Artículo

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

Avegliano, Gustavo ; Politi, Teresa Icon; Costabel, Juan P. ; Kuschnir, Paola ; Trivi, Marcelo Ricardo ; Ronderos, Ricardo

Otros responsables

Fecha

06/2019

Editorial

Lippincott Williams

Revista

Journal Of Cardiovascular Medicine

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Institución organizadora

ISSN

1558-2027

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Inglés

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Resumen

Aims 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. Methods 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. Results 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). Conclusion LVOT obstruction may play a role in the extent of fibrosis in HCM, possibly conditioning greater diastolic dysfunction.

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