Reports of the prevalence of cardiac involvement in patients with AIDS vary from 28% to 73%, with the first case of myocardial KS, found at autopsy in 1983.
Since the introduction of ART, a sharp 
in mortality and morbidity has been observed. New risk factors for coronary heart disease such as increased insulin resistance, dyslipidaemia, and lipodystrophy syndrome, which can be associated with ART, may accelerate underlying arteriosclerosis in HIV-infected patients.
Prior to the introduction of ART, 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, Mycobacterium spp., Cryptococcus neoformans, CMV, tumours (lymphoma, KS). Clinically similar to non-HIV-infected patients, and although usually seen in advanced HIV infection, rarely causes death.
Pericardial aspiration, +/– biopsy may be needed, particularly if no other source of infection found, often culture negative. Should be sent for bacterial, fungal, and TB culture. Histology should be done and special staining for viruses, fungal, and TB carried out.
Treatment is of the underlying cause.
Prior to ART autopsy, evidence was found in 40–52% of those with AIDS, with a specific cause found in <20% (the most common being Toxoplasma gondii, Mycobacterium tuberculosis, Histoplasma and Cryptococcus neoformans). HIV alone can cause myocarditis, HIV or its proteins have been found in the myocardium of patients with or without cardiac disease.
Presents with chest pain and symptoms of cardiac dysfunction. May have abnormal ECG (T-wave inversion common or saddle-shaped ST elevation if associated with pericarditis) in the absence of ischaemic heart disease.
Myocardial biopsy may be indicated, especially if CD4 , severe dysfunction, and no other cause evident.
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 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). Consider drugs and alcohol. The patient will present with shortness of breath, persistent tachycardia, and signs of heart failure. Echocardiogram is of use in diagnosis. Myocardial biopsy may be indicated to identify a cause, but associated with mortality. The overall prognosis is poor.
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%, normally involving lungs, but if on left side, valves may involve the brain, spleen, kidneys, and coronary arteries. They are usually asymptomatic, but rarely may be fatal.
Occurs most commonly in PWIDs, usually affecting the tricuspid valve. The main causative organisms are Staphylococcus aureus (75%) and Streptococcus viridans (20%). Candida, and Aspergillus spp. may rarely cause endocarditis.
Usually presents with fever, sweats, weight loss, peripheral signs of endocarditis (splinter haemorrhages, Osler nodes, Janeway lesions, and Roth’s spots), and co-existing pneumonia (often necrotic with abscess formation), mycotic aneurysms and/or meningitis. A murmur is normally heard. Transthoracic echocardiogram is important, if negative may need to do transoesophageal echocardiogram to confirm diagnosis. 
Mortality in advanced HIV.
Treatment is with IV antibiotics, sensitive S. aureus 4–6 weeks IV flucloxacillin, S. viridans 2–4 weeks amoxicillin.
Chapter 45, ‘Pulmonary vascular disease’, pp. 537–538.
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%, × 50 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 pre-date 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 PWIDs). Echocardiogram may show right ventricular dilatation and right heart vascular studies may be required to confirm the diagnosis. The response to pulmonary vasodilator agents, and anticoagulation therapy is variable. The prognosis is poor compared with 1° pulmonary hypertension. Inconsistent reports of improvement with ART.
Risk of venous thromboembolic disease leading to deep venous thrombosis and consequently pulmonary embolism. Related to changes in coagulation (see Chapter 53, ‘Coagulation disorders’, p. 606).
In autopsy studies, mostly MSM incidence of cardiac KS prior to ART 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.
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 ART and combination chemotherapy.
May be directly caused by HIV with infected monocytes and macrophages, producing atheroma by adhesion or angiitis. There is also evidence of inflammation and T-cell changes leading to increased risk of atherosclerosis, elite controllers of HIV have higher rate of coronary artery plaques than HIV –ve. PLWH on average are more likely to have risk factors for cardiovascular disease, including smoking, hypertension, and dyslipidaemia. Co-infection with HCV increases risk of cardiovascular disease.
Overall the risk of MI is ×2 among HIV +ve vs HIV –ve population. This risk is increased in those with CD4 <200 cells/µl and may not be significantly increased in those with well-preserved CD4 counts. The risk of stroke is also increased.
ART, especially containing 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 MI and death. Although abacavir was implicated in early cohort studies large meta-analysis are less supportive of this. Overall, ART leads to reduced risk of MI and benefits outweigh risk associated with higher lipid levels. ART treatment interruption appears to risk probably through inflammatory mechanisms.
Other cardiovascular risk factors are important to consider, especially cigarette smoking as higher rates have been reported in MSM with HIV infection. Advice on low-fat diets, regular exercise, BP control, lipid-lowering drugs, and smoking cessation are important in patient care (see Chapter 49, ‘Metabolic disorders’, pp. 576–579).
Cardiomyopathy may be caused by zidovudine (also myocarditis), doxorubicin, amphotericin B, and foscarnet, dysrhythmias by ganciclovir and interferon alfa α, and conduction defects by co-trimoxazole, pentamidine, and pyrimethamine.