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Acute Coronary Hemodynamic Response to Cigarette Smoking in Patients with Coronary Artery Disease

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Acute Coronary Hemodynamic Response to Cigarette Smoking in Patients with Coronary Artery Disease JACC Vol. 3, No.4 879 April 1984:879-86 CLINICAL STUDIES Acute Coronary Hemodynamic Response to Cigarette Smoking in Patients With Coronary Artery Disease LLOYD W. KLEIN, MD,* JOHN AMBROSE, MD, FACC, AUGUSTO PICHARD, MD, FACC, JAMES HOLT, MA, RICHARD GORLIN, MD, FACC, LOUIS E. TEICHHOLZ, MD, FACC New York, New York The acute changes in coronary blood flow and coronary group II (p < 0.05). Patients in group IA had a highly resistance that occur in response to cigarette smoking significant increase in coronary resistance as compared have not been accurately determined. To define the fac• with group IB (i 7.0 ± 4.2% versus t 0.9 ± 2.6%) (p tors that affect this response, coronary sinus blood flow < 0.001). Coronary sinus flow tended to decrease ( t 1.2 was measured in 16 patients (group I) with coronary ± 4.6%) in group IA but to increase ( i 3.8 ± 5.1%) artery disease and in 6 patients (group II) without an• in group IB (p = 0.06). giographically detectable coronary disease. Seven pa• It is concluded that smoking increases coronary re• tients (group IA) had severe (2. 75%) proximal left coro• sistance in patients with coronary artery disease. Agreater nary lesions and nine patients (group IB) had significant impact is observed in patients with a severe proximal distal lesions with 50% or less proximal stenoses. Group stenosis than in those with a distal stenosis. It is proposed I had a smaller overall increase ( i 1.6 ± 5.3 %) in coro• that smoking increases coronary artery tone at the site nary sinus blood flow than did group II ( i 7.7 ± 6.1 %) of the stenosis, limiting the coronary flow response pro• (p < 0.05). Coronary resistance increased overall ( i 2.7 portionally to the size of the affected vascular bed. ± 5.3%) in group I but decreased ( t 2.4 ± 3.4%) in Although chronic cigarette smoking produces long-term al• of the coronary vascular response should be measured im• terations in coronary artery reactivity (1), the acute coronary mediately after smoking to best understand its significance. hemodynamic response to smoking remains controversial. Therefore, to study the acute effects of smoking on the Prior observations in human subjects with normal coronary coronary circulation, we measured coronary sinus blood arteries (2,3) and with coronary artery disease (3,4) have flow by the continuous thermodilution technique in patients been conflicting, showing either no change or an increase with and without coronary artery disease while they were in coronary blood flow in response to increased myocardial smoking one cigarette at the time of cardiac catheterization. oxygen demand. In patients with coronary artery disease, neither the extent of the coronary disease nor the state of left ventricular function was considered. Methods In addition, methodologic problems were present in these Patient selection. All patients who were referred for studies (2-4). When coronary flow was determined by the diagnostic cardiac catheterization to evaluate the cause of nitrous oxide extraction technique, measurements of coro• chest pain were eligible for this study. Sixteen patients with nary flow were made up to 40 minutes after smoking one proven coronary artery disease and six patients with normal cigarette. Because the systemic effects of smoking one cig• coronary and left ventricular angiograms form the basis of arette last for approximately 10 minutes (5,6), the duration this study. All patients were either present or past chronic cigarette smokers who gave informed consent before cath• eterization according to a protocol approved by the Mount From the Division of Cardiology, Department of Medicine. and the Department of Biomathematics, Mount Sinai Medical Center, New York, Sinai Medical Center Research Administrative Committee. New York. Manuscript received July 6, 1983; revised manuscript received Patients with the following conditions were excluded from October 19, 1983, accepted October 21, 1983. selection: I) organic heart disease other than coronary artery *Present address and address for reprints: Lloyd W. Klein, MD, Pres• byterian-University of Pennsylvania Medical Center, 39th and Market Streets, disease, 2) nonischemic cardiomyopathy, 3) unstable angina, Philadelphia, Pennsylvania 19104. 4) congestive heart failure, or 5) chest pain during the pro- ©1984 by the American College of Cardiology 0735-1097/84/$3.00 880 KLEIN ET AL. lACC Vol. 3. No.4 CIGARETTE SMOKING AND CORONARY HEMODYNAMICS April 1984:879-86 cedure. Twenty-six patients who fulfilled these criteria agreed Coronary sinus flow was calculated just before and imme• to participate in the study. Coronary sinus blood flow studies diately after smoking during quiet respiration according to could not be perfonned in four of these patients because of the continuous thermodilution method of Ganz et al. (9). technical inability to position the catheter in the coronary The values were obtained as an average over at least a 10 sinus. Thus, 22 patients, 17 men and 5 women with a mean second period. Because of the very small changes observed, age of 53 years (range 40 to 78), were enrolled. the resistance of the thennistors was set for a very large Procedure. Nitrates, beta-adrenergic blocking agents and paper deflection, allowing accurate detennination of small calcium antagonists were withheld for 8 to 12 hours before changes. Coronary sinus blood flow was not measured dur• the procedure. All other medications and caffeine-contain• ing smoking because the deep inhalation involved in smok• ing drinks were withheld for 4 to 6 hours. Patients did not ing creates artifactual changes in the record in some patients. smoke a cigarette for at least 1 hour before the procedure. A representative record is shown in Figure 1. Patients were premedicated with 10 mg oforal diazepam. Rate-pressure product. This was calculated as systolic Aortic and left ventricular pressures were measured during blood pressure x heart rate. the course of the catheterization, and left ventriculography Mean arterial pressure was calculated as [(systolic pres• was perfonned in the right anterior oblique projection. In sure) + 2 (diastolic pressure)] -:- 3. one patient with a 90% left main coronary artery lesion, the Coronary resistance was detennined as mean arterial left ventriculogram was not perfonned and this patient is pressure -:- coronary sinus blood flow. omitted from that portion of the analysis. Routine coronary Arterial-coronary sinus oxygen difference is presented as angiography was completed in each patient before the coro• volume %/1 00 ml. This was calculated by the fonnula: nary sinus flow measurements. An arterial catheter was left [(Arterial oxygen saturation - coronary sinus oxygen sat• in the aorta during the subsequent studies. No further studies uration) X (1.34 X 10 x serum hemoglobin)] -:- 100. were perfonned until at least 15 minutes after completion Left ventricular angiography and coronary arteri• ofthe routine catheterization, so as to minimize any possible ography. The left ventricular angiograms and coronary ar• influence of the vasodilatory effect of contrast medium. teriograms were interpreted by an experienced angiographer A thermodilution catheter was introduced into the coro• who had no knowledge of the results of hemodynamic or nary sinus through a left antecubital fossa vein. A coronary coronary flow measurements. The percent narrowing of a sinus catheter with two thennistors and two pacing elec• lesion was defined as the average visualized in at least two trodes (Wilton Webster Laboratories) was utilized in 15 views. Only the lesion of greatest narrowing in any region patients and a Pepine catheter (7) was utilized in 7 patients. was recorded (Table 1). A significant lesion was defined as Placement of the catheter within the coronary sinus was at least a 50% reduction of luminal diameter, while a critical verified as previously described (8). lesion was defined as a 75% or greater narrowing. Coronary Hemodynamic and flow measurements. Blood pres• collateral vessels were identified as being either present or sure and heart rate. Baseline measurements were obtained absent, and the direction of flow was noted. on an Electronics for Medicine recorder. Heart rate was The proximal left anterior descending artery region was measured by a continuous recording of one electrocardio• defined as that area before either the first large septal or graphic lead, measured over a 20 second period before the first large diagonal branch. The proximal circumflex artery initiation of smoking. Arterial blood pressure was displayed region was defined as that area before the first obtuse mar• and calibrated on a 200 mm Hg scale. ginal branch. Right coronary artery lesions were not in• Arterial and coronary sinus oxygen saturations. Paired cluded in this analysis because the coronary sinus flow method blood samples to measure oxygen saturation were obtained does not usually measure the venous drainage from the right before the start of cigarette smoking. A filtered cigarette, coronary artery territory (10). Ejection fraction was calcu• 1.0 mg nicotine, 16 mg tar, was then smoked by each patient lated by planimetry according to a modification of the method with a continuous recording of the electrocardiogram, ar• of Dodge et al. (11) based on the 30° right anterior oblique terial blood pressure and coronary sinus blood flow. After left ventriculogram. the cigarette was smoked according to the individual's cus• Statistical analysis. The data were maintained and ana• tomary speed and intensity of inhalation, all variables were lyzed using SAS (Statistical Analysis System) on an IBM measured during the next 30 seconds, including repeat paired 370 computer at the City University of New York Com• coronary sinus and arterial oxygen saturation determina• puting Center. Means and standard deviations were calcu• tions. Heart rate and blood pressure were measured at 5 lated for all groups. Student's t tests were perfonned when minute intervals until these variables returned to baseline comparing continuous variables between two groups; chi• values (within 10 to 15 minutes).
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