Comment on: “Quantitative Assessment of Myocardial Perfusion in Physiological and Pathological Hypertrophy Using Myocardial Contrast Echocardiography”

We read with great interest the recent article published by Chunyao et al. evaluating myocardial perfusion differences between physiological and pathological hypertrophy using myocardial contrast echocardiography (MCE) [1]. The study addresses an important clinical challenge and provides promising evidence regarding the potential role of quantitative MCE parameters, particularly the A-value, in differentiating an athlete's heart from hypertension-associated hypertrophy. However, we believe several interpretive limitations deserve further clarification. First, the study may overattribute the observed perfusion differences to the hypertrophy phenotype itself. Coronary microvascular dysfunction in hypertensive heart disease is strongly influenced by systemic hypertension, endothelial dysfunction, vascular remodeling, and altered hemodynamics rather than myocardial hypertrophy alone. Therefore, reduced A-values in the pathological group may reflect broader hypertension-associated vascular dysfunction instead of a unique signature of maladaptive hypertrophy. Camici et al. previously emphasized the multifactorial nature of coronary microvascular dysfunction in hypertrophy and heart failure [2]. Second, the discussion repeatedly links the A-value with capillary density and microvascular remodeling, although no histological validation, positron emission tomography, or cardiac magnetic resonance perfusion imaging was performed. Thus, the study demonstrates indirect perfusion differences rather than direct evidence of structural microvascular alterations [3]. Third, the diagnostic interpretation may be overstated because the ROC-derived cutoff was developed and tested within the same small single-center cohort without external validation. Consequently, the reported diagnostic performance may not be generalizable to broader populations [4]. Finally, the conclusions occasionally refer broadly to “pathological hypertrophy,” despite the study including only hypertension-associated left ventricular hypertrophy. This distinction is important because other pathological hypertrophy states, such as hypertrophic cardiomyopathy or valvular hypertrophy, possess distinct microvascular pathophysiology [5]. Despite these concerns, the study provides valuable preliminary evidence supporting the role of MCE in evaluating myocardial microcirculation. We believe a clearer acknowledgment of these interpretive boundaries would strengthen the clinical and scientific implications of the findings. The author has nothing to report. The author has nothing to report. The author has nothing to report. The author declares no conflicts of interest. The data that support the findings of this study are available in Clinical Cardiology at https://doi.org/10.1002/clc.70285. These data were derived from the following resources available in the public domain: