Join the 200th Anniversary Celebration

Original Article

Effect of Smoking Status on the Long-Term Outcome after Successful Percutaneous Coronary Revascularization

David Hasdai, M.D., Kirk N. Garratt, M.D., Diane E. Grill, M.S., Amir Lerman, M.D., and David R. Holmes, Jr., M.D.

N Engl J Med 1997; 336:755-761March 13, 1997

Abstract

Background

Cigarette smoking is known to be deleterious to patients with coronary artery disease, but the effect of smoking on the clinical outcome of percutaneous coronary revascularization is unknown.

Methods

Patients who had undergone successful percutaneous coronary revascularization at the Mayo Clinic between 1979 and 1995 were divided into nonsmokers (n = 2009), former smokers (those who had stopped smoking before the procedure, n = 2259), quitters (those who stopped smoking after the procedure, n = 435), and persistent smokers (those who smoked before and after the procedure, n = 734).

Results

The maximal follow-up was 16 years (mean [±SD], 4.5±3.4). The nonsmokers and former smokers had similar base-line characteristics and outcomes. The quitters and persistent smokers were younger than the nonsmokers and former smokers and had more favorable clinical and angiographic characteristics. In analyses adjusted for confounding base-line characteristics, the persistent smokers had a greater relative risk of death (1.76 [95 percent confidence interval, 1.37 to 2.26]) and of Q-wave infarction (2.08 [95 percent confidence interval, 1.16 to 3.72]) than the nonsmokers. The quitters and persistent smokers were less likely than the nonsmokers to undergo additional percutaneous coronary procedures (relative risk, 0.80 [95 percent confidence interval, 0.64 to 0.98] and 0.67 [95 percent confidence interval, 0.56 to 0.81], respectively) or coronary bypass surgery (relative risk, 0.72 [95 percent confidence interval, 0.54 to 0.95] and 0.68 [95 percent confidence interval, 0.54 to 0.86], respectively). The persistent smokers were also at greater risk for death than the quitters (relative risk, 1.44 [95 percent confidence interval, 1.02 to 2.11]).

Conclusions

Patients who continued to smoke after successful percutaneous coronary revascularization were at greater risk for Q-wave infarction and death than nonsmokers. The cessation of smoking either before or after percutaneous revascularization was beneficial. Patients undergoing percutaneous revascularization should be encouraged to stop smoking.

Media in This Article

Figure 1Estimated Survival Curves for Smokers Undergoing Percutaneous Coronary Revascularization, According to Subsequent Smoking Status.
Table 1Base-Line Clinical and Angiographic Characteristics of 5437 Patients Undergoing Successful Percutaneous Coronary Revascularization, According to Smoking Status.
Article

Cigarette smoking is a well-established risk factor for the development and progression of coronary heart disease1-4 and is strongly related to morbidity and mortality from cardiovascular causes.5,6 Conversely, the excess risk of cardiovascular events gradually declines after the cessation of smoking.7,8 Previous studies have shown that the cessation of smoking after coronary bypass surgery may have an important beneficial effect on clinical events during long-term follow-up.9,10 However, the effect of smoking status before and after percutaneous coronary revascularization on the long-term outcome is not well established.

The aims of this study were to examine the effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization and to determine whether the cessation of smoking before or after the index intervention affected event-free survival. We performed a retrospective analysis of all patients who had undergone percutaneous coronary revascularization at the Mayo Clinic during a 16-year period.

Methods

During the period from the introduction of coronary balloon angioplasty at the Mayo Clinic, in September 1979, through December 31, 1995, a total of 6600 patients underwent percutaneous coronary revascularization and did not have acute myocardial infarction within 24 hours before the intervention. Complete base-line data were available for 6424 of these patients (97 percent). The 5450 patients (85 percent) in whom the index procedure was clinically successful (as defined below) were the focus of this study.

The Mayo Clinic Registry

Since 1979, all patients undergoing percutaneous revascularization at the Mayo Clinic have been followed according to a protocol approved by the clinic's institutional review board. This registry includes base-line demographic, clinical, and angiographic data. All patients are interviewed in person or by telephone 6 and 12 months after the initial procedure and yearly thereafter. Data from visits and hospitalizations at the Mayo Clinic and other institutions are obtained for review. Patients give written informed authorization for the release of all such information.

Clinical Data

The choice of percutaneous coronary revascularization rather than medical or surgical therapy was made by the attending cardiologist. Initially, only balloon angioplasty was performed, according to conventional techniques.11 Later in the study period, other procedures, such as atherectomy, laser angioplasty, and coronary stenting, were also employed, although balloon angioplasty remained the most common procedure. In cases of multivessel disease, the culprit lesion was generally treated first. Identification of the culprit lesion was based on the findings on electrocardiography, regional left ventricular functional studies, thallium scintigraphy, and coronary angiography.

Follow-up angiography was usually performed only if the attending physician was concerned about recurrent symptoms suggestive of myocardial ischemia. The need for additional coronary revascularization of the target lesion or other segments was also determined by the attending physician. Although all additional percutaneous coronary interventions were documented, data on the segment treated were available only for procedures performed at the Mayo Clinic. The left ventricular ejection fraction was determined by ventriculography at the time of diagnostic angiography in most patients, and during follow-up, as indicated clinically, by echocardiography, radionuclide studies, or left ventricular angiography.

The severity of coronary artery disease was assessed visually by at least two observers using orthogonal views. Single-vessel coronary artery disease was defined as stenosis of at least 70 percent of the diameter of only one major epicardial artery. Two- or three-vessel disease was diagnosed if there were one or two additional major epicardial arteries with at least 70 percent stenosis, respectively. Among patients with 50 percent or more stenosis of the left main coronary artery, those with a right dominant artery were considered to have two-vessel disease and those with a left dominant artery were considered to have three-vessel disease.

Q-wave myocardial infarction was defined as the presence of new Q waves on the electrocardiogram,12 with serum creatine kinase concentrations that were at least three times higher than normal or positive tests for MB isoenzymes, an episode of prolonged angina, or new regional wall-motion abnormalities.

Angina was classified according to the classification system of the Canadian Cardiovascular Society.13 Severe angina was defined as class III or IV.

Complete revascularization was defined as successful dilation of all stenoses of 70 percent or more. Incomplete revascularization was defined as successful dilation of one or more stenoses but with one or more remaining arteries with at least 70 percent stenosis.

The angiographic success of revascularization was defined as a reduction of at least 20 percentage points in the stenosis of at least one lesion, resulting in a residual stenosis of less than 50 percent of the luminal diameter. Clinical success was defined as angiographic success without the in-hospital complications of death, Q-wave myocardial infarction, or referral for coronary-artery bypass grafting.

Death from cardiac causes was defined as death due to myocardial infarction, an arrhythmic event, heart failure, or complications of cardiac surgery or transplantation.

Smoking Status

Patients were queried about their smoking habits at base line and during follow-up; a patient reporting any cigarette smoking in the prior six months was considered a smoker. The study population was divided into four groups on the basis of smoking status at base line: nonsmokers, defined as patients who had never smoked cigarettes regularly; former smokers, those who had quit smoking at least six months before the index procedure; quitters, those who permanently quit smoking immediately after the index procedure; and persistent smokers, those who smoked before and after the index procedure. The small number of patients (13) who first started to smoke during the follow-up period were excluded from our analysis.

End Points

The end points of the study were death from any cause, Q-wave acute myocardial infarction or severe angina, and the need for coronary-artery bypass grafting or repeated percutaneous revascularization.

Statistical Analysis

Continuous data are expressed as means ±SD, and differences among the four groups of patients were tested for significance with one-way analyses of variance. Discrete data are presented as percentages, and comparisons among the groups were made with Pearson's chi-square test. For each of the follow-up events, Cox proportional-hazards analysis was used to estimate the relative risk for former smokers, quitters, and persistent smokers as compared with nonsmokers. The results are presented with 95 percent confidence intervals. The likelihood-ratio test was used to determine significant differences among the groups. A proportional-hazards model was developed for each of the end points by using backward selection. Age, sex, severe angina, prior coronary bypass surgery, prior myocardial infarction, congestive heart failure, history of diabetes mellitus, history of hypertension, complete revascularization, multivessel coronary artery disease, the number of vessels dilated, family history of coronary artery disease, and unstable angina were the covariates used in the modeling process. Once a model was selected, the dichotomous variables for former smokers, quitters, and persistent smokers were added to complete the multivariate model. A group analysis was conducted with only patients who were smokers at the time of the initial intervention (i.e., quitters and persistent smokers). The relative risk of continued smoking, as compared with quitting, was estimated with the use of the same procedure. The adjusted survival curves were generated from the multivariate model by allowing the variable associated with the smoking status to change. The other risk factors in the model were held constant by setting each factor equal to its mean value.

Results

The base-line clinical and angiographic characteristics of the four groups of patients are shown in Table 1Table 1Base-Line Clinical and Angiographic Characteristics of 5437 Patients Undergoing Successful Percutaneous Coronary Revascularization, According to Smoking Status.. Several significant differences were identified. The nonsmokers were older, had had angina for longer periods, and presented with severe angina more frequently than the persistent smokers or quitters, and a larger proportion of nonsmokers were women. In addition, major coexisting conditions such as hypertension and diabetes mellitus were as much as two times as prevalent among the nonsmokers as among the quitters and persistent smokers. The nonsmokers had more extensive coronary artery disease, higher rates of prior coronary bypass surgery, and lower rates of complete revascularization during the index intervention.

The clinical and angiographic characteristics of the former smokers resembled those of the nonsmokers. They were older, had more coexisting conditions, had more extensive coronary artery disease, and had undergone more surgical revascularization procedures than the quitters and persistent smokers. However, the latter patients had higher rates of prior myocardial infarction.

The rate of clinical success of the index procedure was similar in all four groups (approximately 85 percent, data not shown). Among the patients in whom the procedure was successful, 99 percent, 98 percent, 100 percent, and 98 percent of the nonsmokers, former smokers, quitters, and persistent smokers, respectively, reported a substantial improvement in their symptoms at discharge. Patients were followed for up to 16 years after the index procedure (mean, 4.5±3.4 years), with a shorter mean duration of follow-up for the nonsmokers and former smokers (4.4±3.2 and 4.2±3.2 years, respectively) than for the quitters and persistent smokers (5.1±3.7 years and 5.3±3.7 years, respectively).

In the univariable analysis (Table 2Table 2Unadjusted and Adjusted Relative Risks of Major Adverse Events or Repeated Revascularization.), the quitters and persistent smokers had lower risks of death from all causes and severe angina than the nonsmokers. In contrast, the risk of Q-wave myocardial infarction was lower in the nonsmokers than in the persistent smokers. During the follow-up period, percutaneous or surgical revascularization was performed more frequently in the nonsmokers and former smokers than in the other two groups. Six months after the index intervention, 11.8 percent of the nonsmokers, 12.3 percent of the former smokers, 13.4 percent of the quitters, and 8.0 percent of the persistent smokers had undergone additional percutaneous coronary revascularization (P<0.05 for the difference between the persistent smokers and the other three groups). Among the patients who underwent repeated percutaneous coronary revascularization at the Mayo Clinic, revascularization of the same target segment as in the initial procedure was documented in 777 patients. The quitters and persistent smokers had a lower risk of repeated percutaneous revascularization of the same segment than the nonsmokers (relative risk, 0.93 [95 percent confidence interval, 0.71 to 1.22] and 0.65 [95 percent confidence interval, 0.51 to 0.94], respectively).

When the data were adjusted for the base-line variables significantly associated with each end point (Table 2), the persistent smokers had a greater risk of death from all causes (relative risk, 1.76) and Q-wave myocardial infarction (relative risk, 2.08) than the nonsmokers. Both quitters and persistent smokers were less likely to undergo additional percutaneous procedures (relative risk, 0.80 and 0.67, respectively) or surgical procedures (relative risk, 0.72 and 0.68, respectively) than the nonsmokers. The risk of severe angina was similar in all four groups. The relative risk of death from cardiac causes for former smokers, quitters, and persistent smokers as compared with nonsmokers was 1.28 (95 percent confidence interval, 1.04 to 1.58), 1.02 (95 percent confidence interval, 0.63 to 1.64), and 1.44 (95 percent confidence interval, 1.04 to 2.04), respectively.

We calculated the risk of death from all causes among the persistent smokers as compared with the risk among the quitters, after adjusting for significant differences in base-line variables, in order to assess the effect of smoking cessation on long-term mortality. The persistent smokers had a significantly greater risk of overall mortality (relative risk, 1.44; 95 percent confidence interval, 1.02 to 2.11) (Figure 1Figure 1Estimated Survival Curves for Smokers Undergoing Percutaneous Coronary Revascularization, According to Subsequent Smoking Status.). After adjustment of the data for differences in base-line variables, the estimated survival curves for the patients who quit smoking and those who continued to smoke diverged soon after the index percutaneous intervention, and the difference between the two curves increased throughout the follow-up period. The estimated benefit in survival associated with the cessation of smoking increased from 1 percentage point at 1 year (99 percent vs. 98 percent) to 3 percentage points at 5 years (95 percent vs. 92 percent) and to 6 percentage points at 10 years (86 percent vs. 80 percent). As compared with the quitters, the persistent smokers were also at greater risk for death from cardiac causes during the follow-up period (relative risk, 1.49; 95 percent confidence interval, 0.89 to 2.51).

Discussion

A substantial proportion of patients undergoing percutaneous coronary interventions smoke cigarettes. Indeed, in our study, 1169 patients (22 percent) were smokers at the time of the index percutaneous intervention, of whom 734 (63 percent) continued to smoke thereafter. Although the cessation of cigarette smoking is strongly recommended after percutaneous revascularization,14 there are few long-term data on mortality, morbidity, and the need for repeated revascularization in relation to cigarette smoking or its cessation in patients undergoing percutaneous coronary revascularization.

In our study, after adjustment for base-line clinical and angiographic characteristics, the persistent smokers had a greater risk of death or Q-wave myocardial infarction than the nonsmokers during follow-up. The long-term risk of death from any cause was 44 percent greater in the patients who continued smoking than in those who quit. With adjustment for differences in base-line variables, the estimated survival curves for the two groups diverged early after the index percutaneous intervention and continued to diverge throughout the follow-up period. The beneficial effect of smoking cessation on mortality may be due primarily to the reduction in deaths from cardiac causes, since the relative risk of death from cardiac causes was 49 percent higher for the persistent smokers than for the quitters.

The cessation of smoking before percutaneous coronary revascularization was also beneficial. At the time of the procedure, the smokers (both those who quit smoking after the procedure and those who continued to smoke) were approximately 10 years younger than the former smokers and the nonsmokers. The earlier onset of coronary atherosclerosis in the smokers may be attributed to their smoking, since they had fewer coexisting conditions predisposing them to coronary atherosclerosis, such as diabetes mellitus and hypertension, than the former smokers and the nonsmokers. The clinical and angiographic characteristics of the former smokers were similar to those of the nonsmokers, and the two groups accordingly had similar outcomes.

Smoker's Paradox

There is conclusive evidence of the causal role of cigarette smoking in heart disease. Smoking more than doubles the incidence of coronary artery disease and increases mortality from coronary disease by 70 percent.15 It is therefore surprising that in our study, the patients who were smokers at the time of the index percutaneous intervention had fewer adverse events in the univariable analysis than the nonsmokers and former smokers. Barbash et al.16-18 and others19 have reported similar findings in patients receiving thrombolytic therapy for acute myocardial infarction — namely, better outcomes among the smokers. This phenomenon has been coined the “smoker's paradox.”16 The better prognosis for the smokers in these studies was explained, in part, by their younger age and more favorable clinical and angiographic profile. In our study, the risk of death or Q-wave myocardial infarction was as much as two times higher in the smokers, after the outcome data had been adjusted for these differences in base-line characteristics. Thus, this apparent paradox should not be interpreted as a relative benefit of cigarette smoking. On the contrary, because the relatively better clinical and angiographic profile of the smokers is offset by their use of tobacco, these findings underscore the detrimental effect of cigarette smoking.

Repeated Revascularization

During the follow-up period, repeated revascularization procedures, either percutaneous or surgical, were performed more frequently in the patients who were nonsmokers at the time of the index procedure than in those who were smokers. A similar trend has been reported in the Coronary Artery Surgery Study.20 There are several possible explanations for these results. First, differences in the rates of restenosis between smokers and nonsmokers would affect the rate of additional revascularization procedures, at least within six to nine months after the index procedure.21 Cigarette smoking has been reported either to have no effect21,22 or to increase the rate of restenosis23,24 after coronary angioplasty. However, among the relatively few patients in our study for whom data were available on repeated revascularization of the target lesion, the quitters and persistent smokers were at lower risk for repeated revascularization than the nonsmokers. Our study was not designed to assess the rate of restenosis, because follow-up coronary angiography was not routinely performed, and data on the revascularization of target lesions were restricted to patients who underwent repeated revascularization at the Mayo Clinic. Thus, our limited data offer little insight into the effect of cigarette smoking on the rate of restenosis after percutaneous coronary revascularization.

Second, the modification of risk factors — or the lack of modification — may influence decision making about subsequent revascularization procedures. Physicians may be reluctant to perform invasive revascularization procedures in patients who continue to smoke. A policy of not performing revascularization in persistent smokers has been advocated by some clinicians25,26 but is not followed in our institution.

Third, patients in whom revascularization is incomplete during percutaneous coronary interventions often undergo additional revascularization.27 In our study, complete revascularization was achieved in a slightly smaller proportion of nonsmokers (57 percent) than smokers (60 to 64 percent). This small difference does not explain the 20 to 30 percent difference in additional percutaneous and surgical revascularization procedures between smokers and nonsmokers during follow-up.

Fourth, the smokers had higher risks of myocardial infarction and death than the nonsmokers in the multivariable analysis. The morbidity and mortality among the smokers may have precluded further interventions. But this explanation is unlikely, given that the curves for repeated revascularization began to diverge much earlier than the observed differences in morbidity and mortality occurred.

Finally, nonsmokers frequently have coexisting conditions, such as diabetes mellitus and hypertension, which may accelerate the progression of coronary artery disease and necessitate additional revascularization procedures. When the analysis was adjusted for these coexisting conditions, however, the smokers still underwent fewer revascularization procedures during follow-up. Thus, the smaller number of referrals for repeated revascularization procedures in the smokers remains an enigma.

Activity of Coronary Artery Disease

Our results are in accordance with previous studies that have shown that cigarette smoking may accelerate atherogenesis.1-4 The smokers began having angina approximately 10 years earlier than the nonsmokers or former smokers. Furthermore, our data suggest that smokers may be more prone to the development of unstable plaques and hence have more episodes of acute myocardial ischemia. Indeed, the incidence of myocardial infarction before the index percutaneous procedure was approximately 25 percent higher in the smokers, even though they had less extensive coronary artery disease. Moreover, the risk of Q-wave acute myocardial infarction during the follow-up period was as much as two times as high in the smokers as in the nonsmokers. These findings are consistent with the results of a study by Barry et al.,28 who reported substantially more daily episodes of ischemia in smokers with stable angina, as discerned by ambulatory electrocardiography, than in nonsmokers. This increased risk of active ischemia may be related to the procoagulant19,29 and coronary vasoconstrictive effects30 of cigarette smoking.

Conclusions

Considerable resources are devoted to improving the outcome after percutaneous coronary revascularization. In spite of refinements in techniques and pharmacologic therapy, which have resulted in an improved short-term angiographic and clinical outcome after percutaneous coronary interventions, long-term morbidity and mortality have not been shown to be significantly improved.31 Our results demonstrate that after successful percutaneous interventions, patients who continue to smoke have a 44 percent greater risk of death from any cause than those who quit smoking. Successful smoking-cessation programs should thus be beneficial for patients who have undergone successful percutaneous coronary revascularization.

Source Information

From the Division of Internal Medicine and Cardiovascular Diseases, Mayo Clinic and Mayo Foundation, Rochester, Minn.

Address reprint requests to Dr. Holmes at the Division of Internal Medicine and Cardiovascular Diseases, Mayo Clinic, 200 First St. S.W., Rochester, MN 55905.

References

References

  1. 1

    Ross R. The pathogenesis of atherosclerosis -- an update. N Engl J Med 1986;314:488-500
    Full Text | Web of Science | Medline

  2. 2

    Penn A, Batastini G, Soloman J, Burns F, Albert R. Dose-dependent size increases of aortic lesions following chronic exposure to 7,12-dimethylbenz(a)anthracene. Cancer Res 1981;41:588-592
    Web of Science | Medline

  3. 3

    Weintraub WS, Klein LW, Seelaus PA, Agarwal JB, Helfant RH. Importance of total life consumption of cigarettes as a risk factor for coronary artery disease. Am J Cardiol 1985;55:669-672
    CrossRef | Web of Science | Medline

  4. 4

    Waters D, Lesperance J, Gladstone P, et al. Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis: a Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. Circulation 1996;94:614-621
    Web of Science | Medline

  5. 5

    Friedman GD, Dales LG, Ury HK. Mortality in middle-aged smokers and nonsmokers. N Engl J Med 1979;300:213-217
    Full Text | Web of Science | Medline

  6. 6

    Vlietstra RE, Kronmal RA, Oberman A, Frye RL, Killip T III. Effect of cigarette smoking on survival of patients with angiographically documented coronary artery disease: report from the CASS registry. JAMA 1986;255:1023-1027
    CrossRef | Web of Science | Medline

  7. 7

    Rosenberg L, Kaufman DW, Helmrich SP, Shapiro S. The risk of myocardial infarction after quitting smoking in men under 55 years of age. N Engl J Med 1985;313:1511-1514
    Full Text | Web of Science | Medline

  8. 8

    Gordon T, Kannel WB, McGee D, Dawber TR. Death and coronary attacks in men after giving up cigarette smoking: a report from the Framingham Study. Lancet 1974;2:1345-1348
    CrossRef | Web of Science | Medline

  9. 9

    Cavender JB, Rogers WJ, Fisher LD, Gersh BJ, Coggin CJ, Myers WO. Effects of smoking on survival and morbidity in patients randomized to medical or surgical therapy in the Coronary Artery Surgery Study (CASS): 10-year follow-up. J Am Coll Cardiol 1992;20:287-294
    CrossRef | Web of Science | Medline

  10. 10

    Voors AA, van Brussel BL, Plokker HW, et al. Smoking and cardiac events after venous coronary bypass surgery: a 15-year follow-up study. Circulation 1996;93:42-47
    Web of Science | Medline

  11. 11

    Holmes DR Jr. Technical aspects. In: Vlietstra RE, Holmes DR Jr, eds. PTCA, percutaneous transluminal coronary angioplasty. Philadelphia: F.A. Davis, 1987:35-48.

  12. 12

    Blackburn H, Keys A, Simonson E, Rautaharju P, Punsar S. The electrocardiogram in population studies: a classification system. Circulation 1960;21:1160-1175
    Web of Science | Medline

  13. 13

    Campeau L. Grading of angina pectoris. Circulation 1976;54:522-523
    Web of Science | Medline

  14. 14

    Ryan TJ, Bauman WB, Kennedy JW, et al. Guidelines for percutaneous transluminal coronary angioplasty: a report of the American Heart Association/American College of Cardiology Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Percutaneous Transluminal Coronary Angioplasty). Circulation 1993;88:2987-3007
    Web of Science | Medline

  15. 15

    Center for Chronic Disease Prevention and Health Promotion. Reducing the health consequences of smoking: 25 years of progress: a report of the Surgeon General: executive summary. Washington, D.C.: Government Printing Office, 1989. (DHHS publication no. (CDC) 89-8411.)

  16. 16

    Barbash GI, Reiner J, White HD, et al. Evaluation of paradoxical beneficial effects of smoking in patients receiving thrombolytic therapy for acute myocardial infarction: mechanism of the “smoker's paradox“ from the GUSTO-I trial, with angiographic insights. J Am Coll Cardiol 1995;26:1222-1229
    CrossRef | Web of Science | Medline

  17. 17

    Barbash GI, White HD, Modan M, et al. Acute myocardial infarction in the young -- the role of smoking. Eur Heart J 1995;16:313-316
    Web of Science | Medline

  18. 18

    Barbash GI, White HD, Modan M, et al. Significance of smoking in patients receiving thrombolytic therapy for acute myocardial infarction: experience gleaned from the International Tissue Plasminogen Activator/Streptokinase Mortality Trial. Circulation 1993;87:53-58
    Web of Science | Medline

  19. 19

    Grines CL, Topol EJ, O'Neill WW, et al. Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction. Circulation 1995;91:298-303
    Web of Science | Medline

  20. 20

    Emond M, Mock MB, Davis KB, et al. Long-term survival of medically treated patients in the Coronary Artery Surgery Study (CASS) Registry. Circulation 1994;90:2645-2657
    Web of Science | Medline

  21. 21

    Holmes DR Jr, Vlietstra RE, Smith HC, et al. Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA Registry of the National Heart, Lung, and Blood Institute. Am J Cardiol 1984;53:77C-81C
    CrossRef | Web of Science | Medline

  22. 22

    Arora RR, Konrad K, Badhwar K, Hollman J. Restenosis after transluminal coronary angioplasty: a risk factor analysis. Cathet Cardiovasc Diagn 1990;19:17-22
    CrossRef | Medline

  23. 23

    Myler RK, Topol EJ, Shaw RE, et al. Multiple vessel coronary angioplasty: classification, results, and patterns of restenosis in 494 consecutive patients. Cathet Cardiovasc Diagn 1987;13:1-15
    CrossRef | Medline

  24. 24

    Galan KM, Deligonul U, Kern MJ, Chaitman BR, Vandormael MG. Increased frequency of restenosis in patients continuing to smoke cigarettes after percutaneous transluminal coronary angioplasty. Am J Cardiol 1988;61:260-263
    CrossRef | Web of Science | Medline

  25. 25

    Underwood MJ, Bailey JS. Coronary bypass surgery should not be offered to smokers. BMJ 1993;306:1047-1049
    CrossRef | Web of Science | Medline

  26. 26

    Powell JT, Greenhalgh RM. Arterial bypass surgery and smokers. BMJ 1994;308:607-608
    CrossRef | Web of Science | Medline

  27. 27

    Bell MR, Bailey KR, Reeder GS, Lapeyre AC III, Holmes DR Jr. Percutaneous transluminal angioplasty in patients with multivessel coronary disease: how important is complete revascularization for cardiac event-free survival? J Am Coll Cardiol 1990;16:553-562
    CrossRef | Web of Science | Medline

  28. 28

    Barry J, Mead K, Nabel EG, et al. Effect of smoking on the activity of ischemic heart disease. JAMA 1989;261:398-402
    CrossRef | Web of Science | Medline

  29. 29

    Folts JD, Bonebrake FC. The effects of cigarette smoke and nicotine on platelet thrombus formation in stenosed dog coronary arteries: inhibition with phentolamine. Circulation 1982;65:465-470
    CrossRef | Web of Science | Medline

  30. 30

    Martin JL, Wilson JR, Ferraro N, Laskey WK, Kleaveland JP, Hirshfeld JW Jr. Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease. Am J Cardiol 1984;54:56-60
    CrossRef | Web of Science | Medline

  31. 31

    Detre K, Yeh W, Kelsey S, et al. Has improvement in PTCA intervention affected long-term prognosis? The NHLBI PTCA Registry experience. Circulation 1995;91:2868-2875
    Web of Science | Medline

Citing Articles (45)

Citing Articles

  1. 1

    Julia A Critchley, Simon Capewell, Julia A Critchley. 2012. Smoking cessation for the secondary prevention of coronary heart disease. .
    CrossRef

  2. 2

    J. Weil, J. Stritzke, H. Schunkert. (2011) Risikofaktor „Rauchen“. Der Internist
    CrossRef

  3. 3

    Jasvinder A. Singh, Thomas K. Houston, Brent A. Ponce, Grady Maddox, Michael J. Bishop, Joshua Richman, Elizabeth J. Campagna, William G. Henderson, Mary T. Hawn. (2011) Smoking as a risk factor for short-term outcomes following primary total hip and total knee replacement in veterans. Arthritis Care & Research 63:10, 1365-1374
    CrossRef

  4. 4

    J. Wouter Jukema, Jeffrey J. W. Verschuren, Tarek A. N. Ahmed, Paul H. A. Quax. (2011) Restenosis after PCI. Part 1: pathophysiology and risk factors. Nature Reviews Cardiology
    CrossRef

  5. 5

    Paul Frey, David D. Waters. (2011) Tobacco smoke and cardiovascular risk. Current Opinion in Cardiology 26:5, 424-428
    CrossRef

  6. 6

    Stavros Gourgiotis, Stavros Aloizos, Paraskevi Aravosita, Christina Mystakelli, Eleni-Christina Isaia, Christos Gakis, Nikolaos S. Salemis. (2011) The effects of tobacco smoking on the incidence and risk of intraoperative and postoperative complications in adults. The Surgeon 9:4, 225-232
    CrossRef

  7. 7

    Mohammad A. Sherif, Christoph A. Nienaber, Ralph Toelg, Mohamed Abdel-Wahab, Volker Geist, Steffen Schneider, Jochen Senges, Karl-Heinz Kuck, Ulrich Tebbe, Gert Richardt. (2011) Impact of smoking on the outcome of patients treated with drug-eluting stents: 1-year results from the prospective multicentre German Drug-Eluting Stent Registry (DES.DE). Clinical Research in Cardiology 100:5, 413-423
    CrossRef

  8. 8

    Sameer Bashey, Paul Muntner, Annapoorna S. Kini, Ricardo Esquitin, Louai Razzouk, Shiny Mathewkutty, Rachel P. Wildman, April P. Carson, Michael C. Kim, Pedro R. Moreno, Samin K. Sharma, Michael E. Farkouh. (2011) Clustering of Metabolic Abnormalities Among Obese Patients and Mortality After Percutaneous Coronary Intervention. The American Journal of Cardiology 107:10, 1415-1420
    CrossRef

  9. 9

    J. M. van Werkhoven, J. D. Schuijf, A. P. Pazhenkottil, B. A. Herzog, J. R. Ghadri, J. W. Jukema, E. Boersma, L. J. Kroft, A. de Roos, P. A. Kaufmann, J. J. Bax. (2011) Influence of smoking on the prognostic value of cardiovascular computed tomography coronary angiography. European Heart Journal 32:3, 365-370
    CrossRef

  10. 10

    Victor Aboyans, Daniel Thomas, Philippe Lacroix. (2010) The cardiologist and smoking cessation. Current Opinion in Cardiology 22:5, 469-477
    CrossRef

  11. 11

    Alan H. Gradman, Nosheen Javed. 2010. Addictive Disorders in Cardiovascular Medicine. , 251-275.
    CrossRef

  12. 12

    Timothy L. Lash, Morten Schmidt, Annette Østergaard Jensen, Malene Cramer Engebjerg. (2010) Methods to apply probabilistic bias analysis to summary estimates of association. Pharmacoepidemiology and Drug Safety 19:6, 638-644
    CrossRef

  13. 13

    Jae Kean Ryu. (2010) Smoking Interaction with Clopidogrel; Another Smoker's Paradox?. Korean Circulation Journal 40:3, 112
    CrossRef

  14. 14

    Shepard D. Weiner, LeRoy E. Rabbani. (2010) Secondary prevention strategies for coronary heart disease. Journal of Thrombosis and Thrombolysis 29:1, 8-24
    CrossRef

  15. 15

    Yariv Gerber, Laura J. Rosen, Uri Goldbourt, Yael Benyamini, Yaacov Drory. (2009) Smoking Status and Long-Term Survival After First Acute Myocardial Infarction. Journal of the American College of Cardiology 54:25, 2382-2387
    CrossRef

  16. 16

    Shannon Gravely-Witte, Donna E. Stewart, Neville Suskin, Sherry L. Grace. (2009) The association among depressive symptoms, smoking status and antidepressant use in cardiac outpatients. Journal of Behavioral Medicine 32:5, 478-490
    CrossRef

  17. 17

    J.M. Suriñach, L.R. Álvarez, R. Coll, J.A. Carmona, C. Sanclemente, E. Aguilar, M. Monreal. (2009) Differences in cardiovascular mortality in smokers, past-smokers and non-smokers. European Journal of Internal Medicine 20:5, 522-526
    CrossRef

  18. 18

    Leif Erhardt. (2009) Cigarette smoking: An undertreated risk factor for cardiovascular disease. Atherosclerosis 205:1, 23-32
    CrossRef

  19. 19

    David M. Kaylie, Marc L. Bennett, Bryan Davis, C. Gary Jackson. (2009) Effects of smoking on otologic surgery outcomes. The Laryngoscope 119:7, 1384-1390
    CrossRef

  20. 20

    Nael Al-Sarraf, Lukman Thalib, Anne Hughes, Michael Tolan, Vincent Young, Eillish McGovern. (2008) Effect of Smoking on Short-Term Outcome of Patients Undergoing Coronary Artery Bypass Surgery. The Annals of Thoracic Surgery 86:2, 517-523
    CrossRef

  21. 21

    Christopher Bullen. (2008) Impact of tobacco smoking and smoking cessation on cardiovascular risk and disease. Expert Review of Cardiovascular Therapy 6:6, 883-895
    CrossRef

  22. 22

    Patrizio Sarto, Laura Merlo, Giampaolo Pasquetto, Pierluigi Zanco, Pietro Pascotto, Donatella Noventa, Bernhard Reimers. (2008) Competitive sport after coronary angioplasty: suggested eligibility criteria for moderate-high intensity sport. Journal of Cardiovascular Medicine 9:6, 631-635
    CrossRef

  23. 23

    Kirsten H. Long, Henry H. Ting, Erin K. McMurtry, Ryan J. Lennon, Douglas L. Wood, David R. Holmes, Ganesh Raveendran, Charanjit S. Rihal. (2008) A Longitudinal Analysis of Outcomes Associated with Abciximab and Eptifibatide in a Consecutive Series of 3074 Percutaneous Coronary Interventions. Value in Health 11:3, 462-469
    CrossRef

  24. 24

    Birna Bjarnason-Wehrens, Klaus Held, Eike Hoberg, Marthin Karoff, Bernhard Rauch. (2007) Deutsche Leitlinie zur Rehabilitation von Patienten mit Herz-Kreislauferkrankungen (DLL-KardReha). Clinical Research in Cardiology Supplements 2:3, 1-54
    CrossRef

  25. 25

    Robyn L. Richmond, Nicholas Zwar, Rowena Ivers. 2006. Tobacco and Cardiovascular Disease. , 647-688.
    CrossRef

  26. 26

    Kirsten Hall Long, Erin K. McMurtry, Ryan J. Lennon, Anne C. Chapman, Mandeep Singh, Charanjit S. Rihal, Douglas L. Wood, David R. Holmes, Henry H. Ting. (2006) Elective Percutaneous Coronary Intervention Without On-Site Cardiac Surgery. Medical Care 44:5, 406-413
    CrossRef

  27. 27

    Petter Quist-Paulsen, Stian Lydersen, Per S. Bakke, Frode Gallefoss. (2006) Cost effectiveness of a smoking cessation program in patients admitted for coronary heart disease. European Journal of Cardiovascular Prevention & Rehabilitation 13:2, 274-280
    CrossRef

  28. 28

    Henry H. Ting, Ganesh Raveendran, Ryan J. Lennon, Kirsten Hall Long, Mandeep Singh, Douglas L. Wood, Bernard J. Gersh, Charanjit S. Rihal, David R. Holmes. (2006) A Total of 1,007 Percutaneous Coronary Interventions Without Onsite Cardiac Surgery. Journal of the American College of Cardiology 47:8, 1713-1721
    CrossRef

  29. 29

    Dagmara Hering, Virend K Somers, Tomas Kara, Wiesława Kucharska, Pavel Jurak, Leszek Bieniaszewski, Krzysztof Narkiewicz. (2006) Sympathetic neural responses to smoking are age dependent. Journal of Hypertension 24:4, 691-695
    CrossRef

  30. 30

    J CASTILLOMARTIN. (2006) Rehabilitación cardíaca en el síndrome coronario agudo. Rehabilitación 40:6, 318-332
    CrossRef

  31. 31

    J. HERLITZ, J. HOLM, M. PETERSON, B. W. KARLSON, M. HAGLID EVANDER, L. ERHARDT, . (2005) Factors associated with development of stroke long-term after myocardial infarction: experiences from the LoWASA trial. Journal of Internal Medicine 257:2, 201-207
    CrossRef

  32. 32

    Tetsuya Ishikawa, Hidenori Yagi, Takashi Ogawa, Chikara Mori, Hiroshi Takeda, Hiroshi Sakamoto, Makoto Mutoh, Atsushi Seo, Takahiro Shibata, Satoru Yoshida, Kamon Imai, Toshinobu Horie, Seibu Mochizuki. (2005) Deteriorative Effect of Smoking on Target Lesion Revascularization After Implantation of Coronary Stents With Diameter of 3.0 mm or Less. Circulation Journal 69:2, 227-231
    CrossRef

  33. 33

    Soeren Ballegaard, E. Borg, B. Karpatschof, J. Nyboe, A. Johannessen. (2004) Long-Term Effects of Integrated Rehabilitation in Patients with Advanced Angina Pectoris: A Nonrandomized Comparative Study. The Journal of Alternative and Complementary Medicine 10:5, 777-783
    CrossRef

  34. 34

    Herrmann, Howard C., . (2004) Prevention of Cardiovascular Events after Percutaneous Coronary Intervention. New England Journal of Medicine 350:26, 2708-2710
    Full Text

  35. 35

    P.E.M. Lottman, C.J. van Marrewijk, G.A.J. Fransen, R.J.F. Laheij, J. Buth. (2004) Impact of Smoking on Endovascular Abdominal Aortic Aneurysm Surgery Outcome. European Journal of Vascular and Endovascular Surgery 27:5, 512-518
    CrossRef

  36. 36

    Rados??aw Szczech, Dagmara Hering, Krzysztof Narkiewicz. (2004) Smoking and cardiovascular risk. Journal of Hypertension 22:1, 31-34
    CrossRef

  37. 37

    Julia A Critchley, Simon Capewell, Julia A Critchley. 2003. Smoking cessation for the secondary prevention of coronary heart disease. .
    CrossRef

  38. 38

    Barry A. Franklin, J. NORMAN PATTON, GERALD FLETCHER. (2001) Aggressive Secondary Prevention: A Perspective from the Coronary Interventional Setting. Journal of Interventional Cardiology 14:5, 559-562
    CrossRef

  39. 39

    Rudolf M. Snajdar, Steven J. Busuttil, Allen Averbook, Debra J. Graham. (2001) Inhibition of Endothelial Cell Migration by Cigarette Smoke Condensate. Journal of Surgical Research 96:1, 10-16
    CrossRef

  40. 40

    Ron T van Domburg, Karin Meeter, Dorien F.M van Berkel, Rolf F Veldkamp, Lex A van Herwerden, Ad J.J.C Bogers. (2000) Smoking cessation reduces mortality after coronary artery bypass surgery: a 20-year follow-up study. Journal of the American College of Cardiology 36:3, 878-883
    CrossRef

  41. 41

    J Critchley, S Capewell. 2000. Smoking cessation for the secondary prevention of coronary heart disease. .
    CrossRef

  42. 42

    S.H Wilson, P.B Berger, V Mathew, M.R Bell, K.N Garratt, C.S Rihal, J.F Bresnahan, D.E Grill, S Melby, D.R Holmes. (2000) Immediate and late outcomes after direct stent implantation without balloon predilation. Journal of the American College of Cardiology 35:4, 937-943
    CrossRef

  43. 43

    Johan Herlitz, Björn W. Karlson, Margareta Sjölin, Jonny Lindqvist, Thomas Karlsson, Kenneth Caidahl. (2000) Five-year mortality in patients with acute chest pain in relation to smoking habits. Clinical Cardiology 23:2, 84-90
    CrossRef

  44. 44

    W. Warren Suh, Diane E. Grill, David R. Holmes, Malcolm R. Bell, Peter Berger, Kirk N. Garratt. (1999) Clinical, angiographic, and procedural correlates of abrupt vascular closure during coronary intervention: A 10-year experience at Mayo Clinic. Catheterization and Cardiovascular Interventions 47:4, 391-395
    CrossRef

  45. 45

    A.Maziar Zafari, Nanette K. Wenger. (1998) Secondary prevention of coronary heart disease. Archives of Physical Medicine and Rehabilitation 79:8, 1006-1017
    CrossRef