Why the study?
Coronary microvascular dysfunction is an important feature in HCM, but its role in tissue characteristics, LV systolic performance, and clinical manifestations required investigation.
Is coronary microvascular dysfunction associated with adverse tissue characteristics and arrhythmias in patients with hypertrophic cardiomyopathy?
Is coronary microvascular dysfunction associated with adverse tissue characteristics and arrhythmias in patients with hypertrophic cardiomyopathy?
In patients with hypertrophic cardiomyopathy, coronary microvascular dysfunction is associated with increased myocardial fibrosis and a higher risk of atrial fibrillation/flutter.
Does not support routine ischemia assessment in HCM; leaves open whether microvascular dysfunction drives fibrosis and arrhythmias.
Background Coronary microvascular dysfunction (CMD) is an important pathophysiological feature in hypertrophic cardiomyopathy (HCM). Purpose This study investigated the role of CMD in tissue characteristics, left ventricular (LV) systolic performance and clinical manifestations in HCM. Methods This prospective study enrolled patients 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 three-dimensional longitudinal, circumferential and radial strains analysis. Electrocardiogram and 24 hours Holter recording were performed to assess arrhythmias. Results 75P were enrolled, 47 (63%) males, mean age 54.6 (14.8) years; 51 patients (68%) had non obstructive HCM, mean maximum wall thickness (MWT) was 20.2 (4.6)mm, LV ejection fraction 71.6 (8.3)%, ischemic burden 22.5 (16.9)% of LV. Greater MWT was associated the severity of ischemia (β-estimate: 1.809, 95% CI: 1.073; 2.545; p<0.001). Ischemic burden was strongly associated with higher values of native T1 (β-estimate: 9.018, 95% CI: 4.721, 13.315; p<0.001). An association between ischemia and the extent of LGE was found (β-estimate: 2.02, 95% CI: 0.93, 3.10; p<0.001). Ischemia in ≥21% of LV was associated with LGE >15% (AUC 0.766, sensitivity 0.724, specificity 0.659). In multivariable analysis, in the overall population, MWT and LGE were independently associated with ischemia, however the evidence of association between ischemia and extent of LGE became weaker (β-estimate: 1.070, 95% CI: −0.106; 2.245; p=0.074). In subgroup analysis, the association between ischemia and LGE remained significant in individuals with MWT 15–20mm, non-obstructive HCM, female and age <40 years. The severity of ischemia was not associated with markers of LV systolic function, namely LVEF, longitudinal, radial and circumferential strain A strong evidence of association was found between ischemia and atrial fibrillation/flutter (AF/AFL) (OR: 1.481, 95% CI: 1.020,2.152; p=0.039), but no association was verified with non-sustained ventricular tachycardia. Conclusion In HCM, CMD is related to the severity of LV hypertrophy. Ischemia secondary to CMD promotes fibrosis and is associated with an increase in the odds of AF/ALF. Funding Acknowledgement Type of funding sources: None.
No takes yet. Share an insight, caveat, or question.
Rosa et al. (2021) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: