Impact of active smoking on myocardial infarction severity in reperfused ST-segment elevation myocardial infarction patients: the smoker's paradox revisited. (24th January 2016)

• Record Type: Journal Article
• Authors: Symons, Rolf; Masci, Pier Giorgio; Francone, Marco; Claus, Piet; Barison, Andrea; Carbone, Iacopo; Agati, Luciano; Galea, Nicola; Janssens, Stefan; Bogaert, Jan
• Is Part Of: European heart journal. Volume 37:Number 36(2016:Sep.)
• Page Start: 2756
• Page End: 2764
• Publication Date: 2016-01-24
• Subjects: Myocardial infarction -- Left ventricular remodelling -- Cardiovascular risk factors -- Smoker's paradox; Cardiology -- Periodicals; Heart -- Diseases -- Periodicals; 616.12005
• DOI: 10.1093/eurheartj/ehv738
• Languages: English
• ISSNs: 0195-668X

Abstract

Abstract: Aims: 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). Methods and results: 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. Conclusion: 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.