Smokers are surely at higher risk of developing coronary artery diseases, but they have better short-term survival after myocardial infarction. Many patients who quit smoking after ACS return to smoking within 1 year. While cessation is probably the most important thing to do to improve future health.

Aim

This study tends to determine the clinical and the therapeutic particularities of ACS in smokers, to examine their smoking characteristics and to summarize the evidence for smoking cessation among those patients using several smoking cessation therapies.

Methods

A comparative study including 58 smokers (group 1) and 42 non-smokers (group 2), admitted from July 2018 to October 2018 at the cardiology department in La Rabta university hospital, with a diagnosis of ACS including ST-elevation myocardial infarction (STEMI), unstable angina (UA) and non-ST-elevation myocardial infarction (NSTEMI). Diagnosis of the different types of ACS and definitions of data variables were based on the American College of Cardiology clinical data standards. There is no patient-specific exclusion criterion, and all prospective patients with ACS were thus enrolled.

Central obesity was defined as a waist circumference of more than 94 cm in men and more than 80 cm in women. Smoking dependence was evaluated by Fagerstrom inventory, and motivation to cessation was evaluated by Richmond questionnaire. Tobacco cessation strategies were initiated during the hospital stay, then patients were referred to a specialized consultation at Charles Nicolle University hospital. One-month later patients had clinic visits for their ACD, smoking status was assessed too.

One-year mortality and smoking status were obtained by either phone contacts or clinic visits.

Statistical methods

Data were summarized as mean ± Standard Deviation (SD) if they were normally distributed. otherwise, they were summarized as the median and interquartile range (IQR). Differences between groups were assessed using Chi square or Fisher’s exact tests for categorical variables, student’s t tests for continuous and normally distributed variables and the Mann-Whitney U test for skewed variables. Anova was used for the categorical variables with more than two levels. All analyses were considered significant at P < 0.05. The analysis was performed using SPSS software, version 17.

Table1: Baseline characteristics of patient with acute coronary syndrome

SBP: systolic blood pressure, DBP: diastolic blood pressure, HR: heart rate, bpm: beats per minute, CAD: coronary artery disease, NSTEMI: Non-ST segment elevation myocardial infarction, STEMI: ST-segment elevation myocardial infarction, CVA: cerebro vascular accident, TIA: transient ischemic attack, PAD: peripheral artery disease, PCI: percutaneous coronary intervention, CABG: coronary artery bypass graft surgery, COPD: chronic obstructive pulmonary disease, AMI: acute myocardial infarction, CRP: C reactive protein, MCV: Mean corpuscular volume IQR: interquartile range

Results

Characteristics of smokers and non-smokers

The study sample consisted of 100 patients with acute coronary syndrome admitted between July 2018 to October 2018. Of these, 58 (58%) were smokers: G1, and 42 (42%) were non-smokers: G2. Low economic level was noted in 61% of patients and they were mostly from G1 (p = 0,006). Patients were admitted for NSTEMI in 50% of cases, and it was significantly more frequent among non-smokers (p = 0,002). Smokers were mostly diagnosed with AMI (p = 0,001). The baseline characteristics of the study population are presented in Table 1. Mean age was 56 ( ± 9, 64) years with extreme ranging from 33 to 79 years old for G1 and was 64 ( ± 8,47) years with extreme ranging from 46 to 81 years old for G2. Thirty percent of the smokers were aged under 50 years. All patients from G1 were men, while more than a half of G2 (66, 7%) were female. Non-smokers were more likely to have a history of stable angina (7,14%) or NSTEMI (16,66%) than smokers (0%, 10,34%, respectively), while smokers were more likely to have STEMI history (12%). Even though, coronary artery bypass graft was significantly more performed in G2 (p=0,008). G1 patients had fewer cardiovascular risk factors than G2 such as hypertension (p=0,03), dyslipidemia (p=0,01), obesity (p=0,01) and diabetes mellitus (0,001). Nevertheless, patients from G1 had more COPD (10,34%). During the current ACS, typical chest pain was noted in 91% cases in G 1 and 98% of cases in G 2. Triggering factors were not identified in 75% of cases in both groups. At admission, the highest proportion of patients in Killip class >1 was in G2 (21,42%) compared with G1 (6,89%). G1 had higher peak serum CK-MB fraction (p=0,009). Median serum high sensitivity troponin level was higher in G1 (1245 ng/ml) compared to G2 (504 ng/ml). Anemia was more frequent in G2 (p=0,003). Smokers were more likely to have leukocytosis (p < 0,001). Higher frequency of low Global Registry of Acute Coronary Events (GRACE) score category was noted in G1 (p=0,001). Echocardiography was done in all patients. G1 patients were more likely to have better LV function (p=0,006).

Hospital treatment and outcomes

Coronary angiography was performed for all patients according to their hemodynamic status. One-vessel coronary artery disease was found in one-half of patients of G1 (p = 0,04). Smokers were more likely to undergo percutaneous coronary intervention (p = 005), but were less likely to undergo coronary artery bypass grafting than G2 (p = 0,02). Current smokers were also more likely to receive thrombolytics(p = 0,05), and beta-blockers(p = 0,005). (Table 2).

In-hospital death was more important in G2 (15%) than G1 (8%). Major bleeding occurred in 2% of cases in both groups. The risk of 30 days death no longer differed significantly between the two groups

Table 2: In hospital procedures

LV: Left ventricle, PCI: percutaneous coronary intervention, ACE: Angiotensin-converting enzyme inhibitor, CABG: coronary artery bypass graft surgery

Smoking characteristics

Cigarettes consumption was the most frequent type of smoking (86%). Ten per cent of patients used to consume both cigarettes and narghile. Tobacco chewing accounted for 2%. Average age at start of consumption was 21, 13±6,39. Mean duration of smoking was 30,93±10,9 years. Mean consumption was 40,63±23,9 pack/year. More than a half of patients smoked more than 15 pack/year. An increase in cigarette consumption right before the ACS was reported in 55% of cases. Forty percent of patients had at least one cessation experience, and it was medically assisted in 22% of the cases. Cardiac problems were the most reported cause of those attempts (87%) while respiratory problems were reported in 13% of cases. Mean time to relapse was 9,5±2,3 months. Many reasons to relapse were reported, but cafes attendance (77%), withdrawal symptoms (67%), nicotine patches intolerance (65%), smoking friends (65%), and professional problems (43%) were the most frequent. The patients were mostly at high and very high nicotinic dependency (78%), and average dependency according to the Fagerstrom test was 6,5±1,5. Initial motivation on the Richmond Test was 7,78±2,1.Consciousness about the harm caused by tobacco on arteries was the most frequent motivator reported in 83% of cases. Medical obeisance and symptoms remain were reported in 45% of the cases. Medical aid was claimed by 74% of patients. During the hospital stay, 81% of patients continued smoking and 11 patients were quitters, 4 of which decreased daily consumption. Smoking status in hospital was not correlated to dependency (p=0,5), to number of pack/year (p=0,11), to motivation to give up smoking (p=0,33), and to former attempts of tobacco cessation (p=0,9).

Table 3: Smoking types

Table 4: Smoking characteristics

*Percentage calculated for all patients (smokers and non-smokers)

**Percentage calculated for smokers

Tobacco cessation

Tobacco cessation strategies were insured in 98% of the cases during the hospital stay and they were carried on in the smoking cessation consultation later. Only one patient with very high dependency level refused them. Bupropion and varenicline were not available in Tunisia. Only one patient used imported varenicline. Nicotine patches were used in 74%, and homeopathy in 72% of the cases. Behavioral interventions were applicated to 28% of the patients. One month later, only 33% of the patients kept their non-smoker status. Side effects of patches and homeopathy were reported by 54% of patients and thus a good treatment adherence was reported in 24% of cases. Effective attendance in a smoking cessation program was reported by 22% of the patients. After one year, only 28% of the patients were still non-smoker. A model of logistic regression showed that only the young ageat start of tobacco consumption and previous cessation attempts had an impact on the smoking status (Table 6).

Table 5: Tobacco cessation characteristics and outcomes

Table 6: Binomial logistic regression predicting the likelihood of smokers giving up tobacco

Β: Intercept, SE: Standard error, Wald: Wald chi-square test, Df: degree of freedom, Sig: significance, Exp β: Odds ratio, CI: confidence interval

**Percentage calculated for smokers

Discussion

ACS remains a substantial cause of morbidity and mortality.

Few recent data are available regarding the impact of smoking status on presentation and outcome in patients with the spectrum of acute coronary syndromes, particularly among those without persistent ST segment elevation (STEMI), which currently represent the majority of patients with an acute coronary syndrome^[1].

The role of smoking in coronary artery diseases

Atherosclerosis

It has been reported that both active and passive smoking are associated with a consistent increase in intimal-medial thickness of the artery^[2].

Cigarette smoke (CS) exposure impaired endothelium-dependent vasodilation in macro vascular beds such as coronary, which is one of the earliest manifestations of atherosclerotic changes in a vessel^[3]. Nitric oxide (NO) is responsible for the vasodilatory function of the endothelium. It helps regulate inflammation, leukocyte adhesion, platelet activation, and thrombosis. CS was associated with decreased NO availability^[4]. That could have both primary and secondary effects on the initiation and progression of atherosclerosis and on thrombotic events^[5].

CS is associated with an increased level of multiple inflammatory markers including C-reactive protein. Smoking causes a local recruitment of leukocytes on the surface of endothelial cells which is an early event in atherosclerosis^[5].

Smokers have significantly higher serum cholesterol, triglyceride, and low-density lipoprotein^[6].

Thrombosis and platelet dysfunction

Current smokers have higher fibrinogen levels that correlate with the number of cigarettes smoked. Furthermore, higher red blood cell counts, hematocrits, blood viscosity were associated with smoke exposure^[7]. Cigarette smoking is also associated with dysfunctional thrombohemostatic mechanism(s) that promote the initiation and/or propagation of thrombus formation and limit its effective dissolution^[7].

Nonlinear dose effect

Several studies showed a trend for more cardiovascular events in heavier active smokers but it have failed to find a significant dose-dependent correlation between cardiovascular risk and the number of cigarettes smoked or the pack-years of exposure^[8].

Smoking and type of acute coronary syndrome

Many studies stipulate that the proportion of current smokers was higher among patients with ST segment elevation myocardial infarction than among those with non-ST-segment elevation myocardial infarction or unstable angina. Our study showed the same evidence. Indeed, it has already been reported that smoking is associated with ST-segment elevation among patients admitted with acute coronary syndromes.

Smokers paradox

Reports regarding the unexpected favorable outcome of smokers post myocardial infarction has dated back to the pre-thrombolytic era of STEMI^[9]. The main pathogenesis of acute myocardial infarction in smokers has been reported to differ from those of non-smokers. There is documented increase in hematocrits and fibrinogen levels in smokers which predispose them more to intra-coronary thrombosis^[10]. It is thus suggested that the coronary flow limitation is largely due to thrombogenic obstruction with minimal underlying atherosclerotic narrowing. Whereas, in non-smokers it is the atherosclerotic narrowing which is predominant^[11]. With this came the theory of fibrin-rich thrombus in smokers which is said to be more susceptible to thrombolysis/anti-coagulation and theoretically leads to the seemingly better outcome of smokers particularly in the thrombolytic era^[12]. In one study, the response in myocardial reperfusion after thrombolytic therapy in smokers were objectively assessed and compared to non-smokers in a study using TIMI myocardial perfusion grade (TMPG) which showed better response in smokers^[13]. However more recent data in the era of primary PCI showed no significant difference between smokers and non-smokers and smokers benefit equally from PCI and thrombolysis^[14]. Our study was done in the background of IV thrombolysis as the dominant reperfusion strategy for STEMI (24%) that is why smokers had more thrombolysis. we observed that in-hospital death was more important in non-smokers (15%) than smokers (8%). However, this study only looked at the immediate clinical outcome (in-hospital and 30-day post discharge). Some recent data showed that smoking is actually related to increased long term mortality and quitting smoking is associated with improved survival after acute coronary syndromes^[15]. All these data suggest that favorable smokers’ paradox effect is only limited to short term outcome if it does exist at all. Collectively, current data suggests that even though smoking may be associated with a favorable early outcome, the overall picture is still not in favor of smoking especially on long term outcome and post coronary revascularization. This study assessed the smoking status post myocardial infarction and based on the above evidence from the literature, the favorable outcome of smokers are short-lived and hence we continue to strongly advocate the importance of smoking cessation.

Smoking cessation characteristics

In the current paper we explored characteristics that may increase successful smoking cessation, because of the damage and the mortality induced by tobacco consumption in younger patients with a good artery anatomy.

Our study confirms that quitting smoking is extremely difficult for many patients, even after being hospitalized for a life-threatening event, especially for those with a lower education level. Starting smoking at an early age was strongly correlated to failure of cessation experience. Only 33% of the patients succeeded in quitting smoking one month after ACS, which is consistent with success rates in previous studies^[16,17].

On the positive side, however, our study also shows that almost 28% of all smokers succeeded in quitting up to 1 year after ACS. Moreover, of those who quit immediately after the acute event, the majority are successful through 1 year. Our study confirms earlier findings indicating that a clinical event acts as an important motivator and may induce behavioral change^[18], particularly if this event is perceived as life-threatening as is the case with patients’ first ACS^[19]. In accordance with European Society of Cardiology (ESC) guidelines, clinicians may make greater use of this opportunity by addressing the issue before discharge^[20]. These guidelines also recommend that support for cessation of smoking is initiated for all smokers during hospital admission and is continued for a prolonged period after discharge. We have followed those recommendations and 22% of our patients attended a specialized smoking cessation program. However, the majority of successful quitters stop immediately after discharge. It is within their own ability to quit and remain abstinent. Patients were highly and very highly dependent to tobacco (40%, 38%) respectively. However, dependency levels were not correlated to a successful smoking cessation. Some authors claimed that the more a measure of dependence is based exclusively on level of daily smoking, the greater is its ability to predict cessation^[21].

This behavior may be explained by the theory of self-perception^[22]. In our study, 36% of the smokers showed high motivation scores to quit smoking and they felt able to change. This feeling is strengthened when these patients indeed quit smoking after discharge. These patients soon perceive themselves as ‘successful quitters’^[22], which subsequently strengthens them in their resolve to remain abstinent. However, according to the stages of change theory of Prochaska and Diclemente^[23] counseling seems unnecessary and may be even counterproductive^[18]. Our study took place in the cardiologic reanimation department, were first steps of smoking cessation were made, then, patients were referred to a specialized counseling. Only 22% of patients accepted this follow up. Basically, in the decision-making process about smoking cessation interventions, a distinction could be made between types of smokers, such as patients that reduced their daily consumption. This reduction could be considered for smokers who are willing but unable to quit^[25]. This alternative can be advised until these patients are ready for a new attempt^[25]. More research is needed on characteristics of ACS patients who intend to quit smoking during hospitalization, in order to focus on those who are willing to quit but are at risk for relapse after discharge.

Some studies claimed that counseling or pharmacological therapy may not be necessary in patients who did not relapse up to their first outpatient clinic visit. However, in our study, three immediate quitters who remained abstinent up to their first outpatient visit reported a relapse up to 1 year after ACS. The effectiveness of relapse prevention for patients who immediately quit smoking after an acute hospitalization is lacking^[24].

One week after the ACS, only 19% of patients quit smoking (n = 11). Quitters presented for 33% of the cases one month later (n = 19), and they presented 16% after one year. As we observed a number of relapsers, we think that our findings are unclear about the effectiveness of smoking cessation interventions at hospital discharge, because it does not take place in our department. Relapses occurred probably in CABG patients, who may feel the external pressure not to smoke, but have no motivation.

Earlier research has showed that successful quitting is strongly associated with a higher education level and no history of cardio-vascular disease (CVD)^[19]. That has not been verified in our study, probably because of the low economic levels (69%) and the low prevalence of CVD (22.41%).

In our study, bupropion and varenicline were not part of the smoking cessation counseling. They were not available in Tunisia during the study period, although the only medical therapy for which there is compelling evidence regarding relapse prevention is varenicline^[26]. As guidelines recommend offering aids to assist cessation, nicotine replacement therapy, has been prescribed. It has shown to improve the chances of successful quitting, although patients with a recent history of cardiac disease were excluded in these studies^[27]. More research is needed on the effectiveness of pharmacological aids in immediate quitters after an acute life-threatening event.

We conclude that successful quitters stop immediately after their ACS. Patients in this group showed that it was within their own ability to quit, and they did not relapse in 1 year of follow-up. Patients that reduced consumption failed to stop tobacco use. This finding supports the evidence to avoid relapse prevention in ACS patients who stop smoking immediately after the event^[28]. The opportunity of smoking cessation is very strong immediately after ACS and our study reinforces the importance of clinicians’ explicit advice to stop smoking during hospitalization of ACS patients and not after discharge^[28].

Our study demonstrates that anterior cessation experience is the most important characteristic of successful quitters. This group of patients should be well advised because they have higher chance to success.

Smoking cessation strategies in secondary prevention could differentiate between acute and non-acute patients, since an acute event acts as an important motivator for behavioral change. Furthermore, smoking cessation support should differentiate between immediate and late attempts, since relapse prevention seems unnecessary for immediate quitters. However, patients with a late attempt may benefit from more intensive therapy. In our study, we had 11 quitters one week after ACS, 19 quitters one month later. Future research is needed to assess the cost-effectiveness of differentiating between acute or non-acute admissions and immediate or late quit attempts.

Conclusion

The phenomenon of ‘smoker’s paradox’ is a reality among our patients and it is not only related to the favorable baseline characteristics of smokers. Active smokers tend to do better at both in-hospital and 30-days post discharge with significantly lower overall mortality risk compared to those patients who never smoked. The real explanation to this bizarre outcome however, remains unclear but the importance of its therapeutical implication is very important to consider. Smokers should not be treated the same way as non-smokers, especially during the hospital stay for ACS. Their chance smoking cessation is very strong immediately after ACS and explicit medical advice to stop smoking should be done as soon as possible. Patients that quit smoking with no relapse one month later are at low risk of later relapses.

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