Smoking, CMR, and Prognosis After STEMI

Study Questions:

To what extent do infarct size, microvascular dysfunction, edema, myocardial hemorrhage, and prognosis differ by smoking status after acute ST-segment elevation myocardial infarction (STEMI)?

Methods:

The authors conducted a prospective, single-center, observational cohort study at a regional cardiac center. Subjects underwent invasive measurement of microvascular function using a pressure and temperature sensing intracoronary wire after percutaneous coronary intervention for acute STEMI to measure the index of microcirculatory resistance (IMR). Angiograms were analyzed to determine TIMI (Thrombolysis In Myocardial Infarction) flow grade, blush grade, and frame count. Blood was analyzed for troponin T, C-reactive protein, and N-terminal pro–B-type natriuretic peptide (NT-proBNP). A comprehensive cardiac magnetic resonance imaging (MRI) was performed to quantify left ventricular ejection fraction (LVEF), mass, infarct size, microvascular obstruction, myocardial hemorrhage, and edema. Follow-up cardiac MRI was performed to assess for adverse remodeling. Patients were also followed for a primary composite outcome of death from any cause or heart failure (HF) after index hospitalization.

Results:

Enrollment included 324 out of 372 consecutive acute STEMI patients. On average, smokers were younger (55 vs. 65 years old, p < 0.001) and less likely to be hypertensive (27% vs. 41%, p = 0.007). Smokers generally had lower creatinine (p < 0.001), C-reactive protein (p = 0.04), neutrophil and monocyte counts (p < 0.001), and NT-proBNP (p = 0.02). TIMI flow grade was higher in smokers than nonsmokers (p = 0.024), although no differences were seen in blush grade or frame count. ST-segment resolution was also more common at 60 minutes in smokers than nonsmokers. Although nonsignificant, IMR was lower in smokers (22 vs. 27, p = 0.06). On cardiac MRI, infarct size, microvascular obstruction, and LV function were comparable between smokers and nonsmokers prior to adjustment. Hemorrhage was nonsignificantly more frequent in smokers (46% vs. 34%, p = 0.08). After adjustment, smoking was associated with microvascular obstruction (odds ratio [OR], 1.72; p = 0.04), myocardial hemorrhage (OR, 2.55; p = 0.003), and death/HF (OR, 2.2; p = 0.03).

Conclusions:

After adjustment, smoking was associated with more microvascular obstruction, myocardial hemorrhage, and adverse outcomes after STEMI.

Perspective:

This observational, mechanistic study suggests that the smoking paradox wherein smokers have better outcomes after MI than nonsmokers is largely driven by younger age and lower comorbid disease burden among smokers. Indeed, cardiac MRI findings suggest that smokers have worse infarcts with greater burden of adverse prognostic markers (hemorrhage and microvascular obstruction), after accounting for confounders. That many of these observations only became significant after multivariable adjustment warrants some caution in interpretation until results are replicated in other cohorts.

Clinical Topics: Acute Coronary Syndromes, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, ACS and Cardiac Biomarkers, Acute Heart Failure, Chronic Heart Failure, Heart Failure and Cardiac Biomarkers, Interventions and ACS, Interventions and Imaging, Angiography, Magnetic Resonance Imaging, Nuclear Imaging, Hypertension, Smoking

Keywords: Acute Coronary Syndrome, Angiography, C-Reactive Protein, Creatinine, Diagnostic Imaging, Edema, Cardiac, Heart Failure, Hemorrhage, Hypertension, Magnetic Resonance Imaging, Microcirculation, Monocytes, Myocardial Infarction, Natriuretic Peptide, Brain, Percutaneous Coronary Intervention, Primary Prevention, Smoking, Stroke Volume, Troponin T


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