[show abstract][hide abstract] ABSTRACT: Information is limited regarding the functional correlates of intramural scar burden in myopathic hearts. We aimed to explore the use of speckle tracking echocardiography selectively at three intramural locations, to investigate the variance in cardiac strains and their relationship to contrast-enhanced magnetic resonance imaging-derived scar distribution and global left ventricular systolic function.
Fifty-nine patients with evidence of myocardial fibrosis on contrast-enhanced magnetic resonance imaging and 18 healthy subjects underwent speckle tracking echocardiography for measuring subendocardial, midmyocardial, and subepicardial strains in longitudinal, circumferential, and radial directions. Patients were divided into three categories of scar distribution: Group A, endocardial and midmyocardial; Group B, midmyocardial and epicardial; and Group C, transmural. When these patients were compared with 18 healthy control subjects, longitudinal left ventricular deformation was attenuated equally for all three groups, whereas circumferential strain was relatively well preserved. On multivariate analysis, circumferential strain and scar burden were independent determinants of left ventricular ejection fraction (R(2) = 0.57; P = 0.003 for strain burden and P = 0.01 for scar burden).
Longitudinal strains are attenuated independent of myocardial scar location. This alteration in left ventricular deformation is associated with circumferential mechanics becoming a key determinant of global left ventricular pump function in myopathic hearts.
European heart journal cardiovascular Imaging. 10/2011; 13(2):152-8.
[show abstract][hide abstract] ABSTRACT: 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.
The American journal of cardiology 08/2011; 108(9):1322-6. · 3.58 Impact Factor
[show abstract][hide abstract] ABSTRACT: In patients with hypertrophic obstructive cardiomyopathy and dynamic left ventricular outflow tract obstructions, an additional fixed obstruction may uncommonly coexist. In these situations, flow through the aortic valve is usually delayed but typically still throughout the entire ejection period. We describe a case of marked reduction in aortic flow during mid and late systole, diagnosed by Doppler echocardiography, caused by combined hypertrophic obstructive cardiomyopathy and severe calcific bicuspid aortic stenosis.
Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 04/2011; 24(4):471.e1-4. · 2.98 Impact Factor
[show abstract][hide abstract] ABSTRACT: 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.
The American journal of cardiology 11/2010; 106(9):1313-6. · 3.58 Impact Factor
[show abstract][hide abstract] ABSTRACT: We present a case of wide-complex tachycardia occurring during coronary angiography in a patient with a dual chamber pacemaker. This rhythm recurred only during coronary injection of contrast and appeared to be ventricular tachycardia. However, subsequent examination revealed the development of fusion beats followed by fully paced ventricular beats during coronary injection, which only mimicked a potentially dangerous arrhythmia.
Cardiovascular revascularization medicine: including molecular interventions 01/2009; 10(1):60-1.