Twelve Weeks of Successful Smoking Cessation Therapy with Varenicline Reduces Spirometric Lung Age.

Objective We evaluated the short-term effects of smoking cessation therapy with varenicline on the lung function. Methods In this study, 81 subjects received 12 weeks of smoking cessation therapy with varenicline. No changes were made to any previously prescribed medications. A physical examination, blood sampling, and spirometry were performed at the first and last visit. Spirometric lung ages were calculated by a formula based on height and the forced expiratory volume in 1 second. The success group comprised 62 subjects who attained 4-week continuous abstinence confirmed by exhaled carbon monoxide testing; whereas the failure group comprised 19 subjects who did not attain this result. However, the number of cigarettes consumed per day was reduced in all subjects of the failure group. Results The spirometric lung ages significantly improved over the 12-week period in the success group (69.8±24.7 vs. 66.9±24.1, p<0.01); however, spirometric lung ages significantly deteriorated in the failure group (70.5±25.5 vs. 73.7±26.9, p<0.01). The effect sizes (Cohen's d) of spirometric lung age in the success and failure groups were 0.37 and 0.81, respectively. The post-hoc statistical power of the spirometric lung age in the success and failure groups was 0.83 and 0.91, respectively. According to a multiple regression analysis, success in smoking cessation exhibited an independent association with the difference in spirometric lung age between the last visit and baseline (p<0.01). Conclusion These findings suggest that successful smoking cessation therapy with varenicline improves the spirometric lung age in the short term.

Twelve weeks of smoking cessation therapy with varenicline increases the serum levels of apolipoprotein A-I only in the success group.

BACKGROUND: Cigarette smoking adversely affects lipid profiles, and smoking cessation should improve lipid profiles in the long term. However, it remains unclear whether intensive, medication-based smoking cessation therapy can affect lipid profiles in the short term. Thus, we evaluated the short-term effects of smoking cessation therapy with varenicline on lipid profiles. METHODS: Participants included 86 consecutive subjects who received 12 weeks of smoking cessation therapy. All subjects were treated with varenicline, and no changes were made to their current lipotropic and antidiabetic medications during treatment. At first and last visits, lipid profiles and fasting blood glucose and hemoglobin A1c levels were evaluated and physical examination was performed. The success group, comprising subjects who attained exhaled carbon monoxide-confirmed 4-week continuous abstinence, included 69 subjects, whereas the failure group, comprising those who did not achieve complete smoking cessation, included 17 subjects. The number of cigarettes consumed per day was reduced in all subjects in the failure group. RESULTS: Serum apolipoprotein A-I (apoA-I) and high-density lipoprotein cholesterol (HDL-C) levels significantly increased from baseline to 12 weeks in the success group (apoA-I: 151.7 ± 28.0 vs. 158.6 ± 27.3 mg/dL, respectively, p<0.01; HDL-C: 54.6 ± 15.7 vs. 57.9 ± 14.3 mg/dL, respectively, p<0.01); however, there were no statistically significant differences observed in the failure group (apoA-I, 145.9 ± 33.4 vs. 146.8 ± 34.2 mg/dL, respectively, p=0.87; HDL-C, 52.6 ± 15.7 vs. 53.3 ± 16.3 mg/dL, respectively, p=0.80). The effect sizes (Cohen's d) of apoA-I and HDL-C in the success group were 0.42 and 0.46, respectively. The post hoc statistical power values of apoA-I and HDL-C in the success group were 0.94 and 0.96, respectively. CONCLUSION: These findings suggest that successful smoking cessation therapy with varenicline improves serum apoA-I and HDL-C levels in the short term.

Association of low serum levels of apolipoprotein A-I with adverse outcomes in patients with nonischemic heart failure.

BACKGROUND: There is extensive evidence that low serum levels of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apoA-I) predict a worse prognosis in patients with ischemic heart disease. This study examined whether apoA-I levels may also provide prognostic information in patients with nonischemic heart failure. METHODS AND RESULTS: A prospective follow-up study was performed in 117 consecutive patients with nonischemic heart failure for a period of < or = 36 months until the first occurrence of 1 of the following clinical events: all-cause death, cardiac death, and hospitalization with worsening heart failure. Serum levels of apoA-I were measured by immunoturbidimetry. A clinical event occurred during follow-up in 28 (24%) patients. A multivariate Cox proportional hazards analysis showed that lower apoA-I levels (< 103 mg/dL: determined by a receiver-operating characteristic analysis) were significantly associated with an adverse outcome that was independent of creatinine clearance, HDL cholesterol levels, and brain natriuretic peptide levels. ApoA-I was inversely correlated with levels of C-reactive protein and fibrinogen, known inflammatory predictors of poor prognosis in heart failure. CONCLUSIONS: Low levels of apoA-I are independently associated with an adverse prognosis in patients with nonischemic heart failure. ApoA-I may play a beneficial role in nonischemic heart failure partly through an anti-inflammatory action.

Association of high levels of plasma free dopamine with future coronary events in patients with coronary artery disease.

BACKGROUND: There is an intimate relationship between activation of the sympathetic nervous system and myocardial ischemia. This study examined whether plasma levels of dopamine, a precursor of norepinephrine, may provide prognostic information in coronary artery disease (CAD). METHODS AND RESULTS: Plasma levels of free dopamine were measured by high-performance liquid chromatography in 210 consecutive patients with stable CAD. The patients were prospectively followed up for a period of < or =36 months until occurrence of a clinical coronary event. Coronary events occurred in 37 patients during follow-up. In Kaplan-Meier survival analysis, higher dopamine levels (> or =30 pg/ml) resulted in a higher event probability (p<0.01). Multivariate Cox hazards analysis showed that higher dopamine levels were a significant and independent risk factor for future coronary events (hazard ratio 3.3, 95% confidence interval 1.3-8.1, p<0.01). Furthermore, patients with higher dopamine levels had lower left ventricular (LV) ejection fraction and higher levels of brain natriuretic peptide, C-reactive protein, and fibrinogen than those with lower dopamine levels. CONCLUSIONS: Plasma levels of free dopamine are increased in association with a decrease in LV function and an increase in inflammatory risk markers. Higher free dopamine levels are an independent risk factor for future coronary events in CAD patients.