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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 9  |  Issue : 1  |  Page : 30-32

Acute myocardial infarction and HIV infection: A case-based review


1 Department of General Medicine, Sumandeep Vidyapeeth University, Vadodara, Gujarat, India
2 Department of Cardiology, Sumandeep Vidyapeeth University, Vadodara, Gujarat, India

Date of Submission24-Nov-2020
Date of Decision11-Feb-2021
Date of Acceptance11-Feb-2021
Date of Web Publication30-Apr-2021

Correspondence Address:
Dr. Rohit Dhanraj Chordiya
Dhiraj Hospital, SBKS Medical Institute and Research Center, Pipariya, Waghodia, Vadodara - 391 760, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jihs.jihs_33_20

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  Abstract 


Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) is a life-threatening condition. Cardiovascular (CV) complications are not uncommon and are one of the leading causes of death in patients suffering from this infection. This case report is of a patient, tested HIV positive who presented to the hospital with myocardial infarction (MI). The objective of this case review is to highlight CV complication such as MI in HIV/AIDS who did not have common cardiac risk factors such as diabetes mellitus, hypertension, or obesity. Acute MI may be presenting feature of HIV infection and may need timely intervention by combined specialist care.

Keywords: Acute myocardial infarction and human immunodeficiency virus, anterior wall myocardial infarction, antiretroviral therapy, cardiovascular diseases, risk factors for acute myocardial infarction


How to cite this article:
Chordiya RD, Lakhani JD, Mathew C. Acute myocardial infarction and HIV infection: A case-based review. J Integr Health Sci 2021;9:30-2

How to cite this URL:
Chordiya RD, Lakhani JD, Mathew C. Acute myocardial infarction and HIV infection: A case-based review. J Integr Health Sci [serial online] 2021 [cited 2021 Dec 6];9:30-2. Available from: https://www.jihs.in/text.asp?2021/9/1/30/315275




  Introduction Top


Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) has a devastating health effect globally; there are over 36 million people currently living with HIV. It accounts for over 39 million HIV/AIDS-related death, till date.[1] Due to antiretroviral therapy and preventive measures, HIV/AIDS is now considered as a chronic manageable disease.[2]

Cardiovascular disease (CVD) is one of the leading causes of death among the patient suffering from HIV/AIDS, but it is uncommon among younger population. Etiology of CVD in patients with HIV is complex, and possible explanation for CVD in HIV includes traditional risk factor such as dyslipidemia, hypertension, smoking, and metabolic syndrome.[3] In HIV, chronic immune activation also leads to acceleration in the process of atherosclerosis, thereby increasing the risk of myocardial infarction (MI).[4]

Here is a case report of acute coronary syndrome–anterior wall MI (AWMI) in a young HIV positive male without obvious risk factor for CVD.


  Case Report Top


A 38-year-old male was brought to the emergency department for substernal chest pain, palpitation and perspiration which was present for the last 2 h. There was no past history of hypertension or diabetes. He had Bell's palsy (infranuclear facial nerve involvement) 6 months ago and recovered within 1 month. He did not have any other significant past history. He was teetotaler and nonsmoker. His body mass index was 23 kg/m2 with no known cardiac risk factors. Electrocardiogram (ECG) was suggestive of acute extensive anterior wall myocardial infarction (AWMI), right bundle branch block (qRBBB) with ST elevation in the anterior leads and left anterior hemiblock [Figure 1]. Thrombolysis with streptokinase was done, and coronary angiogram (CAG) was planned. During pre-CAG workup, the patient turned out to be HIV positive. Bleeding time, clotting time, prothrombin time, activated partial thromboplatin time, and other tests for coagulation profile were normal. He was further investigated which revealed normal fasting and postprandial blood sugar, HbA1C, and renal function and liver function tests. His lipid profile showed serum cholesterol of 141 mg/dl; triglyceride of 98 mg/dl; low-density lipoprotein (LDL) of 76 mg/dl; very LDL (VLDL) of 20; LDL/high-density lipoprotein of 1.97; and homocysteine of 12 mcmol/L. USG of the abdomen/pelvis showed liver size of 14.6 mm with raised echogenicity, suggestive of nonalcoholic fatty liver. Transthoracic echocardiography was suggestive of hypokinesia of the anteroseptum, apex, and anterior wall with preserved wall thickness with mild tricuspid regurgitation and mild pulmonary arterial hypertension. On the way to cath-lab for CAG, he developed sudden attack of dizziness followed by syncope. On examination, the patient was found to have severe bradycardia followed by which he had cardiac arrest. Lifesaving cardiopulmonary resuscitation was started and urgent transvenous temporary pace maker (TPM) was implanted in the right ventricle apex. CAG was done then after, which was suggestive of recanalized infarct-related artery (nonobstructive CAD in the left anterior descending with mild thrombosis). The patient was given intravenous anticoagulation and tirofiban infusion. The patient was put on BiPAP and ionotrope support. Sinus rhythm was restored, acute left ventricular dysfunction recovered, and TPM was removed after 48 h. The patient was further managed with antiplatelets, low-molecular-weight heparin, and cardioprotective medications. He had good clinical recovery and discharged in healthy condition. He was referred to antiretroviral therapy (ART) center for further workup in relation to HIV and for treatment.
Figure 1: Acute extensive anterior wall myocardial infarction, qRBBB with ST elevation in anterior leads and left anterior hemiblock

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His CD4 count was 78 cells/mm3 at the time of enrollment to ART center. He was treated with combination of tenofovir, lamivudine, and efavirenz with addition of cotrimoxazole chemoprophylaxis. The patient was on regular cardiac medication and also on ART for a month without any complaints.

After 2 months, the patient again was admitted as he had nausea and vomiting of 5 days duration. He had stopped ART on his own. On repeated investigation, all laboratory reports were within normal limits. ECG showed no fresh changes. Echocardiography was done on follow-up which showed evidence of old infarct, ischemic heart disease, dilated inferior vena cava, and severe pulmonary arterial hypertension with PASP by TR jet 58 mmHg. The patient was investigated further for protein C and protein S deficiency which were not found. The patient was managed symptomatically and advised for repeat CD4 count.


  Discussion Top


In our patient, HIV positivity was an incidental finding and his presentation was with AWMI which has resulted in cardiac arrest. Studies have shown that patients infected with HIV have a higher incidence of developing MI. The possible mechanisms by which HIV causes AWMI include low CD4 cell counts, inflammation, altered coagulation, and dyslipidemia.[5] Atherosclerosis-related CVDs are more common in HIV-infected patients.[6],[7] Chronic inflammation and immune dysfunction appear to accelerate the progression of cholesterol plaque erosion and rupture in HIV. There is also an increased activity of macrophages, which contributes to platelet aggregation and can lead to plaque rupture.[5],[6],[7]

HIV infection causes a decrease in CD4 count over time, getting converted to acquired immunodeficiency syndrome; once it is decreased to <200 cells/mm3 or <14%, it may result in opportunistic infections. Both of these may result in endothelial dysfunction making them prone for MI.[8],[9] Decreased CD4 cell count is associated with poor endothelial function which is independent to highly active antiretroviral therapy and has greater role than traditional risk factors.[9] As described above, our patient had no conventional risk factors for CVDs. Fifty percent increased risk of acute MI (AMI) in HIV infection is present independent from recognized risk factors.[5]

Statin therapy along with ART therapy has the potential for interaction. As a result, their combined therapy is less frequently administered in the general population with HIV-infected status. However, recent studies have shown that all statins with the exception of simvastatin and lovastatin can be co-administered with ART. Statins reduce the cholesterol levels and also have shown to reduce chronic immune activation and arterial inflammation in HIV-infected individuals.[10],[11]

To prevent cardiovascular (CV) complications, ART therapy in patients diagnosed with HIV infection as early as possible is recommended, at any level of CD4 cell count.[9] Studies do give link of ART with AMI risk among HIV-positive people. ART can contribute to AMI risk[5],[12],[13] which is related to duration of protease inhibitor (PI) therapy and is found to increase the relative risk of MI, but the same did not apply to nonnucleoside reverse transcriptase inhibitor (NNRTI) therapy.[14],[15] However, ART therapy reduces death due to atherosclerotic events of patients on NNRTI or PI-based therapy compared to patients not on therapy, and thus, recent evidence is in favor of their use.[8]

CV-associated disorders are not uncommon in HIV-infected people, and due to rising prevalence of HIV in population, an integrated and balanced approach by cardiologists with the help of HIV specialist will lead to successful management.[8] So, Timely intervention and integrated approach can be life saving as observed in our case.


  Conclusion Top


AMI may be presenting feature of HIV infection and may need timely intervention by combined specialist care.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Pandey A, Galvani AP. The global burden of HIV and prospects for control. Lancet HIV 2019;6:e809-11.  Back to cited text no. 1
    
2.
Günthard HF, Saag MS, Benson CA, del Rio C, Eron JJ, Gallant JE, et al. Antiretroviral drugs for treatment and prevention of HIV infection in adults: 2016 Recommendations of the International Antiviral Society-USA Panel. JAMA 2016;316:191-210.  Back to cited text no. 2
    
3.
Silverberg MJ, Leyden WA, Xu L, Horberg MA, Chao CR, Towner WJ, et al. Immunodeficiency and risk of myocardial infarction among HIV-positive individuals with access to care. J Acquir Immune Defic Syndr 2014;65:160-6.  Back to cited text no. 3
    
4.
Feinstein MJ, Lloyd-Jones DM. Macrophage inflammation and cardiovascular disease in HIV: Mechanistic insights and future directions. J Infect Dis 2017;215:1343-5.  Back to cited text no. 4
    
5.
Freiberg MS, Chang CC, Kuller LH, Skanderson M, Lowy E, Kraemer KL, et al. HIV infection and the risk of acute myocardial infarction. JAMA Intern Med 2013;173:614-22.  Back to cited text no. 5
    
6.
Paisible AL, Chang CC, So-Armah KA, Butt AA, Leaf DA, Budoff M, et al. HIV infection, cardiovascular disease risk factor profile, and risk for acute myocardial infarction. J Acquir Immune Defic Syndr 2015;68:209-16.  Back to cited text no. 6
    
7.
Drozd DR, Kitahata MM, Althoff KN, Zhang J, Gange SJ, Napravnik S, et al. Increased risk of myocardial infarction in HIV-infected individuals in North America compared with the general population. J Acquir Immune Defic Syndr 2017;75:568-76.  Back to cited text no. 7
    
8.
Dau B, Holodniy M. The relationship between HIV infection and cardiovascular disease. Curr Cardiol Rev 2008;4:203-18.  Back to cited text no. 8
    
9.
Ho JE, Scherzer R, Hecht FM, Maka K, Selby V, Martin JN, et al. The association of CD4+T-cell counts and cardiovascular risk in treated HIV disease. AIDS 2012;26:1115-20.  Back to cited text no. 9
    
10.
Feinstein MJ, Achenbach CJ, Stone NJ, Lloyd-Jones DM. A systematic review of the usefulness of statin therapy in HIV-infected patients. Am J Cardiol 2015;115:1760-6.  Back to cited text no. 10
    
11.
Chauvin B, Drouot S, Barrail-Tran A, Taburet AM. Drug-drug interactions between HMG-CoA reductase inhibitors (statins) and antiviral protease inhibitors. Clin Pharmacokinet 2013;52:815-31.  Back to cited text no. 11
    
12.
Friis-Møller N, Sabin CA, Weber R, d'Arminio Monforte A, El-Sadr WM, Reiss P, et al. Combination antiretroviral therapy and the risk of myocardial infarction. N Engl J Med 2003;349:1993-2003.  Back to cited text no. 12
    
13.
DAD Study Group; Friis-Møller N, Reiss P, Sabin CA, Weber R, Monforte AD, et al. Class of antiretroviral drugs and the risk of myocardial infarction. N Engl J Med 2007;356:1723-35.  Back to cited text no. 13
    
14.
Mary-Krause M, Cotte L, Simon A, Partisani M, Costagliola D; Clinical Epidemiology Group from the French Hospital Database. Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men. AIDS 2003;17:2479-86.  Back to cited text no. 14
    
15.
Kwong GP, Ghani AC, Rode RA, Bartley LM, Cowling BJ, da Silva B, et al. Comparison of the risks of atherosclerotic events versus death from other causes associated with antiretroviral use. AIDS 2006;20:1941-50.  Back to cited text no. 15
    


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