Clin Cardiol. 2026 May;49(5):e70285. doi: 10.1002/clc.70285.
ABSTRACT
OBJECTIVE: To quantitatively evaluate myocardial perfusion levels in patients with physiological and pathological myocardial hypertrophy using myocardial contrast echocardiography (MCE), and to investigate the diagnostic value of MCE parameters for differentiating between these conditions.
METHODS: From June 2023 to December 2024, 25 hypertensive patients with myocardial hypertrophy (pathological hypertrophy group), 25 healthy athletes (physiological hypertrophy group), and 25 healthy controls were enrolled. All participants underwent two-dimensional echocardiography and MCE. Myocardial perfusion parameters-peak intensity (A-value), wash-in slope (β-value), and myocardial blood flow (MBF)-were quantified using a 17-segment model. Differences in perfusion parameters were compared, and receiver operating characteristic (ROC) curve analysis was performed to evaluate diagnostic efficacy.
RESULTS: Compared with controls, the physiological hypertrophy group showed significantly increased peak intensity (A-value) and MBF (p < 0.05), whereas the pathological hypertrophy group exhibited decreased A-value, slope rate (β-value), and MBF (p < 0.05). Intragroup segmental analysis revealed that in pathological hypertrophy, the basal segments had significantly lower A-value and MBF compared to mid and apical segments (p < 0.05). Intermural comparison demonstrated that in both control and physiological hypertrophy groups, the free wall had lower A-value and MBF than the septum (p < 0.05). In contrast, pathological hypertrophy showed reduced A-value but increased β-value in the free wall (p < 0.05). ROC curve analysis identified an optimal cutoff value of A > 8.13 dB (AUC = 0.904) for discriminating exercise-induced physiological hypertrophy from hypertension-induced pathological hypertrophy.
CONCLUSION: MCE enables quantitative assessment of myocardial perfusion in hypertrophic patients. The A value, reflecting microvascular density, serves as a reliable discriminator between physiological and pathological hypertrophy.
PMID:42060780 | DOI:10.1002/clc.70285