Eirik Pettersen

Determinants of Left Ventricular Early-Diastolic Lengthening Velocity Independent Contributions From Left Ventricular Relaxation, Restoring Forces, and Lengthening Load

Background— Peak early-diastolic mitral annulus velocity (e′) by tissue Doppler imaging has been introduced as a clinical marker of diastolic function. This study investigates whether lengthening load (early-diastolic load) and restoring forces are determinants of e′ in addition to rate of left ventricular (LV) relaxation. Methods and Results— In 10 anesthetized dogs, we measured e′ by sonomicrometry and tissue Doppler imaging during baseline, volume loading, caval constriction, dobutamine infusion, and occlusion of the left anterior descending coronary artery. Relaxation was measured as the time constant (&tgr;) of LV pressure decay by micromanometer. Lengthening load was measured as LV transmural pressure at mitral valve opening (LVPMVO). Restoring forces were quantified by 2 different indices: (1) As the difference between minimum and unstressed LV diameter (Lmin−L0) and (2) as the estimated fully relaxed LV transmural pressure (FRPEst) at minimum diameter. In the overall analysis, a strong association was observed between e′ and LVPMVO (&bgr;=0.49; P<0.001), which indicates an independent effect of lengthening load, as well as between e′ and Lmin−L0 (&bgr;=−0.38; P<0.002) and between e′ and FRPEst (&bgr;=−0.31; P<0.002), consistent with an independent contribution of restoring forces. A direct effect of rate of relaxation on e′ was observed in a separate analysis of baseline, dobutamine, and ischemia when postextrasystolic beats were included (&bgr;=−0.06, P<0.01). Conclusions— The present study indicates that in the nonfailing ventricle, in addition to LV relaxation, restoring forces and lengthening load are important determinants of early-diastolic lengthening velocity.

Apical Rotation by Speckle Tracking Echocardiography: A Simplified Bedside Index of Left Ventricular Twist

OBJECTIVE The study objective was to determine whether left ventricular (LV) apical rotation by speckle tracking echocardiography (STE) may serve as a clinically feasible index of LV twist. LV twist has been proposed as a sensitive marker of LV function, but clinical implementation has not been feasible because of the complexity and limitations of present methodologies. METHODS The relationship between apical rotation and LV twist was investigated in anesthetized dogs (n = 9) and a clinical study that included healthy controls (n = 18) and patients (n = 27) with previous myocardial infarction. Rotation by STE was compared with twist measured by magnetic resonance imaging and sonomicrometry in humans and dogs, respectively. RESULTS In dogs, apical rotation by STE correlated well with LV twist over a wide range of loading conditions and inotropic states, and during myocardial ischemia (R = 0.94, P < .01). Similarly, in humans there was a strong correlation between apical rotation and twist (R = 0.88, P < .01) but only a weak correlation between basal rotation and twist (R = 0.53, P < .01). Apical rotation accounted for 72% +/- 14% and 73% +/- 15% of the twisting deformation by magnetic resonance imaging in controls and patients, respectively. In dogs, apical rotation and twist decreased during myocardial ischemia (P < .05). In patients, LV twist and apical rotation were reduced (P < .05) only when LV ejection fraction was less than 50%. CONCLUSION Apical rotation represents the dominant contribution to LV twist, and apical rotation by STE reflects LV twist over a wide range of hemodynamic conditions. These findings suggest that apical rotation by STE may serve as a simple and feasible clinical index of LV twist.

Mechanisms of preejection and postejection velocity spikes in left ventricular myocardium: interaction between wall deformation and valve events.

Background— Normal left ventricular myocardium demonstrates distinct spikes in the velocity trace before and after left ventricular ejection. We tested the hypothesis that the preejection and postejection velocity spikes reflect early systolic shortening and late systolic lengthening that are interrupted by mitral and aortic valve closure, respectively. Methods and Results— In 11 anesthetized dogs, timing of valve closure was determined by pressure variables; left ventricular dimensions were determined by sonomicrometry. Myocardial shortening started 20±10 ms (mean±SD; P<0.001) before mitral valve closure and was interrupted at the time of mitral valve closure (time difference, 4±7 ms). Similarly, myocardial lengthening started 31±15 ms (P<0.001) before aortic valve closure and was interrupted at the time of aortic valve closure (time difference, 0±3 ms). Prevention of mitral (n=4) and aortic (n=4) valve closure by stenting the valves abolished the preejection and postejection velocity spikes, respectively. Echocardiographic measurements of patients (n=15) with severe mitral regurgitation showed that the preejection velocity spike was reduced after prosthetic valve replacement (43±25 versus 32±15 mm/s; P=0.036), indicating that preejection shortening was larger with a leaking valve. Similarly, late systolic lengthening was reduced in patients (n=15) with severe aortic regurgitation after prosthetic valve replacement; minimum postejection velocity spike was increased from −32±11 to −17±11 mm/s; P=0.0003). Asynchronous onset of contraction/relaxation and atrioventricular interaction were investigated as alternative mechanisms of the velocity spikes in dogs and patient groups but were found implausible. Conclusions— This study supports the hypothesis that normal left ventricular preejection and postejection velocity spikes are attributed to valve closures that interrupt early systolic shortening and late systolic lengthening, respectively.

Clinical assessment of left ventricular rotation and strain: a novel approach for quantification of function in infarcted myocardium and its border zones

Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects (n = 15) and patients with myocardial infarction (n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in strain and rotation, we used a mathematical finite element simulation model of the LV. Mean apical rotation and strain by STE were lower in patients than in healthy subjects (9.0 +/- 4.9 vs. 12.9 +/- 3.5 degrees and -13.9 +/- 10.7 vs. -23.8 +/- 2.3%, respectively, P < 0.05). In patients, regional strain was reduced in proportion to segmental infarct extent (r = 0.80, P < 0.0001). Regional rotation, however, was similar in the center of the infarct and in remote viable myocardium. Minimum and maximum rotations were found at the infarct borders: minimum rotation at the border zone opposite to the direction of apical rotation, and maximum rotation at the border zone in the direction of rotation. The simulation model reproduced the clinical findings and indicated that the dissociation between rotation and strain was caused by mechanical interactions between infarcted and viable myocardium. Systolic strain reflects regional myocardial function and infarct extent, whereas systolic rotation defines infarct borders in the LV apical region. Regional rotation, however, has limited ability to quantify regional myocardial dysfunction.

Non-invasive measurement of the response of right ventricular pressure to exercise, and its relation to aerobic capacity

INTRODUCTION Exercise echocardiography assesses exercise-induced pulmonary hypertension. The upper normal limit of right ventricular systolic pressure during exercise is not well established. Our study aims to investigate the response of right ventricular systolic pressure in relation to aerobic capacity. METHODS AND RESULTS Cardiopulmonary exercise testing using a treadmill, and echocardiography during supine cycling, were performed in 113 healthy volunteers aged 13 to 25 years. Maximal right ventricular systolic pressure during evaluable exercise studies obtained in 108 subjects showed a Gaussian distribution only after separating the endurance trained subjects, specifically 12 athletes with Z-score of peak oxygen uptake higher than 2.0, from the normally trained group of 97 subjects. Maximal right ventricular systolic pressure during exercise in the normally trained group showed a mean of 38.0 millimetres of mercury, with standard deviation of 7.2, a median value of 39.0, and a range from 17 to 63, and the 95th percentile was 51 millimetres of mercury. In the athletes, the maximal right ventricular systolic pressure was higher, with a median of 55.5, a range from 28 to 69, this being significant, with p equal to 0.004). Of the 12 athletes, 8 (67%) showed a response of right ventricular systolic pressure to exercise exceeding 50 millimetres of mercury, but only 8 of 97 normally trained subjects (8%) showed a similar response, this also being significant, with p less than 0.001. CONCLUSIONS Our study confirms the great variability in the response of right ventricular systolic pressure to exercise in healthy individuals, with 50 millimetres of mercury representing the upper normal limit. Endurance-trained athletes show higher levels, and two-thirds have abnormal responses exceeding 50 millimetres of mercury.

Identification of Viable Myocardium in Acute Anterior Infarction Using Duration of Systolic Lengthening by Tissue Doppler Strain: A Preliminary Study

BACKGROUND The aim of this study was to investigate whether strain Doppler echocardiography before reperfusion therapy could quantify ischemic dysfunction and predict viable myocardium in acute myocardial infarction as determined by magnetic resonance imaging. METHODS Twenty-six patients (mean age, 60 ± 12 years; seven women) with acute myocardial infarctions who underwent acute percutaneous coronary intervention were examined using strain Doppler echocardiography immediately before the procedure. Percutaneous coronary intervention was performed 296 ± 122 min after the onset of pain. Peak left ventricular systolic longitudinal strain and the duration of systolic lengthening were analyzed. Magnetic resonance imaging was performed 11 ± 5 months after therapy. Scarring exceeding 50% of the segment area was considered nonviable. RESULTS Peak systolic strain fell gradually (becoming less negative) from normal segments to segments with transmural infarction (P < .0001), and the duration of systolic lengthening increased (P < .0001). Myocardial scarring was closely correlated with peak systolic strain (R = 0.76, P < .00001) and the duration of systolic lengthening (R = 0.88, P < .00001). There was a significant correlation between the degree of scarring and time to percutaneous coronary intervention (R = 0.40, P = .045). In segments with systolic lengthening, the improvement in strain after remodeling was significantly higher (5.5 ± 5.1%) than in segments with duration of systolic lengthening > 67% of systole (2.2 ± 3.7%) (P < .001). Receiver operating characteristic curve analyses showed that duration of systolic lengthening > 67.3% could identify nonviable myocardium (sensitivity, 90%; specificity, 94%). CONCLUSIONS In patients with acute myocardial infarctions in the anterior wall, strain measurements can identify myocardium with nontransmural scarring. The duration of systolic lengthening is a novel, easily implemented variable that may identify ischemic but viable myocardium. Myocardial infarctions in other left ventricular regions should be investigated in future studies.

Response to Letter Regarding Article, “Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium: Interaction Between Wall Deformation and Valve Events”

We thank Drs Sengupta and colleagues for their interest in our work.1 Our aim was to understand what causes the pre- and postejection velocity spikes. The main focus of Sengupta et al is to understand why the spikes sometimes cross the zero line, a phenomenon that they name biphasic spikes , as it denotes both a shortening phase (positive velocity) and a lengthening phase (negative velocity). This is an interesting topic, but it was outside the scope of our study.1 The preejection velocity has a spike shape, ie, an upstroke and a downstroke. The upstroke from zero reflects the start of shortening, which pushes blood toward the valve plane and closes the mitral valve. Mitral valve closure then …

Moderate Altitude Increases Right Ventricular Pressure and Oxygen Desaturation in Adolescents with Surgically Closed Septal Defect

OBJECTIVES Abnormal right ventricular systolic pressure response (RVPR) during exercise has previously been demonstrated in patients with septal defects of the heart. Our study investigated whether moderate altitude affects RVPR and oxygen saturation during rest and exercise in patients with surgically closed septal defects. DESIGN Ten patients with surgically closed heart septal defects (six secundum atrial septal defects, four ventricular septal defects) were examined by cardiopulmonary exercise testing and by echocardiography at rest and during supine cycling at sea level. After 2 hours in a hypobaric chamber at 2500 m/8200 ft altitude, exercise echocardiography was repeated. RESULTS During sea level exercise four patients showed abnormal RVPR (>50 mm Hg). Acute hypoxic exposure led to right ventricular systolic pressure increase above 40 mm Hg in two patients. During altitude exercise seven patients showed abnormal RVPR. Average maximal right ventricular systolic pressure was 56.5 ± 12.7 mm Hg and average for the lowest oxygen saturation was 80.0 ± 5.7%. Two patients had simultaneous oxygen desaturation below 80% and right ventricular systolic pressure above 50 mm Hg. CONCLUSIONS Moderate altitude affects right ventricular systolic pressure and oxygen saturation in adolescents with surgically closed ventricular or atrial septal defects. Moderate altitude may induce or aggravate abnormal RVPR and oxygen desaturation during exercise in these patients.