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Ovid: Oxford Handbook of Genitourinary Medicine, HIV, and Aids

Editors: Pattman, Richard; Snow, Michael; Handy, Pauline; Sankar, K. Nathan; Elawad, Babiker Title: Oxford Handbook of Genitourinary Medicine, HIV, and Aids, 1st Edition Copyright ©2005 Oxford University Press > Table of Contents > HIV/AIDS > Chapter 49 – HIV: cardiovascular disorders Chapter 49 HIV: cardiovascular disorders P.478
Introduction Reports of the prevalence of cardiac involvement in patients with AIDS vary from 28–73%, with the first case, myocardial Kaposi’s sarcoma (KS) found at autopsy in 1983. With HAART, cardiac manifestations directly related to HIV have fallen although ↑ cardiovascular problems related to drug side-effects are anticipated. Pericardial effusion Found in about 20% with AIDS. Often small with no haemodynamic consequences, although if large may cause tamponade. Associated with low CD4 count and reported causes include bacteria, especiallyMycobacterium spp., Cryptococcus neoformans, cytomegalovirus, tumours (lymphoma, KS) and multiple unusual organisms. 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. Dilated cardiomyopathy Prevalence in patients with AIDS is 10–30% by echocardiographic and autopsy studies. Associated with advanced disease, low CD4 counts and myocarditis, which may act as a trigger. Several studies have supported a direct role for HIV-1 causing cardiac injury, but the mechanism remains unclear. It may be related to co-infection with cytomegalovirus, coxsackievirus group B, or Epstein–Barr virus. 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, hyper-coagulable 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 though 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, and coexisting pneumonia and/or meningitis with increased mortality in advanced HIV disease in comparison to asymptomatic infection. P.479
Pulmonary hypertension HIV is an independent risk factor for the development of pulmonary hypertension. 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). The response to pulmonary vasodilator agents, antiretroviral drugs, and anticoagulation therapy is variable. Venous thrombosis ↑ risk of venous thrombo-embolic disease leading to deep venous thrombosis and consequently pulmonary embolism. Related to changes in coagulation (see p. 495). Cardiac neoplasia Kaposi’s sarcoma In autopsy studies (mostly homosexual ♂) 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 subepicardial 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. 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), all 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 P.481
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. Other cardiovascular risk factors are important to consider, especially cigarette smoking as higher rates have been reported in homosexual and bisexual men 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. Drug associated Cardiomyopathy may be caused by zidovudine (also myocarditis), doxorubicin, amphotericin B, and foscarnet; dysrhythmias by ganciclovir and α-interferon; conduction defects by co-trimoxazole, pentamidine, and pyrimethamine.

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