Dilated Cardiomyopathy in Patients with HIV Infection: Is there a Role for CMR?

HIV-related disease is recognized as an important cause of dilated cardiomyopathy, with a prevalence of 8-30% [23, 27, 50, 51]. Prior to the introduction of HAART, the annual incidence of dilated cardiomyopathy was estimated at 15.9 per 1,000 patients with HIV infection [27].

Usually observed at the late stage of AIDS, dilated cardiomyopa­thy is associated with a low CD4 count (other clinical predictors, includ­ing ejection fraction, in a cohort of 195 patients who underwent CMR to evaluate for ischemia in the setting of CAD [54]. Even the smallest amount of LGE was pre­dictive of an adverse outcome. Thus, in ischemic and nonischemic myocardial dis­ease, fibrosis is a marker of poor outcome over and above standard clinical markers, including EF. In ischemic cardiomyopathies, it is likely a marker of the burden of CAD and its activity. The extent of infarct scar by CMR is also a better marker of inducible ventricular tachycardia than EF [55]. The presence of fibrosis is more characteristic of nonischemic cardiomyopathy and is thought to be at the root of myocardial re-entry lead­ing to ventricular tachycardia [56]. Fibrosis may also involve the conduction system and lead to dyssynchrony and worsening conges­tive heart failure. Risk stratification in patients with congestive heart failure is a growing necessity in patients with HIV- related cardiomyopathy. It is becoming increasingly apparent that fibrosis may be an important prognostic marker and may identify patients at higher risk of ventricu­lar arrhythmias and cardiac death. CMR has the unique feature of providing a coales­cence of the ability to image fibrosis by late gadolinium-enhanced CMR with an enhanced understanding of its aetiology and prognostic implications.

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