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Table of Contents
REVIEW ARTICLE
Year : 2020  |  Volume : 10  |  Issue : 2  |  Page : 50-55

Heart failure with reduced ejection fraction in people living with human immunodeficiency virus/acquired immunodeficiency syndrome


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

Date of Submission15-Mar-2020
Date of Acceptance08-Apr-2020
Date of Web Publication25-Sep-2020

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


DOI: 10.4103/JICC.JICC_9_20

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  Abstract 


Heart failure is one of those complications of HIV/ AIDS, whose epidemiology has changed grossly after the widespread use of HAART. HIV DCM is multifactorial is the origin. The systolic heart failure can be having an ischemic etiology, or it may be non- ischemic in origin. HIV/ AIDS is no longer considered a contraindication for cardiac transplantation.

Keywords: Dilated cardiomyopathy, heart failure with reduced ejection fraction, human immunodeficiency virus/acquired immunodeficiency


How to cite this article:
Singh S, Singh K. Heart failure with reduced ejection fraction in people living with human immunodeficiency virus/acquired immunodeficiency syndrome. J Indian coll cardiol 2020;10:50-5

How to cite this URL:
Singh S, Singh K. Heart failure with reduced ejection fraction in people living with human immunodeficiency virus/acquired immunodeficiency syndrome. J Indian coll cardiol [serial online] 2020 [cited 2020 Oct 27];10:50-5. Available from: https://www.joicc.org/text.asp?2020/10/2/50/296126




  Introduction Top


Since its discovery, human immunodeficiency virus (HIV) has been surprising us with its various presentations. It is still difficult to manage the disease, when its systemic complications and opportunistic infections have set in. Although there have been remarkable improvements in the diagnosis, prevention, and treatment of the ailments associated with HIV, it can still pose challenge to the treating physician and the patient.

Heart failure (HF) is one of those complications of HIV/acquired immunodeficiency syndrome (HIV/AIDS), whose epidemiology has changed grossly after the widespread use of highly active antiretroviral therapy (HAART). Before the HAART era, it was the most common cardiac complication seen in patients who have HIV/AIDS. HF with reduced ejection fraction (EF) was the most common phenotype back then. As HAART came in, the vast majority of complications which culminated in end-stage heart disease in the form of significant systolic dysfunction declined. The patients who have HIV/AIDS now have HF with preserved EF more commonly.

However, despite these advances in treatment, systolic HF is still a relevant entity affecting patients with HIV/AIDS.[1]

Moreover, the prevalence of HF increases with age, and the highly effective treatment of HIV/AIDS has now enabled these patients to live long enough to suffer from noninfectious diseases.

HF with reduced EF is more difficult to diagnose and treat in HIV/AIDS patients compared to the general population. The reason for this is simple, HIV/AIDS patients may be affected by many entities such as pneumocystis pneumonia, mycobacteria and atypical mycobacteria, or interstitial pneumonia which may be confused with congestive cardiac failure because of the overlapping clinical and radiological appearance.


  Etiology Top


Literature suggests that the HIV dilated cardiomyopathy (DCM) is multifactorial in origin. Systolic HF can be having an ischemic etiology, or it may be nonischemic in origin. The ischemic systolic dysfunction results from accelerated atherosclerosis, increased predisposition to myocardial infarction, cocaine abuse and atherogenic dyslipidemia which is often seen in patients with HIV/AIDS.

The nonischemic causes of systolic dysfunction include opportunistic infections, micronutrient deficiency, autoimmunity, and inflammation.[2],[3]

Direct viral infection

Although controversial, this mode of cardiac affliction has been suggested by recent literature. Previously, the direct role of virus in causing cardiomyopathy was not established. HIV has been found to be a risk factor for the development of HF.[4],[5]

Ongoing viral replication is associated with a higher risk of developing HF.[5]

Inflammation

Inflammation is an important culprit in the pathogenesis of cardiac failure.[6]

Chronic HIV infection results in a persistent inflammatory state which can accentuate cardiovascular disease.[7] The increasing usage of cardiac magnetic resonance imaging has led to document subclinical inflammation in apparently asymptomatic patients.[8],[9]

Other studies have found elevated levels of inflammatory markers such as interleukin (IL)-6, high-sensitivity-C-reactive protein (CRP), and D-dimer in HIV patients who developed cardiovascular disease.[10],[11]

Myocarditis

Myocarditis ultimately culminating into DCM may be one of the possible explanations for the origin of HF in HIV patients. In 19 consecutively admitted patients with HIV/AIDS, nonspecific myocarditis was found in 9 patients on endomyocardial biopsy (EMB).[12] HIV-associated myocarditis has also been demonstrated in CMR studies.[13]

Cardiotropic viral infection

Viral myocarditis can be seen in HIV/AIDS patients with low CD4 + T cell count. It can complicate and present as DCM and HF. Various studies have shown the infection with cardiotropic viruses in cases presenting as acute myocarditis.[14],[15]

Autoimmune mechanisms

Autoimmunity can also cause myocardial injury by the production of pro-inflammatory cytokines.[16] AIDS is a state of immune dysregulation, which is characterized by overproduction of autoantibodies.[17] Making a diagnosis of autoimmune myocarditis has prognostic implications as it is a potentially reversible cause of HF. Frustaci et al. have described a case of biopsy-proven autoimmune myocarditis; steroid administration led to complete recovery of left ventricular cardiac functions.[18]

Antiretroviral therapy-induced myocardial damage

HAART may itself cause myocardial injury.[19] Zidovudine has been found to cause myocardial damage.[20] Similarly, in another retrospective study of close to 400 seropositive patients with HF, it was found that patients on protease inhibitors had higher cardiovascular mortality and recurrent hospitalization for HF.[21] Protease inhibitors have been found to cause myocardial infarction thereby leading to ischaemic left ventricular systolic dysfunction.[22],[23],[24]

Accelerated atherosclerosis and resultant ischemia

It is a well-known fact that HIV infection leads to accelerated atherosclerosis and coronary artery disease. Systolic dysfunction can result from coronary artery disease.[25]

Substance abuse

It has been shown that people living with HIV/AIDS are more likely to have a current or history of tobacco, alcohol, cocaine, heroin, marijuana, or amphetamine abuse than the general population.[26]

Selenium deficiency

There are reports of cardiomyopathy because of selenium deficiency.[27] People living with HIV/AIDS have been found to harbor selenium deficiency.[28] Selenium deficiency should be corrected in such cases.

Sepsis

People living with HIV/AIDS may have sepsis, which, in turn, may be responsible for cardiac dysfunction.[29]


  Clinical Presentation Top


Dyspnea, fatigue, orthopnea, and paroxysmal nocturnal dyspnea are common clinical manifestations. Patients may also complain of right hypochondrial pain because of liver congestion. Systemic examination reveals tachycardias, tachypnea, peripheral edema, cyanosis, raised jugular venous pressure, positive hepatojugular reflex, and a third heart sound.

Current data suggest that patients with high viral load and low CD4+ T cell count are more likely to develop HF.[30]


  Prognosis Top


With the increasing use of HAART, the prognosis of HF has changed dramatically in the past couple of decades. In the pre-HAART era, mortality due to HF was very high. Currie et al., in a pre-HAART era paper, remarked that patients with DCM died earlier than patients without cardiomyopathy because of conditions related to AIDS.[31]

In the past few years, not only there has been an improvement in HAART leading to improvement in the quality of life and lifespan in people living with HIV/AIDS, but also there has been remarkable growth regarding treatment options for HF; the mortality in people living with HIV/AIDS with HF may not be as high as reported in older studies.[32]


  Investigations Top


Cardiac biomarkers

Various cardiac biomarkers can be used in suspected or proven cases of HF. These biomarkers can help in diagnosing, guiding treatment, and prognostication in cases with HF.

Brain natriuretic peptide (BNP) is an inexpensive, one of the most commonly used biomarkers for the assessment of patients with HF. It is released from cardiac myocytes in response to stretch. BNP-level assessment can not only diagnose HF, but it also gives an idea about the severity of the disease and its prognosis.

Neumann et al. studied 802 patients using echocardiography and BNP levels and found that BNP was suitable for the detection of cardiac diseases in people living with HIV/AIDS. In their study, the people who had elevated levels of BNP were likely to be having coronary artery disease, cardiomyopathy, or cardiac failure.[33]

Another study done on HIV-positive patients found a negative correlation between BNP levels and left ventricular systolic functions, like in the general population.[34]

Schuster et al.[35] assessed NT-proBNP levels in the serum of 219 people living with HIV/AIDS without any cardiac or renal disease, not on any HAART regimen, and found that the levels of NT-proBNP negatively correlated with CD4 + T-cell count and positively with viral load, indicating that higher NT-proBNP was able to detect subclinical myocardial damage.

Other studies have resonated the idea of prognostication using natriuretic peptides in people living with HIV/AIDS with HF.[36]

Besides natriuretic peptides, other biomarkers can be useful in prognostication in patients with HF. These include markers of remodeling and inflammation, i.e., CRP, tumor necrosis factor (TNF)-α, Fas, soluble TNF receptors, and ILs (1, 6, and 18). These biomarkers have been evaluated for people living with HIV/AIDS.[37],[38]

Echocardiography

Echocardiography is the cornerstone of evaluation of patients with HF. Various parameters such as left ventricular dimensions and measures of systolic functions can be obtained using echocardiography. Global or regional wall motion abnormalities characteristic of dilated and ischemic cardiomyopathy can be seen. The evidence of back pressure changes due to HF in the form of raised pulmonary arterial systolic pressure can be seen.

Left ventricular EF, which gives significant prognostic information and plays a vital role in selecting patients for device therapy, can be calculated by various methods, including M-mode, 2D, and 3D methods. Any value <50% is considered subnormal.

The novel methods of deformation imaging, i.e., tissue Doppler imaging and speckle tracking, can also help in the detection of subclinical systolic dysfunction.[39],[40],[41]

Cardiac magnetic imaging

CMR is the gold standard imaging modality for the evaluation of left ventricular size and functions. Although costlier than echocardiography and less commonly available in the developing countries, it offers multiple advantages over echocardiography in the assessment of patients. Whenever possible, it should be considered for providing information about ventricular morphology, etiology, and prognosis of HF. CMR in the setting of HF due to coronary artery disease can help in identifying the viable myocardium, i.e., the myocardium which may be stunned or hibernating due to ischemia and can be salvaged with revascularization. It can also diagnose acute myocarditis by looking at the myocardial edema and epicardial and midwall late gadolinium enhancement involving inferolateral wall or septum. It can also help in suspected cases of Chagas' disease. A study found that CMR was able to identify the cardiac pathologies in the majority of people living with HIV/AIDS having elevated BNP levels.[42] Studies have found that even those patients who are asymptomatic have underlying myocardial inflammation, implying that it can help in identifying those patients who will go on to develop left ventricular dysfunction in future.[8],[9],[43] The other markers of remodeling, such as soluble ST2, a marker of fibrosis, and GDF-1, a marker of apoptosis, have been studied in people living with HIV/AIDS.

Endomyocardial biopsy

EMB is reserved for patients who are suspected to be suffering from a disease which requires particular treatment and in whom casual diagnosis cannot be confirmed by traditional noninvasive diagnostic means. It helps in picking up cases suspected of having myocarditis. The drawback of EMB is its invasive nature and chances of missing the area involved in the disease process, for example, myocarditis may not affect the heart in its entirety, hence may be missed in the sampling. Besides, in the context of people living with HIV/AIDS, the procedure is not performed because of low yield and the risk of exposure to health-care workers.[44] The potential advantage of performing an EMB is the identification of the subset of patients who might benefit from the immunotherapy in the form of steroids and intravenous immunoglobulin (IVIg).


  Management Top


Highly active antiretroviral therapy

The widespread use of HAART in the management of HIV/AIDS patients has improved the outcome in patients with DCM. Studies have reported that there has been a decrease in the prevalence of HIV-associated DCM by approximately 30%.[45],[46]

The decline in the number of patients suffering from HIV-associated DCM is because the initiation of HAART in immunocompromised patients prevents myocarditis from occurring. Even if myocarditis has set it, HAART improves the immune status and opportunistic infections which can cause myocarditis.

Besides controlling the opportunistic infections, HAART also improves the chronic inflammation which is present in patients living with HIV/AIDS and is hypothesized to be the culprit in the causation of left ventricular systolic dysfunction.[47]

That HIV is a state of immune dysregulation and is characterized by multiple autoimmune disorders is a known fact. The dysregulated autoimmunity is regarded as one of the underlying mechanisms behind the causation of DCM. Numerous studies have shown that HAART improves immune dysfunction.[48]

Antifailure drugs

Patients with DCM due to HIV/AIDS should receive guideline-directed medical therapy (GDMT) for the management of HF.[49],[50],[51]

A study has shown that people living with HIV/AIDS were less likely to receive diuretics, disease-modifying agents (angiotensin-converting-enzyme inhibitor/angiotensin II receptor blockers [ACE/ARB], beta-blockers), statins, and antiplatelet agents compared to their HIV-negative counterparts.[52]

All the patients should receive angiotensin receptor-neprilysin inhibitor (ARNI)/ACE inhibitor/ARBs along with maximally tolerated doses of either of the three beta-blockers, namely, carvedilol, metoprolol succinate, and bisoprolol. The first ARNI which has been made commercially available is valsartan with sacubitril (1:1 mixture). The ACE inhibitors which have been studied for use in HF include enalapril, captopril, ramipril, and trandolapril. The ARBs extensively studied in HF patients include valsartan, candesartan, and losartan.

Keeping a watch over kidney function test and serum potassium, a mineralocorticoid-receptor antagonist (MRA) such as spironolactone and eplerenone should be added. Loop diuretics should be used for the relief of pulmonary congestion and in cases of decompensation of HF. Ivabradine has been a new addition to the armamentarium in the management of HF. Digoxin has fallen out of favor in the management of HF due to recent advances in the field.

Few drug interactions should be kept in mind while initiating antifailure measures in patients who are receiving HAART. Ivabradine should not be used with protease inhibitors such as ritonavir as the latter can cause cytochrome P450 3A4 enzyme inhibition, increasing the levels of former, leading to excessive sinus bradycardia. Similarly, the patients who are already on protease inhibitors, which require digoxin for the management of HF, should have serum digoxin levels monitored, and the physician should watch for signs of digoxin toxicity.[53]

Statins

Statins have proven to be the magic bullets for the management of cardiovascular diseases. The use of statin in HF is controversial. There is some evidence of benefit from statins in HF with preserved ejection.[54] However, there is insufficient evidence of benefit from statins in HF with reduced EF.[55],[56],[57] As far as the people living with HIV/AIDS with systolic HF on HAART are concerned, some data are justifying the use of statins. The SATURN-HIV trial found that 10 mg of rosuvastatin caused a significant reduction in the levels of NT-proBNP compared to placebo.[58]

Role of immunotherapy

Some authors have used IVIg in the management of HF associated with HIV. Patients who develop DCM as a result of myocarditis benefit from the use of Ig.[59],[60]

Today, the prevalence of HF due to myocarditis is not as common as in the pre-HAART era, so the administration of Ig should be restricted to patients with documented evidence of myocarditis.

Implantable cardioverter-defibrillator in HIV-associated heart failure

Implantable cardioverter-defibrillator (ICD) should be considered for the primary prevention of sudden cardiac death in patients with moderate-to-severe left ventricular dysfunction (EF <30%–35%) and NYHA Class II functional status or worse, with expected survival for at least 1 year. Patients who continue to have depressed EF despite getting GDMT in the form of ARNI/ACEI/ARB with the maximally tolerated beta-blocker, along with an MRA, deserve an ICD. Cardiac resynchronization therapy is recommended for patients in sinus rhythm with wide QRS complex with symptomatic systolic HF (EF <30%–35%).

Howsoever glorified the use of device therapy is in patients with HF, it has been underutilized in people living with HIV/AIDS. Economy is a barrier to access to the device therapy in patients who come from poor socioeconomic background and who are already burdened by the expense of pharmacotherapy.

It has been seen that patients with seropositive status are more likely to have an ICD discharge rate, which is probably due to higher chances of having a positive history of cocaine use and coronary artery disease, compared to a seronegative patient with DCM.[61]

Role of mechanical circulatory support

Mechanical circulatory support devices are mechanical pumps which either assist or replace the function of either or both ventricles. Left ventricular assist devices (LVADs) are used in patients in refractory HF, either as bridge to recovery (BTR), for patients in refractory HF with a reversible etiology; as bridge to transplantation (BTT), for patients with HF with no chances of improvement in left ventricular functions; and as destination therapy (DT) for those with refractory symptoms and ineligibility for transplantation. Studies have shown that both left ventricular assist devices and cardiac transplantation are less commonly used for patients living with HIV/AIDS.[62] LVADs have been used successfully as BTR,[63] BTT,[64],[65] DT.[66]

Cardiac transplantation

The definitive treatment for refractory or end-stage HF is cardiac transplantation. It is offered to patients who have failed medical and interventional therapy and are symptomatic. Allocation is done on a priority basis; those at highest risk of dying are prioritized to receive it earlier. Previously, like all other transplants, HIV/AIDS was considered to be a contraindication for cardiac transplantation. Given the contemporary data,[67],[68],[69] HIV/AIDS is no longer considered a contraindication for cardiac transplantation by the International Society for Heart and Lung Transplantation.[70],[71]

Chen et al.[67] have reported the most extensive series of cardiac transplantation in 35 patients with HIV/AIDS and found no difference in patients' survival and graft survival between HIV-positive and -negative patients.

Two issues, which were like a roadblock to cardiac transplantation in people living with HIV/AIDS are, first, the need for posttransplantation immunosuppression in a patient who is already immunocompromised, and the second is the potential pharmacokinetic interaction between immunosuppressants and enzyme-inducing Non-nucleoside reverse transcriptase inhibitor (NNRTI), for example, efavirenz, which can lead to failure of immunosuppression.

Agüero et al. had suggested that heart transplantation should be considered only for patients who have an undetectable viral load, CD4+ cell count >200, and have been stable on HAART for >1 year. History suggestive of AIDS-defining diagnosis and presence of opportunistic infections preludes the use of cardiac transplantation in this subset of patients.[72]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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