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      Functional Capacity Impairment in Patients with Coronary Artery Disease: Prevalence, Risk Factors and Prognosis

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          Background: Some patients developing heart failure and functional capacity impairment have no history of myocardial infarction (MI), and stable angina pectoris is their principal clinical manifestation of coronary artery disease (CAD). The present study was aimed to evaluate the outcome of CAD-related functional capacity impairment in patients with and without a history of MI over a 7.7-year follow-up. Methods: The study sample comprised 14,283 coronary patients aged 45–74 years, screened for participation in the Bezafibrate Infarction Prevention study. The presence of NYHA functional class II was defined as mild functional capacity impairment and the presence of NYHA functional class III–IV was defined as advanced functional capacity impairment. Results: The patients were divided in two groups: (1) those with a history of MI, 10,307 patients, who formed three subgroups: NYHA I 7,551 patients (73.3%); NYHA II 2,176 patients (21.1%); NYHA III + IV 580 patients (5.6%), and (2) those without a history of MI, 3,976 patients, who also formed three subgroups: NYHA I 2,744 patients (69.0%); NYHA 981 patients (24.7%); NYHA III + IV 251 patients (6.3%). Multivariate analysis identified a history of MI as a consistent predictor of increased all-cause and cardiac mortality for patients with NYHA I, II and III + IV subgroups with escalating significance for patients with advanced functional capacity impairment: hazard ratios of 1.55 (95% CI 1.36–1.75), 1.56 (95% CI 1.30–1.86) and 1.72 (95% CI 1.24–2.40) for all-cause and 1.93 (95% CI 1.60–2.33), 1.73 (95% 1.35–2.20) and 3.22 (95% CI 1.87–5.54) for cardiac mortality, respectively. Conclusions: The prevalence of low functional capacity is similar among coronary patients with and without a history of MI, but their long-term survival differs substantially in favor of the latter. Therefore, two different types of CAD-related advanced functional capacity impairments (post-MI and non-post-MI) can be distinguished.

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          Most cited references 18

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          Apoptosis in the failing human heart.

           R. Reed,  E Quaini,  P Anversa (1997)
          Loss of myocytes is an important mechanism in the development of cardiac failure of either ischemic or nonischemic origin. However, whether programmed cell death (apoptosis) is implicated in the terminal stages of heart failure is not known. We therefore studied the magnitude of myocyte apoptosis in patients with intractable congestive heart failure. Myocardial samples were obtained from the hearts of 36 patients who underwent cardiac transplantation and from the hearts of 3 patients who died soon after myocardial infarction. Samples from 11 normal hearts were used as controls. Apoptosis was evaluated histochemically, biochemically, and by a combination of histochemical analysis and confocal microscopy. The expression of two proto-oncogenes that influence apoptosis, BCL2 and BAX, was also determined. Heart failure was characterized morphologically by a 232-fold increase in myocyte apoptosis and biochemically by DNA laddering (an indicator of apoptosis). The histochemical demonstration of DNA-strand breaks in myocyte nuclei was coupled with the documentation of chromatin condensation and fragmentation by confocal microscopy. All these findings reflect apoptosis of myocytes. The percentage of myocytes labeled with BCL2 (which protects cells against apoptosis) was 1.8 times as high in the hearts of patients with cardiac failure as in the normal hearts, whereas labeling with BAX (which promotes apoptosis) remained constant. The near doubling of the expression of BCL2 in the cardiac tissue of patients with heart failure was confirmed by Western blotting. Programmed death of myocytes occurs in the decompensated human heart in spite of the enhanced expression of BCL2; this phenomenon may contribute to the progression of cardiac dysfunction.
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            Risk Factors for Congestive Heart Failure in US Men and Women

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              The heart failure epidemic: exactly how big is it?


                Author and article information

                S. Karger AG
                December 2003
                16 January 2004
                : 100
                : 4
                : 207-215
                aCardiac Rehabilitation Institute and bBezafibrate Infarction Prevention Study Coordinating Center, NeufeldCardiacResearch Institute, Chaim Sheba Medical Center, Tel-Hashomer, affiliated with Sackler Faculty of Medicine, Tel-AvivUniversity, Tel-Aviv, Israel
                74814 Cardiology 2003;100:207–215
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 5, References: 47, Pages: 9
                General Cardiology


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