Author + information
- Received February 12, 2018
- Revision received May 15, 2018
- Accepted May 17, 2018
- Published online June 3, 2019.
- Caroline Haig, PhDa,∗,
- David Carrick, MD, PhDb,c,∗,
- Jaclyn Carberry, BMedScib,c,
- Kenneth Mangion, MDb,c,
- Annette Maznyczka, MDb,c,
- Kirsty Wetherall, BSca,
- Margaret McEntegart, MD, PhDc,
- Mark C. Petrie, MDc,
- Hany Eteiba, MDc,
- Mitchell Lindsay, MDc,
- Stuart Hood, MDc,
- Stuart Watkins, MDc,
- Andrew Davie, MDc,
- Ahmed Mahrous, MDc,
- Ify Mordi, MDb,c,
- Nadeem Ahmed, MDb,c,
- Vannesa Teng Yue May, MDb,c,
- Ian Ford, PhDa,
- Aleksandra Radjenovic, PhDb,
- Paul Welsh, PhDb,
- Naveed Sattar, MD, PhDb,
- Keith G. Oldroyd, MD(Hons)b,c and
- Colin Berry, MD, PhDb,c,∗ (, )@UofGICAMS
- aRobertson Centre for Biostatistics, University of Glasgow, Glasgow, United Kingdom
- bBritish Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom
- cWest of Scotland Heart and Lung Centre, Golden Jubilee National Hospital, Clydebank, United Kingdom
- ↵∗Address for correspondence:
Prof. Colin Berry, British Heart Foundation, Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, 126 University Place, University of Glasgow, Glasgow G12 8TA, United Kingdom.
Objectives The aim of this study was to mechanistically investigate associations among cigarette smoking, microvascular pathology, and longer term health outcomes in patients with acute ST-segment elevation myocardial infarction (MI).
Background The pathophysiology of myocardial reperfusion injury and prognosis in smokers with acute ST-segment elevation MI is incompletely understood.
Methods Patients were prospectively enrolled during emergency percutaneous coronary intervention. Microvascular function in the culprit artery was measured invasively. Contrast-enhanced magnetic resonance imaging (1.5-T) was performed 2 days and 6 months post-MI. Infarct size and microvascular obstruction were assessed using late gadolinium enhancement imaging. Myocardial hemorrhage was assessed with T2* mapping. Pre-specified endpoints included: 1) all-cause death or first heart failure hospitalization; and 2) cardiac death, nonfatal MI, or urgent coronary revascularization (major adverse cardiovascular events). Binary logistic regression (odds ratio [OR] with 95% confidence interval [CI]) with smoking status was used.
Results In total, 324 patients with ST-segment elevation MI were enrolled (mean age 59 years, 73% men, 60% current smokers). Current smokers were younger (age 55 ± 11 years vs. 65 ± 10 years, p < 0.001), with fewer patients with hypertension (52 ± 27% vs. 53 ± 41%, p = 0.007). Smokers had better TIMI (Thrombolysis In Myocardial Infarction) flow grade (≥2 vs. ≤1, p = 0.024) and ST-segment resolution (none vs. partial vs. complete, p = 0.010) post–percutaneous coronary intervention. On day 1, smokers had higher circulating C-reactive protein, neutrophil, and monocyte levels. Two days post-MI, smoking independently predicted infarct zone hemorrhage (OR: 2.76; 95% CI: 1.42 to 5.37; p = 0.003). After a median follow-up period of 4 years, smoking independently predicted all-cause death or heart failure events (OR: 2.20; 95% CI: 1.07 to 4.54) and major adverse cardiovascular events (OR: 2.79; 95% CI: 2.30 to 5.99).
Conclusions Smoking is associated with enhanced inflammation acutely, infarct-zone hemorrhage subsequently, and longer term adverse cardiac outcomes. Inflammation and irreversible myocardial hemorrhage post-MI represent mechanistic drivers for adverse long-term prognosis in smokers. (Detection and Significance of Heart Injury in ST Elevation Myocardial Infarction. [BHF MR-MI]; NCT02072850)
- cigarette smoking
- magnetic resonance imaging
- myocardial hemorrhage
- myocardial infarction
↵∗ Drs. Haig and Carrick contributed equally to this work.
This work was supported by the British Heart Foundation (grants RE/13/5/30177 and PG/11/2/28474), the National Health Service, and the Chief Scientist Office. Prof. Berry was supported by a senior fellowship from the Scottish Funding Council. Drs. Mangion, Maznyczka, and Welsh are supported by British Heart Foundation fellowships FS/15/54/31639, FS/16/74/32573, and FS/12/62/29889, respectively. Siemens Healthcare provided work-in-progress imaging methods. On the basis of institutional agreements with the University of Glasgow, Prof. Berry has acted as a consultant to Abbott Vascular, Opsens, and Coroventis; and has received travel support from Philips. Prof. Oldroyd has acted as consultant to Abbott Vascular, Boston Scientific, and Volcano Corporation. These companies were not involved in the current research or the manuscript. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 12, 2018.
- Revision received May 15, 2018.
- Accepted May 17, 2018.
- 2019 The Authors