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This report describes a series of symptomatic patients with obstructive hypertrophic cardiomyopathy with significant postprandial hemodynamic changes. This finding was identified by history, clinical examination, and echocardiography in 6 consecutive symptomatic patients referred for the evaluation of ventricular septal reduction therapy. Counseling these patients with dietary changes to include small frequent meals and to increase noncaffeinated fluid intake resulted in reductions in symptoms. In conclusion, severe symptoms in obstructive hypertrophic cardiomyopathy unresponsive to pharmacologic treatment frequently result in referral for definitive septal reduction therapy through surgery or, less frequently, alcohol septal ablation therapy. However, recognition of postprandial exacerbation in symptomatic patients may allow for nonpharmacologic dietary interventions that may obviate the need for more invasive therapies and their associated complications. [ABSTRACT FROM AUTHOR]

Distinguishing the pathologic hypertrophy of hypertrophic cardiomyopathy (HC) from the physiologic hypertrophy of professional football players (PFP) can be challenging when septal wall thickness falls within a "gray zone" between 12 and 16 mm. It was hypothesized that 2-dimensional and speckle-tracking strain (ε) echocardiography could differentiate the hearts of PFPs from those of patients with HC with similar wall thicknesses. Sixty-six subjects, including 28 professional American football players and 21 patients with HC, with septal wall thicknesses of 12 to 16 mm, along with 17 normal controls, were studied using 2-dimensional echocardiography. Echocardiographic parameters, including modified relative wall thickness (RWT; septal wall thickness + posterior wall thickness/left ventricular end-diastolic diameter) and early diastolic annular tissue velocity (e'), were measured. Two-dimensional ε was analyzed by speckle tracking to measure endocardial and epicardial longitudinal ε and circumferential ε and radial cardiac ε. Septal wall thickness was higher in patients with HC than in PFPs (14.7 ± 1.1 vs 12.9 ± 0.9 mm, respectively, p <0.001), while posterior wall thickness showed no difference. RWT was larger in patients with HC than in PFPs (0.68 ± 0.10 vs 0.48 ± 0.06, p <0.001). Longitudinal endocardial ε and radial cardiac ε were significantly higher in PFPs than in patients with HC, while circumferential endocardial ε was no different. RWT was the parameter that most accurately differentiated PFPs from patients with HC. An RWT cut point of 0.6 differentiated PFPs from patients with HC, with an area under the curve of 0.97. In conclusion, a 2-dimensional echocardiographic measure of RWT (septal wall + posterior wall thickness/left ventricular end-diastolic dimension) accurately differentiated PFPs' hearts from those of patients with HC when septal wall thickness was in the gray zone of 12 to 16 mm. Two-dimensional strain analysis identifies variations in myocardial deformation between PFPs and patients with HC with gray-zone hypertrophy. [ABSTRACT FROM AUTHOR]