Harrison's Principles of Internal Medicine, 22nd Edition, Vol. 1 and Vol. 2

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and other predisposing conditions also increases. Although absolute SCD rates increase with age, the proportion of deaths that are due to SCD decreases as other causes of death increase.

Women have a lower incidence of SCD and SCA than men, and women are more likely to present with pulseless electrical activity and to have their SCD occur at home as compared with men. Possibly related to these factors, the SCD rate has not declined as much for younger women compared to men in recent years. Black as opposed to white Americans have higher rates of SCD, are more likely to have unwitnessed arrests and to be found with pulseless electrical activity, and have lower rates of survival. Socioeconomic disparities, with resuscitation being less likely in low-income neighborhoods, are contributing factors but do not appear to account for the entirety of the elevated SCD rate in blacks. Alternatively, individuals of Hispanic ethnicity appear to have lower rates of SCD, despite having a higher prevalence of cardiac risk factors. It appears that the incidence of SCD may be relatively low among Asian populations as well, both within the United States and globally. These gender and racial differences in SCD and SCA incidence and survival are poorly understood and warrant further research.

RISK FACTORS

The presence of overt structural heart disease and or certain types of inherited arrhythmia syndromes markedly elevates SCD risk. Preexisting CHD and HF are the most prevalent predisposing cardiac conditions and are associated with a four to tenfold increase in SCD risk. Correspondingly, SCD shares many of the same risk factors with CHD and heart failure, including hypertension, diabetes, hypercholesterolemia, obesity, and smoking. Diabetes is a particularly strong risk factor for SCD even in patients with established CHD. Hypertension and resultant left ventricular hypertrophy appear to be particularly important markers of SCD risk in blacks, in whom the prevalence of these conditions is greater. Smoking markedly elevates risk, and smoking cessation lowers risk particularly among individuals who have not yet developed overt CHD. Serum cholesterol appears to be more strongly related to SCD at younger ages, and the benefits of cholesterol lowering on SCD incidence have not been firmly established. There also appears to be a genetic component to SCD risk that is distinct from that associated with other manifestations of atherosclerosis. A history of SCD in a first-degree relative is associated with an increased risk for SCD, and with the occurrence of ventricular fibrillation during acute MI, but is not associated with an increased risk for acute MI. These data suggest that genetic factors may predispose to fatal ventricular arrhythmia in the setting of ischemia, rather than to CHD in general.

Obstructive sleep apnea and seizure disorders are also associated with increased SCD risk; the underlying mechanism is not clear but may be due to hypoxia-induced cardiac arrest. Atrial fibrillation also appears to be associated with an increased risk of SCD, which is partly, but not entirely, accounted for by its association with underlying heart disease. Patients with chronic kidney disease are also at higher SCD

risk with annualized SCD rates approaching five point five percent in patients undergoing dialysis. Electrolyte shifts and left ventricular hypertrophy, which are common in this population, have been suggested to play a role. There are also potential dietary influences on SCD risk. Individuals with higher intakes of polyunsaturated fatty acids, particularly n-three fatty acids, and other components of a Mediterranean-style diet have lower SCD risks in observational studies, possibly due to antiarrhythmic effects of dietary components. Low levels of alcohol intake may be beneficial, but heavy intake greater than three drinks per day appears to elevate risk.