Abstract

Introduction: Sudden cardiac death (SCD) is responsible for approximately 380,000 deaths per year. One third of the patients dying of heart disease present with SCD as the first manifestation. There are limited data on the clinico-pathological determinants of SCD. Hypothesis: We hypothesized that, compared to overall deaths, silent coronary atherosclerosis and myocardial fibrosis could be associated with increased frequency of SCDs. Methods: We reviewed the post-mortem data registry from two tertiary care hospitals located at the Buffalo-Niagara Region. Of the 1,314 subjects that underwent comprehensive post-mortem analysis, we identified 187 subjects that died suddenly. For this initial pilot data analysis protocol, we compared the demographic, clinical, electrocardiographic and coronary vascular and myocardial histopathological characteristics of 109 subjects with sudden death vs. 34 age-matched controls with non-sudden death. Results: We found that, of the total 1,314 subjects screened, 14% had SCD. Comparison of age-matched SCD with non-SCD subjects (age in years, SCD: 60±14; non-SCD: 61±20) showed that SCD groups had larger cardiac size (heart weight in grams, SCD: 550±150; non-SCD: 480±117, P=0.03), increased wall thickness (posterior wall thickness in cm, SCD: 1.7±0.4; non-SCD: 1.5±0.2, P=0.01), but reduced LV function reported before the event (LV ejection fraction in %, SCD: 41±17; non-SCD: 58±9, P=0.007). In addition, SCD groups had higher frequency of coronary atherosclerosis (SCD, 76% vs., non-SCD, 52%, P=0.007), and myocardial fibrosis involving both left ventricular free wall (SCD, 47% vs., non-SCD, 26%, P=0.03), and interventricular septum (SCD, 29% vs., non-SCD, 3%, P=0.02). There were no differences on serum electrolytes, circulating biomarkers and the extent of right ventricular fibrosis. Conclusions: The subjects that died suddenly had larger cardiac size, reduced contractile function with myocardial interstitial fibrosis, and silent coronary atherosclerosis. Further studies are in progress to fully examine the clinico-pathological correlates of SCD in our longitudinal study cohorts.

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