BACKGROUND: Smoker\'s paradox usually refers to the observation of a favorable outcome of smoking patients in acute myocardial infarction.
METHODS: From April 2006 to December 2018 a population of 2456 patients with ST segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI) were prospectively enrolled in the MATRIX registry. Ischemic time, clinical, demographics, angiographic data, and 1-year follow-up were collected.
RESULTS: Among 2546 patients admitted with STEMI, 1007 (41 %) were current smokers. Smokers were 10 years younger and had lower crude in-hospital and 1-year mortality (1.5 % vs 6 %, p < 0.0001 and 5 % vs 11 %, p < 0.0001), shorter ischemic time (203 [147-299] vs 220 [154-334] minutes, p = 0.002) and shorter decision time (60 [30-135] vs 70 [36-170] minutes, p = 0.0063). Smoking habit [OR:0.37(95 % CI:0.18-0.75)-p < 0.01], younger age [OR 1.06 (95%CI:1.04-1.09)-p < 0.001] and shorter ischemic time [OR:1.01(95%CI:1.01-1.02)-p < 0.05] were associated to lower in-hospital mortality. Only smoking habit [HR:0.65(95 % CI: 0.44-0.9)-p = 0.03] and younger age [HR:1.08 (95%CI:1.06-1.09)-p < 0.001] were also independently associated to lower all-cause death at 1-year follow-up. After propensity matching, age, cardiogenic shock and TIMI flow <3 were associated with in-hospital mortality, while smoking habit was still associated with reduced mortality. Smoking was also associated with reduced mortality at 1-year follow-up (HR 0.54, 95 % CI [0.37-0.78]; p < 0.001).
CONCLUSIONS: Smoking patients show better outcome after PCI for STEMI at 1-year follow-up. Although \"Smoking paradox\" could be explained by younger age of patients, other factors may have a role in the explanation of the phenomenon.

OBJECTIVE: Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure used to alleviate patients with chronic liver cirrhosis and portal hypertension. Smoking can adversely impact liver function and has been shown to influence liver-related outcomes. This study aimed to examine the impact of smoking on the immediate outcomes of TIPS procedure.
METHODS: The study compared smokers and non-smokers who underwent TIPS procedures in the National Inpatient Sample (NIS) database from the last quarter of 2015 to 2020. Multivariable analysis was used to compare the in-hospital outcomes post-TIPS. Adjusted pre-procedural variables included sex, age, race, socioeconomic status, indications for TIPS, liver disease etiologies, comorbidities, and hospital characteristics.
RESULTS: Compared to non-smokers, smokers had lower risks of in-hospital mortality (7.36% vs 9.88 %, aOR 0.662, p < 0.01), acute kidney injury (25.57% vs 33.66 %, aOR 0.68, p < 0.01), shock (0.45% vs 0.98 %, aOR 0.467, p = 0.02), and transfer out to other hospital facilities (11.35% vs 14.78 %, aOR 0.732, p < 0.01). There was no difference in hepatic encephalopathy or bleeding. Also, smokers had shorter wait from admission to operation (2.76±0.09 vs 3.17±0.09 days, p = 0.01), shorter length of stay (7.50±0.15 vs 9.89±0.21 days, p < 0.01), and lower total hospital cost (148,721± 2,740.7 vs 204,911±4,683.5 US dollars, p < 0.01). Subgroup analyses revealed consistent patterns among both current and past smokers.
CONCLUSIONS: This study compared the immediate outcomes of smokers and non-smokers after undergoing the TIPS procedure. Interestingly, we observed a smokers\' paradox, where smoker patients had better outcomes following TIPS. The underlying causes for this smoker\'s paradox warrant further in-depth exploration.

Smoking is a well-established risk factor for stroke, yet its impact on stroke prognosis remains complex and multifaceted. This systematic review aims to elucidate the relationship between smoking and various stroke outcomes, including response to treatment and long-term recovery. We conducted a comprehensive analysis of four fundamental studies that examined the prognosis of stroke in smokers, focusing on clinical outcomes post-endovascular treatment, response to antiplatelet therapy, incidence of post-stroke delirium, and the effectiveness of thrombolysis treatment. The studies varied in design, including observational, retrospective, and post hoc trial analyses. The review reveals that smoking may paradoxically predict better clinical outcomes in specific treatment scenarios, such as post-endovascular treatment and when using clopidogrel. However, smokers also demonstrated higher rates of ischemic stroke and post-stroke delirium. Notably, the smoker\'s paradox in thrombolysis treatment was not supported. These findings highlight the need for personalized treatment approaches based on smoking status. Smoking has a complex and significant impact on stroke prognosis. While some benefits in specific treatment contexts were observed, the overall evidence strongly advises against smoking due to its adverse health consequences. This review underscores the importance of personalized stroke management in smokers and the integration of smoking cessation programs in post-stroke care. Future research should focus on larger, longitudinal studies to explore these associations further.

Numerous studies indicated that patients with tobacco use disorder (TUD) are inversely associated with mortality in what is known as the smoker\'s paradox. However, limited studies have been conducted on the impact of TUD on the in-hospital mortality rates of patients with secondary pulmonary hypertension (PH, Non-Group 1 PH). Using the 2019 National Inpatient Sample, we identified PH and divided it into TUD and non-TUD to compare the comorbidities and in-hospital mortality between the two after 1:1 propensity-score matching. Of 1,129,440 PH hospitalizations, 12.1 % had TUD. After matching (n=133545, each group), TUD had lower median age (62 vs. 63), higher females (49 vs. 46.6 %), blacks (25.9 vs. 25.3 %), lower household income (40.8 vs. 32.7 %), Medicaid (22.4 vs. 14.8 %), non-elective (93.5 vs. 89.8 %), rural (9.3 vs. 6.7 %), urban non-teaching (17.2 vs 15.8 %) admissions. All CV comorbidities and other substance use were higher in TUD except CHF and valvular heart disease, TUD+ cohort and lower mortality (3.3 vs. 4.2 %, OR 0.78, p<0.001), higher routine discharges (53.8 vs. 51.3 %, p<0.001) and lower total charges ($47155 vs. 51909, p<0.001) than non-TUD. Although PH patients with TUD had a higher comorbidity burden, they had lower in-hospital mortality rates along with lower total charges of hospitalization, mandating real-world data to validate these results. See also the Graphical abstract(Fig. 1).

UNASSIGNED: \"Smoker\'s paradox\" is a controversial phenomenon that describes an unexpectedly favorable short-term outcome of smokers post-percutaneous coronary intervention (PCI). This study aimed to evaluate the effect of smoking status on recurrent major adverse cardiovascular events (MACEs) in patients who recently underwent PCI and to determine whether it was paradoxical.
UNASSIGNED: This study utilized data from the nationwide Thai PCI registry, enrolling patients during 2018-2019. Our study factor was smoking status, classified as current smokers, ex-smokers, and nonsmokers. The outcome of interest was the time to occurrence of a composite of MACEs (i.e., all-cause death, myocardial infarction (MI), stroke, and unplanned revascularization) evaluated at about 1-year post-PCI. A propensity score (PS) model using inverse probability weighting with regression adjustment was used to estimate the effect of smoking on the occurrence of MACE.
UNASSIGNED: Current smokers, ex-smokers, and non-smokers accounted for 23, 32, and 45% of the 22,741 subjects, respectively. Smokers were younger, more frequently male, and had fewer traditional atherosclerotic risk factors. Current smokers presented more frequently with ST-elevation MIs (STEMIs) and cardiogenic shock (54 and 14.6%, respectively) than non-smokers. MACE rates were 1.9, 1.2, and 1.6 per 100 patients per month in the current smokers, ex-smokers, and non-smokers, respectively. After applying a PS, patients with a history of current smoking and ex-smoking developed the onset of recurrent MACEs significantly sooner than non-smokers, with a median time of 4.4 vs. 4.9 vs. 13.5 months (p < 0.001), respectively.
UNASSIGNED: \"Smoker\'s paradox\" was not observed in our patient population. Current smokers and ex-smokers were prone to develop an earlier onset of a post-PCI MACEs than nonsmokers and need a smoke cessation program for further prevention.

BACKGROUND: The effect of smoking on short-term outcomes among patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) is controversial. However, little is known about the impact of smoking on long-term outcomes in patients with stable coronary artery disease (CAD) who receive PCI.
METHODS: A total of 2,044 patients with stable CAD undergoing PCI were evaluated. They were divided into two groups according to smoking status (current smokers vs. non-smokers). Baseline characteristics, exposed risk factors, angiographic findings, and interventional strategies were assessed to compare the long-term clinical outcomes between groups. Predictors for myocardial infarction (MI), all-cause death, cardiovascular (CV) death, and repeated PCI procedures were also analyzed.
RESULTS: Compared with non-smokers, current smokers were younger and mostly male (both P < 0.01). They also had a lower prevalence of chronic kidney disease (CKD) and diabetes (both P < 0.01). Drugs including a P2Y12 receptor inhibitor of platelets (P2Y12 inhibitor), beta-blockers (BB), and statins were used more frequently in current smokers (P < 0.01, P < 0.01, P = 0.04, respectively). Freedom from all-cause death and CV death was lower in the non-smoker group (P < 0.001, P = 0.003, respectively). After adjustment, logistic regression revealed smoking was a major predictor for all-cause death and repeated PCI procedure [hazard ratio(HR): 1.71 and 1.46, respectively].
CONCLUSIONS: Smoker\'s paradox extends to long-term outcome in patients with stable CAD undergoing PCI, which is partially explained by differences in baseline characteristics. However, smoking strongly predicted all-cause mortality and repeated PCI procedures in patients with stable CAD undergoing PCI.

BACKGROUND: The \'smoker\'s paradox\' refers to the observation of favorable prognosis in current smokers following an acute ST elevation myocardial infarction (STEMI) in the era of fibrinolysis, however, several STEMI studies have demonstrated conflicting results in patients undergoing primary percutaneous coronary intervention (p-PCI).
OBJECTIVE: Aim of the current study was to evaluate the impact of cigarette smoking on left ventricular function in STEMI patients undergoing p-PCI.
METHODS: Our population is represented by 74 first-time anterior STEMI patients undergoing p-PCI, 37 of whom were smokers. We assessed left ventricular function by left ventricular ejection fraction (LVEF) on the second day after admission and at 3-month follow-up. Early predictors of adverse left ventricular remodelling after STEMI treated by p-PCI were examined.
RESULTS: Basal demographics and comorbidities were similar between groups. Although the LVEF during the early phase was higher in smokers compared to non-smokers (44.95±7.93% vs. 40.32±7.28%; p=0.011); it worsened in smokers at follow-up (mean decrease in LVEF: -2.70±5.95%), whereas it improved in non-smokers (mean recovery of LVEF: +2.97±8.45%). In univariate analysis, diabetes mellitus, peak troponin I, current smoking, and lower TIMI flow grade after p-PCI, pain-to-door time and door-to-balloon times were predictors of adverse left ventricular remodelling. After multivariate logistic regression analysis, smoking at admission, lower TIMI flow grade after p-PCI, the pain-to-door time and door-to-balloon times remained independent predictors of deterioration in LVEF.
CONCLUSIONS: True or persistent \'smoker\'s paradox\' does not appear to be relevant among STEMI patients undergoing p-PCI. The \'smoker\'s paradox\' is in fact a pseudo-paradox. Further studies with larger numbers may be warranted.

BACKGROUND: Several studies in patients with acute myocardial infarction (AMI) without cardiogenic shock (CS) indicate a better survival in smokers, the so called \"smoker\'s paradox\". For CS, this relationship has not been investigated so far in the primary percutaneous coronary intervention (PCI) era.
METHODS: In a predefined substudy of the Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial and its accompanying registry including patients with CS complicating AMI we investigated differences in outcome of smokers compared to non-smokers. All-cause-mortality at 1year was used as primary endpoint.
RESULTS: Of 772 patients with available smoking status 263 patients were smokers (34%). Smokers were more often male (79% vs. 65%; p<0.001), of younger age (61 [interquartile range IQR 52-70] vs. 73 [IQR 64-79] years; p<0.001), had less comorbidity including arterial hypertension (62% vs. 71%; p=0.007) and diabetes mellitus (26% vs. 38%; p<0.001) and had lower levels of serum creatinine (13% vs. 25%; p<0.001). There was no significant difference between the 2 groups regarding left ventricular ejection fraction, initial revascularization strategy or use of IABP. Smokers had lower rates of mortality at 12months in univariable analysis (43% vs. 59%; p<0.001) but not after adjustment for important confounders using Cox-regression analysis (hazard ratio 0.77, 95% confidence interval 0.59-1.03; p=0.08).
CONCLUSIONS: Smoking is not predictive of outcome in patients with CS complicating AMI. The observed survival benefit in univariable analysis seems to be explained by the younger age and lower risk profile of smokers.

Prior studies have found that smokers undergoing thrombolytic therapy for ST-segment elevation myocardial infarction have lower in-hospital mortality than nonsmokers, a phenomenon called the \"smoker\'s paradox.\" Evidence, however, has been conflicting regarding whether this paradoxical association persists in the era of primary percutaneous coronary intervention.
We used the 2003-2012 National Inpatient Sample databases to identify all patients aged ≥18 years who underwent primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Multivariable logistic regression was used to compare in-hospital mortality between smokers (current and former) and nonsmokers. Of the 985 174 patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention, 438 954 (44.6%) were smokers. Smokers were younger, were more often men, and were less likely to have traditional vascular risk factors than nonsmokers. Smokers had lower observed in-hospital mortality compared with nonsmokers (2.0% versus 5.9%; unadjusted odds ratio 0.32, 95% CI 0.31-0.33, P<0.001). Although the association between smoking and lower in-hospital mortality was partly attenuated after baseline risk adjustment, a significant residual association remained (adjusted odds ratio 0.60, 95% CI 0.58-0.62, P<0.001). This association largely persisted in age-stratified analyses. Smoking status was also associated with shorter average length of stay (3.5 versus 4.5 days, P<0.001) and lower incidence of postprocedure hemorrhage (4.2% versus 6.1%; adjusted odds ratio 0.81, 95% CI 0.80-0.83, P<0.001) and in-hospital cardiac arrest (1.3% versus 2.1%; adjusted OR 0.78, 95% CI 0.76-0.81, P<0.001).
In this nationwide cohort of patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction, we observed significantly lower risk-adjusted in-hospital mortality in smokers, suggesting that the smoker\'s paradox also applies to ST-segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention.

To investigate the influence of cardiovascular risk factors (CV-RFs) on infarct severity and post-infarction left ventricular (LV) remodelling in acutely reperfused ST-segment elevation myocardial infarction (STEMI) patients studied with cardiovascular magnetic resonance (CMR).
Four-hundred seventy-one patients were included in the study. Baseline CMR was performed at 4 ± 1 days after STEMI to assess area-at-risk, infarct size (IS), myocardial salvage index (MSI), microvascular obstruction (MVO), intramyocardial haemorrhage (IMH), LV volumes, and function. Cardiovascular magnetic resonance was repeated 4 months after STEMI (n = 383) to assess adverse LV remodelling (increase of LV end-diastolic volume >20% between baseline and follow-up). Smoking was associated with IMH at baseline even after correction for other factors associated with ischaemia-reperfusion injury including MVO, IS, and MSI (OR: 2.17, 95% CI: 1.17-4.00, P = 0.01). Unexpectedly, smoking was an independent protective predictor against adverse LV remodelling (OR: 0.43, 95% CI: 0.24-0.77, P = 0.005), consistent with the \'smoker\'s paradox\'. However, the presence of IMH at baseline abolished the paradoxical, beneficial effects of smoking with respect to IS, baseline LV function, and post-infarction LV remodelling. No association between other CV-RFs, infarct severity, or post-infarction LV remodelling was observed.
In patients with reperfused STEMI, smoking is strongly and independently associated with IMH at baseline. Nonetheless, consistent with the \'smoker\'s paradox\', smoking was an independent predictor of more favourable post-infarction LV remodelling. However, the paradoxical beneficial effects of smoking were lost in patients with IMH.