Differences in the extent of fibrosis in obstructive and nonobstructive hypertrophic cardiomyopathy

医学 心脏病学 内科学 肥厚性心肌病 射血分数 心肌纤维化 优势比 舒张期 纤维化 多普勒超声心动图 梗阻性心肌病 心室流出道 心肌病 心力衰竭 血压
作者
Gustavo Avegliano,Maria Politi,Juan Pablo Costabel,Paola Kuschnir,Marcelo Trivi,Ricardo Ronderos
出处
期刊:Journal of Cardiovascular Medicine [Lippincott Williams & Wilkins]
卷期号:20 (6): 389-396 被引量:7
标识
DOI:10.2459/jcm.0000000000000800
摘要

Left ventricular outflow tract (LVOT) obstruction is a key feature of hypertrophic cardiomyopathy (HCM) that identifies patients at increased risk of adverse outcomes. Previous studies have hypothesized that LVOT obstruction enhances myocardial fibrosis and increases left ventricular (LV) filling pressures, producing greater clinical deterioration. However, this hypothesis has not been demonstrated in a clinical cohort comparing obstructive and nonobstructive patients.Patients with HCM in whom Doppler echocardiography was performed within 30 days of cardiac MRI were enrolled, using the E/e' ratio to assess LV diastolic function and late gadolinium enhancement to evaluate the extent of fibrosis. Data were assorted according to LVOT obstruction status at rest.The current study enrolled 67 patients who were mostly middle-aged (56.8 ± 13.2 years old) men (75%) with preserved ejection fraction. Obstructive HCM presented a significant association with a high fibrosis extent [odds ratio (OR) 3.33; P = 0.034] which was maintained after adjusting for sex and age (OR 4.37; P = 0.016) but not for maximum LV wall thickness (OR 2.13; P = 0.225). Obstructive HCM was also associated with a clinically significant E/e' ratio more than 14 (OR 7.8; P = 0.001) which decreased slightly after adjusting for age, sex and maximum LV thickness (OR 6.54; P = 0.014). There was a significant association between an E/e' ratio more than 14 and the extent of fibrosis (OR 1.29; P < 0.001) which was maintained after adjusting for age, sex and maximum LV wall thickness (OR 1.36; P = 0.001).LVOT obstruction may play a role in the extent of fibrosis in HCM, possibly conditioning greater diastolic dysfunction.

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