PracticeUpdate: Cardiology - Winter 2018

EDITOR’S PICKS 12

Current Smoking Impacts Prognosis After Acute ST-Segment Elevation Myocardial

Infarction JACC: Cardiovascular Imaging

Take-home message • Patients who underwent emergency PCI following acute STEMI were followed to evaluate the pathophysiology and outcomes among current smokers. Smokers had higher levels of C-reactive protein and neutrophils than nonsmokers on day 1. At 2 days post MI, smoking was a significant independent predictor of infarct zone hemorrhage on imaging. Over a median follow-up of 4 years, smoking was a significant independent predictor of all-cause death, heart failure events, and major adverse cardiovascular events. • Continued smoking following STEMI is associated with increased inflammation and an increased infarct-zone hemorrhage, which results in adverse long-term outcomes.

Abstract OBJECTIVES The aimof this study was tomechanis- tically 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 myocar- dial reperfusion injury and prognosis in smokers with acute ST-segment elevation MI is incom- pletely understood. METHODS Patients were prospectively enrolled during emergency percutaneous coronary inter- vention. Microvascular function in the culprit artery was measured invasively. Contrast-en- hanced 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-seg- ment elevation MI were enrolled (mean age 59 years, 73% men, 60% current smokers). Cur- rent smokers were younger (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-percutane- ous coronary intervention. On day 1, smokers had higher circulating C-reactive protein, neu- trophil, 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 cardio- vascular 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 rep- resent mechanistic drivers for adverse long-term prognosis in smokers. Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction: New Pathophysiological Insights. JACC Cardi- ovasc Imaging 2018 Jul 13;[EPub Ahead of Print], C Haig, D Carrick, J Carberry, et al. www.practiceupdate.com/c/71165

COMMENT By James E. Udelson MD A s far back as 1985, many groups have reported on the “smoker’s paradox” following acute cor- onary syndromes. Patients with ACS who are current smokers in clinical trials and observational databases are often reported to have slightly better outcomes (usually out to 1 year) after ACS, in con- trast to what one might expect. In virtually all of these reports, smokers are much younger than nonsmokers, have less hypertension and diabetes, and have less underlying multivessel CAD. In some of the reports, the apparently better out- come disappears after adjustment for baseline differences, suggesting that a better anatomic and comorbidity profile in smokers may offset the unfavorable effects of smoking per se. Few studies have explored the likely complex mechanisms underlying these observations in depth. Haig and col- leagues, in the current paper, perform highly comprehensive biomarker and cardiac MRI studies (in a highly experi- enced imaging center) in a large group of patients with ST-elevation MI (STEMI) undergoing primary PCI. They followed the patients for outcomes over a median of 4 years, much longer than prior studies. The smoker vs non-smoker demograph- ics were similar to those in other trials. They found slightly better post-PCI TIMI flow status (consistent with prior reports), lower microvascular resistance (of bor- derline significance), better early

" …the much longer follow-up in this study compared with prior studies allowed a clearer picture of how the balance of these

observations associated with true outcomes, and very clearly, the bad outweighs the good.

"

ST-segment resolution, and lower levels of NT-proBNP in smokers, all of which would seem favorable. However, smok- ers had a more unfavorable inflammatory biomarker profile early post-MI, and the early (day 2) cardiac MRI findings showed that smoking status was associated with a higher likelihood of myocardial hemor- rhage, whereas infarct size was similar. Over the long-term follow-up, smoking at the time of the STEMI was associated with death or heart failure events as well as with major adverse cardiac events. This highly comprehensive study goes a long way in advancing our understand- ing of the mechanisms involved in the many observations over the years about post-ACS outcomes in smokers versus nonsmokers. Although very early signals were mixed, the much longer follow-up in this study compared with prior studies allowed a clearer picture of how the bal- ance of these observations associated with true outcomes, and very clearly, the bad outweighs the good.

PRACTICEUPDATE CARDIOLOGY