Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction: New Pathophysiological Insights

TY - JOUR

T1 - Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction

T2 - New Pathophysiological Insights

AU - Haig, Caroline

AU - Carrick, David

AU - Carberry, Jaclyn

AU - Mangion, Kenneth

AU - Maznyczka, Annette

AU - Wetherall, Kirsty

AU - McEntegart, Margaret

AU - Petrie, Mark C.

AU - Eteiba, Hany

AU - Lindsay, Mitchell

AU - Hood, Stuart

AU - Watkins, Stuart

AU - Davie, Andrew

AU - Mahrous, Ahmed

AU - Mordi, Ify

AU - Ahmed, Nadeem

AU - Teng Yue May, Vannesa

AU - Ford, Ian

AU - Radjenovic, Aleksandra

AU - Welsh, Paul

AU - Sattar, Naveed

AU - Oldroyd, Keith G.

AU - Berry, Colin

PY - 2019/6

Y1 - 2019/6

N2 - 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)

AB - 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)

KW - cigarette smoking

KW - magnetic resonance imaging

KW - microcirculation

KW - myocardial hemorrhage

KW - myocardial infarction

KW - prognosis

UR - https://www.scopus.com/pages/publications/85066100594

U2 - 10.1016/j.jcmg.2018.05.022

DO - 10.1016/j.jcmg.2018.05.022

M3 - Article

C2 - 30031700

AN - SCOPUS:85066100594

SN - 1936-878X

VL - 12

SP - 993

EP - 1003

JO - JACC: Cardiovascular Imaging

JF - JACC: Cardiovascular Imaging

IS - 6

ER -