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The BMI is the most frequently used marker to evaluate obesity-associated risks. An alternative continuous index of lipid over accumulation, the lipid accumulation product (LAP), has been proposed, which is computed from waist circumference (WC, cm) and fasting triglycerides (TGs) (mmol/l): (WC - 65) x TG (men) and (WC - 58) x TG (women). We evaluated LAP and BMI as predictors of mortality in a high-risk cohort. Study population included 5,924 new consecutive patients seen between 1995 and 2006 at a preventive cardiology clinic. Fifty-eight percent of patients were discordant for their LAP and BMI quartiles. Patients whose LAP quartile was greater than BMI quartile had higher mortality compared with those with LAP quartile was lower than BMI quartile (8.2 vs. 5.4% at 6 years, P = 0.007). After adjustment for age, gender, smoking, diabetes mellitus, blood pressure, low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol (HDL-C), (ln)LAP was independently associated with mortality (hazard ratio (HR) = 1.46, P < 0.001). BMI was not associated with increased mortality (HR = 1.06, P = 0.39). Adding LAP to a model including traditional risk factors for atherosclerosis increased its predictive value (C statistic 0.762 vs. 0.750, P = 0.048). Adding BMI to the same model did not change its predictive value (0.749 vs. 0.750, P = 0.29). Subgroup analyses showed that LAP predicted mortality in the nondiabetic patients (adjusted HR for (ln)LAP 1.64, P < 0.001), but did not reach significance in the diabetic patients (HR = 1.21, P = 0.11). In conclusion, LAP and not BMI predicted mortality in nondiabetic patients at high risk for cardiovascular diseases. LAP may become a useful tool in clinical practice to stratify the risk of unfavorable outcome associated with obesity.

A common therapeutic approach in patients with type 2 diabetes mellitus who have elevated triglycerides (TGs) is to treat the hyperglycaemia before specifically targeting high TG. The aims of the current study were (i) to determine whether there was a relationship between glycated haemoglobin (HgbA1c) and TG levels at the baseline visit and (ii) to analyse the relationship between DeltaHgbA1c and DeltaTG after treatment.Among 650 consecutive diabetic patients seen in the Cleveland Clinic Preventive Cardiology Department, 372 had both baseline and post-treatment HgbA1c and TG values. We analysed the relationship between baseline HgbA1c and TG as well as between the change in HgbA1c and the change in TG. For analysis, patients were divided into nine groups by tertiles of HgbA1c (or =6.6, 6.7-7.8 and7.8%) and TG (or =1.75, 1.76-3.89 and3.89 mmol/l) at baseline.At baseline, there was a small correlation between HgbA1c and TG (r(2) = 0.051; p0.001). For the entire group, there was a significant correlation between DeltaHgbA1c and DeltaTG from baseline to follow-up (r(2) = 0.077; p0.001). Analyses by tertiles showed that DeltaTG were only associated with changes in two groups: HgbA1c tertile 3 (7.8%) and TG tertiles 2 (r(2) = 0.24; p0.0001) and 3 (r(2) = 0.187; p = 0.003). For every 1% change in the top tertile HgbA1c, there was a 9.3% change in TG (tertile 2) and a 9.8% change in TG (tertile 3).These observations suggest that for patients with diabetes mellitus and elevated TG, the effect of HgbA1c reduction has limited effects on TG reduction. Patients may benefit from TG-specific therapy initiated earlier rather than waiting to see effects of glycaemic control.

Aims To determine the association of serum uric acid with all-cause mortality and hyperglycaemia in patients with Type 2 diabetes. Methods Retrospective cohort analysis of 535 consecutive patients who had uric acid determinations between 1998 and 2004 and whose subsequent vital status was determined at a median of 4.5 years. The association with mortality was analysed with Cox proportional hazards models. The incremental predictive value of uric acid was examined with concordance indexes. The proportional risk of mortality was represented with the Kaplan-Meier survival curves by uric acid quartiles. Results We studied 370 men and 165 women aged 59.3 +/- 11.5 years. Mean uric acid was 371.7 +/- 106.2 micromol/l. Patients with glycated haemoglobin (HbA(1c)) > or = 9% had lower uric acid vs. the rest (342.2 +/- 112.1 vs. 383.5 +/- 106.2, P = 0.002). Overall mortality was 10.8%. For each 59 micromol/l increase in uric acid there was a 41% increase in risk of death (unadjusted analysis). The association of uric acid with mortality remained after adjustment for covariates (hazard ratio = 1.21, 95% confidence interval 1.07-1.45) and after gender subanalyses. Uric acid increased the accuracy of prediction when added to a model including Framingham risk factors, components of metabolic syndrome and fibrinogen (P = 0.03). Mortality was higher in patients taking diuretics vs. the rest (15.9 vs. 7.3%), but uric acid predicted mortality in both subgroups. Conclusions Serum uric acid predicts mortality in Type 2 diabetic patients regardless of gender, HbA(1c), renal function and diuretic use. Intervention studies should determine whether uric acid is a potential therapeutic target or only a marker of mortality risk.

Thyroid hormones have profound effect on the heart and peripheral vasculature. Hypothyroidism is associated with an increase in a number of coronary heart disease (CHD) risk factors including dyslipidemia, hypertension, and elevated levels of homocysteine. Our objective was to assess the effects of hypothyroidism (thyroid-stimulating hormone [TSH]:10 μ U/mL), moderate subclinical hypothyroidism (SCH; TSH: 6.1-10 μ U/mL), and mild SCH (TSH: 3.1-6.0 μ U/mL) on cardiovascular risk factors, CHD prevalence, and all-cause mortality in patients at high risk for CHD seen in a preventive cardiology clinic.All patients seen in the Cleveland Clinic Preventive Cardiology clinic have demographic and laboratory tests including TSH and multiple CHD risk factors obtained at the baseline visit. All data are entered into a database (called PreCIS). The social security death index is queried monthly to determine all-cause mortality.Several CHD risk factors including age, male gender, systolic blood pressure, triglycerides, and fibrinogen were more common in hypothyroid patients. Prevalence of CHD was more common in hypothyroid and moderate SCH patients. All-cause mortality was higher in hypothyroid and moderate SCH patients, but not in mild SCH patients. Higher mortality in these groups was observed in both genders, patients under 65 years of age, and patients not on thyroid replacement therapy, but was not observed in patients over 65 years of age.Hypothyroidism and moderate, but not mild, SCH are associated with increased CHD prevalence and all-cause mortality. These observations suggest patients with moderate, but not mild, SCH and patients at high risk for CHD should be treated with thyroid replacement therapy.

This study examined the relationships among health-related quality of life and risk factors of coronary artery disease (CAD) and all-cause mortality in high-risk cardiac patients seen in a cardiology prevention clinic. At baseline, 1785 patients (age, 53.4+/-13.4 years; 58.8% men) had a medical history, physical examination, and laboratory tests. They completed the Medical Outcomes Study Short Form-36-Item Health Survey (SF-36). Analyses were conducted on associations of 2 SF-36 domain scores (overall physical health [OPH] and overall mental health [OMH]) with CAD biomarkers and all-cause mortality. Lower OPH scores were associated with CAD risk factors including smoking; history of hypertension, diabetes, and peripheral artery disease; the metabolic syndrome; and other novel CAD biomarkers. Lower OMH scores showed similar but weaker associations with CAD risk factors. OPH significantly predicted 5-year mortality in multivariable survival analysis. SF-36, especially OPH, was associated with many risk factors of CAD and significantly predicted mortality.

Objective Uric acid is a product of the activity of xanthine oxidase, an enzyme linked to oxidative stress, endothelial dysfunction, and heart failure. It is unclear whether adding uric acid levels to the assessment of cardiovascular risk might contribute to the improved ability to stratify cardiovascular risk. The purpose of this study was to evaluate the prognostic value of serum uric acid levels in a large cohort of men and women at high risk of cardiovascular disease. Methods Serum uric acid levels were determined in all patients seen for primary/secondary cardiovascular disease prevention at the Cleveland Clinic Section of Preventive Cardiology and Rehabilitation between 1998 and 2004, and all data were entered into the Preventive Cardiology Information System (PreCIS) database. Vital status of the patients was determined through the Social Security Death Index. Death from all causes was summarized across quartiles of uric acid values. Results A total of 3,098 patients (age range 18–87 years) were identified in the database, among whom 43% had cardiovascular disease. There were 156 deaths (5%) during the 14,262 person-years of followup. For each 1-mg/dl increase in the serum uric acid level, there was a 39% increase in the risk of death (by Cox regression analysis). After adjusting for age, sex, smoking status, alcohol consumption, weight, body mass index, waist circumference, blood pressure, history of cardiovascular disease, estimated glomerular filtration rate, levels of cholesterol fractions, and plasma glucose levels, the serum uric acid level continued to predict the risk of death (hazard ratio = 1.26 [95% confidence interval 1.15–1.38], P < 0.001). This association was present regardless of diuretic use. Concordance index (C statistic) analyses showed that uric acid significantly improved the predictive accuracy of a model that included Framingham Heart Study score factors, metabolic syndrome components, and fibrinogen levels. Conclusion Serum uric acid levels are an independent predictor of death in patients at high risk of cardiovascular disease. Further studies are warranted to evaluate its prognostic implications and potential utility in the monitoring of therapy.