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  • Title: Why do patients with chagasic cardiomyopathy have worse outcomes than those with non-chagasic cardiomyopathy?
    Author: Silva CP, Del Carlo CH, Oliveira Junior MT, Scipioni A, Strunz-Cassaro C, Ramirez JA, Pereira Barretto AC.
    Journal: Arq Bras Cardiol; 2008 Dec; 91(6):358-62. PubMed ID: 19142362.
    Abstract:
    BACKGROUND: Heart failure is a highly prevalent disease, the prognosis of which depends on different predictive factors. OBJECTIVE: Chagas disease is a predictor of poor prognosis in patients with chronic heart failure (HF). The purpose of this study is to investigate whether this condition also predicts poor outcome in acutely decompensated patients. METHODS: Four hundred and seventeen patients admitted for decompensated heart failure were studied. Mean age was 51.8 years, and 291 (69.8%) were male. They were divided into two groups: 133 (31.9%) patients with Chagas heart disease (CH) and 284 patients with heart failure of other etiologies. Cytokine and norepinephrine plasma levels were measured in a subgroup of 63 patients (15.1% with Chagas disease). RESULTS: At admission, 24.6% of the patients needed inotropic support, and one-year mortality was 54.7%. Mortality rates were higher in the CH group (69.2% vs. 47.9%, p < 0.001). When data were compared, patients with Chagas disease were younger (47.6 vs. 53.8 years, p < 0.001) and, on average, showed lower systolic blood pressure (96.7 vs. 111.2 mmHg, p < 0,001), ejection fraction (32.7 vs. 36.4%, p < 0.001), and serum Na (134.6 vs. 136.0, p = 0.026), in addition to higher TNF-alpha levels (33.3 vs. 14.8, p = 0.001). The presence of hypotension requiring inotropic support, left ventricular (LV) diastolic diameter, renal function findings, and interleukin-6 and norepinephrine plasma levels did not differ between both groups. CONCLUSION: Chagas disease patients admitted with decompensated heart failure had worse prognoses than patients with heart failure of other etiologies. This may be owing to a greater degree of cardiac impairment (lower ejection fraction) and hemodynamic instability (lower systolic blood pressure and heart rate), increased activation of the renin-angiotensin system (lower sodium), and increased cytokine levels (TNF-alpha).
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