Prognosis in hypertrophic cardiomyopathy observed in a large clinic population

Overall annual cardiac mortality in hypertrophic cardiomyopathy (HC) has been reported to be between 2 and 4%, although these numbers are primarily from retrospective studies of patients referred to large research institutions. A clinic population of 113 patients with HC was prospectively studied to assess cardiac mortality in the overall group and in selected subgroups commonly thought to be at high risk for sudden death. The mean age at diagnosis was 37 ± 16 years. During follow-up, there were 11 cardiac and 2 noncardiac deaths. The annual cardiac mortality was 1% (95% confidence interval 0.2–1.8%). Because of the small number of deaths, relative risk for cardiac death was not significantly different in the presence of young age (≤30 years), family history of HC and sudden death, history of syncope or previous cardiac arrest, or both, ventricular tachycardia on 24-hour Holter monitoring, or septal myotomy/myectomy for refractory symptoms and outflow tract obstruction. It is concluded that HC has a relatively benign prognosis (1% annual cardiac mortality) that is 2 to 4 times less than that previously reported

Hypertrophic cardiomyopathy in a large community-based population: clinical outcome and identification of risk factors for sudden cardiac death and clinical deterioration

AbstractObjectivesThis study evaluates the clinical course and identifies risk factors for sudden cardiac death (SCD) and clinical deterioration in hypertrophic cardiomyopathy (HCM) in a large community-based population. Comparison was made with data from six tertiary referral and six nonreferral institutions.BackgroundHypertrophic cardiomyopathy is a disease with marked heterogeneity in clinical presentation and prognosis. Risk factors for SCD are not well defined in patients free of referral bias.MethodsBetween 1970 and 1999, 225 consecutive patients (mean age [±SD] 41±16 years) were examined and followed at yearly intervals.ResultsForty-four deaths were recorded of which 27 cases were cardiovascular. Fourteen patients died suddenly, six were successfully resuscitated, and seven patients died of congestive heart failure. The annual mortality, annual cardiac mortality, and annual mortality due to sudden death were 1.3%, 0.8%, and 0.6%, respectively. At least one New York Heart Association (NYHA) functional class deterioration was reported in 33% of the patients with a significant (≥50 mm Hg) left ventricular outflow tract (LVOT) gradient in contrast to 7% without obstruction. The presence of syncope was related to SCD (p < 0.05). Younger age and more severe functional limitation distinguishes patients from in hospital-based centers from the ones in community-based centers.ConclusionsHypertrophic cardiomyopathy is a benign disease in an unselected population with a low incidence of cardiac death. Syncope was associated with a higher incidence of SCD and patients with a significant LVOT obstruction were more susceptible to clinical deterioration

Angiotensin II type 2 receptors and cardiac hypertrophy in women with hypertrophic cardiomyopathy

The development of left ventricular hypertrophy in subjects with hypertrophic cardiomyopathy (HCM) is variable, suggesting a ro

935-38 Restenosis After Coronary Angioplasty is Associated with the Activation Status of Circulating Phagocytes Before Treatment

BackgroundThe purpose of this study was to identify biological risk factors for restenosis after PTCA, in order to predict the long-term outcome of PTCA before treatment.Methods and ResultsTo investigate whether blood granulocytes and monocytes could determine luminal renarrowing after PTCA, several characteristics of these phagocytes were assessed before angioplasty in 32 patients who underwent PTCA of one coronary artery and who had repeat angiograms at six months follow-up. The plasma levels 1L-1β, TNF-α, IL-6, fibrinogen, C-reactive protein and LP(a) before angioplasty were assessed as well. We found that the expression of the membrane antigens CD64, CD66 and CD67 by granulocytes was inversely associated with the luminal renarrowing normalized for vessel size (relative loss) at six months after PTCA. while the production of IL-1β by stimulated monocytes was positively associated with the relative loss. Next. these univariate predictors were corrected for the established clinical risk factors, dilation of the LAD, current smoking and angina class.Multiple linear regression analysis showed that luminal renarrowing could be predicted reliably (R2=0.65; P&lt;0.0001) in this patients group on the basis of the vessel dilated and only two biological risk factors that reflect the activation status of blood phagocytes, i.e., the expression of CD66 by granulocytes and the production of IL-lβ by stimulated monocytes.ConclusionsThe results of the present study indicate that activated blood granulocytes prevent luminal renarrowing after PTCA, while activated blood monocytes promote restenosis. To validate this new finding further study in an independent patients group is required