Cardiomyopathy In HIV-infected Patients Research Articles

Retraction. Clinical course of cardiomyopathy in HIV-infected patients with or without encephalopathy related to the myocardial expression of tumour necrosis factor-alpha and nitric oxide synthase.

Retraction. Clinical course of cardiomyopathy in HIV-infected patients with or without encephalopathy related to the myocardial expression of tumour necrosis factor-alpha and nitric oxide synthase.

Cardiovascular manifestations of HIV infection.

Studies published over the past 3 years have tracked the incidence and course of human immunodeficiency virus (HIV) infection in relation to cardiac illness in both children and adults.1 These studies show that subclinical echocardiographic abnormalities independently predict adverse outcomes and identify high-risk groups to target for early intervention and therapy. The Joint United Nations Program on HIV/AIDS estimates that 36.1 million people were living with HIV infection at the end of the year 2000.2 If 8% to 10% of patients develop symptomatic heart failure over a 2- to 5-year period,3 then 3 million cases of HIV-related heart failure will present during that period.1 Cardiovascular manifestations of HIV have been altered by the introduction of highly active antiretroviral therapy (HAART) regimens. On one hand, HAART has significantly modified the course of HIV disease, lengthened survival, and improved the quality of life of HIV-infected patients. On the other hand, the early data have raised concerns that HAART is associated with an increase in both peripheral and coronary arterial diseases.1 The HAART-associated changes are relevant only to the minority of HIV-infected individuals worldwide who have access to HAART. Thus, studies conducted before HAART became available remain globally applicable. In this review article, the principal HIV-associated cardiovascular manifestations will be discussed, with an emphasis on new knowledge about prevalence, pathogenesis, and treatment. HIV disease is recognized as an important cause of dilated cardiomyopathy, with an estimated annual incidence of 15.9 in 1000 before the introduction of HAART3 (Table 1). The importance of cardiac dysfunction is demonstrated by its effect on survival in acquired immunodeficiency syndrome (AIDS). Median survival to AIDS-related death is 101 days in patients with left ventricular dysfunction and 472 days in patients with a normal heart as shown by echocardiography at a similar infection …

Clinical course of cardiomyopathy in HIV-infected patients with or without encephalopathy related to the myocardial expression of tumour necrosis factor-alpha and nitric oxide synthase.

To define whether the development of encephalopathy influences the clinical course of HIV-associated cardiomyopathy (HIV-DCM) in relation to the myocardial expression of tumour necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS). Prospective study. University hospitals and AIDS centres. 115 HIV-infected patients with echocardiographic diagnosis of HIV-associated cardiomyopathy (34 with encephalopathy and 81 without encephalopathy) were followed for a mean of 24 +/- 3.2 months. All patients underwent endomyocardial biopsy for determination of myocardial immunostaining intensity of TNF-alpha and iNOS. Cerebrospinal fluid (CSF) from patients with encephalopathy was examined for the presence of viruses. Patients underwent clinical examination every 3 months and echocardiographic examination every 6 months. The intensity of TNF-alpha and iNOS immunostaining was also evaluated on postmortem cerebral tissue of patients who died of congestive heart failure (CHF). A greater impairment of echocardiographic parameters was observed in patients with HIV-associated cardiomyopathy after development of encephalopathy. These parameters tended to worsen progressively during the follow-up period and were inversely correlated with HIV-1 viral load, CD4 cell count, mini mental status score and the intensity of myocardial and cerebral TNF-alpha and iNOS staining. CSF specimens were available in 29 patients with encephalopathy. HIV-1 sequences were detected in CSF of all these patients with cytomegalovirus sequences in two. The mortality rate for CHF was greater among patients with encephalopathy (73% versus 12%). The development of encephalopathy has an adverse effect on the clinical course of HIV-associated cardiomyopathy. In the relationship between cardiomyopathy and encephalopathy, the activation of iNOS by TNF-alpha may have a significant pathogenetic role in HIV disease.

The natural history and spectrum of idiopathic dilated cardiomyopathy, including HIV and peripartum cardiomyopathy.

Idiopathic dilated cardiomyopathy (IDCM) is an often fatal heart disease characterized by ventricular dilation and reduced systolic function. Despite advances in diagnostic and therapeutic techniques that have enabled earlier identification of patients with IDCM, the etiology of the disease in most patients remains unknown. The current 5-year survival rate for patients with asymptomatic IDCM approaches 80%; this is a significant improvement compared with earlier reports of the natural history of IDCM. Men are more commonly afflicted with IDCM, but women with IDCM tend to present with more advanced disease. Recent analysis of 3-year transplant-free survival reveals no gender differences, however. Survival in children with IDCM is variable; 30% of infants die within 2 years of diagnosis, but 5-year survival for childhood IDCM is 60% to 84%. An association of IDCM with the peripartum period is well recognized. The etiology of peripartum cardiomyopathy remains unknown, and some cases are familial. This disease is reversible in approximately 50% of patients, and in patients with intractable congestive heart failure, cardiac transplantation is a viable treatment option. AIDS has been more recently associated with IDCM. Acute left ventricular dysfunction and consequent dilated cardiomyopathy occur with increased frequency in patients with advanced AIDS. The etiology of dilated cardiomyopathy in HIV-infected patients is presently poorly understood. Survival for patients with AIDS after development of left ventricular dysfunction is extremely poor.

LV-function and development of congestive cardiomyopathy in HIV-infected patients

LV-function and development of congestive cardiomyopathy in HIV-infected patients