defect (VSD). IC, inflow cannula; IVS, interventricular septum; LA, left atrium; LV, left ventricle; OC, outflow cannula; PVSD, post-infarction ventricular septal defect; RA, right atrium; RV, right ventricle; VC, venous cannula.

With kind permission from Elsevier: Pitsis AA, Kelpis TG, Visouli AN, et al. Left ventricular assist device as a bridge to surgery in postinfarction ventricular septal defect. J Thorac Cardiovasc Surg 2008; 135 :951–52

Among the 939 patients of the SHOCK registry, the incidence of VSR was 5.85%. VSR occurred at a median of 16 hours after MI. Although VSR patients had less severe CAD, they had higher in-hospital mortality (87% vs 61%, P < 0.001). The survival was 19% in surgically treated patients and 4.2% in medically treated patients [28]. Currently, the reported mortality rates with early surgery fluctuate between 20% and 40% [6].

Infarctectomy techniques (including the excision of the infarct area and direct or patch closure) have been used, but an exclusion, rather than an excision, technique preserves better the ventricular volume and geometry (see Figure 54.2). Described by David, it involves endocardial patch repair resembling the Dor technique of ventricular endoaneurysmorrhaphy. David et al. applied this reparative technique during the acute phase of MI, with excellent results (operative mortality of 14%, 6-year actuarial survival of 66 ± 7%) [29]. Results in other centres have been mixed.

Mitral regurgitation after myocardial infarction

MR is common after STEMI and usually occurs 2–7 days after MI. There are three mechanisms of acute MR in this setting: (1) annular dilatation , (2) papillary muscle displacement and (3) (trunk or tip) papillary muscle rupture. The first two mechanisms are parts of the post-infarction ventricular remodelling [7]. In most patients, acute MR is due to papillary muscle displacement, rather than rupture.

In papillary muscle rupture, emergency surgery is the treatment of choice [6]. Mitral valve (MV) replacement is often required, while MV repair has been increasingly reported and may be a better option in selected patients and “experienced hands” [6]. CABG should be performed, as needed [6, 7]. During the preparation for surgery, stabilization with medical treatment and IABP is applied [6, 7]. Improved results, with a hospital mortality decreased to 20%, may be achieved by early surgery that prevents further myocardial injury, organ failure, and death [7].

In our experience, there is a good chance of successful MV repair when the papillary muscle rupture occurs towards the muscle tip, because the presence of fibrous tissue in this area allows more secure suturing. When there is a partial tip rupture (one of the usually two papillary muscle heads is ruptured), a competent valve can easily be achieved by suturing of the ruptured head to the intact one (see Figure 54.3). An undersized annuloplasty with a rigid complete ring reducing the anteroposterior diameter is indicated to relieve the strain of the repaired papillary muscle. Conversely, repair of a basal papillary muscle rupture is not secure, being associated with a high risk of dehiscence; thus, mitral valve replacement is probably indicated (see Figure 54.3) [30, 31].

Figure 54.3 Partial (black arrow) and complete (yellow arrows) papillary muscle rupture.

Figure 54.3
Partial (black arrow) and complete (yellow arrows) papillary muscle rupture.

With kind permission from Springer Science + Business Media: Pitsis AA, Anagnostopoulos CE. Acute heart failure: is there a role for surgery? Heart Fail Rev 2007; 12 :173–8 (top row) and Karger Publishers: Pitsis AA, Boudoulas H. Mitral regurgitation in acute heart failure: the role of echocardiography. Cardiology 2009; 113 (4):246–8 S (bottom row).

The severity of functional MR after MI may decrease with PCI and/or aggressive medical treatment. If surgery is required due to persistent ischaemia or refractory HF, MV repair by downsized annuloplasty ring is usually performed or less frequently MV replacement [7].

CABG should be performed at the time of surgical repair of mechanical complications of MI, as needed [6, 7]. Angiography is indicated in surgical candidates with VSR and/or MR. In FWR, CABG should also be done if the coronary anatomy is known, but usually there is no time to perform coronary angiography, because of the unstable patient condition.

Role of surgery in acute heart failure due to valvular disease

Valvular heart disease (VHD) may cause or aggravate HF [8]. In the EHFS II survey, VHD was an underlying disease in 34.4% of all patients hospitalized with AHF, and a precipitating factor in 26.8% [32].

AHF in patients with VHD may be of new onset (de novo) in acute native or prosthetic valve disease, or may occur as acute decompensation of CHF in patients with chronic VHD. Patients with HF and concomitant VHD represent a high-risk population [8], in which therapeutic interventions are underused. Several surgical risk scores (EuroSCORE I, EuroSCORE II, STS score, etc.) may help in risk stratification and decision-making in patients considered for surgery [11]. While these scores may overestimate the surgical risk (in particular the EuroSCORE I markedly overestimates the 30-day mortality), they do not include factors such as the presence of patent CABG grafts, porcelain aorta, frailty, cognitive and functional capacity that play a significant role, particularly in the elderly. Critical preoperative status, urgent/emergent and salvage operation, LV dysfunction, higher functional class, and active endocarditis are associated with increased operative mortality. Other risk factors include older age, female gender, concomitant CAD, pulmonary hypertension, comorbidities, and previous cardiac operation(s) [8, 11, 33] .

Transthoracic echocardiography (TTE) is recommended to establish the diagnosis of VHD and identify patients suitable for surgical correction (I B) [33]. Transoesophageal echocardiography (TOE) should be considered in suboptimal TTE quality or suspicion of thrombosis, prosthetic valve dysfunction or endocarditis. Intraprocedural TOE is used to guide and evaluate the results of (surgical or transcatheter) valve interventions.

Coronary angiography is indicated in candidates of valve surgery with severe VHD and any of the following LV systolic dysfunction, suspected myocardial ischaemia, history of cardiovascular disease, presence of ≥ 1 cardiovascular risk factors, and in men>40 years, and postmenopausal women (I C). Coronary angiography is also recommended for evaluation of moderate to severe secondary MR (I C) [11 “CT angiography should be considered as an alternative to coronary angiography before valve surgery in patients with severe VHD and low probability of CAD or in whom conventional coronary angiography is technically not feasible or associated with a high risk” (IIa C) [6]. CABG should be performed, as needed [6, 7]. During the preparation for surgery, stabilization with medical treatment and IABP is applied [6, 7]. Improved results, with a hospital mortality decreased to 20%, may be achieved by early surgery that prevents further myocardial injury, organ failure, and death [7].

In our experience, there is a good chance of successful MV repair when the papillary muscle rupture occurs towards the muscle tip, because the presence of fibrous tissue in this area allows more secure suturing. When there is a partial tip rupture (one of the usually two papillary muscle heads is ruptured), a competent valve can easily be achieved by suturing of the ruptured head to the intact one (see Figure 54.3). An undersized annuloplasty with a rigid complete ring reducing the anteroposterior diameter is indicated to relieve the strain of the repaired papillary muscle. Conversely, repair of a basal papillary muscle rupture is not secure, being associated with a high risk of dehiscence; thus, mitral valve replacement is probably indicated (see Figure 54.3) [30, 31].

Figure 54.3 Partial (black arrow) and complete (yellow arrows) papillary muscle rupture.

Figure 54.3
Partial (black arrow) and complete (yellow arrows) papillary muscle rupture.

With kind permission from Springer Science + Business Media: Pitsis AA, Anagnostopoulos CE. Acute heart failure: is there a role for surgery? Heart Fail Rev 2007; 12 :173–8 (top row) and Karger Publishers: Pitsis AA, Boudoulas H. Mitral regurgitation in acute heart failure: the role of echocardiography. Cardiology 2009; 113 (4):246–8 S (bottom row).

The severity of functional MR after MI may decrease with PCI and/or aggressive medical treatment. If surgery is required due to persistent ischaemia or refractory HF, MV repair by downsized annuloplasty ring is usually performed or less frequently MV replacement [7].

CABG should be performed at the time of surgical repair of mechanical complications of MI, as needed [6, 7]. Angiography is indicated in surgical candidates with VSR and/or MR. In FWR, CABG should also be done if the coronary anatomy is known, but usually there is no time to perform coronary angiography, because of the unstable patient condition.

Role of surgery in acute heart failure due to valvular disease

Valvular heart disease (VHD) may cause or aggravate HF [8]. In the EHFS II survey, VHD was an underlying disease in 34.4% of all patients hospitalized with AHF, and a precipitating factor in 26.8% [32].

AHF in patients with VHD may be of new onset (de novo) in acute native or prosthetic valve disease, or may occur as acute decompensation of CHF in patients with chronic VHD. Patients with HF and concomitant VHD represent a high-risk population [8], in which therapeutic interventions are underused. Several surgical risk scores (EuroSCORE I, EuroSCORE II, STS score, etc.) may help in risk stratification and decision-making in patients considered for surgery [11]. While these scores may overestimate the surgical risk (in particular the EuroSCORE I markedly overestimates the 30-day mortality), they do not include factors such as the presence of patent CABG grafts, porcelain aorta, frailty, cognitive and functional capacity that play a significant role, particularly in the elderly. Critical preoperative status, urgent/emergent and salvage operation, LV dysfunction, higher functional class, and active endocarditis are associated with increased operative mortality. Other risk factors include older age, female gender, concomitant CAD, pulmonary hypertension, comorbidities, and previous cardiac operation(s) [8, 11, 33] .

Transthoracic echocardiography (TTE) is recommended to establish the diagnosis of VHD and identify patients suitable for surgical correction (I B) [33]. Transoesophageal echocardiography (TOE) should be considered in suboptimal TTE quality or suspicion of thrombosis, prosthetic valve dysfunction or endocarditis. Intraprocedural TOE is used to guide and evaluate the results of (surgical or transcatheter) valve interventions.

Coronary angiography is indicated in candidates of valve surgery with severe VHD and any of the following LV systolic dysfunction, suspected myocardial ischaemia, history of cardiovascular disease, presence of ≥ 1 cardiovascular risk factors, and in men>40 years, and postmenopausal women (I C). Coronary angiography is also recommended for evaluation of moderate to severe secondary MR (I C) [11 “CT angiography should be considered as an alternative to coronary angiography before valve surgery in patients with severe VHD and low probability of CAD or in whom conventional coronary angiography is technically not feasible or associated with a high risk” (IIa C) [11], such as acute aortic dissection, large aortic vegetation in the proximity of the coronary ostia, occlusive prosthetic valve thrombosis with unstable haemodynamic condition, etc.

Indications for CABG in patients with a primary indication for valve surgery

Among patients with a primary indication for aortic/mitral valve surgery, CABG is indicated for patients with a coronary artery diameter stenosis ≥ 70% (I C), while CABG should be considered for patients with a coronary artery diameter stenosis 5070% (Iia C) [11].

Acute heart failure in chronic VHD

Chronic valvular stenosis or regurgitation (particularly aortic stenosis and mitral insufficiency) can be the primary cause or an aggravating factor of AHF [8]. In acutely decompensated patients with an indication for surgery, emergent operation should be avoided, if possible; optimal medical management of heart disease and comorbidities should be offered preoperatively (but without adding unnecessary delay).

In the absence of specific guidelines for the treatment of patients with HF and coexisting VHD (as the main cause or a precipitating/aggravating factor of HF), individualized evaluation and multidisciplinary clinical judgement should be guided by the HF guidelines [8] and the VHD guidelines [11, 34].

Severe chronic aortic stenosis

Chronic aortic stenosis (AS) is currently the most common VHD leading to surgery or catheter intervention in Europe and North America. AS is usually calcific, encountered mainly in the elderly, congenital in younger patients, and rarely rheumatic. Aortic stenosis due to calcific degeneration has an increasing prevalence due to aging of population, while progressive stenosis may occur earlier in congenitally bicuspid aortic valves. Severe, symptomatic AS has a very poor spontaneous prognosis, thus early intervention (surgical or transcatheter) is strongly recommended [11].

Indications for surgical or transcatheter intervention in chronic aortic stenosis (2017 ESC/EACTS VHD guidelines)

According to the 2017 ESC/EACTS guidelines “Intervention is indicated in symptomatic patients with severe, high-gradient aortic stenosis (mean gradient >_40mmHg or peak velocity >_4.0 m/s)” (I B) [11]. High-gradient AS (mean gradient > 40mmHg, valve area < 1 cm2) can be assumed severe irrespective of LVEF and flow, which can be normal or reduced. In symptomatic patients with severe AS and mean pressure gradient >40 mmHg, there is “virtually” no lower LVEF limit for intervention, whether surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI) [11].

A challenging issue in patients with AS and reduced LVEF is the “low flow- low gradient” entity (LVEF < 50%, valve area <1 cm2, mean pressure gradient <40 mmHg), i.e. AS with reduced mean gradient due to decreased transaortic flow, resulting from low stroke volume [8, 11]. Low-dose dobutamine stress echocardiography is recommended in patients with “low flow–low gradient” AS and reduced ejection fraction to distinguish between truly severe AS and pseudosevere AS, the later defined by an increase of the valve area to > 1.0 cm2 with flow normalization. Dobutamine echocardiography also helps to evaluate the contractile or flow reserve (increase of stroke volume > 20%), the presence of which has a positive prognostic value [8, 11]. Among patients with low-flow, low gradient (< 40 mmHg) AS and reduced LVEF, intervention is indicated in patients with evidence of flow (contractile) reserve, excluding pseudosevere AS (I C), while intervention should be considered in patients without flow reserve, particularly if CT calcium scoring confirms severe AS (IIa C). Although the interventional mortality (with both SAVR and TAVI) is higher in patients without flow reserve, intervention improves the clinical status and the LVEF [11].

“Intervention should not be performed in patients with severe comorbidities when the intervention is unlikely to improve quality of life or survival” (III C) [11].

The choice of intervention mode (SAVR or TAVI) should be based on individual evaluation of technical suitability, estimated risks and benefits with each modality, the local expertise and outcomes. (I C) [11] considering the patients’ values, and preferences (I A) [34].

Surgery for severe AS

Among patients fulfilling the criteria for intervention, “SAVR is recommended in patients at low surgical risk,” i.e. predicted surgical mortality by the STS or EuroSCORE II < 4% or the logistic EuroSCORE I < 10% (the EuroSCORE I overestimates 30-day mortality), and absence of other risk factors not included in these risk scores, such as frailty, porcelain aorta, or chest radiation (I B). Other factors that favour SAVR include younger age (< 75 years), suspicion of endocarditis, unfavourable access for TAVI, short distance between coronary ostia and aortic valve annulus, size of aortic valve annulus out of range for TAVI, aortic root morphology and/or valve morphology unfavourable for TAVI (bicuspid aortic valve, severe calcification with rapid progression), thrombi in the aorta or the LV, additional cardiac conditions requiring consideration of surgical treatment, such as severe coronary artery disease requiring CABG, severe primary mitral valve and/or tricuspid valve disease, ascending aortic aneurysm, and septal hypertrophy requiring myectomy.

Surgical aortic valve replacement (AVR) is also indicated in patients with severe AS undergoing CABG, or surgery of the ascending aorta or another valve (I C) [11].

TAVI for severe AS

Among patients fulfilling the criteria for intervention, TAVI is indicated for patients who are not suitable for SAVR, as judged by the Heart Team (I B). In patients with high surgical risk (STS or EuroSCORE II ≥ 4% or other high-risk factors: frailty, porcelain aorta, radiation), “the decision between SAVR and TAVI should be made by the Heart Team according to the individual patient characteristics, with TAVI being favoured in elderly patients (≥ 75 years) suitable for transfemoral access” (I B). Other factors that favour TAVI are: severe comorbidity leading to prohibitive surgical risk, restricted mobility or other conditions that may hamper rehabilitation after surgery, previous cardiac surgery, patent coronary artery bypass grafts at risk during sternotomy, expected patient – prosthesis mismatch, and severe chest deformation or scoliosis (see Figure 54.4).

Figure 54.4 Transapical aortic valve-in-valve implantation (SAPIEN THV (Edwards Lifesciences, Irvine, CA) in a Toronto stentless valve (St Jude Medical, Inc, St Paul, MN))—TOE. (A) Preoperative. (B) Post-operative and fluoroscopy of: (a) valve positioning; (b) valve deployment; (c) final result.

Figure 54.4
Transapical aortic valve-in-valve implantation (SAPIEN THV (Edwards Lifesciences, Irvine, CA) in a Toronto stentless valve (St Jude Medical, Inc, St Paul, MN))—TOE. (A) Preoperative. (B) Post-operative and fluoroscopy of: (a) valve positioning; (b) valve deployment; (c) final result.

With kind permission from Elsevier: Kelpis TG, Mezilis NE, Ninios VN, et al. Minimally invasive transapical aortic valve-in-a-valve implantation for severe aortic regurgitation in a degenerated stentless bioprosthesis. J Thorac Cardiovasc Surg 2009; 138:1018–20.

Percutaneous aortic balloon dilation (valvotomy) may be considered as a bridge to SAVR or TAVI in symptomatic patients with severe AS (IIb C) [33, 34] who require urgent non-cardiac surgery or in patients with severe AS who are haemodynamically unstable (IIb C) [11].

Severe chronic mitral regurgitation

Chronic mitral regurgitation (MR) is the second most frequent VHD encountered in Europe. Chronic MR can be classified in primary (structural) and secondary (functional) MR [11]. Surgery in primary MR is curative and clearly indicated. On the contrary, surgery in secondary MR is not curative and has an uncertain role if there are no options for revascularization.

Severe chronic primary MR

Primary MR [11, 33] (or organic [11] or degenerative [33] MR) is characterized by intrinsic structural abnormalities of one or more components of the valve apparatus that are directly affected, usually due to myxomatous degeneration in younger population, or fibroelastic deficiency in older population, and less frequently due to rheumatic disease, endocarditis, connective tissue disorders, congenital cleft mitral valve, radiation, etc. [33]. Myxomatous degeneration (Barlow’s valve) is characterized by gross redundancy and thickening of both leaflets (“floppy” leaflets), annular dilation, and chordal elongation [33]. Fibroelastic deficiency is characterized by lack of connective tissue that leads to leaflet and chordal thinning and eventually chordal rupture [33]. These structural differences have surgical implications [33], particularly when MV repair is considered.

Chronic primary MR causes LV volume overload, which, if prolonged and severe, results in progressive myocardial damage, HF, and death. Correction of primary MR is curative [33].

Quantitative echocardiographic criteria for the definition of severe primary MR include effective regurgitant orifice area (EROA) ≥ 40 mm2, regurgitant volume ≥ 60 ml/beat, and LV/LA enlargement [11]. Other parameters that should be evaluated include LV function, geometry, size, and ejection fraction, left atrial volume, systolic pulmonary artery pressure, RV size and function, tricuspid regurgitation and tricuspid annular dimensions [11].

The occurrence of HF symptoms in patients with severe primary MR is a strong indication for surgery.

MV repair and MV replacement in chronic primary MR

Despite the absence of randomized comparisons, it is generally accepted that MV repair, when feasible, is preferred to MV replacement [11]. Preoperative and intraoperative transoesophageal echocardiography (TOE), including three-dimensional echocardiography, is essential in precise evaluation of valve anatomy and function, feasibility and monitoring of repair [8, 11, 33]. Decision about the reparability of the regurgitant MV and the choice of the repair strategy is based on echocardiographic evaluation, according to Carpentier functional classification (based on leaflet opening and closing motions) and segmental valve analysis (localization of dysfunction), as well as assessment of the annular dimensions, and the presence of calcification. Successful and durable repair is feasible in degenerative MR due to segmental valve prolapse. The reparability of MR due to rheumatic lesions, extensive valve prolapse, leaflet and/or extensive annular calcification is more challenging. Demanding operations of MV repair should be performed in high-volume experienced centers with records of low operative mortality and high durability of MV repair [11].

According to the 2017 ESC/EACTS VHD guidelines [11], in patients with severe primary MR, MV repair should be preferred when durable results are expected (I C). According to the 2017 AHA/ACC VHD guideline [34], in patients with chronic severe primary MR and indication for surgery, MV repair is recommended in preference of replacement in MR limited to the posterior leaflet (I B), and in MR of the anterior or both leaflets when successful and durable repair can be accomplished (I B). MV replacement should not be performed in isolated severe primary MR limited to less than one half of the posterior leaflet unless attempted MV repair was unsuccessful (III (harm) B) [34]. When MV repair is not feasible, MV replacement with preservation of the subvalvular apparatus is favoured [11].

Indications for MV surgery in chronic severe primary MR by degree of LV dysfunction

There is consensus that MV surgery is recommended in symptomatic patients with chronic severe primary MR and LVEF >30% (I B) [11, 33, 34].

According to the 2017 AHA/ACC VHD guideline [34] MV surgery “may be considered in symptomatic patients with chronic severe primary MR” and LVEF ≤30%” (IIb C) (usefulness/effectiveness unknown/unclear/less well established). According to the 2017 ESC/EACTS VHD guidelines [11], MV repair “should be considered in patients with severe primary MR, severe LV dysfunction (LVEF <30% and/or LVESD >55 mm) refractory to medical therapy,” low comorbidity, and high likelihood of successful repair” (IIa C), while MV replacement “may be considered in patients with severe primary MR, severe LV dysfunction (LVEF <30% and/or LVESD >55 mm) refractory to medical therapy” with low likelihood of successful repair and low comorbidity (IIb C) (usefulness/efficacy less well established) [11].

Severe chronic secondary MR

In chronic secondary (functional) MR the valve leaflets and chordae are structurally normal, but MR is caused by geometrical distortion of the valve apparatus and “imbalance between closing and tethering forces on the valve secondary to alterations in LV geometry” caused by ischaemic or non-ischaemic dilated cardiomyopathy [11]. Papillary muscle displacement and annular dilatation result in leaflet tethering, while reduced contractility and/or dysynchrony result in reduced closing forces; both mechanisms leading to insufficient leaflet coaptation and MR [33]. Valve insufficiency is just one component of the HF aetiology; LV dysfunction and adverse remodelling, due to CAD or idiopathic dilated cardiomyopathy, pre-exist and may progressively deteriorate. Thus, in contrast to the curative role of surgery in primary MR, repair of secondary MR is not curative of HF [33]. The surgical treatment of chronic secondary MR is challenging, having higher mortality than that of the primary MR [8].

Echocardiography is essential to establish the diagnosis. Quantitative echocardiographic criteria for definition of severe secondary MR include effective regurgitant orifice area (EROA) ≥ 20 mm2 and regurgitant volume ≥ 30 ml/beat (the thresholds to define severe secondary MR are controversial, lower thresholds than those defining severe primary MR have been proposed to define severe secondary MR (ACC/AHA 2014, ESC/EACTS 2017), due to their association with poor prognosis, with adverse outcomes at smaller EROA, perhaps because a small regurgitant volume represents a large regurgitant fraction due to low total stroke volume) [11, 33]. Higher thresholds similar to those defining primary MR are also proposed (ACC/AHA, 2017) [34]. Secondary MR is a dynamic condition (dependent on preload, afterload, and LV function). The severity of MR should be reassessed after optimization of medical treatment. In patients undergoing CABG, the evaluation of ischaemic MR severity should be made before surgery, as it may be significantly reduced by general anaesthesia. An acute volume challenge and increase in afterload may help in intraoperative MR assessment [11].

Coronary angiography is recommended for the evaluation of moderate to severe secondary MR (I C) [11]. Surgery has a distinct role in secondary ischaemic MR if there are revascularization options (target vessels suitable for CABG and viable myocardium). On the contrary, the role of isolated MV surgery for chronic secondary MR is uncertain if there are no revascularization options.

Surgery in severe chronic secondary MR with revascularization option

MV surgery is indicated in patients with severe chronic secondary MR and LVEF>30%, who are undergoing CABG (I C) [11]; combined MR surgery and CABG should be considered in symptomatic patients with severe chronic secondary MR and LVEF <30% if revascularization is an option and there is evidence of viable myocardium (IIa C) [11] or if revascularization is required for angina refractory to medical treatment (IIa C) [8]. Atrial ablation and closure of the left atrial appendage may be considered at the time of MV surgery in the presence of atrial fibrillation [8].

MV repair and MV replacement in chronic secondary MR

Although there has been a trend favouring MV repair by an undersized annuloplasty, rather than MV replacement for patients with chronic secondary MR [35], the benefit of MV repair is unclear [8, 33]. MV repair with downsized annuloplasty is associated with relatively lower perioperative morbidity and mortality, and the “presumed” benefits of preservation of the subvalvular apparatus to LV systolic function. However, repair is associated with high rate of recurrent MR, while excess downsizing may result in functional mitral stenosis. Chordal-sparing MV replacement provides more durable correction of MR but is associated with higher perioperative mortality, and higher risks of long-term thromboembolism, endocarditis, and structural valve deterioration [35].

A recent multicenter RCT that randomly assigned 251 patients with severe ischemic MR to either MV repair or chordal-sparing MV replacement (with or without concomitant CABG in both groups), showed that there were no significant between-group differences in LV reverse remodeling, survival, composite of major adverse cardiac or cerebrovascular events, functional status, or quality of life at 12 months. Replacement provided more durable MR correction. At 2 years there was no significant between-group difference in LV reverse remodeling or survival (2-year mortality 19.0% in the repair group vs. 23.2% in the replacement group, p=0.39). The rate of MR recurrence was significantly higher in the repair group (58.8% vs. 3.8%, P<0.001), resulting in more HF-related adverse events and cardiovascular admissions [35].

The optimal surgical technique of secondary MR treatment remains controversial.

According to the 2017 ESC/EACTS guidelines, “while MV repair with an undersized complete ring to restore leaflet coaptation and valve competence is the preferred technique, MV replacement should be considered in patients with echocardiographic risk factors for residual or recurrent MR” (ungraded recommendation) [11].

According to the 2017 ACC/AHA VHD guidelines, “It is reasonable to choose chordal-sparing MV replacement over downsized annuloplasty repair if operation is considered for severely symptomatic patients (NYHA class III to IV) with chronic severe ischemic MR (stage D) and persistent symptoms despite GDMT (guideline directed medical treatment) for HF” (IIa B-R) [34].

Surgery in severe chronic secondary MR without revascularization option

Indications for surgery in severe secondary MR are “particularly restrictive” when concomitant CABG is not an option, due to significant operative mortality, high rates of recurrence and absence of proven survival benefit [11].

According to ACC/AHA VHD guidelines, MV repair or MV replacement “may be considered for severely symptomatic patients (NYHA class III to IV) with chronic severe secondary MR (stage D) who have persistent symptoms despite optimal GDMT for HF (IIb B) [33, 34].

According to ESC guidelines, in patients with severe chronic secondary MR, who remain symptomatic despite optimal medical management (including CRT if indicated), have LVEF >30%, and no indication for revascularization, MV surgery may be considered if the surgical risk is low (IIb C), while a percutaneous edge-to-edge procedure may be considered if the valve anatomy is suitable and the surgical risk is high, avoiding futility (IIb C) [11]. Isolated surgery for severe, non-ischaemic functional MR in patients with LVEF <30% may be considered in selected cases in order to avoid or postpone transplantation (IIb C) [8]. In patients without option for revascularization, with severe secondary MR and LVEF <30% who remain symptomatic despite optimal medical management (including CRT if indicated), the Heart Team may consider: MV surgery, percutaneous edge-to-edge procedure, implantation of a ventricular assist device (VAD), or heart transplantation, according to individual patient characteristics. (IIb C) [11]. Generally, valve intervention is not indicated when the LVEF < 15%.

MV surgery for severe primary or secondary MR as a concomitant procedure

MV repair or MV replacement “is indicated in patients with chronic severe primary MR undergoing cardiac surgery for other indications” (I B) [33, 34].

MV surgery “is reasonable for patients with chronic severe secondary MR (stages C and D) who are undergoing CABG or AVR” (IIa C) [33, 34].

Acute heart failure due to acute VHD

Acute valve insufficiency is among the most frequent primary cardiac causes of acute (de novo) HF. Acute regurgitation (or severe exacerbation of pre-existing regurgitation) of native of prosthetic valves occurs abruptly more commonly than acute stenosis. Acute regurgitation of left-sided heart valves is poorly tolerated and if severe enough results in acute HF refractory to medical treatment, while acute VHD of the right-sided valves has a generally less dramatic presentation. Acute valve regurgitation can result from infective endocarditis (through various mechanisms), calcific degeneration of native or bioprosthetic valves (with tear usually occurring adjacent to an akinetic calcified area). blunt trauma, iatrogenic injury, suture dehiscence after surgical valve replacement (causing paravalvular leak), rheumatic fever, ergotamine abuse, systemic lupus erythematosus, carcinoid heart disease, chest radiation, etc. Acute primary mitral regurgitation (MR) can be caused by papillary muscle rupture after MI, or chordal rupture, occurring mainly in elongated or thinned chordae in the course of chronic primary MR. Acute functional MR may be secondary to acute ischaemia, acute myocarditis, or acute dilated cardiomyopathy. Acute aortic regurgitation (AR) can be caused by aortic dissection affecting the ascending aorta (Stanford classification type A, De Bakey classification types I and II). Refractory AHF in severe acute VHD due to structural valve lesions of native valves necessitates immediate surgery. the most common indications being acute primary MR, and acute AR. Urgent or emergency surgery is indicated in acute obstructive thrombosis or failure of prosthetic valves causing AHF, while early surgery is indicated in infective valve endocarditis causing AHF [8, 11, 33, 34].

Acute primary mitral regurgitation

Severe acute MR, such as massive MR in complete papillary muscle rupture after MI, is poorly tolerated and necessitates urgent surgery [6, 7]. Urgent surgery may be indicated even in partial papillary muscle rupture with haemodynamic stability, due to the risk of sudden progression to complete rupture [33]. (Acute MR after MI is discussed in mechanical complications of MI at a previous section of this chapter).

In chordal rupture (due to endocarditis or primary degenerative MR, particularly fibroelastic deficiency, and rarely rheumatic valve disease) the severity of symptoms depends on the number and the location or the ruptured chordae. In moderate MR, stabilization can be achieved after an initial symptomatic period, due to compensation mechanisms, but in most patients, surgery is required for symptomatic relief, establishment of normal haemodynamics, treatment of the underlying disease, and prevention of chronic pulmonary hypertension and chronic HF. In ruptured chordae tendineae, MV repair is usually feasible and preferred over MV replacement. The timing of surgery is determined by the severity of regurgitation, the hemodynamic status, and the overall clinical condition. In underlying IE earlier surgery is generally preferred [33]. (The indications for surgery in infective valve endocarditis are discussed in the relevant section following in this chapter.)

Acute aortic regurgitation

Acute aortic regurgitation (AR) may result from aortic root or valve abnormalities, mainly aortic dissection or infective endocarditis (IE). Less frequently it may be iatrogenic, or a result of blunt chest trauma [33]. (Infective valve endocarditis and aortic dissection are discussed in relevant sections.) Generally, in symptomatic acute severe AR, urgent/emergent surgery is indicated [33]. IABP is contraindicated in significant AR and/or aortic dissection [11, 33].

Acute heart failure in infective endocarditis

IE has an in-hospital mortality of 15–20%, which is higher in the presence of valve dysfunction and HF symptoms. HF is the most frequent [11] and the most severe complication of IE, being the most important predictor of mortality. Sudden death may occur in patients with IE causing HF symptoms, particularly in aortic valve involvement. HF is an indication for early surgery in IE [36].

Mechanical complications of IE that precipitate HF and may require surgical intervention include native or prosthetic valve stenosis and/or regurgitation, mitral or aortic annular abscesses, and rarely intracardiac or aortocardiac fistulae. Valve stenosis may be caused by vegetations obstructing the valve orifice of native or bioprosthetic valves or interfering with the opening of mechanical valves. Transvalvular and/or paravalvular regurgitation is caused by several mechanisms, including: leaflet erosion/ rupture/ fenestration of native or bioprosthetic valves, paravalvular leak of prosthetic valves (more often encountered in mechanical rather than bioprosthetic valves), incomplete closure of mechanical valves due to vegetations, chordal rupture of the MV, mitral valve “aneurysm” (localized protrusion), rupture of mitral annulus abscess penetrating into the left atrium, annular aortic abscess causing AR, etc.).

HF is observed in 42–60% of cases of left-sided native valve endocarditis [36]. In patients with IE complicated by HF, surgical treatment is associated with decreased mortality in comparison to medical treatment (in-hospital mortality 21% versus 45%; 1-year mortality 29.1% versus 58.4%) [33].

According to the 2017 AHA/ACC VHD guidelines [34], in infective endocarditis multidisciplinary decision making about timing of surgical intervention is recommended (I B)]. Early surgery (during initial hospitalization and before completion of a full antibiotic course) is indicated in patients with IE and (native or prosthetic) valve dysfunction causing HF symptoms (I B), or in the presence of complications, such as heart block, annular or aortic abscess, and destructive penetrating lesions (I B) [34].

According to the 2015 ESC IE guidelines [36], in patients with IE and HF, early consultation with a cardiac surgeon, and multidisciplinary decision-making is recommended. Emergency (within 24 hours) surgery is indicated in aortic or mitral native valve endocarditis (NVE) or prosthetic valve endocarditis (PVE) with severe acute regurgitation, obstruction or fistula causing refractory pulmonary oedema or CS (I B). Urgent (within a few days to less than 1 week) surgery is indicated in “Aortic or mitral NVE or PVE with severe regurgitation or obstruction causing symptoms of HF or echocardiographic signs of poor haemodynamic tolerance” (I B) [36]. Unless severe co-morbidity exists, surgery for NVE or PVE is indicated even in CS [36].

Surgical treatment in the presence of severe destructive IE lesions is a surgical challenge. Thus, early surgery is indicated not only in the presence of HF but also in left sided IE caused by resistant organisms, in persistent or relapsing infection, or persistent vegetations despite appropriate antimicrobial treatment [34]. “Complete removal of pacemaker or defibrillator systems, including all leads and the generator, is reasonable in patients undergoing valve surgery for valvular IE” (IIa C) [34]. Radical debridement and appropriate antibiotic treatment minimize the risk of recurrence. Use of stentless biological valves or homografts in the aortic position may be beneficial, but in the absence of robust evidence there is no consensus on the choice of valve.

Acute heart failure in acute prosthetic valve disease

Prosthetic valve disease is encountered with increasing frequency due to the aging of population, increasing application of valve interventions, and increasing post-intervention survival. Prosthetic valve disease includes acute thrombosis, prosthetic valve failure, and infective endocarditis.

Symptomatic prosthetic valve thrombosis is observed predominantly with mechanical valves, but it may occur in bioprosthetic valves, in which asymptomatic and subclinical leaflet thrombosis may be frequent, particularly after TAVI [34].

Acute mechanical prosthetic valve thrombosis

Mechanical valves are prone to acute thrombosis, which can cause acute stenosis or regurgitation (interfering with mechanical valve opening or closure). In prosthetic valve thrombosis, there is usually recent history of inadequate anticoagulation. In developed countries, the prevalence of mechanical valve thrombosis is 0.3–1.3% per patient-year, while it is lower with bioprosthetic valves [33].

According to the 2017 ESC/EACTS VHD guidelines [11], “urgent or emergency valve replacement is recommended for obstructive thrombosis” of mechanical prosthetic valves “in critically ill patients without serious comorbidity” (I C). Fibrinolysis should be considered when surgery is not available or is very high risk or for thrombosis of right-sided prostheses. (IIa C). In non-obstructive prosthetic valve thrombosis, surgery should be considered for large (> 10mm) thrombus complicated by embolism (IIa C) [11].

Emergency re-operation in haemodynamically compromised patients results in high mortality (30-day mortality of 10–15%, reduced to < 5% in patients with NYHA class I/II symptoms). Fibrinolysis is associated with lower mortality (overall 30-day mortality of 7%), but a success rate of 75%, thromboembolism rate of 13%, bleeding rate of 6% (including cerebral bleeding of 3%) and a higher rate of thrombosis recurrence [11, 34]. A recently reported “echocardiogram-guided slow-infusion low-dose fibrinolytic protocol” resulted in success rates >90%, embolic event rates <2%, and major bleeding rates <2% [34].

According to 2017 ACC/AHA VHD guideline [34], “Urgent initial treatment with either slow-infusion low-dose fibrinolytic therapy or emergency surgery is recommended for patients with a thrombosed left-sided mechanical prosthetic heart valve presenting with symptoms of valve obstruction” (I B non-randomized data). The decision between surgery and fibrinolysis should be individualized and decision making should be shared with patients and care-givers. Parameters favouring surgery are: readily available surgical expertise, low surgical risk, contraindication to fibrinolysis, recurrent valve thrombosis, NYHA class IV, large clot (>0.8 cm2), left atrial thrombus, need for concomitant CABG, other valve disease requiring surgery, possible pannus, and patient choice favoring surgery. Absence of these parameters and/or presence of the opposite (e.g. lack of surgical expertise, high surgical risk, first-time thrombosis, NYHA class I-III, small thrombus, etc.) favor thrombolysis [34].

Bioprosthetic valve thrombosis

Bioprosthetic valve thrombosis may occur after TAVI or surgical AVR. It may be asymptomatic (despite causing reduced leaflet motion and increased transvalvular gradients), it may lead to slow progression of stenosis over months to years after implantation, but it may also result in thromboembolism or obstruction [11, 34].

According to 2017 ESC VHD guidelines anticoagulation using a vitamin K antagonist (VKA) and/or unfractionated heparin (UFH) “is recommended in bioprosthetic valve thrombosis before considering reintervention” (I C) [11]. According to the 2017 ACC/AHA VHD guideline, initial treatment with a VKA is reasonable in suspected or confirmed bioprosthetic valve thrombosis in hemodynamically stable patients with no contraindications to anticoagulation (IIa C Limited Data). Surgery or thrombolysis may still be required for patients who are haemodynamically unstable or have advanced and refractory HF, a large mobile thrombus, or high risk for embolism [34].

Non-thrombotic prosthetic valve failure

Repeat valve replacement is the mainstay treatment for severe symptomatic prosthetic valve failure, leading to HF, intractable haemolysis or being related to infective endocarditis. Surgery is indicated in severely symptomatic patients with stenosis and/or transvalvular or paravalvular regurgitation of mechanical or bioprosthetic valves.

According to the 2017 VHD guidelines, repeat valve replacement is indicated in severe symptomatic (mechanical or biological) prosthetic valve stenosis (IC) [34]. Reoperation is recommended in symptomatic patients with significant increase of transprosthetic gradient of bioprosthetic valves (after exclusion of thrombosis) (I C) [11]. Surgery is recommended in operable patients with severe prosthetic or paraprosthetic regurgitation of mechanical valves causing HF (or intractable haemolysis) (I B) [34]. Reoperation is recommended in symptomatic patients with severe (transprosthetic) regurgitation of bioprosthetic valves (I C) [11]. Reoperation is recommended if paravalvular leak of prosthetic valves “is related to endocarditis or causes haemolysis requiring repeated blood transfusions or leading to severe symptoms” (I C) [11]. (Indications for surgery in infective prosthetic valve endocarditis have been discussed at a previous section of this chapter.)

In the absence of infective endocarditis, transcatheter interventions may be reasonable for selected patients. Transcatheter valve-in-valve implantation should be considered in bioprosthetic aortic valve failure (stenosis and/or regurgitation) in severely symptomatic patients who have high or prohibitive risk of reoperation judged by the Heart Team, when improvement in hemodynamics is anticipated (IIa B) [34] (or) depending on the size and the type of prosthesis (IIa C) [11], (haemodynamic benefit being expected in larger-sized prostheses). Evidence is provided by non-randomized studies, while long-term results are not available yet. “Transcatheter valve-in-valve implantation has also been successfully performed for failed surgical bioprostheses in the mitral, pulmonic, and tricuspid positions” [34], but experience is limited [11].

Percutaneous repair of clinically significant paravalvular leaks in (biological or mechanical) prosthetic valves may be considered as an alternative to reoperation in patients with high surgical risk and suitable anatomical features, when performed in experienced centers (IIa, B, ACC/AHA, [34]), after Heart Team decision (IIb C, ESC/EACTS) [11]).

Role of surgery in acute heart failure due to acute aortic disease

Acute aortic dissection (AD) type A (Stanford classification) is frequently associated with cardiac complications, including AR, tamponade, ischaemia or MI, HF, and CS Urgent surgery is recommended in type A AD (I B), which, if not operated, has a mortality of 50% within the first 48 hours. Despite the high rates of perioperative mortality (25%) and neurologic complications (18%), surgery is the treatment of choice, reducing the 1-month mortality from 90% to 30%. In acute type A AD and organ malperfusion, a hybrid approach should be considered (IIa B). Treatment of intramural haematoma (IMH) is similar to that of AD [37].

In acute contained rupture of thoracic aortic aneurysm urgent surgical repair is recommended (I C), while in the presence of favourable anatomy and available expertise thoracic endovascular aortic repair (TEVAR) should be preferred over open surgery (I C) [37].

Role of surgery in acute pulmonary embolism

Pulmonary embolism (PE) with shock or hypotension is associated with high risk of early death, and is defined as high-risk PE [38]. Immediate primary reperfusion with systemic thrombolysis is the treatment of choice for high-risk acute PE (I B) [38]. In contraindicated or failed thrombolysis surgical embolectomy is recommended (I C), while percutaneous catheter-directed treatment should be considered as an alternative to surgery (IIa C). Multidisciplinary decision making is advised [38].

In intermediate-high-risk PE, close monitoring is recommended to allow early detection of haemodynamic decompensation (I B); in imminent decompensation, thrombolysis should be considered (IIa B), while surgical embolectomy (IIb C) or percutaneous embolectomy (IIb B) may be considered if the anticipated bleeding risk of systemic thrombolysis is high [38].

Acute PE superimposed on chronic thromboembolic pulmonary hypertension should be treated by pulmonary thrombendarterectomy [38].

Role of surgery in pericardial disease

Tamponade is one of the most common acute primary cardiac causes of AHF [8]. Common causes of tamponade are pericarditis, tuberculosis, iatrogenic trauma, and malignancy. Urgent pericardiocentesis or cardiac surgery is recommended to treat cardiac tamponade” (I C) and symptomatic moderate to large pericardial effusions unresponsive to medical therapy (I C) [39]. Pericardial fluid drainage of the, preferably by needle pericardiocentesis, under echocardiographic or fluoroscopic guidance, should be performed without delay in unstable patients. Alternatively, surgical drainage is performed, especially in situations such as purulent pericarditis, loculated pericardial effusion, or urgent situations with intrapericardial bleeding [39].

In cardiac tamponade due to penetrating heart/chest trauma, immediate thoracotomy is indicated (I B); pericardiocentesis as a bridge to thoracotomy may be considered (IIb C) [39].

Surgical ventricular remodelling

In patients with chronic HF and systolic LV dysfunction (LVEF<35%) “myocardial revascularization should be considered in the presence of viable myocardium” (IIa C) and/or to relief angina symptoms [1]. CABG was recommended for patients with LM or LM equivalent (I C); or significant LAD stenosis and multivessel CAD, in order to reduce mortality and hospitalization for cardiovascular causes (I B) [1]. When revascularization is required in patients with HFrEF “the choice between CABG and PCI should be made by the Heart Team”, after careful evaluation of clinical status and coronary anatomy, expected completeness of revascularization, coexisting VHD and co-morbidities” [8].

Surgical ventricular restoration, reconstruction, or remodeling of the anteroseptal LV wall (aiming to exclude scarred tissue and restore the LV volume and shape), along with revascularization (and MV repair, as required), have been applied in patients with ischaemic cardiomyopathy, with good results according to observational data (see Figure 54.5). The Hypothesis 2 substudy of the STICH RCT [40] failed to show differences between the groups of isolated CABG and CABG plus ventricular reconstruction regarding the composite of death or re-hospitalization for cardiac causes, functional class, or exercise tolerance. The 30-day all-cause mortality was 5%, and the all-cause mortality at a median of 48 months was 28% in each group. A LVESVI < 70 ml/m2 after CABG plus ventricular reconstruction was associated with improved survival compared with isolated CABG [40].

Figure 54.5 Surgical ventricular remodelling with the use of bovine pericardial patch (yellow arrow), combined with bypass grafting (green arrow) and mitral valve repair with an undersized annuloplasty (black arrow) in a patient with decompensated heart failure due to ischaemic cardiomyopathy.

Figure 54.5
Surgical ventricular remodelling with the use of bovine pericardial patch (yellow arrow), combined with bypass grafting (green arrow) and mitral valve repair with an undersized annuloplasty (black arrow) in a patient with decompensated heart failure due to ischaemic cardiomyopathy.

According to the 2014 ESC/EACTS revascularization guidelines [1], “LV aneurysmectomy during CABG should be considered in patients with a large LV aneurysm, if there is a risk of rupture, large thrombus formation or the aneurysm is the origin of arrhythmias” (IIa C), while “CABG with surgical ventricular restoration may be considered in patients with a scarred LAD territory, especially if a postoperative LVESVI <70 mL/m² can be predictably achieved” (IIb–B). According to the 2013 ACCF/AHA HF guideline [41], surgical reverse remodeling or LV aneurysmectomy may be considered in selected HFrEF patients for specific indications such as intractable HF and ventricular arrhythmias (IIb B).

Surgical ventricular reconstruction is not recommended for routine use [8] and has a very limited role in the acute setting. Cardiomyoplasty, partial left ventriculectomy, and external ventricular restoration are not recommended for the treatment of HF and have been abandoned.

Mechanical circulatory support

Short- and long-term MCS may be applied when conventional treatment of HF fails [8, 27, 41–57]. Non-durable (short-term) MCS, “including percutaneous and extracorporeal ventricular assist devices (VADs), is reasonable as a “bridge to recovery” or “bridge to decision” for carefully selected patients with HFrEF with acute, profound hemodynamic compromise” (IIa B) [41]. Short-term MCS is applied in acute (de novo) HF or ADCHF (see Box 54.1) [27, 4146]. A bridging to decision can describe the short-term support strategy implemented in acutely and critically ill patients (AHF/CS, resuscitated cardiac arrest), to prevent imminent death, achieve haemodynamic stabilization, and end-organ perfusion, and provide time for evaluation, including neurological assessment, in order to decide about further treatment. Medical and/or surgical treatment of the underlying disease (see Figure 54.2), adjunctive therapy, and ventricular unloading during short-term MCS may lead to recovery; otherwise HTx or long-term MCS may be considered in suitable candidates [27, 4146] (see Box 54.2).

The results of short-term MCS are highly dependent on the pre-implantation patient profile. Initiation before irreversible myocardial and end-organ injury and treatment of the underlying disease are of paramount importance [27, 4146].

Long-term (durable) MCS is mainly applied in end-stage CHF due to ischaemic or non-ischaemic cardiomyopathy [4751] (see Figure 54.6), as a bridge to transplantation (BTT), bridge to transplantation candidacy (BTC), destination therapy (DT), and very rarely as a bridge to recovery (BTR) or rescue therapy (see Boxes 54.3 and 54.4) [4751].

Figure 54.6 Immediate post-operative chest X-rays (CXRs) of two patients with end-stage heart failure, implanted with the Jarvik 2000 LVAD as destination therapy (black arrows). (A) CXR of a patient suffering from idiopathic dilated cardiomyopathy (who had been implanted with an implantable cardioverter–defibrillator (ICD) in the past, white arrow). (B) CXR of a patient suffering from ischaemic cardiomyopathy (who had been implanted with a biventricular ICD, white arrow). Device therapy is becoming increasingly common for the treatment of refractory heart failure.

Figure 54.6
Immediate post-operative chest X-rays (CXRs) of two patients with end-stage heart failure, implanted with the Jarvik 2000 LVAD as destination therapy (black arrows). (A) CXR of a patient suffering from idiopathic dilated cardiomyopathy (who had been implanted with an implantable cardioverter–defibrillator (ICD) in the past, white arrow). (B) CXR of a patient suffering from ischaemic cardiomyopathy (who had been implanted with a biventricular ICD, white arrow). Device therapy is becoming increasingly common for the treatment of refractory heart failure.

BTT describes the MCS strategy aiming to keep alive transplant candidates at high-risk of death while on the waiting list, until a donor organ becomes available. BTC involves application of MCS to patients with one or more relative contraindications to transplantation that are deemed potentially reversible or treatable (pulmonary hypertension, cancer, obesity, tobacco use, etc.) [52]. BTR involves application of long-term MCS until myocardial recovery is sufficient for device removal. BTR with long-term devices is applied electively (as an isolated procedure or in combination with other treatments) after careful patient selection [49]. DT is permanent or life-long MCS, without a predefined ultimate goal. It has been traditionally applied in non-transplant eligible patients with refractory end stage heart failure, to prolong life as an alternative to heart transplantation [4754] (Box 54.4).

The long-term support strategies may overlap and change during the support period. In Europe, only 10% of patients BTT with an LVAD are actually transplanted within the first year and “lifelong LVAD therapy, despite eligibility for transplantation, has become a clinical reality” [8].

In the most recent era, the support strategy for patients entered in the INTERMACS registry was DT in 45%, BTT in 25.8%, BTC in 28%, BTR in 0.3%, and rescue therapy in 0.4% of patients [53].

General indications for referral for MCS include LVEF <25% and NYHA class III–IV despite guideline directed medical treatment (GDMT), including CRT if indicated, with either high predicted 1- to 2-year mortality or dependence on continuous parenteral inotropic support [41]. Patient selection requires an experienced multidisciplinary team [41].

Among patients with end-stage HFrEF despite OMT including (non-surgical) device therapy, an LVAD should be considered (a) in transplant-eligible patientsto improve symptoms, and reduce the risks of HF-hospitalization and premature death (BTT), (IIa C) and (b) in non-transplant-eligible patients to reduce the risk of premature death (IIa B) (DT) [8].

The INTERMACS registry has long described profiles for classification of advanced HF in relation to indication for long-term MCS [4753]. In the more recent era, the pre-implantation profiles of patients entered in the registry were: INTERMACS profile 1: (critical CS) in 15.5%; INTERMACS profile 2: (“sliding on (IV) inotropes”) in 34.9%; INTERMACS profile 3: (stable but (IV) inotrope-dependent) in 33%; INTERMACS profile 4 (resting symptoms, “frequent flyer”) in 13.1%; INTERMACS profile 5: (exertion-intolerant, “housebound”) in 2.1%; INTERMACS profile 6: (exertion-limited, “walking wounded”) in 0.6%; and INTERMACS profile 7: advanced NYHA class III: in 0.3% of registered patients [53].

The improved results of long-term MCS (survival of 80% at 1 year and 70% at 2 years) mainly reflect application of long-term continuous-flow LVADs but also improved patient selection earlier application of support, and improved patient management. Despite earlier application, more than 80% of patients currently receiving long-term MCS in the USA are on inotropic support (INTERMACS profiles 1, 2, and 3). Long-term MCS with biventricular assist devices (BIVADs) or the total artificial heart (TAH) is rarely applied and is associated with decreased survival. Isolated right ventricular assist devices (RVADs) are extremely rarely applied. Earlier application of continuous flow LVADs (before severe RV failure, CS and/or severe end-organ impairment) is advised [4754]. Destination therapy is increasingly applied, but it is not recommended for patients with biventricular failure. Long-term biventricular support with two implantable continuous-flow devices may offer a chance to prolonged survival in transplant-ineligible patients with refractory biventricular failure, but further investigation is required (see Figure 54.7) [50]. A recent RCT showed favorable preliminary results regarding reduced thrombogenicity of a magnetically levitated continuous centrifugal-flow LVAD versus its predecessor continuous axial-flow LVAD [54].

Figure 54.7 Planned long-term biventricular MCS (total ventricular assist) with two Jarvik 2000 continuous axial flow intraventricular pumps, first applied on 25 March 2009. Elective single-stage, off-pump, beating heart (without ventricular fibrillation (VF)) implantation of two pumps through a left thoracotomy, which provided good access to the LV apex and to the diaphragmatic surface of the RV, close to the acute margin and the RV apex, without major cardiac distortion, facilitating implantation without haemodynamic compromise. Furthermore, it was advantageous in a patient with previous CABG through a median sternotomy and patent skeletonized bilateral ITA grafts beneath the sternum. After feasibility of implantation and good exposure were shown in this patient (first patient), the same implantation method was adapted in the second patient. (A) Head and neck and chest radiographs of the first patient. One tunnel was created for both power cables, and two pedestals were screwed to the left post-auricular and supra-auricular area of the skull. LVAD pump inside the LV; RVAD pump inside the RV. (B) Schematic representation of the implantation of two Jarvik 2000 pumps for long-term biventricular MCS. The LVAD pump inflow is “facing” the mitral valve. The RVAD pump inflow is “facing” the pulmonary valve. The LVAD outflow graft is anastomosed to the descending thoracic aorta. The RVAD outflow graft is anastomosed to the left pulmonary artery. (C) Photograph of the first patient on the 42nd day of support. Exit of power cables. The LVAD power cable pedestal (LP) is fixed at a high point of the left post-auricular area, and the RVAD power cable pedestal (RP) is fixed superiorly and posteriorly to it. The pedestal fixation areas need not be strictly post-auricular. In both places, the skull had sufficient thickness (>8.8 mm), as measured on preoperative CT. Fixation to the skull (which is an area of increased vascularity) ensured excellent wound healing, with minimal care. LP, left pedestal; LVAD, left ventricular assist device; RP, right pedestal; RV, right ventricular; RVAD, right ventricular assist device.

Figure 54.7
Planned long-term biventricular MCS (total ventricular assist) with two Jarvik 2000 continuous axial flow intraventricular pumps, first applied on 25 March 2009. Elective single-stage, off-pump, beating heart (without ventricular fibrillation (VF)) implantation of two pumps through a left thoracotomy, which provided good access to the LV apex and to the diaphragmatic surface of the RV, close to the acute margin and the RV apex, without major cardiac distortion, facilitating implantation without haemodynamic compromise. Furthermore, it was advantageous in a patient with previous CABG through a median sternotomy and patent skeletonized bilateral ITA grafts beneath the sternum. After feasibility of implantation and good exposure were shown in this patient (first patient), the same implantation method was adapted in the second patient. (A) Head and neck and chest radiographs of the first patient. One tunnel was created for both power cables, and two pedestals were screwed to the left post-auricular and supra-auricular area of the skull. LVAD pump inside the LV; RVAD pump inside the RV. (B) Schematic representation of the implantation of two Jarvik 2000 pumps for long-term biventricular MCS. The LVAD pump inflow is “facing” the mitral valve. The RVAD pump inflow is “facing” the pulmonary valve. The LVAD outflow graft is anastomosed to the descending thoracic aorta. The RVAD outflow graft is anastomosed to the left pulmonary artery. (C) Photograph of the first patient on the 42nd day of support. Exit of power cables. The LVAD power cable pedestal (LP) is fixed at a high point of the left post-auricular area, and the RVAD power cable pedestal (RP) is fixed superiorly and posteriorly to it. The pedestal fixation areas need not be strictly post-auricular. In both places, the skull had sufficient thickness (>8.8 mm), as measured on preoperative CT. Fixation to the skull (which is an area of increased vascularity) ensured excellent wound healing, with minimal care. LP, left pedestal; LVAD, left ventricular assist device; RP, right pedestal; RV, right ventricular; RVAD, right ventricular assist device.

With kind permission from Elsevier: Pitsis AA, Visouli AN, Ninios V, Kremastinos DT. Total ventricular assist for long-term treatment of heart failure. J Thorac Cardiovasc Surg. 2011;142(2):464–7.

Heart transplantation

HTx remaines the gold standard of treatment for patients with end-stage heart failure who remain symptomatic, despite OMT. A milestone in the history of HTx was the introduction in the 1980s of cyclosporine, which dramatically reduced acute rejection and infection [55].

HTx has failed to provide an epidemiologically significant impact in the treatment of end-stage heart failure due to critical shortage of donor hearts [63]. The overall number of HTx reported to the International Society for Heart and Lung Transplantation (ISHLT) followed a descending curve between 1993 and 2004, but since 2005 there has been a slow progressive increase, attributed to increased volumes in North America and particularly countries beyond North America and Europe [64] (see Figure 54.8). A total of 4,746 HTx (including 4,157 adult HTx but excluding combined heart-lung transplants) were performed in 2014 and reported to the ISHLT [58]. The increased volume of HTx represents the combined effect of increased reporting and the absolute increase in transplant volumes. It is estimated that approximately 66% of worldwide thoracic transplant activity is reported to the ISHLT. (Thus, it can be inferred that more than 7,000 HTx are performed yearly worldwide [58].)

Figure 54.8 Number of adult and paediatric heart transplants reported to the ISHLT by year (1982–2014) and geographic region. ISHLT 33rd Adult Heart Transplantation Report, 2016 [64].
With kind permission from Elsevier Lund LH, Edwards LB, Dipchand AI, et al; International Society for Heart and Lung Transplantation. The Registry of the International Society for Heart and Lung Transplantation: thirty-third Adult Heart Transplantation Report-2016; Focus Theme: Primary Diagnostic Indications for Transplant. J Heart Lung Transplant. 2016;35(10):1158–69.

Figure 54.8
Number of adult and paediatric heart transplants reported to the ISHLT by year (1982–2014) and geographic region. ISHLT 33rd Adult Heart Transplantation Report, 2016 [64].

With kind permission from Elsevier Lund LH, Edwards LB, Dipchand AI, et al; International Society for Heart and Lung Transplantation. The Registry of the International Society for Heart and Lung Transplantation: thirty-third Adult Heart Transplantation Report-2016; Focus Theme: Primary Diagnostic Indications for Transplant. J Heart Lung Transplant. 2016;35(10):1158–69.

In Europe, the yearly transplant volume remains relatively stable since 2002, and the median waiting time of listed patients is 16 months. More than 60% of patients are transplanted in high-urgency status, while the mortality on the Eurotransplant waiting list was approximately 22% in 2013 [8].

Evaluation for HTx “is indicated for carefully selected patients with stage D HF despite GDMT, device, and surgical management” (I C) [41].

Indications for consideration of transplantation are end-stage HF with severe symptoms and poor prognosis, without remaining alternative treatment options. Motivated, well informed, and emotionally stable patients, capable of complying with the intensive post-transplant treatment are suitable candidates [8].

According to the 2016 ISHLT updated listing criteria for HTx [52], cardiopulmonary stress testing (I B), HF prognostic scores (IIb C), right heart catheterization (RHC) (I C), evaluation of reversibility of pulmonary hypertension, comorbidities, frailty, substance abuse, and psychosocial assessment should be performed before listing for transplantation.

A peak oxygen consumption (VO2) <10 ml/kg/min is an indication for transplantation, while peak VO2 between 10 ml/kg/min and 14 ml/kg/min along with major limitation of daily activities is a probable indication for transplantation [52].

HF prognostic scores should be performed along with cardiopulmonary exercise testing. Listing solely based on prognostic scores should not be performed (III C) [52].

RHC should be performed on all adult HTx candidates and repeated periodically until transplantation (I C) [58]. Pulmonary hypertension and increased pulmonary vascular resistance (PVR) refractory to medical treatment may be contraindications to HTx, depending on severity. If the pulmonary artery systolic pressure (PAS) is >50 mmHg, and either the transpumonary gradient (TPG) is >15mmHg or the PVR is >3 Wood units, reversibility of pulmonary hypertension should be actively sought (by acute vasodilator challenge (I C), continuous haemodynamic monitoring under treatment including vasodilators such as inhaled nitric oxide (I C), and ultimately with LV unloaded by IABP and/or LVAD. Haemodynamics should be reevaluated after 3 to 6 months of LVAD implantation “to ascertain reversibility of pulmonary hypertension” (IIa C) [52].

Irreversible pulmonary hypertension, advanced age (>70 years), obesity (BMI >35 kg/m2), cancer, uncontrolled diabetes with end-organ damage, irreversible renal dysfunction (estimated Glomerular Filtration Rate <30 ml/min/1.73 m2), clinically severe symptomatic cerebrovascular disease, peripheral arterial disease limiting rehabilitation without revascularization option, frailty, active tobacco use, alcohol or drug abuse, poor social support insufficient to achieve compliancy at the outpatient setting, severe cognitive-behavioral disabilities [52], active uncontrolled infection, systemic disease with multiorgan involvement, and other serious comorbidities with poor prognosis [8] are contraindications to HTx.

Advanced age is not an absolute contraindication. Carefully selected patients >70 years may be considered (IIb C) [52] and are rarely transplanted [56]. Most comorbidities are relative contraindications depending on severity and potential reversibility. MCS as a BTC should be considered for patients with potentially reversible or treatable comorbidities” (IIb C) [52].

Currently, more than 50% of transplant recipients are bridged to HTx with MCS, while the percentage is much higher in some centers [64]. BTT especially with continuous-flow implantable LVADs, has contributed to increased survival and crash-free survival on the waiting list. Post-transplant survival is not adversely affected by pre-transplant MCS, with the notable exception of patients BTT with extracorporeal membrane oxygenation, in whom the post-transplant survival is distinctly worse [56].

The unadjusted survival of adult heart recipients is progressively increasing. The median survival of patients transplanted between 1982–1991 was 8.5 years, it increased to 10.4 years in patients transplanted between 1992–2001, and further increased to 11.9 years in patients transplanted between 2002–2008 [64]. For recipients who live beyond the first year, the mean survival is 13 years [56].

Conclusion

AHF due to ACS should be managed by emergent or urgent revascularization with PCI or CABG, based on clinical and anatomical criteria. Clinical criteria, mainly the risk for imminent irreversible myocardial necrosis requiring emergent reperfusion on an ‘as soon as possible’ basis or accelerated haemodynamic instability, favour PCI. Anatomical criteria, mainly the need for complete reperfusion and durable revascularization, in the presence of complex multivessel disease, favour CABG. In clinical practice, there is a progressive shift to an increased application of PCI, rather than CABG, in most anatomical and clinical settings of ACS [18].

Primary PCI is the preferred mechanical revascularization modality for STEMI patients [1, 6, 7]. CABG may be applied to lesions that are not amenable to PCI (bypassing the lesion, instead of dealing with it) [1, 2, 47].

NSTE-ACS represent the majority among all ACS and, despite a generally less severe presentation, are associated with high morbidity and mortality, similar to that of STEMI after the first month. Unstable NSTE-ACS patients should be managed as STEMI patients [5, 8]. In stabilized NSTE-ACS patients, the indications for PCI or CABG are generally the same as in stable CAD [4, 5]. Thus, in the presence of multivessel disease, CABG should be considered in all stabilized NSTE-ACS patients and preferred in diabetic patients [1, 4, 5]. In clinical practice, CABG is applied in about 10% among all NSTE-ACS patients and in more than 20% of NSTE-ACS patients with multivessel disease [1, 4, 5].

CS represents the rarest and most severe form of ACS, having the highest in-hospital mortality. Immediate PCI is recommended for patients with CS and suitable coronary anatomy, while emergency CABG is recommended if the coronary anatomy is not suitable for PCI or after failed PCI. Complete revascularization is advised. CABG is rarely applied (in about 5% of patients). CS in the presence of mechanical complications of MI is associated with a higher mortality than CS due to ventricular failure; corrective surgery is indicated (with or without MCS), and CABG should be offered at the time of surgical repair [1, 2, 6, 7].

Thus, urgent or emergency CABG may be indicated in selected patients with multivessel disease and AHF complicating ACS, particularly at the two extremes of the spectrum, e.g. in stabilized NSTE-ACS patients (when major irreversible myocardial injury has not yet occurred, and time is provided for surgery) and in severely ill patients with CS (when the early time frame for optimal revascularization is lost in most cases). In the presence of mechanical complications of MI, prompt surgery is clearly indicated [1, 2, 47].

Surgery should be considered in patients with severe (native or prosthetic) aortic or mitral valve disease that causes or aggravates/precipitates AHF. Although surgery yields better results in patients with moderate LV dysfunction, it should also be considered in patients with advanced LV dysfunction refractory to OMT, particularly in patients with a lower surgical risk. TAVI for severe AS has emerged as an alternative to surgical AVR, being favoured in elderly patients with high surgical risk who are suitable for transfemoral access. In the absence of infective endocarditis, transcatheter valve-in-valve implantation should be considered for the treatment of bioprosthetic valve failure. The decisions between surgical or transcatheter interventions should be made by the Heart Team [11, 34]. Early surgery is indicated in infective valve endocarditis causing HF. Urgent or emergency valve replacement is recommended for obstructive mechanical valve thrombosis, while fibrinolysis should be considered [11].

Urgent surgery is recommended in type A acute aortic dissection [37]. Surgical embolectomy is recommended for high-risk acute PE in contraindicated or failed thrombolysis [38]. Urgent pericardiocentesis or cardiac surgery is recommended for cardiac tamponade [39].

LV aneurysmectomy during CABG should be considered in selected patients with a large LV aneurysm at risk of rupture, large thrombus formation, or causing ventricular arrhythmias. Partial left ventriculectomy, cardiomyoplasty, and external ventricular restoration should not be done [1, 8, 40, 41].

Short-term MCS is applied in profoundly compromised patients with AHF, with results depending on the severity of the pre-implantation profile. Long-term continuous flow LVADs are increasingly applied. Better patient selection, earlier intervention (before CS, severe RV, and end-organ dysfunction), and improved technology of long-term LVADs resulted in substantially improved 1- and 2-year survival (of 80% and 70%, respectively). Magnetically levitated LVADs may contribute to further improvement [8, 41–59].

Cardiac transplantation remains the gold standard of the surgical treatment of end-stage CHF, having progressively improving results, but limited epidemiological impact. Urgent transplantation in the setting of AHF (particularly in the setting of ADCHF) is possible, but BTT with inotropes or MCS is usually required [47, 52, 56].

Personal perspective

Accumulating evidence, including RCTs (SYNTAX, FREEDOM, BEST), shows that, in patients with complex left main (LM) and/or multivessel disease and a stable clinical status or with UA, CABG offers more complete and durable revascularization than PCI and is associated with better results.

Nevertheless, when “time is muscle”, “timely use of a reperfusion therapy is likely more important than the choice of therapy” [7]. Thus, in the acute setting of ongoing STEMI, PCI is the treatment of choice. When more time is provided, as in stabilized NSTE-ACS, and when the optimal time for revascularization is lost, as in most cases of CS, complete revascularization with CABG should be considered in the presence of complex LM and/or multivessel disease. Rescue/salvage revascularization in acute terminal collapse is the most challenging goal that may be managed with a rapid implementation of invasive techniques. Salvage primary stenting of the LM can be lifesaving and, in our opinion, is strongly indicated in life-threatening situations, when the likelihood of death, before the patient can even reach the operating theatre, is high. In less acute states, stenting of the LM should be highly selective, concerning only suitable lesions, in the absence of additional complex multivessel disease, in patients with high operative risk. In the presence of CS with mechanical complications of AMI, prompt cardiac surgery is the only potentially lifesaving modality for the time being.

AHF due to valvular disease (more commonly, acute decompensation in chronic AS or MR, and acute de novo HF in acute AR or MR) is best treated with surgery (AVR and MV repair). For elderly patients with AS, high surgical risk and other risk factors, such as frailty or porcelain aorta, TAVI is indicated.

Short-term MCS can be lifesaving in AHF refractory to conventional treatment. Long-term MCS represents a rapidly expanding field, with a dramatically improved 1- and 2-year survival. In CHF, long-term MCS should be applied before CS and severe RV dysfunction. Further improvement in device technology, regarding reduced thrombogenicity and the feasibility of full implantation for long-term treatment is desirable. Cardiac transplantation remains the gold standard, being limited by donor organ availability.

Finally, regeneration of the heart with heart cell therapies might have a clinical application someday for the treatment of the failing myocardium.

Further reading

American Heart Association. ACC/AHA joint guidelines. Available at: <http://my.americanheart.org/professional/StatementsGuidelines/ByTopic/TopicsA-C/ACCAHA-Joint-Guidelines_UCM_321694_Article.jsp>.

European Society of Cardiology. ESC practice guidelines by topic. Available at: <http://www.escardio.org/Guidelines>.

Interagency Registry for Mechanically Assisted Circulatory Support. INTERMACS research. Available at: <http://www.uab.edu/medicine/intermacs/research>.

International Society for Heart and Lung Transplantation Guidelines. Available at: <http://www.ishlt.org/guidelines/>.

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