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 Guide Editors
 Editor In Chief
    Joel E. Gallant, MD, MPH

Pharmacology Editor
    Paul Pham, PharmD, BCPS

Zambia Guideline Team
   Peter Mwaba MMed PhD FRCP
   Alywn Mwinga MMed
   Isaac Zulu MMed MPH
   Velepie Mtonga MMed
   Albert Mwango MBChB
   Jabbin Mulwanda MMed FCS
 

 

 

Diagnosis>Organ System>
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Cardiac Manifestations of HIV Infections

Christopher Hoffman, M.D. and Paul G. Auwaerter, M.D.
04-16-2009

  • Epidemiology of HIV-related cardiomyopathy in Zambia is unknown.
  • Heart failure in sub-Saharan Africa largely due to non-ischaemic causes with hypertensive heart disease, rheumatic heart disease, and endemic cardiomyopathy accounting for most cases.
  • Key differences in cardiomyopathy epidemiology between developed world and Africa include contribution of endomyocardial fibrosis and the increased contribution of some infectious diseases such as TB to cardiomyopathies in Africa.
  • Endomyocardial fibrosis is a restrictive cardiomyopathy of children and young adults which occurs mainly in equatorial Africa and is a significant contributor to cardiomyopathy in Africa. Relationship to HIV is unknown.
  • In HIV+ African pts, TB appears to be the main cause of pericardial effusions, and HIV is a significant risk factor for developing tuberculosis pericarditis.
  • Some diagnostic tools, such as echocardiography, pericardiocentesis, BNP, Holter monitor, V/Q scanning, angiography, and RV cath, are of limited availability in Zambia.
  • If CHF Dx'd, management is largely as recommended below.
  • Nesiritide and prostacyclin not available in Zambia.

REFERENCES

Zambia Information Author: Larry William Chang, MD, MPH

PATHOGENS

CLINICAL

  • Cardiovascular malignancyKS may cause cardiac tumors, pericardial lesions but usually clinically silent. Lymphoma rare.
  • Dilated cardiomyopathy: Generally defined as <50% EF on echo with LV dilation. Affected 30-40% of AIDS patients pre-HAART, now est. 3%-15%. May present with CHF, palpitations/arrythmia, syncope. Sudden death rare.
  • Endocarditis: HIV infection and low CD4 count have been both associated with increased risk of infective endocarditis (mostly occurs among IDUs). Common organisms: S. aureus & Streptococcus viridans. Most pts have similar presentations and survival, although 30% increased mortality in end-stage AIDS vs. matched asymptomatic HIV+ pts.
  • Myocarditis: most causes undefined, direct role of HIV unclear. OI found in <20% (see pathogens), along with occasional coxsackie virus, EBV, CMV cases. Noninfectious causes may include hypersensitivity/drug reactions (AZT), cocaine, thyrotoxicosis.
  • Pericardial effusion: common (~11%) in untreated AIDS patients, lower on HAART. Most small, etiology unknown. Identifiable causes include TB, pyogenic bacteria, Nocardia, and primary effusion body lymphoma. Presence in AIDS equates with median survival 6 mos.
  • Pericarditis: may cause tamponade, bodes poor prognosis. Causes: mycobacterial > pyogenic > lymphoma > KS > viral > fungal.
  • Pulmonary hypertension: surprisingly common, 1/200 incidence including RV hypertrophy/dilation. Causes include recurrent bronchopulmonary infections, IDU, thromboembolic disease, cirrhosis. Association with HHV-8 defined. Common Sx include cough, chest pain, fatigue and hemoptysis.
  • Coronary artery disease: HIV leads to a pro-inflammatory state and endothelial dysfunction increasing risk for coronary artery disease (data especially strong among pts with treatment interruption). ABC implicated with increased MI risk (doubles MI risk among high risk group). Other CAD risks: tobacco, HTN, low HDL-C, diabetes mellitus, age, family history, & obesity.

DIAGNOSIS

  • CHF: Obtain echo, ECG, TSH. Brain natriuretic peptide (BNP) may assist with clinical assessment. Role of myocardial Bx not defined, consider selectively. Consider evaluation for CAD (ischemic cardiomyopathy).
  • Pericardial effusion: Obtain echo, consider pericardiocentesis with hemodynamic compromise or if concerned about active infection.
  • Arrhythmia: Baseline ECG for QTc prolongation, Holter monitor, electrolytes, Mg. Consider echo to look for structural heart disease. Survey medications for likely causes (pentamidine most famous, associated with torsade de pointes) or drug interactions (PIs, digoxin etc).
  • Pulmonary HTN: Doppler evaluation of right-sided pressures by echo, but RV cath remains gold standard. R/O secondary causes (LV dysfn, hypoxemia, COPD). CT angiography now preferred for PE evaluation, although V/Q scanning or angiography occasionally necessary in some cases, especially chronic PE.
  • Coronary artery disease: stress testing, coronary angiography, lipid panel, glucose tolerance testing. 

TREATMENT

CHF

  • No clear documented benefit of ART.
  • Rapid onset bodes poor prognosis: >50% mortality over 6-12 mos.
  • Consider D/C of cardiotoxic drugs (e.g., AZT), drug and alcohol cessation, optimize BP control.
  • Asymptomatic: ACE inhibitors (eg, start lisinopril 2.5-5.0 mg once daily PO, titrate to 20-40 mg/d).
  • Sx (dyspnea, fatigue): ACE inhibitor/ARB + daily diuretic (furosemide 20-40 mg PO, bumetanide 0.5-1.0 mg PO, titrate to dry weight); Add beta-blocker when not volume overloaded (carvedilol 3.125-25 mg twice-daily target or metoprolol 6.25 mg twice-daily, 50 mg bid target or metoprolol XL 12.5 mg once daily, to 100 mg once daily target).
  • Spironolactone 25 mg PO once daily titrate to 3 times daily yields mortality benefit for advanced CHF; consider eplerenone 25-50 mg once daily (potential for drug interaction with PIs) for those intolerant of spironolactone.
  • Digoxin 0.125-0.25 mg PO once daily. May help reduce hospitalizations, but no mortality benefit.
Pericardial Disease

  • Attempts at aspiration +/- pericardial Bx generally driven by hemodynamic issues and need to obtain diagnosis.
  • Effect of ART on pericardial effusions not known.
  • Chronic inflammation may cause constriction, requiring surgical stripping of pericardium.
Pulmonary Hypertension

  • Obtain specialty consultation
  • Oxygen supplementation to correct hypoxemia
  • Diuretics may help reduce right-sided volume overload, but use with caution; avoid reduced preload can cause hypotension.
  • Anticoagulation may be used even without documented emboli as use improves long-term outcomes.
  • If acute pulmonary vasoreactivity documented, calcium channel blockers or other vasodilators may give favorable longer term benefit.
  • Severe pulmonary HTN: consider prostacyclin (epoprostenol) by continuous IV infusion.
  • ART may improve pulmonary hypertension. 
Coronary Artery Disease

  • Risk factor modification (stop smoking, increase exercise, control glucose & BP, continue HART, switch from ABC or drugs causing dyslipidemia and/or insulin resistance if possible. 
  • Aspirin, lipid lowering therapy (if on protease inhibitor use pravastatin, atorvastatin or rosuvastatin), beta-blockers. 

OTHER INFORMATION

  • Pre-HAART autopsy series: cardiac lesions identified in 25-75% of patients with AIDS. Cases of myocarditis >80% undefined etiology.
  • Rates of coronary artery disease, atherosclerosis may be increased in HIV+ pts on PIs (see Lipodystrophy, Hypertriglyceridemia).

Basis for Recommendations

  • Hunt SA, Abraham WT, Chin MH, et al.; ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society.; Circulation; 2005; Vol. 112; pp. e154-235;
    ISSN: 1524-4539;
    PUBMED: 16160202
    Rating: Basis for recommendation
    Comments:Current treatment guidelines for heart failure.

REFERENCES


 
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