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Relationship between microcirculatory dysfunction, myocardial fibrosis and arrhythmias in hypertrophic cardiomyopathy
Session:
Sessão de Comunicações Orais - Doenças do Miocárdio
Speaker:
Silvia Aguiar
Congress:
CPC 2020
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
17. Myocardial Disease
Subtheme:
17.3 Myocardial Disease – Diagnostic Methods
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Sílvia Aguiar Rosa; Luís Lopes; António Fiarresga; Boban Thomas; Gonçalo Branco; Ricardo Pereira; Catarina Barão; Luís Baquero; Rui Cruz Ferreira; Miguel Mota Carmo
Abstract
<p><strong>Background: </strong>Microcirculatory dysfunction constitutes one of the most important pathophysiological features in hypertrophic cardiomyopathy (HCM). Chronic and recurrent myocardial ischemia may lead to fibrosis, which constitutes an arrhythmic subtract.</p> <p> </p> <p><strong>Objective</strong>: To analyze the relationship between coronary microcirculatory dysfunction and: a) myocardial fibrosis assessed by cardiovascular magnetic resonance (CMR); b) supraventricular and ventricular arrhythmias.</p> <p> </p> <p><strong>Methods: </strong>The present study prospectively included HCM adult patients (P) who underwent CMR, including parametric mapping, perfusion imaging during regadenoson-induced hyperemia and late gadolinium enhancement (LGE) assessment. Supraventricular and ventricular arrhythmias were documented by 12 lead electrocardiogram and 24hours Holter monitoring. Epicardial coronary artery disease was excluded by computed tomography or invasive coronary angiography. For perfusion assessment, the myocardium was divided into 32 subsegments (16 AHA segments subdivided into an endocardial and epicardial layer, excluding segment 17). Ischemic burden was calculated as the number of involved subsegments, assigning 3% of myocardium to each subsegment.</p> <p> </p> <p><strong>Results: </strong>38 P were enrolled (55% male, mean age 56.9±14.2 years). Asymmetric septal hypertrophy was seen in 20P (53%), apical in 14P (37%), concentric in 4P (10%), with maximal wall thickness (MWT) of 20.5±4.9mm; 26% with evidence of LVOT obstruction.</p> <p>Ischemic burden was greater in concentric hypertrophy comparing with the remaining patterns, and correlated with the severity of left ventricular hypertrophy (LVH), by MWT and LV mass (table1). Higher ischemic burden was correlated with higher values of native T1 mapping (Spearman correlation factor 0.540; p<0.001)(table1). A correlation between ischemic burden and amount of fibrosis quantified by LGE was also noted (Spearman correlation factor 0.414; p<0.011)(table1).</p> <p>Regarding arrhythmic events, P with documented atrial fibrillation presented more severe ischemia compared with P in sinus rhythm. Despite no difference in perfusion was noted between P with and without non-sustained ventricular tachycardia (NSVT) (table1), P with significant hypoperfusion and LGE trend to have more NSVT(figure1).</p> <p> </p> <p><strong>Conclusion: </strong>In HCM patients, the severity of microcirculatory dysfunction was associated with more extensive myocardial fibrosis and atrial fibrillation. The combination of significant ischemia and fibrosis trend to increase the occurrence of NSVT.</p>
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