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 - http://www.scopus.com/inward/record.url?scp=85066100594&partnerID=8YFLogxK
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 -