Vital exhaustion not a risk factor for sudden cardiac death
Vital exhaustion (VE)—defined as lack of energy, increased fatigue and irritability, and feelings of demoralization—does not contribute to an increased risk of sudden cardiac death (SCD), according to a US study.
The present investigation used data from a biracial (black and white) cohort of 13,923 individuals aged 45 to 64 years at baseline from the ARIC (Atherosclerosis Risk in Communities) study. VE, measured using the Maastricht questionnaire, was low among 4,464, moderate among 4,869 and high among 4,590 participants. Those with high VE were particularly older and more likely to exhibit cardiovascular disease risk factors. [Heart 2017;doi:10.1136/heartjnl-2017-311825]
A total of 457 SCD events occurred during a median follow-up of 21.2 years, with the incidence rate higher in the high vs low and moderate VE groups (1.98 vs 1.45 and 1.47 per 1,000 person-years).
The highest VE tertile was associated with a 48-percent increase in the risk of SCD (hazard ratio [HR], 1.48; 95 percent CI, 1.17 to 1.87; p=0.001) in a Cox proportional hazards model controlling for age, sex and race/centre. However, this association disappeared after adjustment for established cardiovascular disease risk factors (HR, 0.94; 0.73 to 1.20; p=0.609). Results were robust to various definitions of SCD.
SCD was defined as follows: 1) a sudden pulseless condition presumed due to a ventricular tachyarrhythmia in a previously stable individual without evidence of a noncardiac cause (eg, drug overdose, stroke, aortic aneurysm rupture, other acute bleeding, pulmonary embolism, acute respiratory failure or trauma); 2) fatal coronary heart disease (CHD) within 1 hour of symptom onset; and 3) fatal CHD within 24 hours of symptom onset.
Contrary to previous reports of an association between VE and various cardiovascular disease endpoints, including the ARIC study, the present data do not show an association between VE and SCD over either short- or long-term follow-up on adjustment, the investigators pointed out. [Ann Epidemiol 2004;14:416–24; Am J Cardiol 2010;105:1661–5; Eur Heart J 2015;36:1385–93]
“While it is possible that our differing conclusions may be attributable to the outcome definition, our conclusions were predominately consistent for several SCD endpoints,” they said, while acknowledging the difficulty of ascertaining SCD and the absence of a uniform agreement on how to operationally define SCD.
“[B]ased on our findings, it may be more accurate to view VE as possible precursor to more prevalent cardiovascular disease events than as a predictor specific to SCD,” the investigators said.
More studies are warranted to further examine the relation of psychosocial stressors with SCD, they added.