Abstract
Purpose
The ‘smoker’s paradox’ refers to the observation of favorable prognosis in current smokers following an acute myocardial infarction (AMI). Initial positive findings were in the era of fibrinolysis, with more contemporary studies finding conflicting results. We sought to determine the presence of a ‘smoker’s paradox’ in a cohort of ST Elevation Myocardial Infarction (STEMI) patients identified via field triage, treated with primary percutaneous coronary intervention (pPCI).
Methods
This was a single center retrospective cohort study identifying consecutive STEMI patients presenting for pPCI via field triage. The primary end points were all cause mortality, major adverse cardiac events (MACE), major bleeding, in-hospital cardiac arrest and length of stay (LOS).
Results
A total of 382 patients were included in the study. Current smokers were more likely to be younger (p < 0.00001), male (p < 0.001) and have fewer comorbidities, including renal impairment (p < 0.01) and a history of AMI (p < 0.05). Current smokers also had a shorter ischemic time (p < 0.05), were less likely to have collateral circulation (p < 0.05), and more likely to have signs of pulmonary edema at presentation (p < 0.05). There was no difference between smoking groups and all cause mortality (p = 0.67), MACE (p = 0.49), major bleeding (p = 0.49) or in-hospital cardiac arrest (p = 0.43). Current smokers had a shorter LOS (p < 0.05). In multivariate analysis smoking status did not correlate with primary outcomes.
Conclusion
The ‘smoker’s paradox’ does not appear to be relevant among STEMI patients undergoing pPCI, identified via field triage. The previously documented ‘smoker’s paradox’ may have been an indication of patient characteristics and the historical treatment of STEMI with thrombolysis. Further studies with larger numbers may be warranted.
1
Introduction
It has been previously suggested that smokers undergoing treatment for acute myocardial infarction (AMI) have a favorable prognosis compared with non-smokers, a phenomenon known as the ‘smoker’s paradox’ . This finding was shown in a number of early studies, in the era pre-dating thrombolysis , as well as in the era of fibrinolysis . Subsequent contemporary studies in the era of primary percutaneous coronary intervention (pPCI) have found conflicting evidence . The apparent survival benefit in smokers was observed as early as 30 days , and has persisted in 3 years follow up . These improved mortality rates have been attributed to various factors, including a greater thrombus burden in smokers, leading to greater efficacy of fibrinolysis , as well as demographic differences, particularly smokers’ younger age and fewer co-morbidities .
The primary objective of initial treatment for ST elevation myocardial infarction (STEMI) is to limit ischemic times, with more recent emphasis shifting to reducing first medical contact to TIMI grade 3 flow time . Field triage identifies patients in the community with STEMI, transferring them directly to the cardiac catheterization laboratory, bypassing emergency departments. Field triage is now considered the gold standard of care in STEMI patients, as it has been shown to reduce total ischemic time and improve clinical outcomes .
Given the majority of patients with STEMI are now being treated by pPCI, often via field triage, it is important to determine whether previous epidemiological findings, such as the ‘smoker’s paradox’ are an indicator of previous treatment strategies, or continue to be observed in a contemporary cohort undergoing current evidence based best practice. We sought to determine whether the ‘smoker’s paradox’ has any contemporary relevance on clinical outcomes in a cohort of patients all undergoing pPCI for STEMI via field triage.
2
Methods
This was a single centered retrospective study conducted from May 2004 to December 2010 at Royal North Shore Hospital, a large tertiary center in northern Sydney. All consecutive STEMI patients field triaged directly to the cardiac catheterization laboratory were identified. Patients were included if they had EKG changes consistent with STEMI. Exclusion criteria were patients who presented with incomplete data sets and out of hospital cardiac arrests. Upon field diagnosis of STEMI, all patients received sublingual nitroglycerin, oral aspirin (300 mg) and clopidogrel loading (300–600 mg) prior to transfer to the cardiac catheterization laboratory. Angiography was performed according to standard procedure, with either a femoral or radial artery approach taken. Assessment of coronary stenosis was visual, and the treatment strategy thereafter was at the discretion of the treating interventional cardiologist. The presence of collateral flow was noted if there was complete collateral filling of the epicardial vessel of the infarct related artery, as previously described . Post pPCI, heparin up to a dose of 75–100 IU/kg was given intravenously while the use of glycoprotein IIb/IIIa receptor blockers was at the operator’s discretion. Coronary stenting was used if deemed appropriate, with a policy to treat the infarct-related artery only. Emergency cardiac surgery was available on-site. Revascularization was deemed successful after TIMI-3 flow was achieved.
2.1
Data collection and measures
Patients were followed for 30 days from admission. Baseline demographic data were collected prospectively from all patients. Peri-procedural data, inpatient course, length of admission and outcomes were prospectively recorded. Study end points were 30 day all cause mortality, major adverse cardiac events (MACE), major bleeding and in hospital cardiac arrest. MACE was defined as the composite of mortality, re-infarction, cerebrovascular accident or the requirement for repeat revascularization.
Smoking status was based on self reported history. A patient was considered to be a current smoker if they had regularly smoked within the last 12 months. Previous smokers were those who had not smoked in the preceding 12 months prior to presentation. Time to first medical contact was calculated from symptom onset to calling the emergency services number. Total ischemic time was calculated from symptom onset to TIMI 3 flow time.
2.2
Data analysis
Categorical variables were expressed as frequencies and percentages of the cohort, while continuous variables were expressed as medians with interquartile range. Chi-square test was used to assess the differences in baseline demographics, clinical characteristics and in-hospital outcomes between smokers, former smokers and non-smokers, for categorical variables. For continuous variables, the Kruskal–Wallis test was used. Multivariate logistic regression analysis was used to determine the predictors of the primary endpoints, and to correct for confounders, with univariate predictors with a p < 0.05 entered into the multivariate model. The odds ratio (OR) of primary endpoints in the current- and former- smoker groups was calculated using non-smokers as a reference. Significance was accepted at a value of p < 0.05. Statistical analysis was performed using SPSS for Windows release 17.0 (SPSS, Inc., Chicago, Illinois).
2
Methods
This was a single centered retrospective study conducted from May 2004 to December 2010 at Royal North Shore Hospital, a large tertiary center in northern Sydney. All consecutive STEMI patients field triaged directly to the cardiac catheterization laboratory were identified. Patients were included if they had EKG changes consistent with STEMI. Exclusion criteria were patients who presented with incomplete data sets and out of hospital cardiac arrests. Upon field diagnosis of STEMI, all patients received sublingual nitroglycerin, oral aspirin (300 mg) and clopidogrel loading (300–600 mg) prior to transfer to the cardiac catheterization laboratory. Angiography was performed according to standard procedure, with either a femoral or radial artery approach taken. Assessment of coronary stenosis was visual, and the treatment strategy thereafter was at the discretion of the treating interventional cardiologist. The presence of collateral flow was noted if there was complete collateral filling of the epicardial vessel of the infarct related artery, as previously described . Post pPCI, heparin up to a dose of 75–100 IU/kg was given intravenously while the use of glycoprotein IIb/IIIa receptor blockers was at the operator’s discretion. Coronary stenting was used if deemed appropriate, with a policy to treat the infarct-related artery only. Emergency cardiac surgery was available on-site. Revascularization was deemed successful after TIMI-3 flow was achieved.
2.1
Data collection and measures
Patients were followed for 30 days from admission. Baseline demographic data were collected prospectively from all patients. Peri-procedural data, inpatient course, length of admission and outcomes were prospectively recorded. Study end points were 30 day all cause mortality, major adverse cardiac events (MACE), major bleeding and in hospital cardiac arrest. MACE was defined as the composite of mortality, re-infarction, cerebrovascular accident or the requirement for repeat revascularization.
Smoking status was based on self reported history. A patient was considered to be a current smoker if they had regularly smoked within the last 12 months. Previous smokers were those who had not smoked in the preceding 12 months prior to presentation. Time to first medical contact was calculated from symptom onset to calling the emergency services number. Total ischemic time was calculated from symptom onset to TIMI 3 flow time.
2.2
Data analysis
Categorical variables were expressed as frequencies and percentages of the cohort, while continuous variables were expressed as medians with interquartile range. Chi-square test was used to assess the differences in baseline demographics, clinical characteristics and in-hospital outcomes between smokers, former smokers and non-smokers, for categorical variables. For continuous variables, the Kruskal–Wallis test was used. Multivariate logistic regression analysis was used to determine the predictors of the primary endpoints, and to correct for confounders, with univariate predictors with a p < 0.05 entered into the multivariate model. The odds ratio (OR) of primary endpoints in the current- and former- smoker groups was calculated using non-smokers as a reference. Significance was accepted at a value of p < 0.05. Statistical analysis was performed using SPSS for Windows release 17.0 (SPSS, Inc., Chicago, Illinois).
3
Results
In the study period a total of 388 consecutive patients with a diagnosis of STEMI presented for pPCI via field triage. Six patients were excluded due to incomplete data set, resulting in a study cohort of 382 patients.
In the study population, 113 (29.6%) were current smokers, 95 (24.9%) were former smokers, while 174 (45.5%) identified themselves as lifelong non-smokers. The mean age for current smokers was 57.2, 66.1 in former smokers and 68.5 years in non-smokers (p < 0.0001) with 47.8% of current smokers aged 18–54. 79.7% of current smokers, and 85.3% of former smokers were male, while women were more likely to be non-smokers (34.5%; p < 0.001). Co-morbidities were mostly spread throughout the population, although non-smokers were more likely to have a past history of AMI (17.8%) and renal impairment (8%) as compared to previous smokers (22.1% and 9.5% respectively) and current smokers (8.8% and 0% respectively) (p < 0.05; p < 0.01 respectively). Current smokers had a shorter median symptom onset to seeking medical help time (28 min) as compared to former (34.5 min) and non-smokers (46 min); p < 0.05. Current smokers also had a shorter median symptom onset to TIMI 3 flow time (ischemic time) of 125 min as compared to former (127 min) and non-smokers (148 min); p < 0.05.
At presentation, non-smokers were less likely to have evidence of pulmonary edema (63.2%), as determined by a Killip class of I, as compared to current and former smokers (76.1% and 76.8% respectively); p < 0.05. There was no significant difference in the location of the culprit artery. However, current smokers were significantly less likely to have collateral arterial supply from the culprit vessel (0%) as compared to non-smokers (3.4%); p < 0.05. Former smokers had the highest rate of collaterals at 11%. There was no significant difference in the number of vessels diseased at presentation.
There was no difference in 30 day all cause mortality between the smoking groups, with 1 death (0.9%) in current smokers, 2 (2.1%) in former smokers, and 4 (2.3%) in non-smokers (p = 0.67). Similarly, there was no significant difference in MACE (p = 0.49), major bleeding (p = 0.49) or cardiac arrest (p = 0.43). Current smokers did however have a shorter median length of hospital stay (3 days) as compared to former and non-smokers (3 and 3.5 days respectively), p > 0.05 ( Table 1 ).
| Current Smoker | Former Smoker | Non Smoker | p-value | |
|---|---|---|---|---|
| n = 382 | n = 113 (29.6%) | n = 95 (24.9%) | n = 174 (45.5%) | |
| Age median, years (IQR) | 56 (48–65) | 66 (55.5–70) | 69 (59–79) | < 0.00001 |
| 18–54 | 54 (47.8%) | 23 (24.2%) | 29 (16.7%) | < 0.00001 |
| 55–64 | 27 (23.9%) | 21 (22.1%) | 34 (19.5%) | |
| 65–74 | 19 (16.8%) | 21 (22.1%) | 50 (28.7%) | |
| ≥ 75 | 13 (11.5%) | 30 (31.6%) | 61 (35.1%) | |
| Body Mass Index (kg/m 2 ) | 27 (24.8–29.9) | 25.9 (23.9–29.3) | 26.1 (23.4–29.3) | 0.10 |
| Women | 23 (20.3%) | 14 (14.7%) | 60 (34.5%) | < 0.001 |
| Past History | ||||
| Hypertension | 44 (38.9%) | 48 (50.5%) | 82 (47.1%) | 0.24 |
| Hypercholesterolemia | 55 (48.7%) | 40 (42.1%) | 92 (52.9%) | 0.24 |
| Diabetes | 13 (11.5%) | 18 (18.9%) | 25 (14.4%) | 0.32 |
| AMI | 10 (8.8%) | 21 (22.1%) | 31 (17.8%) | < 0.05 |
| CVA | 3 (2.6%) | 5 (5.3%) | 14 (8%) | 0.16 |
| Renal Impairment | 0 (0%) | 9 (9.5%) | 14 (8%) | < 0.01 |
| CABG/PCI | 15 (13.3%) | 18 (18.9%) | 32 (18.4%) | 0.47 |
| Time to Medical Contact, min median (IQR) | 28 (14,77) | 34.5 (16, 103) | 46 (14, 143) | < 0.05 |
| Ischemic Time, min median (IQR) | 125 (91.75–167.5) | 127 (99.25–208.75) | 148 (104–223) | < 0.05 |
| Clinical Presentation | ||||
| Killip Class I | 86 (76.1%) | 73 (76.8%) | 110 (63.2%) | < 0.05 |
| Killip Class II–IV | 27 (23.9%) | 22 (23.2%) | 64 (36.8%) | |
| Affected Artery | ||||
| LAD | 36 (31.9%) | 39 (41%) | 67 (38.5%) | 0.38 |
| LCx | 15 (13.3%) | 11 (11.6%) | 23 (13.2%) | 0.91 |
| LM | 0 (0%) | 1 (1%) | 1 (0.6%) | 0.57 |
| RCA | 60 (53.1%) | 44 (46.3%) | 80 (46) | 0.41 |
| SVG | 2 (1.8%) | 0 (0%) | 2 (1.1%) | 0.45 |
| Number of affected vessels | ||||
| Single | 61 (54.0%) | 49 (51.5%) | 90 (51.7%) | 0.90 |
| Double | 29 (25.7%) | 24 (25.3%) | 42 (24.15%) | 0.95 |
| Triple | 23 (20.3%) | 22 (23.2%) | 42 (24.15%) | 0.75 |
| LV Ejection Fraction, median (IQR) | 50% (40–55) | 45% (40–55) | 45% (40–50) | 0.37 |
| Collaterals | 0 (0%) | 3 (11%) | 2 (3.4%) | < 0.05 |
| Outcomes | ||||
| Mortality | 1 (0.9%) | 2 (2.1%) | 4 (2.3%) | 0.67 |
| MACE | 8 (7.1%) | 5 (5.3%) | 16 (9.2%) | 0.49 |
| Major Bleeding | 3 (2.6%) | 2 (2.1% | 8 (4.6%) | 0.49 |
| Cardiac Arrest | 8 (7.1%) | 3 (3.2%) | 11 (6.3%) | 0.43 |
| Length of Stay, days median (IQR) | 3 (2–4) | 3 (2–5) | 3.5 (2–7) | < 0.05 |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
