OBJECTIVE:To evaluate the risks imposed by tobacco smoking, in particular, bidi smoking, in the development of lung cancer.METHODS:Two hundred eighty-four histologically confirmed patients of bronchogenic carcinoma and 852 controls matched for age, sex, and socioeconomic status were interviewed according to a predesigned questionnaire. Effects of individual variables defining the various aspects of tobacco smoking, in particular, bidi smoking, were assessed using logistic regression models.RESULTS:81.3% cases of bronchogenic carcinoma were ever smokers as compared with 42.2% among controls. The odd ratios for ever smoking, bidi smoking, and cigarette smoking were 5.9 (confidence interval [CI] 4.3, 8.4), 6.1 (CI 4.3, 8.7), and 5.3 (CI 2.7, 10.4), respectively.CONCLUSION:Bidi smoking poses a very high risk for lung cancer even more than that of cigarette smoking.

No abstract

The immediate haemodynamic dose response effects of beta blockade (propranolol: 2 to 16 mg) were compared with those of combined alpha beta blockade (labetalol: 10 to 80 mg) in a randomised study of 20 patients with stable angina pectoris. After control measurements, the circulatory changes induced by four logarithmically cumulative intravenous boluses of each drug in equivalent beta blocking doses were evaluated at rest, after which comparison of the effects of the maximum cumulative dose of each was undertaken during a four minute period of supine bicycle exercise. Propranolol, at rest, induced significant dose related reductions in heart rate and cardiac output, with reciprocal increases in the systemic vascular resistance and pulmonary artery occluded pressure; systemic arterial pressure was unchanged. Labetalol was followed by significant dose related decreases in systemic blood pressure and vascular resistance associated with a significant increase in cardiac output; heart rate and pulmonary artery occluded pressure were unchanged. The slope of the left ventricular pumping function curve relating output to filling pressure from rest to exercise was significantly depressed by propranolol but unchanged after labetalol. The less deleterious effects on left ventricular haemodynamic performance after alpha beta blockade in contrast to beta blockade alone in ischaemic heart disease may be attributable to the concomitant reduction in left ventricular afterload associated with the alpha blocking activity of labetalol.

A population based hybrid design combining element ofcohort and cross-sectional approach was used to develop a simple clinical algorithm to predict individual probability of developing hypertension (systolic BP > 140 mm lis and lor diastolic BP > 90 mmHg). 3615 soldiel'5 initially normotensive at the time of induction into high altitude, were studied by systematic random sampling. Multiple logistic regression analysis showed a high significant association between hypertension and age, body mass index (BMI), tobac:c:o smoking and alcohol consumption. Using the constant/coefficient values obtained from the logistic model and the receiver operating charaderistic:s (ROC) curve analysis, the following predictive rule was developed -"To the agein yean, add (BMix 3.86); also add 5.53 if he is a smoker; and add 19.81 ifhe consumes alcohol. Ifthe total exceeds 143, the individual is at high risk ofdeveloping hypertension. This algorithm carries a sensitivity of68.3% and specificity of 78.5%. ; 50: 175-180 MJAFll994

The differences between slow calcium blocking agents with respect to effects on heart rate, myocardial contractility and atrioventricular conducting time are well described; the relevance of such differences to the treatment of patients with impaired left ventricular function due to coronary heart disease is uncertain. The haemodynamic effects of equivalent hypotensive doses of nifedipine and verapamil were therefore compared in 20 patients with severe angina pectoris associated with angiographically documented coronary artery disease. 2 The plasma concentrations of nifedipine (mean 57 + 19; range 27-77 nglml) and verapamil (mean 147 + 14; range 117-260 ngtml) at the time of the haemodynamic measurements were of an order usually associated with substantial pharmacodynamic activity. 3 Sitting at rest nifedipine resulted in reduction in systemic arterial pressure (P < 0.05) and vascular resistance (P < 0.01); both the heart rate (P < 0.01) and cardiac output (P < 0.05) increased without any significant change in the left heart filling pressure. In contrast, verapamil, which similarly reduced systemic blood pressure (P < 0.05) and vascular resistance (P < 0.01), increased cardiac output (P < 0.05) and left heart filling pressure (P < 0.05) without any change in heart rate. 4 During upright bicycle exercise both drugs attenuated the angina induced in all subjects during the control exercise period. Despite reductions in systemic blood pressure and vascular resistance the cardiac output was unaltered on either drug at the same workload as in the control assessment. The reduction in exercise blood pressure following nifedipine induced a reflex tachycardia; this was not present, despite the similar hypotensive action, after verapamil. The pulmonary artery occluded pressure during exercise increased on verapamil but was unchanged following nifedipine. 5 Although both drugs reduced systemic blood pressure and left ventricular afterload, it is unlikely that the symptomatic improvement noticed by the majority of the patients can be explained on this basis. The present study suggested that verapamil, due to the attenuation of exercise tachycardia, ought to have amplified anti-anginal activity compared with nifedipine; however, the lesser depression of left ventricular function on the latter suggested that nifedipine may be a safer therapeutic choice in patients whose angina pectoris is complicated by some impairment of left ventricular function.