Afección cardíaca en la infección por virus de la inmunodeficiencia humana tipo 1
Cardiac involvement in HIV-1-infected patients includes pericardial effusion/pericarditis, dilated cardiomyopathy, myocarditis, tumour infiltration and pulmonary hypertension (PH). HIV-1 infection can affect the heart by different mechanisms such as immune alterations, opportunistic infections (HIV-1 itself and/or other microorganisms) and tumours, as well as drug toxicity (because of highly active antiretroviral therapy HAART and/or therapy of the opportunistic complications) and/or use of illicit drugs. The identification of cardiac involvement in HIV-1 infection may be difficult due to the frequent coexistence of pulmonary infections and other systemic complications, so that symptoms may erroneously be attributed to them. After the introduction of HAART, the incidence of cardiac involvement has decreased, but at the same time the risk of development of atherosclerosis and ischemic heart disease has increased. Studies about the incidence of cardiovascular disease and mortality in HIV-1-infected patients are limited by short periods of follow-up. Objectives: 1) To assess the prevalence of morphologic and functional cardiac involvement as well as of myocardial damage in HIV-1-infected patients by means of transthoracic echocardiography and (111)In-antimyosin scintigraphy, respectively. 2) To identify possible predictors of cardiac involvement. 3) To assess the incidence of hard cardiac events (heart failure, acute myocardial infarction AMI or cardiac death) and predictors of global mortality. Material and methods: Ninety-six consecutive patients at different stages of HIV-1 infection and from all groups at risk for the infection were included. None of the patients had known or suspected structural heart disease. All patients underwent echocardiography and cardiac (111)In-antimyosin scan. A subgroup of patients who presented altered results was reassessed six months later. Subsequently, a retrospective registration of hard cardiac events and global mortality was performed after a mean of follow-up of 7±3 years. Results: Twenty-five (26%) patients showed echocardiographic alterations, and 11 patients (11.5%) had abnormal (111)In-antimyosin scans. Most of the echocardiographic alterations corresponded to mild valvular heart disease, however, on account of the clinical relevance, it is important to point out that: two patients had left ventricle LV dilatation and mitral regurgitation (one of them with severe LV dilatation and mild tricuspid regurgitation added); one patient had basal septal akinesia suggestive of an old AMI and mild mitral regurgitation; one patient had mild LV hypertrophy and hypokinesia and paradox movement of the septum; and two patients had PH with right ventricle RV dilatation and tricuspid regurgitation (one of them with primary PH and global hypokinesia of the RV with moderate tricuspid regurgitation). No significant association between echocardiography and (111)In-antimyosin scintigraphy was found. The duration of the infection, although not significant, tended to be longer for those patients with normal (111)In-antimyosin scans. Echocardiographic alterations of four patients who also showed abnormal (111)In-antimyosin scans corresponded to a patient with small nonspecific pericardial effusion with myopericardial involvement, one patient with mild mitral and tricuspid regurgitation, and two patients with myocarditis. In two patients who showed abnormal (111)In-antimyosin scintigraphy but normal echocardiography, there was recent treatment with adriamycin in one of them, and active addiction to cocaine in the other. Seven patients with abnormal (111)In-antimyosin scans underwent a second scintigraphy 6 months after beginning HAART or insisting on the importance of adherence to this therapy. (111)In-antimyosin uptake decreased in all of them (with contractility improvement in those patients who previously presented wall motion disorders). At the end of the study, 25 patients developed lipodystrophy syndrome and 10 patients developed metabolic alterations, with no significant association between them. Follow-up was not possible in 15 patients (15.6%), but three episodes of AMI were registered in young patients, as well as 20 (20.8%) deaths of noncardiac origin (one corresponding to the patient with primary PH). Only the age and CD4 cell count <200/?l in the inclusion period were significant predictors of global mortality in single-variable and multivariable Cox proportional hazard model. Conclusions: Transthoracic echocardiography and (111)In-antimyosin scintigraphy allow the detection of silent cardiac involvement in HIV-1-infected patients. (111)In-antimyosin scintigraphy allows early detection of ongoing myocardial damage before the appearance of functional consequences. The prevalence of myocardial damage in HIV-1-infected patients in the first years of HAART is 11.5%. Global ventricular dysfunction and myocardial damage improve after 6 months of treatment of myocarditis or after the beginning of HAART or insisting on the importance of adherence to this therapy, which suggests a beneficial effect of antiretroviral treatment over cardiac involvement. Cardiac involvement in patients who receive HAART does not relate with the analytical parameters usually used for the follow-up of HIV-1-infected patients. Early diagnosis and subsequent follow-up of HIV-1-infected patients may have an important role in the prevention of myocardial damage, since it allows the beginning of HAART in the optimum moment. Echocardiographic and scintigraphic alterations are not predictors of mortality risk in HIV-1-infected patients. Primary pulmonary hypertension is associated with bad outcome.
Advisor:Domingo Pedrol, Pere; Carrió Gasset, Ignasi
School:Universitat Autónoma de Barcelona
Source Type:Master's Thesis
Keywords:417 departament de medicina
Date of Publication:06/10/2008