Echocardiography of the heart in the HIV disease

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Last updated: September 2, 2019

Echocardiographyis useful for assessing left ventricular systolic function in this populationand echocardiography should be performed in any patient at elevatedcardiovascular risk, with any clinical manifestations of cardiovasculardisease, or with unexplained or persistent pulmonary symptoms or viral co-infectionsat baseline and every 1 to 2 years thereafter, or as clinically indicated.RecentEchocardiographic Study in Nigeria.Olusegun-Joseph et.al Identified by echocardiography earlyabnormalities in 100 treatment-naïve patients.

Significant echocardiographicabnormalities found  included  systolic dysfunction  and diastolic dysfunction . Otherabnormalities were pericardial effusion in 47% and dilated cardiomyopathy . One patient each had aortic root dilatation,mitral valve prolapse and isolated right heart dilatation and dysfunction.

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Theyconcluded that cardiac abnormalities are more common in HIV-infected peoplethan in normal controls. A careful initial and periodic cardiac evaluation todetect early involvement of the heart in the HIV disease is recommended.Anelectrocardiogram (ECG) can reveal nonspecific conduction defects orrepolarization changes. The chest radiograph has low sensitivity andspecificity for congestive heart failure in patients with HIV infection.

Insmall studies of HIV-infected patients and large populations of patientswithout HIV infection, brain natriuretic peptide levels have been inverselycorrelated with left ventricular ejection fraction and can be useful in thedifferential diagnosis of congestive cardiomyopathy in HIV-infected patients.COURSEOF DISEASE. Patientswith asymptomatic left ventricular dysfunction (fractional shortening less than28 percent, with global left ventricular hypokinesis) may have transient diseaseby echocardiographic criteria.

PROGNOSIS.Mortalityin HIV-infected patients with cardiomyopathy is increased, independently of CD4count, age, sex, and HIV risk group. The median survival to AIDS-related deathwas 101 days in patients with left ventricular dysfunction and 472 days inpatients with a normal heart at a similar stage of infection before HAARTtherapy.

Rapid-onsetcongestive cardiac failure has a grim prognosis in HIV-infected adults andchildren, with more than 50 percent of patients dying from primary cardiacfailure within 12 months of presentation. Chronic-onset heartfailure may respond better to medical therapy in these patients.THERAPYTherapyfor dilated cardiomyopathy associated with HIV infection is generally similarto therapy for non-ischaemic cardiomyopathy and includes diuretics, digoxin,beta blockers, aldosterone antagonists, and angiotensin-converting enzymeinhibitors, as tolerated. Opportunisticor other infections should be sought aggressively and treated to improve orresolve the cardiomyopathy. Right ventricular biopsy may be useful foridentifying infectious causes of failure and for suggesting targeted therapy.After medical therapy is begun, serial echocardiographic studies shouldbe performed at 4-month intervals.Monthlyimmunoglobulin infusions in HIV-infected children have minimized leftventricular dysfunction, increased left ventricular wall thickness, and reducedpeak left ventricular wall stress , suggesting that impaired myocardial growthand left ventricular dysfunction can be immunologically mediated. Hearttransplantation has been reported in one HIV-infected man believed to haveanthracycline-related cardiomyopathy.

At24 months of follow-up, his course was complicated by more frequent and highergrade episodes of rejection than average, but otherwise it was relativelyuneventful and productive. Clinical and echocardiographic findings havesuggested that diastolic dysfunction is relatively common in long-termsurvivors of HIV infection. Left ventricular diastolic dysfunction may precedesystolic dysfunction. Recent evidence suggests that treating HIV infectionwith ART may reduce the risk of CVD, even at higher CD4 T-cell counts; however,the definitive answer to this question will come from clinical trials andlong-term observational studies. Newer generation protease inhibitors,chemokine receptor 5 antagonists, and integrase inhibitors do not appear to beassociated with the adverse cardiometabolic risks of older drugs. In additionto the well established risk of coronary heart disease, emerging evidence nowsuggests that chronic HIV infection is associated with higher risk of ischemicstroke, heart failure, and arrhythmias.

These epidemiologic studies have associatedimmunodeficiency and active viral replication with higher CVD risk. Novelmethods of imaging subclinical vascular disease continue to implicateinflammation and immune activation as likely mediators of CVD among patientswith HIV. FUTURE PERSPECTIVESAslongevity improves in HIV-infected patients, cardiovascular disease willpredominate as a cause of mortality and will surface as a vital area ofresearch. Research may translate to other populations if HIV can be used as amodel of chronic immunosuppression in a large population. Understanding geneticpredispositions to QT prolongation may guide therapy, and understanding thecauses of cardiomyopathy may benefit diverse research efforts, such as theeffects of cytokine, mitochondrial, and neurohormonal pathways.

Observationsof increased mortality related to left ventricular mass and very mild leftventricular dysfunction may enhance diagnostic testing in at-risk populationsaffected by other poorly understood cardiomyopathies.

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