Chlamydia pneumoniae and luminal narrowing after coronary angioplasty.

OBJECTIVES: Numerous studies have linked Chlamydia pneumoniae with atherosclerotic vessel disease and a trend for an association of the bacteria with restenosis after percutaneous transluminal coronary angioplasty (PTCA) has also been observed. The aim of this study was to assess the role of Chlamydia pneumoniae in the luminal narrowing taking place after PTCA. DESIGN: A noninterventional 6-month follow-up study. SETTING: A university hospital. SUBJECTS: A total of 122 patients with angiographically proven coronary heart disease (CHD) referred for PTCA. INTERVENTIONS: None. MAIN OUTCOME MEASURES: The degree of luminal narrowing in the coronary arteries following coronary angioplasty. RESULTS: The levels of C. pneumoniae antibodies (IgG, IgA and IgM classes) and immune complexes were not associated with luminal narrowing after PTCA in multivariate analyses whilst smoking, plasma endothelin levels and diabetes were. The serologic parameters did not change during the follow up either. CONCLUSIONS: These results do not support a role for C. pneumoniae in luminal narrowing following PTCA.

Influence of continued smoking and some biological risk factors on restenosis after percutaneous transluminal coronary angioplasty.

OBJECTIVES: To identify possible biological risk factors for restenosis following successful percutaneous transluminal coronary angioplasty (PTCA) in patients having single or multivessel disease. The effect of continued smoking on restenosis was also evaluated. DESIGN: In this prospective smoking controlled study all subjects had a routine angiographic restudy after 6 months. The biological risk factors assessed before angioplasty were adrenaline, endothelin, fibrinogen, lipoprotein (a) and tissue plasminogen activator. SUBJECTS: The study population consisted of 122 patients of whom 25% were current smokers. MAIN OUTCOME MEASURES: Angiographic restenosis was defined as at least 50% diameter stenosis on the follow-up angiogram after an initially successful procedure. RESULTS: Restenosis was observed in 43% of patients. The restenosis rate was significantly lower among current smokers, but they were significantly younger and also had significantly less dilated stenoses. Multivariate analysis revealed the number of dilated stenoses, the mean inflation time, post-PTCA percentage diameter stenosis and left anterior descending coronary artery to be predictive of restenosis, while continued smoking was not. When only the lesion with the greatest loss in luminal diameter of each patient was considered, the multiple linear regression analysis revealed high endothelin level to be predictive of restenosis. CONCLUSIONS: This study revealed high endothelin levels to be predictive of luminal narrowing after angioplasty. In addition, the number of dilated stenoses, the mean inflation time, post-PTCA percentage diameter stenosis and stenosis location in the left anterior descending artery were found to be predictive of restenosis. However, continued smoking after angioplasty did not emerge as a risk factor for restenosis.

Smoking induced differences in autonomic responses in military pilot candidates.

The effects of smoking on autonomic function, the renin-angiotensin-aldosterone system, plasma catecholamine and 11-dehydro-thromboxane B2 values were studied in 37 young male military pilot candidates, 19 smokers and 18 non-smokers. There was a higher diastolic blood pressure at rest and higher systolic blood pressure after 5 min during the orthostatic test in smokers. Smokers also had higher diastolic blood pressure levels after exercise in the hand-grip test. Smokers had a lower Valsalva ratio and higher tachycardia ratio in the modified Valsalva manoeuvre, suggesting a degree of autonomic dysfunction. Plasma renin levels at rest and plasma noradrenaline levels after hand-grip test were significantly higher in smokers, implying increased sympathetic activity and enhanced activation of the renin-angiotensin system. Our findings indicate that smoking in fit young men increases sympathetic activity and changes physiological responses to autonomic tests.

Enalapril versus atenolol in the treatment of hypertensive smokers.

A randomised crossover study has been done to compare the antihypertensive efficacy of enalapril and atenolol in 45 smoking, hypertensive men. Treatment was started with enalapril 20 mg/d or atenolol 50 mg/d and, if necessary, the doses were doubled after 4 weeks to achieve a sitting diastolic blood pressure < or = 95 mm Hg, after which hydrochlorothiazide was added, if necessary. Both drugs lowered blood pressure significantly. However, enalapril was more efficient in lowering both systolic and diastolic blood pressure; the mean difference was significant after both 4 and 8 weeks in the sitting systolic (11.6 mm Hg and 7.9 mm Hg) and diastolic (3.3 mm Hg and 3.0 mm Hg) pressures and in the erect systolic pressures (8.2 mm Hg and 7.2 mm Hg), and after 8 weeks in the supine systolic pressure, too (8.9 mm Hg). The effect on enalapril was especially marked in moderate (< 20 cigarettes/day) smokers. The need for diuretics was also significantly less in the enalapril group. It appears that angiotensin-converting enzyme inhibitors may be superior to beta-adrenoceptor blockers in the treatment of hypertensive smoking patients.

Cigarette smoking alters sympathoadrenal regulation by decreasing the density of beta 2-adrenoceptors. A study of monitored smoking cessation.

We report the effects of monitored smoking cessation on adrenergic regulation in chronic smokers. The beta 2 adrenoceptor density of mononuclear leukocytes (MNLs) and plasma catecholamines was analyzed before cessation and 2, 3, and 8 weeks after cessation. We found a progressive increase in beta-adrenoceptor density after smoking cessation. During smoking the beta-adrenoceptor density was 1.456 +/- 83 (mean +/- SEM) binding sites per cell (n = 10), whereas 3 weeks after cessation the density was 1,774 +/- 157 sites per cell (n = 10; p less than 0.05), and at 8 weeks, 1,900 +/- 227 sites per cell (n = 8; p less than 0.05), representing an overall increase of 23%. Smoking cessation had no effect on binding affinity nor on lymphocyte subgroup distribution. The density of MNL cell beta-adrenoceptors in age-matched nonsmoking men was higher, at 1,896 +/- 271 sites per cell, than that of the chronic smokers before cessation, 1,419 +/- 117 sites per cell (n = 14; p less than 0.01). Plasma epinephrine decreased as a result of cessation from 0.36 pmol/ml (0.26-0.44, 95% confidence interval; baseline) to 0.26 pmol/ml (0.20-0.32) at 8 weeks (p less than 0.05), and norepinephrine decreased from 2.09 pmol/ml (1.38-2.80) to 1.69 pmol/ml (1.14-2.24; p = 0.06). We conclude that stopping smoking progressively increases beta 2-adrenoceptor density on MNL cells. Eight weeks after cessation the adrenoceptor density reaches the corresponding level of nonsmokers. These reversible changes in adrenergic regulation after smoking cessation may be associated with the relatively rapid reduction in cardiovascular disease risk among ex-smokers.