ObjectiveIn this study, we evaluated obesity as a single risk factor for coronary artery disease (CAD), along with the synergistic effect of obesity and other risk factors.MethodsA retrospective study of 7,567 patients admitted to hospital for chest pain from 2005 to 2014 and underwent cardiac catheterization. Patients were divided into two groups: obese and normal with body mass index (BMI) calculated as ≥30 kg/m2 and <25, respectively. We assessed the modifiable and non-modifiable risk factors in obese patients and the degree of CAD.ResultsOf the 7,567 patients who underwent cardiac catheterization, 414 (5.5%) had a BMI ≥30. Of 414 obese patients, 332 (80%) had evidence of CAD. Obese patients displayed evidence of CAD at the age of 57 versus 63.3 in non-obese patients (p<0.001). Of the 332 patients with CAD and obesity, 55.4% had obstructive CAD versus 44.6% with non-obstructive CAD. In obese patients with CAD, male gender and history of smoking were major risk factors for development of obstructive CAD (p=0.001 and 0.01, respectively) while dyslipidemia was a major risk factor for non-obstructive CAD (p=0.01). Additionally, obese patients with more than one risk factor developed obstructive CAD compared to non-obstructive CAD (p=0.003).ConclusionHaving a BMI ≥30 appears to be a risk factor for early development of CAD. Severity of CAD in obese patients is depicted on non-modifiable and modifiable risk factors such as the male gender and smoking or greater than one risk factor, respectively.

BackgroundNiacin induces the release of vasodilating prostaglandins, for which receptors are present within the pulmonary arterial circulation. We hypothesized that immediate-release niacin would reduce right ventricular systolic pressure in patients with pulmonary hypertension in a randomized, double-blinded, single-dose provocation study.MethodsWe recruited inpatient subjects with a Doppler echocardiogram showing a peak tricuspid regurgitation (TR) jet velocity of 2.7 m/s or greater, and who were free of known pulmonary vascular disease. Subjects were randomized in a 1:2:2 ratio to receive a single dose of either placebo, niacin 100 mg or niacin 500 mg, respectively. TR jet velocities were measured immediately before, and 1 hour post dose, corresponding to peak niacin absorption and prostaglandin release. The primary endpoint was the change in mean TR jet velocity measured over ten successive cardiac cycles.ResultsThe baseline mean estimated right ventricular systolic pressure (RVSP) for all 49 subjects (25 male) was 51.9 ± 12.1 mm Hg. The primary endpoint of mean change in TR jet velocity was 0.016 ± 0.065 m/s in the placebo group, compared to −0.017 ± 0.065 m/s with niacin 100 mg, and −0.063 ± 0.038 m/s with niacin 500 mg (P = 0.63). The change in maximum estimated RVSP across the three drug groups was 0.2 ± 1.6 mm Hg, −1.3 ± 1.8 mm Hg and −2.2 ± 1.2 mm Hg (P = 0.62). In exploratory pairwise analysis in the high-dose niacin group (500 mg), the reduction in mean RVSP was from 50.9 ± 9.4 mm Hg to 48.7 ± 10.0 mm Hg (P = 0.09).ConclusionsA single dose of immediate-release niacin (100 mg or 500 mg) had no significant effect on RVSP 1 hour post administration. A nonsignificant dose-dependent trend for a modest reduction in RVSP, most notable in the 500 mg group, was noted.(ISRCTN number 12353191, registered April 23, 2015).Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-015-1013-6) contains supplementary material, which is available to authorized users.

IntroductionCoronary Artery Disease (CAD) is a major cause of morbidity and mortality worldwide, and although mortality is decreasing, prevalence of CAD is increasing. A number of modifiable risk factors (smoking) and non-modifiable risk factors (gender, age) have well established association with CAD, whereas other potential risk factors (such as obesity) are less well established. In this study, we evaluated the obesity as a single risk factor for CAD and evaluated the synergistic effect of obesity with the other risk factors.MethodA retrospective study of 7,567 patients admitted to hospital for chest pain from 2005–2014 and underwent cardiac catheterization. Patients were divided into two groups: obese and normal with body mass index (BMI) calculated as ≥30 kg/m2 and ≤25, respectively. Patients with BMIs between 26 and 29 were excluded. We assessed the modifiable and non-modifiable risk factors in obese patients and the degree of CAD with coronary angiography as obstructive CAD (left main stenosis of ≥50% or any stenosis of ≥70%), non-obstructive CAD (≥1 stenosis ≥20% but no stenosis ≥70%) and normal coronaries.ResultsOf the 7,567 patients who underwent cardiac catheterization, 414 (5.5%) had a BMI ≥30. Of 414 obese patients, 332 (80%) had evidence of CAD. Obese patients displayed evidence of CAD at the age of 57 versus 63.3 in non-obese patients (p<0.001).Of the 332 patients with CAD and obesity, 55.4% had obstructive CAD versus 44.6% with non-obstructive CAD. In obese patients with CAD, Male gender and history of smoking were major risk factors for development of obstructive CAD (p=0.001 and 0.01, respectively) while dyslipidemia was a major risk factor for non-obstructive CAD (p 0.01). Additionally, obese patients with more than one risk factor; developed obstructive CAD compared to non-obstructive CAD (p=0.003). Approximately 40% presented with STEMI, 30% with NSTEMI and 30% had stable angina as a primary diagnosis.Of the 332 obese patients with CAD, 24% received medical treatment, 58% underwent percutaneous coronary intervention (PCI) and 18% obtained coronary artery bypass grafting (CABG).In a gender comparison, average age of CAD in obese males were 55 years of age compared to 59 in females (p <0.001). Approximately 67% of males underwent PCI (OR: 2.4, 95% CI: 1.5–3.6, p<0.001) and 24% obtained CABG (OR: 3, 95% CI: 1.6–5.6, p<0.001), whereas in obese females 43% received medical therapy (OR: 9, 95% CI: 5–17, p<0.001).ConclusionHaving a BMI ≥30 appears to correlate as a risk factor for early development of CAD. Severity of CAD in obese patients is depicted on non-modifiable and modifiable risk factors such as the male gender and smoking or greater than one risk factor, respectively. Early lifestyle modification and education may provide benefit in striving to aid decreasing incidents of CAD and possibly lowering cardiovascular events.