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Table of Contents
Year : 2020  |  Volume : 10  |  Issue : 2  |  Page : 43-49

Cardiovascular abnormalities in people living with HIV/AIDS

1 Department of Cardiology, Fortis Escorts Heart Institute, New Delhi, India
2 Department of Paediatrics, Lal Bahadur Shastri Hospital, New Delhi, India

Date of Submission13-Nov-2019
Date of Decision27-Dec-2019
Date of Acceptance27-Dec-2019
Date of Web Publication25-Sep-2020

Correspondence Address:
Dr. Shailesh Singh
M-429, Ashiana Colony, Lucknow - 226 012, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_47_19

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HIV/ AIDS affects the heart late in the course of the disease. Many of these complications arise not because of the disease but because of the treatment of the disease itself. The various complications which may be seen include left ventricular systolic dysfunction, accelerated atherosclerosis, leading to coronary artery disease, and stroke, infective endocarditis, and pulmonary hypertension.

Keywords: Coronary artery disease, HIV/AIDS, infective endocarditis, pulmonary hypertension, stroke, systolic dysfunction

How to cite this article:
Singh S, Singh K. Cardiovascular abnormalities in people living with HIV/AIDS. J Indian coll cardiol 2020;10:43-9

How to cite this URL:
Singh S, Singh K. Cardiovascular abnormalities in people living with HIV/AIDS. J Indian coll cardiol [serial online] 2020 [cited 2021 Dec 6];10:43-9. Available from:

  Introduction Top

HIV/AIDS affects the heart late in the course of the disease. Many of these complications arise not just because of the disease but also secondary to the treatment of the disease itself. In the pre highly active antiretroviral therapy (HAART) era, people living with HIV/AIDS (PLHA) had a poor quality of life and significantly high mortality because of the various opportunistic infections and malignancies. Over the last few decades, there have been advances in the way we diagnose and treat this illness as well as the various opportunistic infections and malignancies associated with it leading to significant reductions in morbidity and mortality rates. As the mortality due to infections has declined, the average lifespan of PLHA has increased resulting in increased mortality attributable to acquired heart diseases.[1] The time is not far away when acquired cardiovascular diseases (CVDs) will be the most common cause of death in PLHA in developing countries also.

The reduction in mortality and prevention of infectious diseases because of HAART has not come without a cost. The metabolic abnormalities resulting from the use of the HAART are implicated in pathogenesis for atherosclerotic CVDs.[2] With the use of HAART getting increasingly aggressive because of the lower threshold of HAART initiation, adverse cardiovascular effects of the drugs are expected to increase.

Various studies have studied the prevalence of cardiac complications in HIV-infected adults and children. Recent studies have found that the use of HAART has not only changed the prevalence of cardiac complications but has also changed the manner in which the heart is involved in the disease. In the preantiretroviral therapy (ART) era, dilated cardiomyopathy was said to be the most common cardiac disease in PLHA; however, the incidence and prevalence of dilated cardiomyopathy has decreased with the increasing use of HAART. A recent study done in North India reported that approximately 24% of patients had a cardiac abnormality. Left ventricular diastolic dysfunction was the most common abnormality, which was seen in 22% of total patients. Only 12% of patients had dilated cardiomyopathy.[3] Studies have also shown that PLHA develop myocardial infarction at a younger age than the general population.[4] Patients are also prone to develop atherosclerotic cerebrovascular disease because of the same risk factors.[5]

In this article, we will discuss common cardiovascular complications of HIV.

  Coronary Artery Disease and Myocardial Infarction in HIV Top

Multiple studies have proved the fact that PLHA are plagued by accelerated atherosclerosis. There are multiple causes of accelerated atherosclerosis in PLHA. The PLHA are more likely to have a history of alcoholism, smoking, and cocaine consumption. Besides these traditional risk factors, the role of chronic inflammation, drug-induced metabolic abnormalities such as dysglycemia and dyslipidemia, direct vascular injury by HIV itself has been implicated.

Atherosclerosis is no longer considered to be a deposition disease. It has been proven to be an inflammatory disease.[6],[7],[8],[9] Pro-inflammatory cytokines, for example, tumour necrosis factor-α and interleukin-1 and chronic mononuclear inflammatory cells have been found to be increased in atherosclerosis.[6],[9]

The lower the CD4+ T-cell count of the patient, the greater the likelihood of having an inflammatory state. In the HIV outpatient study, CD4 cell count ≤500 cells/mm 3 was found to be an independent risk factor for incident CVD.[10]

Coagulation abnormalities have been found in HIV. HIV has been considered to be a hypercoagulable condition by many authors, which, can lead to atherosclerotic cardiovascular and cerebrovascular diseases.[11]

HAART may also increase cardiovascular risk. Studies have found that some antiretroviral agents can cause diabetes and dyslipidemia resulting in increased cardiovascular risk.[12]

Some of the patients, especially those who belong to low- middle-income countries, who have been initiated on HAART develop lipodystrophy syndrome. It is characterized by a redistribution of fat, i.e., lipohypertrophy leading to centripetal obesity and lipoatrophy over face and extremities. Insulin resistance and dyslipidemia are seen in the majority of these patients. Various agents used in HAART regimes can result in various types of lipid abnormalities, some can cause elevation of total cholesterol and low-density lipoprotein (LDL), some can alter the levels of HDL, whereas some can cause hypertriglyceridemia.[13],[14] The role of elevated triglycerides in atherosclerosis has been a matter of debate until recently.[15]

The Data Collection on Adverse events of Anti-HIV Drugs (D:A:D) Study, done in over 25,000 patients infected with HIV-1, pointed out that HAART is associated with an increased risk of myocardial infarction. Patients exposed to HAART had a 26reater rate of myocardial infarction, compared to those who were not exposed. The risk increased with increasing duration of exposure to HAART.[16],[17] Studies have found abacavir and didanosine to be associated with higher risk of myocardial infarction, whereas other nucleoside reverse transcriptase inhibitors (NRTIs) like zidovudine, tenofovir, stavudine and lamivudine or the non-NRTIs (NNRTIs) like nevirapine, efavirenz were not found to be associated with myocardial infarction (MI).[17]

The association between protease inhibitors and myocardial infarction can be attributed to the vast number of metabolic complications of the drug group. Among the antiretrovirals, the highest incidence of dyslipidemia has been reported with protease inhibitors. Protease inhibitors [17],[18] can lead to marked elevation of triglycerides and total cholesterol and LDL cholesterol levels. Different protease inhibitors have different effects on lipids. Ritonavir has the worst effect on lipids profile, whereas indinavir or nelfinavir can only cause a modest increase in total cholesterol levels with no significant change in triglycerides. On the other hand, elevation of cholesterol levels is not seen with saquinavir.

Efavirenz, an NNRTI, can lead to elevation of triglycerides and total cholesterol levels. Among the NRTIs stavudine is most notorious for causing dyslipidemia, it can lead to significant elevation of triglycerides and total cholesterol and LDL cholesterol levels. Zidovudine can also lead to elevated total cholesterol and LDL cholesterol.

Other NRTI, for example, tenofovir, abacavir, and lamivudine do not cause much changes in lipid profile.[19],[20]

Abacavir does not cause dysglycemia or dyslipidemia; still, it has been found to be associated with an increased risk of CVD. Studies have found that abacavir increased the risk of CVDs, probably by causing vascular inflammation.[20] The newer groups such as the CCR5 inhibitor (Maraviroc) and Integrase inhibitors (Raltegravir) have relatively neutral effects on lipid profile.[19],[20]

  Screening and Management of Coronary Artery Disease Top

As in the general population, the risk of coronary artery disease (CAD) in PLHA can be estimated using the Framingham Risk Assessment score. The D:A:D risk calculator has been designed especially for PLHA.[21]

PLHA presenting with an acute myocardial infarction should receive guideline-directed medical, interventional and surgical management.[22],[23]

However, screening the patients for silent CAD is challenging. Stress testing in the form of exercise stress test, stress echocardiography or direct visualization of ischemia by stress nuclear imaging may be done in high-risk cases. All patients should have a periodic assessment of lipids. Statins may be considered for primary prevention of atherosclerotic CVDs. There has been an increasingly important role for CT angiography and coronary artery calcium score in the assessment of CAD.[24]

  Left Ventricular Systolic Dysfunction Top

Left ventricular systolic dysfunction in PLHA can be because of ischemic cardiomyopathy or nonischemic dilated cardiomyopathy. Both of these have a similar clinical presentation. Patients present with a history of dyspnea on exertion, orthopnea or paroxysmal nocturnal dyspnea. Clinical examination may reveal pulsus alternans, bilateral basal crepitations, and third heart sound. Ischemic left ventricular dysfunction occurs because of accelerated atherosclerosis as already discussed above.

Studies have found that approximately 12%–23% patients develop left ventricular systolic dysfunction in patients who have HIV/AIDS.[3],[25],[26] A vast majority of HIV/AIDS patients who develop nonischemic dilated cardiomyopathy have a CD4+ T cell counts <100. Studies have confirmed this association.[3],[27] However, with use of HAART getting more rampant, this once most common cardiac affliction in HIV/AIDS patients has decreased in frequency.[27]

Various theories have been proposed to explain the etiopathogenesis of HIV/AIDS-associated nonischaemic left ventricular dysfunction. It has been postulated that left ventricular systolic dysfunction in PLHA can result from a direct effect of HIV on myocardium, viral myocarditis (due to viruses like Epstein-Barr virus, cytomegalovirus [CMV], adenovirus, coxsackievirus) or nutritional deficiencies (selenium), drug-induced injury (zidovudine, cardiotoxic anticancer agents used for opportunistic Infection), injury due to illicit drugs such as cocaine, chronic inflammation, or autoimmunity.

  Management Top

Evaluation of Patient with HIV/AIDS presenting with heart failure should include both noninvasive as well as invasive tests. The noninvasive investigations include hematological profiling as well as blood biochemistry (kidney function tests, liver function tests, serum electrolytes, biomarkers of heart failure, i.e., B-type natriuretic peptide [BNP], N-terminal pro BNP ), X-ray chest, electrocardiogram, and echocardiography. Not only are these investigations useful in diagnosing the problem; they also help in prognostication of the illness. The higher the value of natriuretic peptides, the poorer the long-term prognosis. Similarly, a lower ejection fraction indicates a higher chance of recurrent hospitalization and poor outcomes. In selected patients, cardiac magnetic resonance imaging maybe useful for assessing the extent and etiology of left the ventricular systolic function. Further invasive investigations include coronary angiography to rule out an ischemic etiology of heart failure, and endomyocardial biopsy.

PLHA with systolic dysfunction should be prescribed guideline-directed medical therapy, which should include a diuretic, either an angiotensin-converting enzyme inhibitors or aldosterone receptor blockers or angiotensin receptor/neprilysin inhibitors along with maximally tolerated doses of either of three beta-blockers, i.e., metoprolol succinate, carvedilol or bisoprolol. A mineralocorticoid should be added to the treatment regimen while keeping a watch over kidney functions and serum potassium. Addition of digoxin may benefit selected patients. Nutritional supplementation should be ensured. Infectious causes of heart failure should be treated aggressively. Patients should be considered for device therapy, in the form of an automated implantable cardioverter defibrillator and cardiac resynchronization therapy for advanced heart failure. Left ventricular assist devices and cardiac transplantation should be offered for cases with resistant heart failure.[28],[29],[30]

  Prognosis Top

The severe systolic dysfunction that was a hallmark of pre-ART HIV-associated cardiomyopathy carried a grim prognosis.[26],[31],[32],[33],[34],[35],[36] HAART has not only changed the epidemiology of the disease but also, it is short-term and long-term prognosis.[34]

  Left Ventricular Diastolic Dysfunction Top

Studies have found that left ventricular diastolic dysfunction can be seen in patients with hypertension, obesity, CAD, old myocardial infarction, and cardiomyopathies; diabetes; and systolic dysfunction. The prevalence of diastolic dysfunction increases with increasing age. The increased susceptibility to ischemia due to accelerated atherosclerosis and systolic dysfunction are also responsible for relaxation abnormality of left ventricle.[37],[38]

Left ventricular diastolic dysfunction is seen in a large number of with HIV/AIDS, the number of which is still rising because of an increasing lifespan. Studies have also found that because of higher chances of smoking and myocardial infarction in PLHA, left ventricular diastolic dysfunction may be more prevalent in PLHA.[39]

Longer duration of infection with HIV has also been implicated in the pathogenesis of left ventricular diastolic dysfunction.[40] An increase in left ventricular mass index seen in patients of HIV/AIDS may indicate an underlying diastolic dysfunction. It is also possible that HIV or other associated viral infection may directly affect the myocardium.[41],[42] Studies have shown that the chronic inflammatory state which is seen in PLHA can also predispose the patient to diastolic dysfunction.[43] An association between advanced immunodeficiency and diastolic dysfunction has been reported in some studies.[39],[42] Few studies have found an association between low CD4 + T-Cell count and left ventricular diastolic dysfunction.[39] Like most cardiac ailments, HAART is implicated in the pathogenesis of diastolic dysfunction. Drugs like zidovudine [41] and protease inhibitors [44] have been found to be associated with diastolic dysfunction.

  Pericardial Involvement in HIV/AIDS Top

Various types of pericardial disease may be seen in patients with HIV/AIDS; it may include effusions with or without cardiac tamponade or chronic constrictive pericarditis.

Pericardial effusion is a common cardiac manifestation of HIV/AIDS. Up to half of the patients had been found to have a pericardial effusion in the pre-HAART era. However, in contemporary studies, very few patients were found to have pericardial involvement.[3],[45] HIV infection should be suspected and ruled out whenever a young patient presents with pericardial effusion or tamponade.

Pericardial effusion in HIV/AIDS patients is multifactorial in origin. Opportunistic infections by many bacteria like Staphylococcus, Streptococcus, Mycobacterium; viruses like HSV, CMV; fungi like Cryptococcus and parasites like Toxoplasma have been found to be the causative organism. Opportunistic malignancies like lymphoma [46] and Kaposi's sarcoma [47] have also been found to cause a pericardial effusion. In some cases, pericardial effusion can be noninfective in origin, e.g., as a part of anasarca in advanced heart failure. Asit is caused by opportunistic infections and opportunistic malignancies; it is usually seen in patients with end-stage disease and those having a lower CD4+ T-cell count.

Because of the same reason the prevalence of pericardial effusion has declined in recent times after the widespread use of HAART. There is no apparent correlation between the clinical stage of HIV infection and severity of pericardial involvement.[48]

Patients with acute pericarditis may present with pleuritic chest pain which may radiate to the trapezius ridge, which worsens on assuming a supine position, along with dyspnea. A pericardial rub can be heard on auscultation. Patients with pericardial effusion may be completely asymptomatic in cases of gradually increasing pericardial collection including large effusions. In large effusions, the apex cannot be palpated, the left border of heart does not correspond to the cardiac apex on percussion, and the cardiac sounds may not be audible. Patients who develop cardiac tamponade have the classic Beck's triad, i.e., hypotension, muffled heart sounds, and raised jugular venous pressure.

Tubercular pericardial infection is worth mentioning separately. In developing countries, tuberculosis is very common. Patients with advanced immunodeficiency usually present with extrapulmonary tuberculosis. The tubercular affliction of the pericardium has been recognized as a complication seen in patients with very low CD4 + T cell count. Tubercular pericardial infection is usually secondary. The primary focus of the disease may be in the lungs, which may or may not clinically manifest. Tubercular pericardial infection may result in acute pericarditis, pericardial effusion which may be hemorrhagic, cardiac tamponade, or chronic constrictive pericarditis. Tubercular pericarditis or tubercular pericardial effusion can be a part of disseminated tuberculosis or miliary tuberculosis, both of which increase in prevalence as immunodeficiency worsens. Tubercular pericardial infection requires a high index of suspicion as the classical signs and symptoms of tuberculosis may not be present in the patients. Hemorrhagic tubercular pericardial effusion should be differentiated from malignant effusions. The chances of patients developing immune reconstitution inflammatory syndrome should be kept in mind while initiating antiretrovirals and anti-tubercular drugs. Nontubercular mycobacteria have also been implicated in pericardial effusion in PLHA.[49]

Electrocardiography can provide clues to the presence of pericardial disease. Low voltage complexes and PR depression can be seen. Echocardiography reveals the presence of an effusion and may give clues to the presence of tamponade. Pericardiocentesis with pericardial fluid analysis as well as pericardial biopsy should be carried out to find the infective or malignant cause of pericardial effusion. Patients may be considered for a pericardial window in case of large recurrent effusions. The studies have found that the presence of pericardial effusion is associated with increased mortality. However, in some patients, it has been found to resolve spontaneously.

  Arrhythmia Top

Patients with HIV/AIDS may develop arrhythmias like atrial fibrillation (AF) or flutter. Patients with HIV/AIDS may harbor one or more risk factors for AF like increased left ventricular mass, ischemic heart disease or myocardial infarction because of accelerated atherosclerosis, dilated cardiomyopathy, myocarditis, pericarditis, constrictive pericarditis, cardiac tumors, severe pulmonary hypertension (PH), centripetal obesity due to lipodystrophy, and persistent inflammatory state. Furthermore, PLHA are more likely to have a history of excessive alcohol intake (“holiday heart syndrome”). Studies have found the association between low CD P4+ T-cell count and increased risk of atrial fibrillation/ artial flutter (AF/AFL) among HIV+ persons.[50]

AF should be managed by rate-controlling drugs along with anticoagulation or by rhythm controlling agents. The drugs used for controlling the ventricular rate include atrioventricular node blocking agents like beta blockers, calcium channel blockers verapamil and diltiazem, digoxin, and amiodarone. The drugs usually used for anticoagulation in hospital settings include unfractionated heparin and low molecular weight heparin. Oral anticoagulants like Vitamin K antagonist, which include, warfarin and acenocoumarol may be prescribed to the patients on an outpatient basis with the advice to monitor the PT/INR. Recently, the rising use of direct oral anticoagulants (DOACs) like Apixaban, rivaroxaban, and dabigatran, has decreased the need for serial monitoring of coagulation profile. The commonly used drugs for rhythm control for AF include flecainide, dofetilide, propafenone, ibutilide or amiodarone. Patients with hemodynamic compromise and without a left atrial/left atrial appendage clot should be managed by direct-current cardioversion.

The optimal strategy for anticoagulation in the HIV-infected persons with AF is unknown. The threshold for anticoagulation based on CHA2DS2-VASc scores should be low. Studies have found that warfarin may be less effective in preventing thromboembolic events in PLHA with HIV/AIDS.[51]

Experience with DOACs in PLHA with AF/AFL is limited because of a smaller number of studies.[52] Potential drug–drug interactions should be kept in mind while prescribing them for patients receiving HAART.[53]

Patients may develop long QT syndrome because of multiple drugs being used for treatment and prophylaxis of opportunistic infections, like fluoroquinolones, trimethoprim-sulfamethoxazole, pentamidine, azole group of antifungals. Long QT may result in Torsades de pointes (TdP), a polymorphic ventricular tachycardia. Besides these drugs, ganciclovir has been implicated as a causative agent of ventricular tachycardia.[54]

For the management of ventricular tachycardia in the setting of a prolonged QT interval, anti-arrhythmic of Class IA, Class IC, and Class III should be avoided as it may lead to further prolongation of QT interval. IV magnesium sulfate is the treatment of choice for TdP. Direct-current cardioversion should be used in case of hemodynamic collapse.

  Pulmonary Artery Hypertension Top

PH is defined as mean pulmonary arterial pressure of more than or equal to 25 mm Hg at rest. PAH associated with HIV has been classified as Class 1 PH. Approximately 0.5% of HIV patients are affected by PAH. The incidence of PAH in HIV does not depend on the CD4+ cell count of the patients. Furthermore, unlike various other cardiac complications in PLHA, the PAH has not changed with the widespread use of HAART. The exact mechanism causing the elevated mean pulmonary artery pressure is unknown. PAH Possibly results from effects of HIV viral proteins, HIV induced immune activation, left ventricular Diastolic dysfunction.[55],[56]

Pathologic studies have revealed that plexogenic arteriopathy of the pulmonary vasculature is seen in the patients with HIV–PAH.

Clinically HIV-PAH presents with a history of dyspnea, fatigue and exercise intolerance. A history of syncope, distension of abdomen, and pedal edema are not uncommon. Physical examination may reveal, left parasternal heave, loud P2, right ventricular S4, and systolic ejection murmur at the pulmonary area and signs of right ventricular failure such as raised jugular venous pressure, hepatojugular reflex, tender hepatomegaly, ascites, and pedal edema.

A few differences exist between idiopathic PAH (IPAH) and HIV-PAH. Patients with HIV PAH are younger than those with IPAH. Studies have found that HIV-PAH carries a poorer prognosis than IPAH.[57],[58],[59]

Patients with HIV-PAH should be managed similarly to those with IPAH.[60] Patients should be given anticoagulation, and calcium channel blockers along with PH-specific therapy which includes sildenafil, bosentan or prostaglandin analogues. Potential drug interaction between ambrisentan and ritonavir should be kept in mind. Inhalational oxygen, Bilevel Positive Airway Pressure (BiPAP), or continuous positive airway pressure should be used in acute decompensation. Diuretics can be considered for right heart failure and volume overload.

  Infective Endocarditis Top

Infective endocarditis is defined as the formation of prototypic lesions, i.e., vegetations, which are made up of bacteria, inflammatory cells, fibrin and platelets on the endocardial surface of the heart, or the native or prosthetic heart valve or a congenital heart defect.

Infective endocarditis in patients with HIV/AIDS may be caused by bacteria like Staphylococcus aureus or Staphylococcus epidermidis, or Streptococcus.  Salmonella More Details endocarditis is unique to patients with HIV/AIDS. Fungi like Candida, Cryptococcus and Aspergillus have been found to cause infective endocarditis in PLHA. Fungal bloodstream infection and endocarditis has decreased in frequency after the widespread use of HAART and is now confined to the subset of patients with advanced immunodeficiency.[61] PLHA with a history of intravenous drug abuse are prone to develop right-sided infective endocarditis. A study found that in patients with mortality was increased in those patients with right-sided infective endocarditis who had HIV/AIDS and had lower CD4+ T cell count, a larger size of vegetations, and fungal etiology.[62]

Patients with infective endocarditis may clinically present with a history of fever, a new murmur or change in the character of preexisting murmur, and heart failure. Specific signs like Roth spots, Janeway lesions, splinter hemorrhages and Osler's node may be seen. Isolation of the organism by serial blood cultures and echocardiography form the cornerstone of the diagnostic workup of a case of infective endocarditis. Studies have been undertaken to evaluate if Dukes criteria have similar accuracy in diagnosing infective endocarditis in PLHA compared to HIV negative patients. It was found that the sensitivity and specificity of Duke's criteria did not differ with serostatus of the patients.[63]

The management of infective endocarditis in PLHA is not different from those with seronegative status. Patients should be aggressively managed with antibiotics, antifailure measure, and valve replacement should be considered.[64]

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