Effects Of Long-term Cigarette Smoking Research Articles

Long-Term Effects of Cigarette Smoking on All-Cause Mortality and Cardiovascular Outcomes in Thai Population: Results From a 30-Year Cohort Study.

Despite the overwhelming evidences on the health consequences of smoking, studies in Asian population in low-to-middle income countries are very limited. Baseline data of a prospective cohort study were collected in year 1985. Endpoints regarding all-cause mortality and major adverse cardiovascular events (MACE) were followed for 30 years. Cox proportional hazard models were used for analysis. Participants had an average age of 43 years, 23% were female, and 43% were current smokers. All-cause mortality was significantly higher in ex-smokers (hazard ratio [HR] 1.32) and current smokers (HR 1.70) when compared with never smokers. Participants with any history of smoking had significantly higher risk of developing MACE. Furthermore, all-cause death, cardiovascular death, and MACE increased with increasing pack years. Statistically significant dose-response relationships were established. Therefore, cigarette smoking increased the risk of all-cause mortality, cardiovascular mortality, and MACE in Thai population. Results emphasized the importance of tobacco control in Thailand.

The Effect of Cigarette Smoking during Pregnancy on Endocrine Pancreatic Function and Fetal Growth: A Pilot Study.

Cigarette smoking in pregnancy is a common cause of fetal growth restriction. We aimed to investigate endocrine pancreatic function of mother-infant dyads in relation to cigarette smoking, as a possible mechanism for the poor fetal growth. Prospective study of smoking mothers (10 cigarettes or more per day, self-reported to the midwife) and non-smoker control mothers during their first pregnancy. Insulin, glucose, C-peptide, HbA1C, fructosamine, prolactin, serotonin, and cortisol were measured in maternal blood at 24-26 weeks and in umbilical cord blood at birth. Cotinine was also measured in cord blood. Of 37 smokers and 36 non-smokers recruited, cord blood was obtainable from 38 babies (19 in each group). In utero cigarette exposure was associated with lower birthweight (3,035 ± 490 versus 3,405 ± 598 g, p = 0.005), with linear modeling of the smoking cohort showing a 41 g reduction for every increase of one cigarette smoked per day (95% CI -71 to -11 g, p = 0.010). There were no differences between groups in indices of maternal or perinatal endocrine pancreatic dysfunction. Heavier smoking independently correlated with higher maternal fasting levels of glucose (p = 0.044) and C-peptide (p = 0.011). We did not observe any significant associations between the daily number of cigarettes and any of the cord blood parameters. We also looked for differences between cohorts based on infant gender. Serotonin levels were higher in smoking mothers with male fetuses (p = 0.01 to p = 0.004). Endocrine pancreatic dysfunction does not appear to be a major contributing factor to nicotine-associated fetal growth restriction. The higher serotonin levels in smoking mothers carrying male infants is of uncertain significance but could be a manifestation of gender differences in susceptibility to the long-term effects of cigarette smoking.

Effects of Habitual Cigarette Smoking on Retinal Circulation in Patients With Type 2 Diabetes.

To examine the long-term effects of cigarette smoking on retinal circulation in patients with type 2 diabetes. Seventy-four patients with type 2 diabetes mellitus and minimal (no or mild nonproliferative) diabetic retinopathy (DR) were evaluated. These patients with type 2 diabetes were divided into three groups based on their smoking history: current smokers (n = 19), past smokers (n = 20), and never smoked (n = 35). The retinal circulatory parameters were measured with laser Doppler velocimetry and were compared among the groups. There were significant decreases in the retinal blood flow (RBF; 8.9 ± 2.9 vs. 11.6 ± 3.1 μL/min, P = 0.009) with decreased blood velocity (V; 29.6 ± 6.8 vs. 37.8 ± 9.0 mm/s, P = 0.003) but no difference in the vessel diameter (D; 112.0 ± 11.9 vs. 113.7 ± 8.6 μm, P = 0.57) in the current smokers compared with those who never smoked. There were no differences in the RBF, blood V, and vessel D in the past smokers compared with those who never smoked and current smokers. Multiple regression analysis showed that the creatinine level was correlated negatively with the RBF and that current smoking was significantly and independent correlated with decreased RBF. Our results indicated that the blood V and RBF in the retinal arterioles may decrease in patients with type 2 diabetes who are chronic smokers, suggesting that chronic smoking may be associated with decreased RBF, probably via lower blood V in the retinal arterioles in early-phase DR.

A Qualitative Study of Smoking Behaviors among Newly Released Justice-Involved Men and Women in New York City.

Long-term effects of cigarette smoking result in an estimated 443,000 deaths each year, including approximately 49,400 deaths due to exposure to secondhand smoke. Tobacco is a major risk factor for a variety of chronic health problems, including certain cancers and heart disease. In this article, authors present qualitative findings derived from individual interviews with men and women who were incarcerated in New York state and New York City. Participants were 60 racially and ethnically diverse men and women ages 21 through 60 (M = 46.42, SD = 6.88). Of the participants interviewed, 91.7 percent released from a smoke-free correctional facility resumed cigarette smoking and 8.3 percent remained abstinent. Daily consumption ranged from smoking four cigarettes to 60 cigarettes. The four themes that emerged from the study were (1) lifetime exposure to cigarette smoking influences smoking behavior; (2) cigarettes help relieve stress and are pleasurable; (3) there is a relationship between access, availability, and relapse; and (4) smoking cessation strategies are available. Negative influences from participants' families and peers, stressful housing situations, and mandated programs emerged from this study as key challenges to abstaining from smoking cigarettes. Involving family members and partners in smoking cessation interventions could influence newly released justice-involved men and women not to resume cigarette smoking and possibly maintain long-term abstinence.

The relation of circulating YKL-40 to levels and decline of lung function in adult life

YKL-40 is a chitinase-like protein that, in cross-sectional clinical studies, has been associated with severe asthma and COPD in smokers. To determine the longitudinal relation of circulating YKL-40 to levels and decline of lung function in the general population. We used longitudinal data from up to 13 surveys from the population-based TESAOD study which was conducted in Tucson, Arizona between 1972 and 1996. In cross-sectional analyses, we also used data from 3 Spanish centers of the multicenter ECRHS study (ECRHS-Sp). Serum YKL-40 was measured at baseline in TESAOD and in survey 2 in ECRHS-Sp using ELISAs. Multivariate linear regression was used to test associations of serum YKL-40 to concomitant lung function. In TESAOD, random coefficients models were used to test associations of serum YKL-40 to subsequent decline of lung function. Data on YKL-40 and lung function were available from 1088 TESAOD and 854 ECRHS-Sp adult participants (59% and 51% females; respectively). In adjusted multivariate meta-analyses, being in the highest YKL-40 quartile was associated cross-sectionally with significant deficits in FEV1 and FVC %predicted. In adjusted longitudinal analyses, TESAOD participants in the top YKL-40 quartile had an FEV1 decline that was 5 ml/yr (p = 0.05) faster than subjects in the third quartile, 5 ml/yr (p = 0.02) faster than subjects in the second quartile, and 10 ml/yr (p < 0.001) faster than subjects in the lowest YKL-40 quartile. These longitudinal effects were particularly strong in smokers and absent in never smokers. After adjusting for covariates, as compared with the other three quartiles combined, the top YKL-40 quartile was associated with a 9 ml/yr (p = 0.001) faster FEV1 decline among smokers, while no significant effects were found among never smokers (2 ml/yr, p = 0.35). Circulating YKL-40 is associated with levels and decline of lung function in the general population and may be a biomarker of susceptibility to the long-term effects of cigarette smoking.

On Lung Function and Interactions Using Genome-Wide Data

On Lung Function and Interactions Using Genome-Wide Data

Dysfunction of high-density lipoprotein and its apolipoproteins: New mechanisms underlying cardiometabolic risk in the population at large

We review the metabolic and residual cardiovascular risk existing in populations with prevailing metabolic syndrome (MetS) or in people prone to impaired glucose tolerance. Evidence is presented that enhanced systemic inflammation, or oxidative stress associated with elevated plasma triglyceride-rich lipoproteins and their remnants, and excess oxidized lipoprotein(a) phospholipids underlie this risk. The adverse risk profile is augmented by loss of the anti-inflammatory, anti-oxidative and atheroprotective properties of high-density lipoprotein and its apolipoproteins (apo). Common clinical manifestations are atherogenic dyslipidemia and hypertriglyceridemia with elevated apoB or hypertriglyceridemic waist phenotype. These manifestations are often accompanied by such inflammatory mediators/markers as elevated serum apoE, C-reactive protein, complement C3, and uric acid levels. Compared with men, peri- and postmenopausal women are more commonly and more strongly affected by multiple inflammation mediators. The long-term effects of cigarette smoking are not adverse in such women, but instead, serve as protection against obesity and other health issues. ApoA-I may become dysfunctional in either gender, even in the absence of MetS and diabetes. The public health implications of this cardiometabolic risk are huge. Much research is needed on this topic to further clarify the impact of apoA-I dysfunction, to elucidate the underlying genetics and mechanisms, and to determine preventive measures and optimal management. Avoiding (abdominal) obesity via lifestyle modifications, including dietary changes, improving physical inactivity, and limiting smoking and alcohol consumption, are mainstay measures in the prevention and management of pro-inflammatory states and HDL dysfunction. Omega-3 fatty acids are a good adjunct to lower plasma triglycerides. When further treatment is needed, extended-release niacin or fibrates, with or without statins, are the best options.

Diverging sex-specific long-term effects of cigarette smoking on fasting insulin and glucose levels in non-diabetic people

ObjectivesWe determined in non-diabetic persons the associations of current smoking with future glucose and insulin concentrations. Design and methodsMiddle-aged non-diabetic adults (n=1071) were studied in whom these values were measured at baseline and 5.2-years later. ResultsAge-adjusted fasting insulin concentrations in 137 smoking men remained lower than never smokers at both surveys. While age-adjusted fasting glucose values in male never smokers declined at follow-up (p=0.037), they rose in male smokers. In 94 female smokers, age-adjusted fasting insulin values marginally declined, and fasting glucose was reduced (by 0.09mmol/L, p=0.055) during follow-up. In contrast in never-smoking women, insulin and glucose concentrations rose (p<0.001 in both). Age-adjusted insulin levels in former smokers exhibited similar trends as never smokers. Trends were essentially unchanged when adjustment included body mass index. Current male smokers demonstrated evidence of reduced insulin sensitivity, female smokers of improved one, as assessed by QUICKI. ConclusionSmoking among Turks induces at long-term lower fasting insulin levels which represent improved insulin sensitivity in women, yet a reduced one in men.

Short and long-term effects of cigarette smoking independently influence exhaled nitric oxide concentration in asthma

The fractional concentration of nitric oxide in exhaled breath (FeNO) is elevated in asthma. FeNO measurement has been proposed as a noninvasive index of disease activity. Cigarette smoking suppresses FeNO, which limits its use in smokers. To identify and model short-term and long-term influences of cigarette smoking on FeNO. The smoking history, FeNO, and fractional concentration of carbon monoxide in exhaled breath (FeCO) were measured in 53 subjects with asthma and 51 control subjects. A mathematical model of the short-term and long-term effects of cigarette smoking on FeNO was derived. Subjects with asthma had higher FeNO than controls ( P < .001). Smokers had increased FeCO ( P < .001). The short-term effect (hours since last cigarette) was associated with increased FeNO ( P < .01) and decreased FeCO ( P < .05). The long-term effect (years smoked) was associated with decreasing FeNO only in the subjects with asthma ( r = -0.62; P = .005). These short-term and long-term effects were independent and were combined in a model predicting FeNO, predicted log 10 FeNO = 1.23 - 0.58 e -0.34t - 0.00000103 x (lifetime cigarettes), where t = hours since the last cigarette. This gave a convincing prediction of FeNO ( r = 0.83; P < .0001). Short-term and long-term effects of smoking influenced the measurement of FeNO. We defined a model that describes these effects. The use of this formula may improve the value of FeNO measurements in smokers with asthma.

Documentation of slow coronary flow by the thrombolysis in myocardial infarction frame count in habitual smokers with angiographically normal coronary arteries

The thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. In this study we aimed to evaluate the effects of long-term cigarette smoking on the TIMI frame count in patients with angiographically proven normal coronary arteries. Between May 2001 and January 2002, 41 habitual smokers and 41 sex-matched nonsmokers with angiographically proven normal coronary arteries were included in the study. The TIMI frame count was determined for each major coronary artery in each patient. The TIMI frame count of the smoking group was significantly higher than that of nonsmokers for all three coronary arteries: left anterior descending (corrected), 39 +/- 13 vs 22 +/- 8; right coronary artery, 35 +/- 13 vs 24 +/- 11; and left circumflex artery, 37 +/- 13 vs 25 +/- 8 (P < 0.001 for all). The smokers tended to be younger than nonsmokers (46 +/- 7 vs 49 +/- 9 years; P = 0.07). We have found that smokers with angiographically normal coronary arteries have a higher TIMI frame count than nonsmokers with angiographically normal coronary arteries. An increased TIMI frame count can be regarded as an index of the harmful effects of smoking on coronary circulation regardless of the underlying mechanism.

Long-term effects of cigarette-smoke exposure on plasma testosterone, luteinizing hormone and follicle-stimulating hormone levels in male rats.

To determine the effects of long-term cigarette smoking on the levels of plasma testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in male adult rats and to examine morphological and histological changes in the testes. Cigarette smoke was generated by a smoking-machine and 12 rats were exposed to cigarette smoke diluted with 90% air for 60 days (2 h/day). Twelve rats were exposed to room air only under similar conditions as controls. The concentrations of plasma testosterone, LH and FSH were measured before and after exposure using a radio-immunoassay and the testes were examined histologically. In rats exposed to smoke, the mean plasma testosterone level decreased significantly but there were no significant changes in testosterone in the control rats. The mean plasma LH and FSH levels of the two groups did not change significantly after exposure. In rats exposed to smoke, histological examination of the testes showed fewer Leydig cells and degeneration of the remaining cells. These results indicate that the decrease in plasma testosterone levels induced by exposure to smoke was not associated with changes in plasma gonadotrophin levels. The decrease in testosterone levels may be related to the toxic effects of smoke on Leydig cells.

Differences in psychomotor reaction time in male monozygotic twins discordant for lifetime cigarette smoking.

The effects of long-term cigarette smoking on psychomotor reaction time were investigated among 8 pairs of monozygotic male twins highly discordant for lifetime smoking (means 32.4 versus 0.6 pack-years). The men had no diagnosed cardiovascular disease or other major diseases, musculoskeletal complaints, or vision problems that might interfere with reaction time testing. The twins had similar education, work, and exercise histories; alcohol and coffee consumption and exposure to solvents were examined as possible confounds. Direct comparison of cotwins also controlled for age, genetics, and possible early environmental factors. Simple and choice reaction time were measured in the dominant hand and in both feet. The decision-time component of total reaction time was of primary interest. On average, long-term smokers had slower decision times than their nonsmoking twins; however, the differences were small (5 to 14%) and were not statistically significant for four of the six decision-time measures, perhaps due to the lack of power with only eight twin pairs. Further study may confirm our evidence suggesting that long-term cigarette smoking impedes reaction time, a key measure of function of the central nervous system.

Effects of Long-Term Cigarette Smoking on Endothelium-Dependent Responses in Humans

Endothelial injury is a central feature of vascular disease induced by cigarette smoking and may act as a precursor for future atherosclerosis. Using forearm occlusion plethysmography, we studied the vascular responses to methacholine (an endothelium-dependent vasodilator) and sodium nitroprusside (an endothelium-independent vasodilator) infused into the brachial artery of 35 long-term cigarette smokers and 16 nonsmoking subjects. NG-monomethyl-l-arginine (L-NMMA), a stereospecific inhibitor of nitric oxide production, was used to inhibit synthesis of nitric oxide in the endothelium. The reactive hyperemic response at peak and during recovery to the temporary interruption of forearm blood flow was also compared between groups. Smokers had elevated carboxyhemoglobin levels compared with nonsmokers (5.1 ± 2.1% vs 0.8 ± 0.4%; p <0.001). No differences were found in the peak or late hyperemic responses between groups. In smokers, the incremental infusions of methacholine and sodium nitroprusside increased forearm blood flow from 3.6 ± 1.2 to 12.9 ± 9.0 ml·min−1·100 ml−1 and from 4.0 ± 1.5 to 9.3 ± 4.0 ml·min−1·100 ml−1, respectively, compared with 3.2 ± 1.0 to 13.5 ± 5.6 ml·min−1·100 mL−1 and from 2.9 ± 0.7 to 8.6 ± 4.2 ml·min−1·100 ml−1 in nonsmoking subjects (p = NS). L-NMMA (4 μmol/min for 5 minutes) significantly reduced forearm blood flow in both smokers and nonsmokers from 4.1 ± 1.4 to 3.4 ± 1.2 ml·min−1·100 ml−1 and 3.8 ± 0.7 to 2.3 ± 0.5 mL·min−1·100 ml−1, respectively (p <0.01 for both); and the decrement in forearm blood flow in nonsmokers was significantly greater than that recorded in smoking subjects (p <0.05). In this study, long-term cigarette smokers exhibited an impairment in basal, but not stimulated, nitric oxide-mediated vasodilation.

Prediction of smoking behavior in Japanese young adults

Eighty-eight second grade students of a senior high school in Saitama prefecture in Japan participated in a prospective study to predict cigarette smoking behavior 3.5 years later. Predictor variables include sex, knowledge, beliefs and attitudes toward smoking, previous smoking behavior, and smoking behavior of their families. Stepwise discriminant analyses revealed that 90% of the smokers and 65% of the non-smokers were correctly classified. In this model, previous smoking behavior proved to be the best predictor. Attitude toward adult male's smoking, sex and smoking behavior of subjects' families were also related. These four variables explained 35% of the variance in smoking behavior. As for stepwise discriminant analyses among those who had not smoked at baseline, 78% of the smokers and 76% of the non-smokers were correctly classified. Attitude toward adult male's smoking, sex, knowledge about long-term effects of cigarette smoking and smoking behavior of their families entered the model in this order. These four variables explained 37% of the variance. Implications of this study for smoking prevention programs in Japan are discussed.

Short- and long-term effects of cigarette smoking on heart rate variability

The short- and long-term effects of cigarette smoking on autonomic cardiac regulation were investigated by power spectral analysis of heart rate variability under controlled respiration (15/ min). The short-term effects were examined in 9 smokers without evidence of cardiopulmonary disorders after an overnight abstinence from smoking. The heart rate spectral component reflecting the respiratory sinus arrhythmia (0.25 Hz), a quantitative index of vagal cardiac control, decreased 3 minutes after smoking 1 cigarette (p = 0.0061) and the component reflecting Mayer wave sinus arrhythmia (0.04 to 0.15 Hz), which includes sympathetically mediated activity, increased after 10 to 17 minutes (p = 0.0124). The long-term effects were examined in 81 normal subjects comprising 25 nonsmokers, 31 moderate (1 to 24 cigarettes/ day) smokers and 25 heavy (>25 cigarettes/day) smokers after an overnight abstinence. Although the magnitude of the Mayer wave component was unaffected by the smoking status, the respiratory component in the supine position was smaller in the young (≤30 years) heavy smokers than in the young nonsmokers or moderate smokers (p = 0.0078). Also, postural changes in the components, a decrease in the respiratory component and an increase in the Mayer wave component with standing, were observed in the nonsmokers but not in the heavy smokers. These results suggest that smoking causes an acute and transient decrease in vagal cardiac control, and that heavy smoking causes long-term reduction in vagal cardiac control in young people and blunted postural responses in autonomic cardiac regulation.

Long-term effects of cigarette smoking and moderate alcohol consumption on coronary artery diameter: Mechanisms of coronary artery disease independent of atherosclerosis or thrombosis?

Epidemiologic studies have shown that cigarette smoking (increased risk) and moderate alcohol consumption (decreased risk) have opposite effects in coronary artery disease. To investigate whether they act via the common mechanism of affecting the coronary diameter, 31 white men with arteriographically normal coronary arteries were evaluated. Histories of cigarette smoking (never smoked, exsmoker, or current smoker) and alcohol consumption (nonuser or low user versus moderate users with an average of one drink per day) were analyzed for an association with coronary diameters. Nonsmokers had larger left main and left anterior descending diameters than either exsmokers or current smokers (p = 0.0001 and 0.004). Moderate alcohol users had large left main and left anterior descending diameters than nondrinkers (p = 0.009 and 0.01). Neither association was removed after adjustment for the other risk factor. These data suggest that smoking and moderate alcohol use have significant, independent, and opposite effects on long-term coronary diameter. These effects may be important mechanisms through which these behaviors alter the risk of coronary artery disease.

Effects of chronic smoking on testosterone metabolism in dogs

The effects of long-term cigarette smoking on androgen hydroxylases and peripheral hormones were studied in male beagles. In the testis, chronic smoking of high nicotine/tar cigarettes was associated with decreased activity of the 7α-hydroxylase active on testosterone (68% of control, P < 0.05). Testicular 6β and 16α-hydroxylases were not altered. The hepatic androgen 6β-hydroxylase activity in control animals was approximately 6 times the testis levels and was stimulated markedly by smoking. This increase ranged from 221% in the low nicotine/tar group ( P < 0.02) to 304% in the high nicotine/tar group ( P < 0.006). Serum testosterone levels were reduced to 54% of control ( P < 0.02) and prostate size to 44% ( P < 0.001) of control with heavy smoking. Serum LH levels were elevated with smoking. These results suggest that chronic cigarette smoking increased hepatic metabolism of testosterone. In addition, serum testosterone levels and prostate size decreased and LH levels increased. Whether the hepatic and the endocrine effects are causally related cannot be determined from this preliminary study.

Cigarette smoking and voice fundamental frequency

The effects of long-term cigarette smoking were examined in a series of phonatory tasks. The results indicated that a significant difference existed between the fundamental frequency of the male smokers and the male nonsmokers in the oral reading and spontaneous speech tasks. Differences between the ƒ 0 values of the female smokers and nonsmokers in these tasks were not significant, but the same trends were noted. Results of the ƒ 0 analysis of the sustained vowel phonations were not significant, but showed the same trend; that is, the smokers had lower fundamental frequency values than the nonsmokers.

Myocardial effects of long-term cigarette smoking: Relative roles of carbon monoxide and nicotine

In a prior study of an animal model exposed to long-term cigarette smoking, left ventricular performance was observed to decline in association with morphologic evidence of collagen accumulation. Because controversy has existed as to whether nicotine or carbon monoxide is the major pathogenetic agent in cigarette smoking, 18 young adult male beagles with chronic tracheostomy were placed in three groups of six dogs each: Group 1 served as a control group; group 2 received seven cigarettes of low nicotine content (0.2 mg/cigarette), which effected a peak carboxyhemoglobin level approximating 5/100 ml, similar to that of regular cigarettes; and group 3 received nicotine twice daily intramuscularly in an amount equivalent to seven cigarettes/day. In the intact anesthetized state, heart rate, left ventricular end-diastolic pressure and volume (indicator dilution) did not differ among the three groups. To assess relative myocardial wall stiffness, saline solution was infused into the left ventricular chamber. A significantly higher end-diastolic pressure and tension were elicited in group 3, suggesting a decrease in left ventricular compliance. No such change was observed in either group 1 or 2. Only long-term nicotine use was associated with increased hydroxyproline content in the left ventricular myocardium, suggesting a basis for enhanced stiffness. An index of left ventricular contractility was derived from the peak rate of rise of left ventricular pressure ( dP dt ), normalized for preload and afterload. Groups 1 and 2 showed no difference in this index (2.18 ± 0.3 versus 2.15 ± 0.18 muscle lengths/s per cm) at similar levels of aortic pressure, but the index was significantly lower (1.28 ± 0.12, p < 0.01) in group 3. Thus, the effects of long-term cigarette use on the myocardium appear to be predominantly dependent on nicotine rather than on carbon monoxide.

Cardiovascular effects of long-term cigarette smoking and nicotine administration

The nature of the cardiovascular risk in cigarette smokers has not been characterized. To compare the relative effects of long-term smoking and nicotine administration on the cardiovascular system, 18 month old beagle littermates were prepared with a permanent tracheostomy. They were classified into three groups: I, seven control dogs; II, nine dogs that smoked seven cigarettes/day; and III, eight dogs that received an equivalent amount of nicotine. After a period of up to 22 months, the animals were catheterized under anesthesia for assessment of left ventricular function and volumes by indicator-dilution technique. Heart rate, stroke volume, left ventricular end-diastolic pressure and volume and intraventricular conduction times did not differ significantly in the three groups. Left ventricular ejection fraction was 44 ± 3 percent (mean ± standard error of the mean) in the control group, 35 ± 3 percent in the dogs that smoked cigarettes ( P < 0.05) and 27 ± 3 percent in those given nicotine ( P < 0.01) despite similar values for end-diastolic variables in the three groups. The first derivative of left ventricular pressure ( dP dt ) normalized for pre- and afterload was 2.4 ± 0.2 cm/sec −1 in the control group, 1.41 ± 0.12 in the cigarette-smoking group ( P < 0.005) and 1.34 ± 0.08 in the nicotine group ( P < 0.01). Although mean aortic pressure was significantly elevated in both the smoking (127 ± 5 mm Hg) and nicotine (27 ± 10 mm Hg) groups, there was no significant correlation with the contractility indexes. Reduction of afterload to normal levels did not affect the abnormal ventricular performance. Hypertrophy, inflammation and abnormalities of cell ultrastructures were not present, and myocardial lipid and cation composition were normal. Since interstitial fibrosis was evident in both experimental groups, an alteration of elastic elements may be operative. These cardiovascular abnormalities appear to be predominantly dependent on the nicotine of cigarettes.