A prospective study of statin use and mortality among 67,385 blacks and whites in the Southeastern United States.

PURPOSE: The primary objective of this study is to examine the race-specific associations between statin use and overall mortality, as well as cardiovascular and cancer mortality, among blacks and whites in the Southeastern United States (US). Little is known about these associations in blacks. PATIENTS AND METHODS: The Southern Community Cohort Study is an ongoing, prospective cohort study, which enrolled from 2002 through 2009 nearly 86,000 participants aged 40-79 years. We used Cox regression models to estimate race-specific hazard ratios (HRs) and 95% confidence intervals (CI) for overall and cause-specific mortality associated with statin use based on self-reported hypercholesterolemia and treatment at cohort entry. Mean age at cohort entry was 51.4 years in blacks (n=48,825) and 53.5 years in whites (n=18,560). Sixty-one percent of participants were women. Whites were more likely to have self-reported hypercholesterolemia (40% versus 27%, P<0.001), and to report being treated with either statins (52% versus 47%, P<0.001) or combination lipid therapy (9% versus 4%, P<0.001) compared with blacks, regardless of sex. During follow-up (median: 5.6 years) 5,199 participants died. Compared with untreated hypercholesterolemic individuals, statin use was associated with reduced all-cause mortality (adjusted HR [aHR] 0.86; 95% CI 0.77-0.95) and cardiovascular disease mortality overall (aHR 0.75; 95% CI 0.64-0.89) and among whites (aHR 0.67; 95% CI 0.50-0.90), blacks (aHR, 0.80; 95% CI 0.65-0.98), men (aHR 0.70; 95% CI 0.55-0.90), and women (aHR 0.79; 95% CI 0.63-0.99) (P>0.05 for race and sex interaction). Statin use was not associated with cancer mortality overall or in subgroup analyses. CONCLUSION: Regardless of race or sex, self-reported statin use was linked to reduced all-cause and cardiovascular disease mortality. However, factors contributing to the modestly lower statin use and markedly lower prevalence of self-reported hypercholesterolemia among blacks remain to be determined.

Confounders of vasovagal syncope: orthostatic hypotension.

A syncope evaluation should start by identifying potentially life-threatening causes, including valvular heart disease, cardiomyopathies, and arrhythmias. Most patients who present with syncope, however, have the more benign vasovagal (reflex) syncope. A busy syncope practice often also sees patients with neurogenic orthostatic hypotension presenting with syncope or severe recurrent presyncope. Recognition of these potential confounders of syncope might be difficult without adequate knowledge of their presentation, and this can adversely affect optimal management. This article reviews the presentation of the vasovagal syncope confounder and the putative pathophysiology of orthostatic hypotension, and suggests options for nonpharmacologic and pharmacologic management.

Confounders of vasovagal syncope: postural tachycardia syndrome.

Most patients who present to a cardiologist with syncope have vasovagal (reflex) syncope. A busy syncope practice often also sees patients with postural tachycardia syndrome, often presenting with severe recurrent presyncope. Recognition of this syncope confounder might be difficult without adequate knowledge of their presentation, and this can adversely affect optimal management. Postural tachycardia syndrome can often be differentiated from vasovagal syncope by its hemodynamic pattern during tilt table test and differing clinical characteristics. This article reviews the presentation of postural tachycardia syndrome and its putative pathophysiology and presents an approach to nonpharmacologic and pharmacologic management.