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Coronary Flow in Hypertrophic Obstructive Cardiomyopathy-Immediate Effects of Alcohol Septal Ablation
Vojko V Misevic1,2, Ana N Golocevac1, Kosta S Krupnikovic1
1Institute for Cardiovascular Diseases "Dedinje", Belgrade, Serbia.
Background:
Hypertrophic cardiomyopathy is associated with alterations in coronary microvascular function which have variable pathophysiologic mechanisms, and variable reversibility acutely and chronically following alcohol septal ablation (ASA).
Aims:
The aim of this study was to examine immediate changes in absolute coronary blood flow before and after ASA using continuous thermodilution.
Methods:
Consecutive eligible patients without obstructive coronary artery disease undergoing ASA in a single center were enrolled in the study. Absolute coronary blood flow (Q) was measured using continuous thermodilution technique before and immediately after ASA and was used to calculate coronary flow reserve (CFR) and resistance (R).
Results:
Twenty-three patients, aged 57.9 ± 12.6 years, 47.8% female, underwent ASA. Left ventricular outflow tract gradient decreased from a median of 101 mmHg [IQR 77-133] to a median of 19 mmHg [16-36 mmHg] (p < 0.01). Comparing the state before and after ASA, no changes were observed in average resting (0.126 ± 0.064 vs. 0.129 ± 0.081 L/min) or hyperemic (0.264 ± 0.136 vs. 0.248 ± 0.116 L/min) coronary blood flow, or between resting (868 ± 564 vs. 929 ± 618 mmHg/[L/min]) or hyperemic (351 ± 172 vs. 345 ± 126 mmHg/[L/min]) resistance (p > 0.05 for all). The majority of patients n = 16 (69.6%) had an abnormal CFR (≤ 2.5) prior to ASA. Mean CFR was 2.31 ± 1.02 before and 2.35 ± 1.04 after ASA (p = 0.808 for difference). Thirteen patients experienced CFR improvement by 10%, and they had significantly lower hyperemic Q (0.219 ± 0.087 vs. 0.336 ± 0.171 L/min, p = 0.041) and CFR (1.86 ± 0.76 vs. 2.85 ± 1.19, p = 0.041) before ASA, compared to those who didn't.
Conclusions:
Patients with obstructive hypertrophic cardiomyopathy are a heterogeneous population with variable immediate microvascular response to ASA.
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