Prevalence of and Risk Factors for Autopsy-Determined Atherosclerosis Among US Service Members, 2001-2011
ABSTRACT Autopsies of US service members killed in the Korean and Vietnam wars demonstrated that atherosclerotic changes in the coronary arteries can appear early in the second and third decades of life, long before ischemic heart disease becomes clinically apparent.
To estimate the current prevalence of coronary and aortic atherosclerosis in the US armed forces.
Cross-sectional study of all US service members who died of combat or unintentional injuries in support of Operations Enduring Freedom and Iraqi Freedom/New Dawn between October 2001 and August 2011 and whose cardiovascular autopsy reports were available at the time of data collection in January 2012. Prevalence of atherosclerosis was analyzed by various demographic characteristics and medical history. Classifications of coronary atherosclerosis severity were determined prior to data analysis and designed to provide consistency with previous military studies: minimal (fatty streaking only), moderate (10%-49% luminal narrowing of ≥1 vessel), and severe (≥50% narrowing of ≥1 vessel).
Prevalence of coronary and aortic atherosclerosis in the US armed forces and by age, sex, self-reported race/ethnicity, education, occupation, service branch and component, military rank, body mass index at military entrance, and International Classification of Diseases, Ninth Revision, Clinical Modification, diagnoses of cardiovascular risk factors.
Of the 3832 service members included in the analysis, the mean age was 25.9 years (range, 18-59 years) and 98.3% were male. The prevalence of any coronary atherosclerosis was 8.5% (95% CI, 7.6%-9.4%); severe coronary atherosclerosis was present in 2.3% (95% CI, 1.8%-2.7%), moderate in 4.7% (95% CI, 4.0%-5.3%), and minimal in 1.5% (95% CI, 1.1%-1.9%). Service members with atherosclerosis were significantly older (mean [SD] age, 30.5 [8.1] years) than those without (mean [SD] age, 25.3 [5.6] years; P < .001). Comparing atherosclerosis prevalence among with those with no cardiovascular risk factor diagnoses (11.1% [95% CI, 10.1%-12.1%]), there was a greater prevalence among those with a diagnosis of dyslipidemia (50.0% [95% CI, 30.3%-69.7%]; age-adjusted prevalence ratio [PR], 2.09 [95% CI, 1.43-3.06]), hypertension (43.6% [95% CI, 27.3%-59.9%]; age-adjusted PR, 1.88 [95% CI, 1.34-2.65]), or obesity (22.3% [95% CI, 15.9%-28.7%]; age-adjusted PR, 1.47 [95% CI, 1.10-1.96]), but smoking (14.1% [95% CI, 8.0%-20.2%]) was not significantly associated with a higher prevalence of atherosclerosis (age-adjusted PR, 1.12 [95% CI, 0.73-1.74]).
Among deployed US service members who died of combat or unintentional injuries and received autopsies, the prevalence of atherosclerosis varied by age and cardiovascular risk factors.
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ABSTRACT: 3-Hydroxy-3-methyl-glutarylCoA reductase inhibitors, or statins, are a mainstay in the treatment of patients with established coronary artery disease (CAD) because of their proven efficacy in reducing cardiovascular death, myocardial infarction, and coronary revascularization procedures in this patient population. Statin therapy has also proven successful in the primary prevention of CAD. However, the absolute reduction in cardiovascular events is lower in primary prevention than in secondary prevention trials, and many of the primary prevention trials enrolled a significant number of patients with established cardiovascular disease and/or other high-risk features, such as diabetes mellitus. For these reasons we do not recommend widespread treatment of the general adult population with a statin. Rather, we advocate a strategy which involves collection of standard clinical data and the use of validated risk-prediction tools to stratify patient risk and limit initiation of a statin to those who are more likely to benefit from such therapy.Missouri medicine 110(4):339-41.
- JAMA The Journal of the American Medical Association 12/2012; 308(24):2624-5. DOI:10.1001/jama.2012.164971 · 30.39 Impact Factor
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ABSTRACT: Residual risk, the ongoing appreciable risk of major cardiovascular events (MCVE) in statin-treated patients who have achieved evidence-based lipid goals, remains a concern among cardiologists. Factors that contribute to this continuing risk are atherogenic non-low-density lipoprotein (LDL) particles and atherogenic processes unrelated to LDL cholesterol, including other risk factors, the inherent properties of statin drugs, and patient characteristics, ie, genetics and behaviors. In addition, providers, health care systems, the community, public policies, and the environment play a role. Major statin studies suggest an average 28% reduction in LDL cholesterol and a 31% reduction in relative risk, leaving a residual risk of about 69%. Incomplete reductions in risk, and failure to improve conditions that create risk, may result in ongoing progression of atherosclerosis, with new and recurring lesions in original and distant culprit sites, remodeling, arrhythmias, rehospitalizations, invasive procedures, and terminal disability. As a result, identification of additional agents to reduce residual risk, particularly administered together with statin drugs, has been an ongoing quest. The current model of atherosclerosis involves many steps during which disease may progress independently of guideline-defined elevations in LDL cholesterol. Differences in genetic responsiveness to statin therapy, differences in ability of the endothelium to regenerate and repair, and differences in susceptibility to nonlipid risk factors, such as tobacco smoking, hypertension, and molecular changes associated with obesity and diabetes, may all create residual risk. A large number of inflammatory and metabolic processes may also provide eventual therapeutic targets to lower residual risk. Classically, epidemiologic and other evidence suggested that raising high-density lipoprotein (HDL) cholesterol would be cardioprotective. When LDL cholesterol is aggressively lowered to targets, low HDL cholesterol levels are still inversely related to MCVE. The efflux capacity, or ability to relocate cholesterol out of macrophages, is believed to be a major antiatherogenic mechanism responsible for reduction in MCVE mediated in part by healthy HDL. HDL cholesterol is a complex molecule with antioxidative, anti-inflammatory, anti-thrombotic, antiplatelet, and vasodilatory properties, among which is protection of LDL from oxidation. HDL-associated paraoxonase-1 has a major effect on endothelial function. Further, HDL promotes endothelial repair and progenitor cell health, and supports production of nitric oxide. HDL from patients with cardiovascular disease, diabetes, and autoimmune disease may fail to protect or even become proinflammatory or pro-oxidant. Mendelian randomization and other clinical studies in which raising HDL cholesterol has not been beneficial suggest that high plasma levels do not necessarily reduce cardiovascular risk. These data, coupled with extensive preclinical information about the functional heterogeneity of HDL, challenge the "HDL hypothesis", ie, raising HDL cholesterol per se will reduce MCVE. After the equivocal AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides: Impact on Global Health Outcomes) study and withdrawal of two major cholesteryl ester transfer protein compounds, one for off-target adverse effects and the other for lack of efficacy, development continues for two other agents, ie, anacetrapib and evacetrapib, both of which lower LDL cholesterol substantially. The negative but controversial HPS2-THRIVE (the Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events) trial casts further doubt on the HDL cholesterol hypothesis. The growing impression that HDL functionality, rather than abundance, is clinically important is supported by experimental evidence highlighting the conditional pleiotropic actions of HDL. Non-HDL cholesterol reflects the cholesterol in all atherogenic particles containing apolipoprotein B, and has outperformed LDL cholesterol as a lipid marker of cardiovascular risk and future mortality. In addition to including a measure of residual risk, the advantages of using non-HDL cholesterol as a primary lipid target are now compelling. Reinterpretation of data from the Treating to New Targets study suggests that better control of smoking, body weight, hypertension, and diabetes will help lower residual risk. Although much improved, control of risk factors other than LDL cholesterol currently remains inadequate due to shortfalls in compliance with guidelines and poor patient adherence. More efficient and greater use of proven simple therapies, such as aspirin, beta-blockers, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, combined with statin therapy, may be more fruitful in improving outcomes than using other complex therapies. Comprehensive, intensive, multimechanistic, global, and national programs using primordial, primary, and secondary prevention to lower the total level of cardiovascular risk are necessary.Vascular Health and Risk Management 01/2013; 9:617-670. DOI:10.2147/VHRM.S37119