Plaque disruption was observed in 38% of women with myocardial infarction but no obstructive coronary artery disease, indicating alternate mechanisms of injury.
Women ≥18 years of age presenting with acute myocardial infarction without angiographically obstructive coronary artery disease (no lesion with ≥50% diameter stenosis)
Intravascular ultrasound (IVUS) and cardiac magnetic resonance imaging (CMR)
Mechanisms of myocardial infarction (plaque disruption on IVUS, late gadolinium enhancement or T2 signal hyperintensity on CMR)surrogate
In women with myocardial infarction and no obstructive coronary artery disease, plaque disruption and ischemic myocardial injury are common mechanisms identified by IVUS and CMR.
Absolute Event Rate: 0% vs 0%
Background— There is no angiographically demonstrable obstructive coronary artery disease (CAD) in a significant minority of patients with myocardial infarction, particularly women. We sought to determine the mechanism(s) of myocardial infarction in this setting using multiple imaging techniques. Methods and Results— Women with myocardial infarction were enrolled prospectively, before angiography, if possible. Women with ≥50% angiographic stenosis or use of vasospastic agents were excluded. Intravascular ultrasound was performed during angiography; cardiac magnetic resonance imaging was performed within 1 week. Fifty women (age, 57±13 years) had median peak troponin of 1.60 ng/mL; 11 had ST-segment elevation. Median diameter stenosis of the worst lesion was 20% by angiography; 15 patients (30%) had normal angiograms. Plaque disruption was observed in 16 of 42 patients (38%) undergoing intravascular ultrasound. There were abnormal myocardial cardiac magnetic resonance imaging findings in 26 of 44 patients (59%) undergoing cardiac magnetic resonance imaging, late gadolinium enhancement (LGE) in 17 patients, and T2 signal hyperintensity indicating edema in 9 additional patients. The most common LGE pattern was ischemic (transmural/subendocardial). Nonischemic LGE patterns (midmyocardial/subepicardial) were also observed. Although LGE was infrequent with plaque disruption, T2 signal hyperintensity was common with plaque disruption. Conclusions— Plaque rupture and ulceration are common in women with myocardial infarction without angiographically demonstrable obstructive coronary artery disease. In addition, LGE is common in this cohort of women, with an ischemic pattern of injury most evident. Vasospasm and embolism are possible mechanisms of ischemic LGE without plaque disruption. Intravascular ultrasound and cardiac magnetic resonance imaging provide complementary mechanistic insights into female myocardial infarction patients without obstructive coronary artery disease and may be useful in identifying potential causes and therapies. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00798122.
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Harmony R. Reynolds
General Cardiology
Monvadi B. Srichai
Cardiac Imaging
Sohah N. Iqbal
Columbia University Irving Medical Center
Circulation
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Reynolds et al. (Wed,) reported a other. Plaque disruption was observed in 38% of women with myocardial infarction but no obstructive coronary artery disease, indicating alternate mechanisms of injury.
synapsesocial.com/papers/69813047229fc2169ebc21f8 — DOI: https://doi.org/10.1161/circulationaha.111.026542