Left ventricular (LV) twist represents a phenomenon that links systolic contraction with diastolic relaxation and plays a major role in cardiac physiology; thus, the study of twist mechanics is of particular interest in hypertrophic cardiomyopathy (HC). Three-dimensional speckle tracking echocardiography (3D-STE) has the potential to overcome the limitations of 2-dimensional imaging and provide a greater understanding of LV twist in HC. We aimed to examine LV twist mechanics in HC using 3D-STE. Echocardiograms from subjects with a diagnosis of HC were examined for 3D-STE analysis. Age- and gender-matched healthy subjects were tested as a control group. Forty patients with HC (age 37 ± 16 years; 42.5% women) and 40 control subjects (age 35 ± 10 years; 42.5% women) were examined. Compared with the controls, the patients with HC showed increased peak LV twist (16.5 ± 4.7° vs 12.0 ± 3.9°, p <0.001) mainly because of increased apical rotation of those with LV outflow tract obstruction (obstruction, 12.7 ± 4.4° vs nonobstruction, 9.7 ± 2.8°, p = 0.02). In addition, the patients with HC displayed onset of torsion recoil occurring closer to the aortic valve closure (94 ± 6% vs 85 ± 6%, p <0.001; time normalized by the length of systole), limited completion of untwist during early diastole (31 ± 12% vs 62 ± 15%, p <0.001), and delayed peak untwist velocity (22 ± 7% vs 13 ± 9%, p <0.001; time normalized by the length of diastole). In conclusion, the evaluation of twist mechanics using 3D-STE provides novel insight regarding alterations in LV mechanics in patients with HC. Elucidating the characteristics of the wringing motion of the heart might help to broaden the understanding of the hyperdynamic contraction and impaired relaxation observed in these patients.
Left ventricular (LV) twist represents a phenomenon that links systolic contraction with diastolic relaxation and plays a major role in cardiac physiology. Speckle tracking echocardiography (STE), based on tracking and measurement of tissue displacement, has the potential for accurate and reliable assessment of myocardial mechanics, providing a relatively simple, noninvasive approach to the study of LV rotation and twist. The presence, in patients with hypertrophic cardiomyopathy (HC), of a supranormal ejection fraction within a clearly diseased myocardium, and important limitations of transmitral velocities and tissue Doppler imaging for the estimation of filling abnormalities has generated interest in evaluating the usefulness of STE for HC, where its application might help to widen the understanding of the complex pathophysiology of HC. Despite interest in STE for the assessment of HC through rotational and twist parameters, the available data are quite scarce and limited to a few reports, all of which used 2-dimensional technology, with the inherent limitation of tracking out-of-plane tissue motion. The aim of the present study was to describe LV twist mechanics in HC using 3-dimensional (3D)-STE.
Methods
We examined outpatients referred to our echocardiography laboratory from the Hypertrophic Cardiomyopathy Center (Tufts Medical Center, Boston, Massachusetts). Inclusion required a diagnosis of HC (the demonstration of a hypertrophied nondilated left ventricle [in adults, a wall thickness of ≥15 mm; in children, a wall thickness >+2 SDs of normal values according to body surface area ] ) and the absence of hypertension, diabetes mellitus, or any other cardiac or systemic disease that could produce the magnitude of hypertrophy evident. In addition, sinus rhythm had to be present at echocardiography. Left ventricular outflow tract obstruction was considered when an at rest or provocable (Valsalva maneuver) gradient of ≥30 mm Hg was detected. The patients were questioned in detail about their history and symptoms of coronary artery disease and were excluded if they provided any history suggesting this condition or if evidence of coronary artery disease was identified by a review of the medical records. Patients demonstrating wall motion abnormalities on the standard echocardiogram were also excluded. In addition, as a part of the routine assessment of HC in our institution, 18 of 40 enrolled patients (those without at rest or Valsalva-induced obstruction) underwent a treadmill echocardiographic test to evaluate for exercise-provocable obstruction. All these patients reached the target heart rate, with neither ST-segment changes nor wall motion abnormalities on the peak exercise echocardiogram. Finally, patients with previous septal myectomy or alcohol septal ablation were excluded. Normal age- and gender-matched volunteers were examined as controls (±5 years matching for age and exact matching for gender). They were selected as normal subjects after a detailed history was obtained regarding possible health issues, with an absence of complaints compatible with cardiac disease and no history of hypertension, diabetes mellitus, or any other systemic disease. They were excluded as controls if any of the following was detected on the standard echocardiogram: significant valvulopathy; abnormal cardiac chamber size; or ejection fraction <50%. The institutional review board approved the present study.
Echocardiograms were performed with the Artida 4D System scanner (Toshiba Medical Systems, Tustin, California) in the tissue harmonic mode. The PST-30SBT transducer was used for standard 2D/Doppler measurements and the matrix array PST-25SX transducer for acquisition of 3D data sets. The latter consisted of an apical full volume created by the combination of 6 wedge-shaped subvolumes from 6 consecutive cardiac cycles during a single breath-hold; 2 to 4 data sets with a temporal resolution of 20 to 25 volumes per second were obtained from each patient to subsequently select that of the best quality for off-line processing.
The full-volume 3D data sets were analyzed using the 3D Wall Motion Tracking software (Toshiba Medical Systems) by an expert in the interpretation of echocardiographic images. First, the apical 4- and 2-chamber views and the 3 short axis views were automatically selected at end-diastole. Then, the foreshortened images were avoided by looking for the largest long axis dimensions. The transversal axes were modified as appropriate to optimize their orientation throughout the cardiac cycle. Next, the LV endocardial surface at end-diastole was automatically traced; only in the cases in which the software algorithm did not identify the surface correctly, manual tracing was used. Finally, myocardial tissue displacement was tracked throughout the cardiac cycle. The left ventricle was divided into 16 segments. The curves and values of LV rotation and twist and the timing of these parameters were provided by the software. Untwist and untwist rate were calculated by the investigators using the following formulas:
Untwist = [ ( P L V T − T w i s t 1 ) / P L V T ] × 100
Untwist rate = ( T w i s t 1 − P L V T ) / [ ( t 1 − t P L V T ) / 1000 ]
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