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Coronary microvascular dysfunction is associated with tissue changes and myocardial deformation impairment in hypertrophic cardiomyopathy – a magnetic resonance imaging study
Session:
CO 21 - Miocardiopatias
Speaker:
Silvia Aguiar
Congress:
CPC 2021
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; Boban Thomas; António Fiarresga; Ana Luísa Papoila; Marta Alves; Inês Cruz; Ricardo Pereira; Gonçalo Branco; Luis Baquero; Rui Cruz Ferreira; Miguel Mota Carmo; Luís Rocha Lopes
Abstract
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Background: Fibrosis and impairment of left ventricular (LV) performance are associated with worse prognosis in hypertrophic cardiomyopathy (HCM).</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Objectives: a) to assess the role of coronary microvascular dysfunction (CMD) in promoting edema and fibrosis in HCM; b) to evaluate the impact of CMD on LV myocardial deformation in HCM.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Methods: This prospective study enrolled patients (P) with HCM without obstructive epicardial coronary artery disease. Each patient underwent cardiovascular magnetic resonance (CMR), including parametric mapping, perfusion imaging during regadenoson-induced hyperemia, late gadolinium enhancement (LGE) and <span style="color:black">three-dimensional </span><span style="color:black">longitudinal, circumferential and radial strains analysis. </span>CMD was assessed by <span style="background-color:white">perfusion imaging. The myocardium was divided into 32 subsegments (16 AHA segments subdivided into an endocardial and epicardial layer, excluding segment 17) and the ischemic burden was calculated as the number of involved subsegments, assigning 3% of myocardium to each subsegment. </span>Myocardial fibrosis was assessed by native T1, extracellular volume (ECV) and LGE. T2 was used to evaluate edema<span style="background-color:white">. </span>Linear regression models were used. A level of significance α=0.05 was used, although p-values <0.100 were still considered in the multivariable analyses.</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Results: 75P, 47 (62.7%) males, mean age 54.6(14.8)years. 24 P (32.0%) had obstructive HCM, mean maximal wall thickness (MWT) was 20.1(4.6)mm, LV mass 97.2(30.5)g/m<sup>2</sup>, LV ejection fraction 71.6(8.3)%, ischemic burden <span style="color:#010205">22.5(16.0)% of LV</span>. Greater MWT was associated with more severe ischemia (β-estimate:1.81, 95%CI:<span style="color:#010205">1.07;2.55, p<0.001).</span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#010205">In the multivariable analysis, ischemia was related with native T1 and LGE (table 1). </span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#010205">Increased ischemic burden was associated with impaired longitudinal strain </span>(β-estimate:0.08, 95%CI:0.<span style="color:#010205">01;0.14, p=0.017). No relationship was found between ischemia and radial and circumferential strain.</span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#010205">Conclusion: CMD is associated with myocardial fibrosis and impaired myocardial deformation in HCM.</span></span></span></p> <p> </p> <p><strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#010205">Table 1. Multivariable linear regression for factors related with tissue characteristics.</span></span></span></strong></p> <p> <strong> <span style="font-size:11.0pt"><span style="font-family:"Calibri","sans-serif"">Β-estimate 95% confidence interval p-value</span></span></strong></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Native T1 (ms)</strong></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><u>Ischemia (% of LV)</u> 1.227 0.833 to 1.622 <0.001</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Non obstructive HCM -12.198 -26.430 to 2.034 0.092</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>ECV (%)</strong></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><u>Ischemia (% of LV)</u> 0.001 0.000 to 0.001 0.054</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Diabetes 0.026 -0.001 to 0.053 0.055</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>LGE (%of LV)</strong></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><u>Ischemia (% of LV)</u> 0.002 0.094 to 0.309 <0.001</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Dyslipidemia -3.215 -6.936 to 0.507 0.089</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>T2 (ms)</strong></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><u>Ischemia (% of LV)</u> 0.028 -0.001 to 0.058 0.061</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Non obstructive HCM -1.294 -2.389 to -0.199 0.021</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Dyslipidemia 1.521 0.484 to 2.558 0.005</span></span></p> <p> </p>
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