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Hypertrophic cardiomyopathy (HCM) is characterized by extreme clinical heterogeneity, ranging from sudden cardiac death to long-term disease progression and heart failure-related complications. Myocardial ischemia, occurring at the microvascular level, is a major determinant of clinical expression and outcome. Accordingly, the severity of this microvascular dysfunction has been shown to represent an early and powerful predictor of unfavorable outcome in HCM. The assessment of microvascular function in vivo is technically challenging, although critical to a truly comprehensive evaluation and risk stratification of HCM patients. Available technologies include positron emission tomography and cardiac magnetic resonance (CMR). Studies of regional myocardial blood flow using positron emission tomography have demonstrated that the vasodilator response to dipyridamole is impaired in most HCM patients, not only in the hypertrophied ventricular septum but also in the less hypertrophied or non-thickened left ventricu

作者:贾镭;Franco Cecchi;Iacopo Olivotto;Massimo Baldi;Martin S. Maron;Barry J. Maron

来源:中华心血管病杂志 2009 年 37卷 12期

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| 浏览:232 | 下载:60
作者:
贾镭;Franco Cecchi;Iacopo Olivotto;Massimo Baldi;Martin S. Maron;Barry J. Maron
来源:
中华心血管病杂志 2009 年 37卷 12期
Hypertrophic cardiomyopathy (HCM) is characterized by extreme clinical heterogeneity, ranging from sudden cardiac death to long-term disease progression and heart failure-related complications. Myocardial ischemia, occurring at the microvascular level, is a major determinant of clinical expression and outcome. Accordingly, the severity of this microvascular dysfunction has been shown to represent an early and powerful predictor of unfavorable outcome in HCM. The assessment of microvascular function in vivo is technically challenging, although critical to a truly comprehensive evaluation and risk stratification of HCM patients. Available technologies include positron emission tomography and cardiac magnetic resonance (CMR). Studies of regional myocardial blood flow using positron emission tomography have demonstrated that the vasodilator response to dipyridamole is impaired in most HCM patients, not only in the hypertrophied ventricular septum but also in the less hypertrophied or non-thickened left ventricu