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The differentiation of left ventricular (LV) hypertrophic phenotypes is challenging in patients with normal ejection fraction (EF). The myocardial contraction fraction (MCF) is a simple dimensionless index useful for specifically identifying cardiac amyloidosis (CA) and hypertrophic cardiomyopathy (HCM) when calculated by cardiac magnetic resonance. The purpose of this study was to evaluate the value of MCF measured by three-dimensional automated, machine-learning-based LV chamber metrics (dynamic heart model [DHM]) for the discrimination of different forms of hypertrophic phenotypes. We analyzed the DHM LV metrics of patients with CA ( = 10), hypertrophic cardiomyopathy (HCM, = 36), isolated hypertension (IH, = 87), and 54 healthy controls. MCF was calculated by dividing LV stroke volume by LV myocardial volume. Compared with controls (median 61.95%, interquartile range 55.43-67.79%), mean values for MCF were significantly reduced in HCM-48.55% (43.46-54.86% < 0.001)-and CA-40.92% (36.68-46.84% < 0.002)-but not in IH-59.35% (53.22-64.93% < 0.7). MCF showed a weak correlation with EF in the overall cohort (R = 0.136) and the four study subgroups (healthy adults, R = 0.039 IH, R = 0.089; HCM, R = 0.225; CA, R = 0.102). ROC analyses showed that MCF could differentiate between healthy adults and HCM (sensitivity 75.9%, specificity 77.8%, AUC 0.814) and between healthy adults and CA (sensitivity 87.0%, specificity 100%, AUC 0.959). The best cut-off values were 55.3% and 52.8%. The easily derived quantification of MCF by DHM can refine our echocardiographic discrimination capacity in patients with hypertrophic phenotype and normal EF. It should be added to the diagnostic workup of these patients.
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http://dx.doi.org/10.3390/jcm12175525 | DOI Listing |
JCI Insight
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Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
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Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh Swanson School of Engineering, Pittsburgh, PA, USA; Orland Bethel Family Musculoskeletal Research Center, University of Pittsburgh School of Med
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Department of Engineering Mechanics, School of Ocean and Civil Engineering, Shanghai Jiao Tong University, Shanghai, 200240, China.
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