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Background: To evaluate supplement use, most notably ephedra, which has been temporally associated with sudden death. Animal models suggest increased myocardial irritability may predispose to primary arrhythmic death. Methods: Clinical, pathological, and investigative records from the Office of the Armed Forces Medical Examiner's Cardiovascular Death Registry were reviewed. Forty-eight cases of those with known supplement use were compared to 144 age-, gender-, and socioeconomic-matched controls in a 1:3 case:control manner. Results: Of the 48 sudden deaths temporally associated with supplement use, the mean age was 34.2 ± 10.0 years and predominantly male (n = 44, 91.7%). The underlying cause of death was fatal atherosclerotic coronary disease in 18 (37.5%), sudden unexplained death in 16 (33.3%), and hypertrophic cardiomyopathy in six (12.5%). Compared with controls, there were no statistically significant differences in adjudicated cause of death. On autopsy, there were no differences in cardiac mass, ventricular wall thickness, or presence of atherosclerosis in those known to be taking identified supplements compared to a control population. In the subject ≥35 years, and known to be taking supplements, there was a significant increase in causality of death as due to sudden unexplained death (relative risk = 5.1 [95% confidence interval, 1.4–18.7]). Conclusions: Active surveillance of mortality in an autopsy-derived series of young adults finds atherosclerotic coronary disease and idiopathic sudden death are common etiologies of death when taking supplements, but no cardiac structural or histologic mechanism to suggest different pathologic process than a matched control population. (PACE 2012; 35:1332–1337)

Although studies have indicated that the levels of catecholamines increase during sepsis, it remains unknown whether the elevated levels of epinephrine, norepinephrine, and dopamine observed in early sepsis are sustained during late, hypodynamic stages of sepsis. In this study, rats were subjected to sepsis by cecal ligation and puncture (CLP, i.e., polymicrobial sepsis). Immediately after CLP or sham operation, animals received 3 mL/100 g body weight normal saline subcutaneously. At .5, 2, 10 (i.e., early sepsis), or 20 h (late sepsis) after CLP, blood samples were drawn and the plasma was separated. Plasma levels of epinephrine, norepinephrine, and dopamine were determined using a [3H]-radioenzymatic assay. The results indicate that plasma levels of epinephrine, norepinephrine, and dopamine increased significantly as early as .5 h after CLP. The increase in catecholamine levels persisted throughout the study periods. Thus, circulating levels of catecholamines were elevated in both early and late stages of polymicrobial sepsis. These results suggest that the increased catecholamine levels at .5-10 h after CLP may contribute to the hypermetabolic conditions that occur during early, hyperdynamic sepsis. However, there is a lack of an association between the elevated plasma catecholamine levels and hypometabolic/hypodynamic state in late sepsis.

To evaluate supplement use, most notably ephedra, which has been temporally associated with sudden death. Animal models suggest increased myocardial irritability may predispose to primary arrhythmic death.Clinical, pathological, and investigative records from the Office of the Armed Forces Medical Examiner's Cardiovascular Death Registry were reviewed. Forty-eight cases of those with known supplement use were compared to 144 age-, gender-, and socioeconomic-matched controls in a 1:3 case:control manner.Of the 48 sudden deaths temporally associated with supplement use, the mean age was 34.2 ± 10.0 years and predominantly male (n = 44, 91.7%). The underlying cause of death was fatal atherosclerotic coronary disease in 18 (37.5%), sudden unexplained death in 16 (33.3%), and hypertrophic cardiomyopathy in six (12.5%). Compared with controls, there were no statistically significant differences in adjudicated cause of death. On autopsy, there were no differences in cardiac mass, ventricular wall thickness, or presence of atherosclerosis in those known to be taking identified supplements compared to a control population. In the subject ≥35 years, and known to be taking supplements, there was a significant increase in causality of death as due to sudden unexplained death (relative risk = 5.1 [95% confidence interval, 1.4-18.7]).Active surveillance of mortality in an autopsy-derived series of young adults finds atherosclerotic coronary disease and idiopathic sudden death are common etiologies of death when taking supplements, but no cardiac structural or histologic mechanism to suggest different pathologic process than a matched control population.

The purpose of this study was to define the incidence and characterization of cardiovascular cause of sudden death in the young.The epidemiology of sudden cardiac death (SCD) in young adults is based on small studies and uncontrolled observations. Identifying causes of sudden death in this population is important for guiding approaches to prevention.We performed a retrospective cohort study using demographic and autopsy data from the Department of Defense Cardiovascular Death Registry over a 10-year period comprising 15.2 million person-years of active surveillance.We reviewed all nontraumatic sudden deaths in persons 18 years of age and over. We identified 902 subjects in whom the adjudicated cause of death was of potential cardiac etiology, with a mean age of 38 ± 11 years. The mortality rate for SCD per 100,000 person-years for the study period was 6.7 for males and 1.4 for females (p0.0001). Sudden death was attributed to a cardiac condition in 715 (79.3%) and was unexplained in 187 (20.7%). The incidence of sudden unexplained death (SUD) was 1.2 per 100,000 person-years for persons35 years of age, and 2.0 per 100,000 person-years for those ≥ 35 years of age (p0.001). The incidence of fatal atherosclerotic coronary artery disease was 0.7 per 100,000 person-years for those35 years of age, and 13.7 per 100,000 person-years for those ≥ 35 years of age (p0.001).Prevention of sudden death in the young adult should focus on evaluation for causes known to be associated with SUD (e.g., primary arrhythmia) among persons35 years of age, with an emphasis on atherosclerotic coronary disease in those ≥ 35 years of age.