HIV: cardiovascular disorders
Introduction
Reports of the prevalence of cardiac involvement in patients with AIDS vary from 28% to 73%, with the first case of myocardial Kaposi’s sarcoma (KS), found at autopsy in 1983. Since the introduction of HAART, a sharp ↓ in mortality and morbidity has been observed. New risk factors for coronary heart disease such as increased insulin resistance, dyslipidemia, and lipodystrophy syndrome, which are associated with HAART, may accelerate underlying arteriosclerosis in HIV-infected patients.
Pericardial effusion
Prior to the introduction of HAART, the frequency of this complication was estimated to be 5–46%, and fibrinous pericarditis has been identified at autopsy in 9–62% of deceased AIDS patients. It is often small with no haemodynamic consequences, although if large it may cause tamponade. It is associated with low CD4 count and reported causes include bacteria, especially Mycobacterium spp and also Cryptococcus neoformans, cytomegalovirus, tumours (lymphoma, KS). Clinically similar to non-HIV infected patients, and although usually seen in advanced HIV infection rarely causes death.
Myocarditis
Prior to HAART autopsy evidence was found in ~33% of those with AIDS, with a specific cause found in <20% (the most common being Toxoplasma gondii, Mycobacterium tuberculosis, and C.neoformans). HIV alone can probably cause myocarditis, as HIV or its proteins have been found in the myocardium of patients with or without cardiac disease. Myocardial biopsy may be indicated, especially if CD4 ↓.
Dilated cardiomyopathy
Prevalence in patients with AIDS is 10–30% by echocardiographic and autopsy studies. Associated with advanced disease. Several studies have supported a direct role for HIV-1 as the cause of cardiac injury, but the mechanism remains unclear. Other viruses such as group B coxsackie virus, CMV, or EBV have been implicated (found in >80% of heart histology specimens). The patient will present with shortness of breath, persistent tachycardia, and signs of heart failure. Echocardiogram is of use in diagnosis. The overall prognosis is poor.
Endocarditis
Non-bacterial thrombotic endocarditis
Friable fibrinous clumps of platelets and red blood cells adherent to cardiac valves (usually tricuspid in HIV infection) without an inflammatory reaction. Occurs in 3–5% of those with AIDS, usually aged >50 years. Associated with malignancy, hypercoagulable states, and chronic wasting disease. Emboli may occur in up to 42%, involving the brain, lung, spleen, kidneys, and coronary arteries. They are usually asymptomatic, but rarely may be fatal.
Infective endocarditis
Occurs most commonly in injecting drug users (IDUs), usually affecting the tricuspid valve. The main causative organisms are Staphylococcus aureus (75%) and Streptococcus viridans (20%). Usually presents with fever, sweats, weight loss, peripheral signs of endocarditis, and coexisting pneumonia and/or meningitis. A murmur is normally heard and may be TR in setting of IDU. Echocardiogram is important, followed by transoesophageal echo-cardiogram. ↑ mortality in advanced HIV.
Pulmonary hypertension
HIV is an independent risk factor for the development of pulmonary hypertension. The true incidence is not known, but reported incidence in symptomatic patients is 0.3-0.5%, i.e. more than 50 times that in the general population. The precise pathogenesis is unknown. The stage of HIV infection is unrelated to the development and progression of pulmonary hypertension and it may predate the diagnosis of HIV disease. Found most commonly in young ♂. Progressive dyspnoea followed by ankle oedema are the usual presenting features. Diagnosed after excluding other causes, e.g. thrombo-embolism, talc granuloma (particularly in IDUs). Echocardiogram may show RV dilatation and right heart vascular studies may be required to confirm the diagnosis. The response to pulmonary vasodilator agents, antiretroviral drugs, and anticoagulation therapy is variable. The prognosis is poor compared with 1° pulmonary hypertension. Inconsistent reports of improvement with HAART.
Venous thrombosis
↑ risk of venous thromboembolic disease leading to deep venous thrombosis and consequently pulmonary embolism. Related to changes in coagulation (
Chapter 51, Haematological disorders p. [link]).
Cardiac neoplasia
Kaposi’s sarcoma
In autopsy studies, mostly ♂ who have sex with ♂ (MSM) incidence of cardiac KS prior to HAART was 12–28% (usually part of disseminated involvement). Typical cardiac sites are the visceral layer of serous pericardium or sub-epicardial fat (especially beside a major coronary artery). Clinical features are often negligible. May cause pericardial effusion which can produce cardiac tamponade requiring emergency paracentesis. If suspected, diagnosis can be confirmed by biopsy through a pericardial window which also provides decompression.
Non-Hodgkin’s lymphoma
Usually part of disseminated neoplasia rather than primary cardiac lymphoma (very rare). Typically high grade with spread often early in those with AIDS. Any heart chamber may be involved but right atrium is the most common. Usually no specific symptoms but may present with progressive congestive heart failure, pericardial effusion, cardiac arrhythmia, or cardiac tamponade. Nodular or polypoid lymphomas may appear, predominantly involving the pericardium with variable myocardial infiltration. Their removal may alleviate mechanical obstruction. Prognosis is poor, although clinical remission has been observed with combination chemotherapy.
Vascular disease
May be directly caused by HIV with infected monocytes and macrophages producing atheroma by adhesion or angiitis. HAART, especially containing protease inhibitors (PIs), except atazanavir, may cause hyperlipidaemia leading to atherosclerosis and thrombosis. Hyperlipidaemia is found to a lesser extent with the nucleoside/nucleotide reverse transcriptase inhibitors (especially stavudine) and the non-nucleoside reverse transcriptase inhibitors. Insulin resistance (associated with PIs) is an independent risk factor for myocardial infarction and death. The risk of myocardial infarction is ~3 times that of ♂ in the general population if PIs are used for ≥30 months. Abacavir and didanosine have also been associated with ↑ cardiovascular risk. Abacavir has been associated with a 1.9-fold increased risk from other NRTIs; this is enhanced in those with an already high cardiovascular risk. Other cardiovascular risk factors are important to consider, especially cigarette smoking as higher rates have been reported in MSM with HIV infection. Therefore advice on low-fat diets, regular exercise, blood pressure control, lipid-lowering drugs, and smoking cessation are important in patient care.