Metabolic Syndrome and the Risk of Coronary Heart Disease in 367 Patients Treated With Second-Generation Antipsychotic Drugs

Christoph U. Correll, M.D.; Anne M. Frederickson, M.D.; John M. Kane, M.D.; and Peter Manu, M.D.

Objective: To examine the relationship between presence of metabolic syndrome and the risk of coronary heart disease (CHD) events (angina pectoris, myocardial infarction, and sudden cardiac death) in patients treated with second-generation antipsychotic medications.

Method: 367 adults treated with second-generation antipsychotics randomly selected from consecutive psychiatric admissions to a single hospital between August 1, 2004, and March 1, 2005, underwent assessments evaluating the presence of metabolic syndrome. The 10-year risk of CHD events was calculated according to the Framingham scoring system for age, smoking, total cholesterol, high-density lipoprotein (HDL)-cholesterol, blood pressure, and history of diabetes and was compared in patients with and without the metabolic syndrome.

Results: Metabolic syndrome, present in 137 patients (37.3%), was associated with a significantly greater age- and race-adjusted 10-year risk of CHD events, i.e., 11.5% vs. 5.3% for men (risk ratio = 2.18, 95% CI = 1.88 to 2.48, p < .0001) and 4.5% vs. 2.3% for women (risk ratio = 1.94, 95% CI = 1.65 to 2.23, p = .0005). The increased risk of CHD events in patients with metabolic syndrome remained significant after the exclusion of diabetic patients. In a logistic regression analysis of variables independent of the Framingham scoring system, triglyceride levels (p < .0001), waist circumference (p = .035), and white race (p = .047) were significantly associated with the 10-year risk of CHD events (R² = 0.134; p < .0001).

Conclusions: These data confirm the high prevalence of metabolic syndrome in patients receiving second-generation antipsychotics, indicate that metabolic syndrome doubles the 10-year risk of CHD events in this population, and emphasize the importance of the "hypertriglyceridemic waist" for the identification of psychiatric patients at high risk of CHD.

(J Clin Psychiatry 2006;67:575-583)

Received Aug. 30, 2005; accepted Jan. 9, 2006. From The Zucker Hillside Hospital, North Shore-Long Island Jewish Health System, Glen Oaks, N.Y. (all authors), and Albert Einstein College of Medicine, Bronx, N.Y. (Drs. Kane and Manu).

Supported by The Zucker Hillside Hospital Advanced Center for Intervention and Services Research for the Study of Schizophrenia (MH074543-01) grant from the National Institute of Mental Health, Bethesda, Md.

Dr. Correll has been a consultant to AstraZeneca, Bristol-Myers Squibb, and Eli Lilly and has served on the speakers/advisory boards of AstraZeneca, Bristol-Myers Squibb, and Janssen. Dr. Kane has been a consultant to Janssen, Pfizer, Eli Lilly, and Bristol-Myers Squibb and has received honoraria from Abbott, Bristol-Myers Squibb, and Janssen. Drs. Frederickson and Manu report no additional financial or other relationships relevant to the subject matter of this article.

The authors thank Bernadette M. Riordan, Zaimoon N. Hack, and Leslie Randolph of The Zucker Hillside Hospital for assistance with primary data collection.

Corresponding author and reprints: Peter Manu, M.D., Medical Services, Zucker Hillside Hospital, 75-59 263rd St., Glen Oaks, NY 11004 (e-mail: pmanu@lij.edu).