Factors affecting real-time, cross-sectional echocardiographic imaging of perimembranous ventricular septal defects

Recent studies suggest good prospective accuracy for two-dimensional echocardiographic imaging of ventricular septal defects (VSD). We obtained two-dimensional images with high-frequency, high-resolution scanners from 36 patients proved by cardiac catheterization to have perimembranous VSD. In 20 patients, the VSD was an isolated lesion and in 16 it was associated with other forms of heart disease. VSDs were imaged in long-axis, apical four-chamber and subcostal echocardiographic views. The smallest VSD imaged was 2 mm in diameter on echo; the largest, 23 mm. The imaged size of VSDs was larger at end-diastole than at end-systole by paired t test on all views (all p less than 0.005). VSD size also varied between views, with no predictive relationship except between apical and subcostal four-chamber views in diastole (r = 0.71, p less than 0.005). This agreed with qualitative direct observations of an ellipsoid or irregularly shaped VSD in operated patients. Echocardiographically measured VSD size normalized for either aortic root size or for patient weight could be used to separate isolated VSDs with large shunts (Qp/Qs greater than 2:1) from those with small shunts. Review of 250 two-dimensional echocardiographic studies from patients proved not to have a VSD revealed 28 planes of imaging with false-positive VSD. None of the false-positive VSDs was imaged consistently on all views. Additionally, a "T" artifact (broadening of septal edges around a VSD) has been found to be a reliable marker of true VSD imaging. To best quantify VSD size and to avoid false-positive diagnoses, it is necessary to use multiple views and to consider the marked changes in VSD size that occur between diastole and systole.     

The effect of left ventricular pressure or volume overload on ventricular dimension in children. Left ventricular volume determination from one or two ventricular dimensions

The effect of pressure or volume overload on the geometry of the left ventricle (LV) was determined in order to examine the feasibility and accuracy of LV volume determinations from one minor axis or two dimensions (one minor axis and the longest length). The longest length (LL) and minor axis (MA) in both the anteroposterior (AP) view and lateral (LAT) view were determined from the LV cine silhouette in patients with normal LV volume and pressure (group 1), LV pressure (LVP) overload group (LVP greater than 140 mm Hg, group 2), and LV volume overload group (LV end-diastolic volume greater than 124% of normal, group 3). The ratio of the MA to the LL, which represents the spherical configuration of the LV, was less than "normal" in group 2, and higher than "normal" in group 3. In all groups the LV was less spherical at end-systole than at end-diastole. Additionally, the (MA)3 had a different relationship to true LV volume (biplane LV volume) in the three groups and from diastole to systole in each group. Left ventricular volume calculation from one minor axis was associated with a large error. In contrast, left ventricular volume can be accurately determined from two ventricular dimensions using either the anteroposterior or lateral ventricular image (r larger than or equal to 0.97).     

Cases of multiple ventricular septal defects

We had 4 cases with multiple ventricular septal defects (VSDs) in complexed congenital heart disease. One of four had two separate VSDs detected by two dimensional echocardiography before operation. Second of four had additional infundibular muscular VSD which was detected by echocardiography in the intensive care unit (ICU) after patch closure of a perimembranous VSD. The third case had two additional VSDs of inlet muscular and subaortic septum detected by transesophageal and direct echocardiography during reoperation, beside a subpulmonary VSD which was originally diagnosed before Jatene operation for double outlet right ventricle. The fourth case had multiple trabecular muscular VSDs diagnosed by postoperative angiography soon after Rastelli operation. Since these additional multiple VSDs compromise the postoperative hemodynamics if those are unrecognized, it is indispensable to detect all VSDs before operation, using transthoracic and transesophageal echocardiography.     

Anatomic features and surgical strategies in double-outlet right ventricle

BACKGROUND: The objective of this study was to review anatomic features and surgical strategies in children with double-outlet right ventricle (DORV) and to assess risk factors for early mortality. METHODS AND RESULTS: Records were reviewed of all children with DORV undergoing surgery between 1978 and 1993. Noncomplex patients (group 1) had atrioventricular (AV) concordance, a single ventricular septal defect (VSD), balanced ventricles, no straddling AV valves, and no major pulmonary artery anomaly. Group 2 (complex) comprised all remaining patients. Independent risk factors analyzed included location of the main VSD, presence of additional VSDs, coarctation, ventricular outflow obstruction, ventricular hypoplasia, age at operation, operation before 1985, previous palliation, and type of definitive operation. Of 193 patients, 117 were in group 1 and 76 in group 2. In 148 patients, biventricular repair was undertaken, including 111 of 117 group 1 patients and 37 of 76 group 2 patients. Early mortality was higher among group 2 patients undergoing biventricular repair than among group 1 patients (8 of 37 versus 4 of 111, P<.005) and higher than group 2 patients undergoing a Fontan procedure (none of 29, P<.01). Aortic arch obstruction, operation before 1985, and multiple VSDs were significant risk factors for mortality. Age <1 month (P<.05) and multiple VSDs (P<.005) were independent risk factors after definitive repair. Up-to-date follow-up is available on 144 surviving patients, with 127 (88%) in New York Heart Association class I and the remaining 17 in class II. Overall 10-year survival probability was 81%, whereas probability of survival, free from reoperation (after definitive surgery), was 65% at 10 years. CONCLUSIONS: Biventricular repair can be achieved in most patients with DORV with low risk. In complex DORV, a Fontan procedure is associated with a lower surgical mortality.     

3-Hydroxy-3-methylglutaryl coenzyme A lyase: targeting and processing in peroxisomes and mitochondria

Murine models of left ventricular (LV) hypertrophy recently have been developed. We tested the accuracy of 2-dimensional (2D) echocardiographic measurement of LV mass with high-frequency imaging in mice. Ten anesthetized mice (weight 20 to 31 g, aged 1 to 5 months) were examined with a 15-MHz transthoracic linear-array transducer. End-diastolic myocardial area (A)(epicardial - endocardial) from the parasternal short-axis view at the midpapillary level and LV length (L) from the parasternal long-axis view were measured to calculate LV mass with the area-length method (1.05 [5/6 x A x L]) and data were compared with LV-mass with the 2D guided M-mode method. Within 3 days of echocardiography, the hearts were removed and weighed after potassium-induced cardiac arrest. Two-dimensional echocardiographic measurement with a 15-MHz transducer was performed in all mice. LV chamber dimensions included end-diastolic septal (0.80 +/- 0.12 mm) and posterior wall thickness (0.76 +/- 0.13 mm), end-diastolic dimension (3.64 +/- 0.28 mm), and end-systolic dimension (2.34 +/- 0.32 mm). Echocardiographic LV mass with the area-length method, 2D guided M-mode method, and autopsy LV weight were 80.8 +/- 16.1 mg, 97.6 +/- 17.8 mg, and 78.8 +/- 13.2 mg, respectively. A strong correlation existed between LV weight (x ) and echocardiographic LV mass (y ) with the area-length method: y = 0.745x + 18.9, r =0.908, standard error of estimate (SEE) = 5.9 mg, P <.0005. This correlation was stronger than that of LV weight (x ) and echocardiographic LV mass (y ) with the 2D guided M-mode method: y = 0.577x + 22.6, r =0.779, SEE = 8.8 mg, P =.008. These data suggest that serial in vivo measurements of LV mass with the 2D area-length method may be more accurate than M-mode methods in experimental murine models of LV pathology.     

Accuracy of formulae for calculating left ventricular volumes of the equine heart

Echocardiography may be an accurate method of measuring left ventricular (LV) volumes and mass of the horse's heart. If so, studies of the heart size and hypertrophy would be possible. This study evaluated geometric models of the external and internal LV shapes, to determine which could be applied to echocardiographic measurements. We preserved 30 horses' hearts and measured their dimensions and cross sectional areas. These measurements were entered into seven formulae representing different geometric models of the ventricle and its chamber. We derived a correction factor to estimate the long axis as a fixed proportion of the external diameter, so that volumes could be determined from an M-mode or a cross sectional echocardiogram. Statistical analysis of the regressions of known volumes against calculated volumes measured by water displacement, demonstrated that the ellipsoid formula using cross sectional areas was very accurate in representing the external shape of the left ventricle (slope = 1.01 r2 = 96.3) and its chamber (slope = 0.83, r2 = 94.3). Myocardial volume, measured by subtracting internal (chamber) volume from external volume, was also calculated accurately (slope = 1.01, r2 = 96.5). The ellipsoid formula using directly measured diameter was only slightly less accurate. LV mass could be calculated by applying the specific gravity of equine myocardium, 1.05, to the myocardial volume. Formulae recommended for evaluating are, with M-mode echocardiography: [equation: see text] and with 2D echocardiography [equation: see text] where De is the external diameter, Di is the internal diameter, Ae the external area and Ai the internal area.     

Experience with the Ultrex and Ultrex Plus inflatable penile prosthesis: new implantation techniques and surgical outcome

OBJECTIVE: To construct nomograms of the size of the fetal orbit and lens during gestation. SUBJECTS: The study group included 349 normal pregnant women at 14-36 weeks' gestation. METHODS: Routine biometric measurements were obtained in all the participants; these included biparietal diameter, head and abdominal circumferences, measurements of the long bones and the diameters of the fetal orbit and lens. The orbital and lens circumference measurements were also related to gestational ages. RESULTS: A linear growth function was observed between gestational age (GA) and orbital diameter (r = 0.94; p < 0.00001; y = -0.66 + 0.5 x GA), orbital circumference (r = 0.94; p < 0.00001; y = -2.1 + 1.5 x GA) and orbital area (r = 0.94; p < 0.00001; y = -98.1 + 8.3 x GA). Significant correlation was also found between femoral length (FL) and orbital diameter (r = 0.95; p < 0.00001; y = 3.3 + 1.9 x FL), orbital circumference (r = 0.95; p < 0.00001; y = 10.3 + 5.9 x FL) and orbital area (r = 0.93; p < 0.00001; y = -28.2 + 32.2 x FL). A linear growth function was observed between orbital circumference and biparietal diameter (r = 0.94; p < 0.00001) and head circumference (r = 0.95; p < 0.00001). A linear growth function was also observed between gestational age and the diameter of the lens (r = 0.89; p < 0.00001; y = 0.88 + 1.4 x GA) the circumference of the lens (r = 0.89; p < 0.00001; y = 2.78 + 0.4 x GA) and the area of the lens (r = 0.89; p < 0.00001; y = -7.95 + 1.0 x GA). The correlation was found between the ratios of the diameters, circumferences and areas of the lens and the orbit. CONCLUSIONS: These results provide normative data of the growth of the fetal orbit and lens and may aid future studies relating to fetal eye anomalies.     

Left ventriculotomy for closure of muscular ventricular septal defects. Treatment of choice

Closure of muscular ventricular septal defects (VSDs) through the right atriotomy or right ventriculotomy may be difficult. These VSDs are often located behind the hypertrophied trabeculae carnae or papillary muscle. Residual or recurrent VSD may result from the difficult approach. Between March 1971 and December 1975, we have used the left ventriculotomy near the apex for closure of muscular VSDs in ten children. The patients' ages ranged from five months to eight years and three months. The diagnosis was established by cardiac catheterisation and left ventricular angiocardiogram in all patients. Six patients had multiple VSDs; in four patients VSD in the muscular septum was present (three apical, one midseptal). Operations were performed on cardiopulmonary bypass with moderate hypothermia and intermittent anoxic arrest. VSDs in the membranous septum were closed through the right atrium. Muscular VSDs were approached through a small vertical incision in the left ventricle near the apex. The postoperative course was uneventful in eight patients. Two patients, aged 16 months and eight years, died; histology showed grade IV pulmonary vascular disease in both. All survivors are well four months to five years after the operation, without clinical evidence of residual or recurrent VSD.     

Relationship between systolic and diastolic function of the left ventricle in patients with impaired relaxation of the left ventricle without symptoms of heart failure. Attempt at quantitative estimation of diastolic function in the impaired relaxation stage

Diastolic dysfunction of left ventricle appears very often in patients with coronary artery disease (CAD) and hypertension (HT) and is a main cause of heart failure in 30-40% of all cases. Relation between systolic and diastolic function of left ventricle (LV) is commonly known but not documented well enough. Moreover, no quantitative classification of diastolic dysfunction is still available. AIM OF THE STUDY: To find out the relations between the parameters of systolic and diastolic function of LV in patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure and to make up the quantitative classification of diastolic dysfunction in the stage of impaired relaxation of LV. METHODS: Investigations were carried out in 57 patients (mean age 55.5 +/- 11.5) with angiographically proven CAD and in 91 patients (mean age 56.3 +/- 10.6) with HT and angiographically excluded CAD, all without regional myocardial contractility abnormalities and valvular heart diseases. Control group consisted of 54 healthy subjects (mean age 55.4 +/- 11.4). During 2D echocardiography examination left ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD) and left atrial dimension (LA) were obtained. Using Doppler method transmitral inflow indices: E velocity (E), A velocity (A), E velocity integral (E-VTI), A velocity integral (A-VTI), total velocity integral (T-VTI), E deceleration time (DT), isovolumic relaxation time (IVRT) and aortic flow velocity integral (Ao-VTI) were measured. Only patients with E/A < or = 1 and--to exclude pseudonormalization of mitral inflow--with DT > or = 140 ms were qualified to the study. We proposed diastolic dysfunction ratio (DDR) calculated from formula: DDR = E/A x E-VTI/T-VTI. Using AFVI, LV outflow diameter, heart rate (HR) and body surface area cardiac index (CI) was calculated. RESULTS: In studied group there were significantly higher values of LA, A, IVRT, DT and lower values of E, E/A, E-VTI and DDR compared to controls. There were no significant differences between these groups in HR, LVEDD, LVESD, T-VTI and CI. No significant differences in any of studied parameters were found between subgroups with CAD and HT. Among healthy subjects in subgroup with abnormal mitral inflow pattern (E/A < or = 1) there were significantly higher values of LA, IVRT, DT and lower values of DDR than in sugroup with normal one. Both subgroups did not differ in LVEDD, LVESD, CI. In the studied group there was positive correlation between DDR and CI (r = 0.69, p < 0.001), DDR and IVRT (r = 0.71, p < 0.001), DDR and DT (r = 0.61, p < 0.001), CI and E (r = 0.34, p < 0.01), CI and IVRT (r = 0.52, p < 0.001), CI and DT (r = 0.42, p < 0.001), CI and E/A (r = 0.54, p < 0.001), CI and E-VTI (r = 0.43, p < 0.001). In the control group significant correlation was found only between DDR and IVRT (r = 0.64, p < 0.02) and between DDR and DT (r = 0.52, p < 0.02) but not between DDR and CI. Using DDR DD was divided into 3 classes: class I with DDR > 0.47, class II with 0.47 > or = 0.30, and class III with DDR < 0.30. Applying of such intervals of values of DDR determined the groups which significantly differed between themselves in CI, IVRT and DT. CONCLUSIONS: (1) In patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure there is relation between parameters of systolic and diastolic function of LV: the more advanced diastolic dysfunction, the more impaired systolic function. (2) In healthy subjects there is no relation between parameters of systolic and diastolic function of LV. (3) DDR is a good indicator of quantitative estimation of diastolic dysfunction in the stage of impaired relaxation of LV.     

Apical muscular ventricular septal defects between the left ventricle and the right ventricular infundibulum. Diagnostic and interventional considerations

BACKGROUND: Effective transcatheter or surgical closure of apical muscular ventricular septal defects (VSDs) requires accurate delineation of variable and often complex anatomy. These defects have generally been considered as communications between the apexes of both left and right ventricles. METHODS AND RESULTS: Among 50 consecutive patients with multiple muscular VSDs referred for transcatheter device closure between October 1987 and April 1993, a subset of 10 patients (aged 7 days to 28 years) with apical muscular VSDs shared a unique set of anatomic characteristics: (1) large and often single opening in the left ventricle; (2) multiple right ventricular openings in the anterior aspect of the apical septum; and (3) separation of the right ventricular apical region into which the VSDs open from the rest of the right ventricular inflow and outflow by prominent muscle bundles. Additional analysis of the anatomy by use of echocardiography and cineangiography showed that these muscular defects were between the left ventricular apex and right ventricular infundibular apex. In 6 patients, the transcatheter devices used to create a septum in these hearts were placed in the right ventricle, straddling muscle bundles that separated the apical VSD from the rest of the right ventricular inflow and outflow, resulting in incorporation of a portion of the right ventricular infundibular apex into the physiological left ventricle. Three patients had devices placed between the apexes of the left ventricle and the infundibulum. The defect closed spontaneously within the right ventricle in 1 patient. One patient died after surgery for tetralogy of Fallot in situs inversus. The remaining 9 patients were all clinically well at the time of their most recent follow-up visit (follow-up duration, 32 +/- 11 months). This distinct type of apical VSD was identified by echocardiography in 20 of 274 patients who were followed up clinically for muscular VSDs. CONCLUSIONS: Left ventricular-infundibular apical VSDs constitute a distinct morphological type of muscular VSD that can be distinguished by echocardiography and cineangiography. In selected cases, the infundibular apex can be separated from the rest of the right ventricular inflow and outflow to eliminate flow across these defects.     

Quantitative two-dimensional echocardiographic assessment of regional wall motion during transient ischemia and reperfusion in the rat

Nonlethal myocardial ischemia produces profound and long-lasting effects on regional ventricular function and metabolism (myocardial stunning) and protects against myocardial infarction from subsequent prolonged ischemia (ischemic preconditioning). Two-dimensional echocardiography (2DE) is an essential tool for quantitative analysis of regional and global left ventricular (LV) function during myocardial ischemia and reperfusion and the study of these phenomena. However, the inability to perform 2DE in the open-chest rat heart has seriously limited the use of this model. To investigate the effect of transient coronary occlusion on segmental wall motion and LV geometry, we employed a 20 MHz intravascular ultrasound catheter placed on the epicardial surface of the rat heart (n = 15) to yield 2DE images suitable for quantitative analysis. Three 2-minute left coronary occlusions were made, separated by 5 minutes of reperfusion, with imaging during occlusion and at 5 and 60 minutes of reperfusion. Ischemic and nonischemic wall thicknesses, LV cross-sectional area, estimated LV volume, and the fractional changes of these parameters were measured. In eight animals these values were also compared with necropsy measurements of wall thickness, LV cross-sectional area, and volume. LV and right ventricular structures were well visualized in short-axis cross-sectional images in all animals, and images suitable for quantitative analysis were obtained in 92% of the periods. Coronary occlusion caused immediate, marked LV cavitary expansion, which rapidly returned to normal by 5 minutes of reperfusion. Active systolic thickening of the anterior wall at baseline (47% +/- 3%) became passive thinning during occlusion (-6% +/- 2%) and recovered partially, to 30% +/- 3% at 5 minutes of reperfusion and 42% +/- 4% at 60 minutes (p < 0.0005 at 5 minutes of reperfusion vs baseline; p not significant at 60 minutes). Recovery of thickening after 5 minutes of reperfusion was not different after the first versus third occlusion (23% +/- 4% vs 30% +/- 3%; p = 0.19). Measurements made by 2DE correlated well with those made by necropsy, although wall thickness was slightly thicker by 2DE. We conclude that epicardial echocardiography with an intravascular ultrasound catheter provides quantifiable 2DE images in this model and yields accurate information on segmental wall thickening and ventricular geometry not available by other techniques. Left coronary occlusion in the rat is associated with marked global and segmental LV expansion, which rapidly reverses with reperfusion. Postischemic regional wall motion abnormalities are present after coronary occlusion as brief as 2 minutes and can be measured accurately. The effect of multiple brief occlusions is not cumulative.(ABSTRACT TRUNCATED AT 400 WORDS)     

Evaluation of left ventricular early diastolic performance by color tissue Doppler imaging of the mitral annulus

A noninvasive assessment of left ventricular (LV) diastolic performance by tissue Doppler imaging was performed in 56 patients (8 patients with atypical chest pain, 42 with coronary artery disease with a previous myocardial infarction, and 6 without a previous myocardial infarction) who underwent cardiac catheterization. Mitral annular velocity (MAV) during early ventricular diastole was obtained by M-mode color tissue Doppler imaging at the posterior corner of the mitral annulus. In each patient, the negative peak of the first derivative of LV pressure decay (peak -dP/dt) and a time constant of LV relaxation (tau) were calculated from the LV pressure waves obtained by a catheter-tip micromanometer. LV end-systolic volume index was measured from contrast left ventriculography. MAV during early diastole was significantly correlated with tau (r = -0.73, p <0.001), peak -dP/dt (r = 0.58, p <0.001), and LV end-systolic volume index (r = -0.63, p <0.001). On multivariate regression analysis with MAV during early diastole, tau and LV end-systolic volume index were selected as prime determinants (r = 0.80, p <0.001). These findings suggest that MAV during early diastole has a direct relation to LV elastic recoil as well as to LV relaxation. MAV during early diastole gives important information regarding LV behavior in late systole to early diastole where LV early diastolic performance is determined.     

Effects of low doses of ionizing radiation and induced hypothyroidism on the course of pregnancy and the development of the offspring in rats

OBJECTIVES: To determine the appropriate indications and timing for surgery in children with either a perimembranous or a subarterial type of ventricular septal defect (VSD) associated with aortic cusp prolapse. DESIGN: Retrospective review of children with VSD and associated aortic cusp prolapse with or without aortic regurgitation. This review was based on data obtained from clinical findings, two-dimensional echocardiography, cardiac catheterization and angiocardiography. SETTING: Tertiary health care facility with two-dimensional and colour Doppler echocardiographic and cardiac surgery facilities, and a catheterization laboratory. PATIENTS: Forty-eight patients were found to have perimembranous or subarterial VSDs in association with aortic cusp prolapse with or without aortic regurgitation. INTERVENTIONS: All 48 patients had high resolution two-dimensional and colour Doppler echocardiography. Of the 19 patients who underwent surgical closure of their VSD, five also had an aortic valvuloplasty and one had an aortic valve replacement. Cardiac catheterization was performed in 16 of the 19 surgical patients and 12 of the 29 nonsurgical patients. MEASUREMENTS AND MAIN RESULTS: Annual clinical and echocardiographic assessments in the nonsurgical group did not demonstrate increasing aortic insufficiency. Two children in the nonsurgical group showed spontaneous resolution of aortic insufficiency. In the surgical group, four children with VSD and clinical aortic insufficiency had surgery at less than five years of age; two were found to be regurgitant-free, one had trivial clinical aortic insufficiency and the other had echocardiography-only insufficiency. Of the seven surgical patients older than five years with VSD and clinical aortic insufficiency, four were found to be regurgitant-free, one had echocardiography-only regurgitation and two were unchanged. Two children undergoing surgery with VSD and no aortic insufficiency had postoperative echocardiography-only regurgitation, presumably related to cusp deformity from presurgical prolapse. Children with large VSDs with or without aortic cusp prolapse required surgery for indications of shunt size and pulmonary resistance. CONCLUSIONS: For children with small perimembranous VSDs and cusp prolapse, surgery is indicated only if there is clinical evidence of aortic regurgitation and progressive left ventricular enlargement.     

Quantification of mitral regurgitation by automated cardiac output measurement: experimental and clinical validation

OBJECTIVES: To develop and validate an automated noninvasive method to quantify mitral regurgitation. BACKGROUND: Automated cardiac output measurement (ACM), which integrates digital color Doppler velocities in space and in time, has been validated for the left ventricular (LV) outflow tract but has not been tested for the LV inflow tract or to assess mitral regurgitation (MR). METHODS: First, to validate ACM against a gold standard (ultrasonic flow meter), 8 dogs were studied at 40 different stages of cardiac output (CO). Second, to compare ACM to the LV outflow (ACMa) and inflow (ACMm) tracts, 50 normal volunteers without MR or aortic regurgitation (44+/-5 years, 31 male) were studied. Third, to compare ACM with the standard pulsed Doppler-two-dimensional echocardiographic (PD-2D) method for quantification of MR, 51 patients (61+/-14 years, 30 male) with MR were studied. RESULTS: In the canine studies, CO by ACM (1.32+/-0.3 liter/min, y) and flow meter (1.35+/-0.3 liter/min, x) showed good correlation (r=0.95, y=0.89x+0.11) and agreement (deltaCO(y-x)=0.03+/-0.08 [mean+/-SD] liter/min). In the normal subjects, CO measured by ACMm agreed with CO by ACMa (r=0.90, p < 0.0001, deltaCO=-0.09+/-0.42 liter/min), PD (r=0.87, p < 0.0001, deltaCO=0.12+/-0.49 liter/min) and 2D (r=0.84, p < 0.0001, deltaCO=-0.16+/-0.48 liter/min). In the patients, mitral regurgitant volume (MRV) by ACMm-ACMa agreed with PD-2D (r= 0.88, y=0.88x+6.6, p < 0.0001, deltaMRV=2.68+/-9.7 ml). CONCLUSIONS: We determined that ACM is a feasible new method for quantifying LV outflow and inflow volume to measure MRV and that ACM automatically performs calculations that are equivalent to more time-consuming Doppler and 2D measurements. Additionally, ACM should improve MR quantification in routine clinical practice.     

Left ventricular systolic torsion and early diastolic filling by echocardiography in normal humans

This study describes a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic twist in humans and relates this measure to early ventricular filling. LV twist is the counterclockwise rotation of the left ventricle during systole when viewed from the apex. The effect of ventricular twist has been postulated to store potential energy, which ultimately aids in diastolic recoil, leading to ventricular suction. The generated negative early diastolic pressures may augment early ventricular filling. We measured ventricular twist in 40 patients with normal transthoracic echocardiograms. End-systolic twist was determined by measuring rotation of the anterolateral papillary muscle about the center of the ventricle. LV filling was assessed by analysis of transmitral Doppler flow velocities. The mean value obtained was 9 +/- 7 degrees of rotation. Twist measurements were highly reproducible with an intraobserver correlation coefficient of r = 0.881, p <0.001. The magnitude of ventricular twist was strongly correlated positively with acceleration of the mitral E-wave (r = 0.75; p <0.0001) and negatively with the mitral E-wave acceleration time (r = -0.83; p <0.0001).     

Diastolic function parameters and atrial arrhythmias in patients with arterial hypertension

OBJECTIVE: To investigate in patients with arterial hypertension (HT) the extent of left ventricular (LV) hypertrophy and diastolic function in relation to atrial arrhythmias. PATIENTS AND METHODS: In 112 hypertensive patients (40 women, 72 men; mean age 50 +/- 6.6 years) with a mean systolic blood pressure for the cohort of 170 +/- 5 mmHg, their first invasive coronary angiography was performed between July 1995 and October 1997 because of angina pectoris and/or an abnormal stress electrocardiogram. After excluding coronary heart disease LV dimensions and diastolic function were measured by echocardiography; in 59 of the 112 patients LV hypertrophy was demonstrated. In addition, long-term blood pressure monitoring, exercise and long-term electrocardiography, late-potential analysis and measurement of heart rate variability were undertaken. The control group consisted of 51 patients without arterial hypertension after exclusion of coronary heart disease. RESULTS: Even in the hypertensive patients without LV hypertrophy diastolic LV function and ergometric exercise capacity were reduced. The risk of LV arrhythmias was significantly higher in patients with LV hypertrophy than those without and in the control group, as measured by the complexity of atrial arrhythmias (P < 0.001), the incidence of abnormal late potentials (P < 0.001) and reduction in heart rate variability (29.3 +/- 5.3 ms vs 47.8 +/- 12.1 ms vs 60.7 +/- 6.6 ms; P < 0.001). There were similar results regarding severe complex atrial arrhythmias (38.5 vs 15.0 vs 0%; P < 0.001). The incidence of atrial arrhythmias correlated with the LV diameter (r = 0.68, P < 0.001), LV morphological dimensions and diastolic function (isovolumetric relaxation time r = 0.44, P < 0.001) and the ratio of early to late diastolic inflow (r = 0.46; P < 0.001). CONCLUSIONS: Hypertensive patients have a higher risk of atrial and ventricular arrhythmias, depending on the degree of LV hypertrophy. But atrial arrhythmias, in contrary to ventricular arrhythmias, are also closely related to abnormalities in LV diastolic function.     

A novel monoclonal antibody permitting recognition of NKT cells in various mouse strains

OBJECTIVES: The purpose of this study was to determine whether restrictive left ventricular (LV) filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. BACKGROUND: We recently demonstrated a diastolic ventricular interaction in approximately 50% of a series of patients with chronic heart failure, as evidenced by paradoxic increases in LV end-diastolic volume despite reductions in right ventricular end-diastolic volume during volume unloading achieved by lower body negative pressure (LBNP). We reasoned that such an interaction would impede LV filling in mid and late diastole, but would be minimal in early diastole, resulting in a restrictive LV filling pattern. METHODS: Transmitral flow was assessed using pulsed wave Doppler echocardiography in 30 patients with chronic heart failure and an LV ejection fraction < or = 35%. Peak early (E) and atrial (A) filling velocities and E wave deceleration time were measured. Left ventricular end-diastolic volume was measured using radionuclide ventriculography before and during -30-mm Hg LBNP. RESULTS: Nine of the 11 patients with and 2 of the 16 patients without restrictive LV filling patterns (E/A > 2 or E/A 1 to 2 and E wave deceleration time < or = 140 ms) increased LV end-diastolic volume during LBNP (p = 0.001). The change in LV end-diastolic volume during LBNP was correlated with the baseline A wave velocity (r = -0.52, p = 0.005) and E/A ratio (r = 0.50, p = 0.01). CONCLUSIONS: Restrictive LV filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. Volume unloading in the setting of diastolic ventricular interaction allows for increased LV filling. Identifying patients with chronic heart failure and restrictive filling patterns may therefore indicate a group likely to benefit from additional vasodilator therapy.     

Left ventricular diastolic properties of hypertensive patients measured by pulsed tissue Doppler imaging

Examination of left ventricular (LV) diastolic dysfunction in hypertensive patients has been based on parameters obtained from the transmitral flow velocity during pulsed Doppler echocardiography. However, these parameters are affected by loading conditions. We evaluated LV diastolic function along the longitudinal and transverse axes by pulsed tissue Doppler imaging (TDI) in 50 hypertensive (HT) patients and 36 age-matched healthy volunteers (N). Transmitral flow velocity was recorded by pulsed Doppler echocardiography. LV posterior wall motion velocity along the longitudinal and transverse axes also was recorded by pulsed TDI. In both groups, peak early diastolic velocity of the LV posterior wall (Ew) along the transverse axis (N: 15.8+/-5.2 cm/s, HT: 12.2+/-4.4 cm/s) was higher than that along the longitudinal axis (N: 12.7+/-3.1 cm/s, HT: 9.5+/-3.3 cm/s). Peak atrial systolic velocity of the LV posterior wall (Aw) along the longitudinal axis (N: 9.1+/-1.8 cm/s, HT: 9.7 +/-2.6 cm/s) significantly exceeded that along the transverse axis (N: 8.0+/-2.2 cm/s, HT: 8.4+/-2.4 cm/s) in both groups. The Ews were lower and the Aws were higher along both axes in the patient group than in the control group. The time intervals from the aortic component of the second heart sound to the peak of the early diastolic wave (IIA-Ews) along both the transverse (N: 142+/-18 ms, HT: 154+/-19 ms) and longitudinal (N: 151 16 ms, HT: 162+/-20 ms) axes were longer in the patient group. In 29 patients, Ews along both axes correlated negatively (transverse: r = -0.80, P < .0001; longitudinal: r = -0.71, P < .0001) and IIA-Ews correlated positively (transverse: r = 0.81, P < .0001; longitudinal: r = 0.74, P < .001) with the time constant of the LV pressure decay during isovolumic diastole. The Aws along both axes in the 24 patients without pseudonormalization in transmitral flow velocity correlated positively (transverse: r = 0.60, P < .001; longitudinal: r = 0.74, P < .0001) with the LV end-diastolic pressure. In conclusion, LV relaxation and filling along the longitudinal and transverse axes were impaired in many patients with hypertension. Pulsed TDI was useful for evaluating LV diastolic dynamics in this disease.     

Hydrochlorothiazide is superior to isradipine for reduction of left ventricular mass: results of a multicenter trial. The Isradipine Study Group

OBJECTIVES: We sought to determine the efficacy of isradipine in reducing left ventricular (LV) mass and wall thickness in hypertensive patients. BACKGROUND: LV hypertrophy on the echocardiogram is a strong predictor of cardiovascular events. Reduction of LV mass may be a desirable goal of drug therapy for hypertension. However, although thiazide diuretic drugs have been advocated as first-line therapy for hypertension, their efficacy in reducing LV mass has been questioned. METHODS: Patients with mild to moderate diastolic hypertension and LV mass in excess of 1 SD of normal values were randomized to isradipine (n = 89) or hydrochlorothiazide therapy (n = 45). Evaluations were obtained at baseline, after 3 and 6 months of treatment and 2 weeks after treatment was stopped. RESULTS: At 6 months, LV mass decreased by 43 +/- 45 g (mean +/- SD) with hydrochlorothiazide (p < 0.001) but only by 11 +/- 48 g with isradipine (p = NS; between-group comparison, p < 0.001). Two weeks after drug therapy was stopped, LV mass remained 24 +/- 41 g lower than that at baseline in the hydrochlorothiazide group (p = 0.003) but only 7 +/- 50 g lower in the isradipine group (p = NS). Septal and posterior wall thicknesses were significantly and equally reduced with both isradipine and hydrochlorothiazide. Greater LV mass reduction with hydrochlorothiazide was related to a 2.8 +/- 3.3-mm reduction of LV cavity size with hydrochlorothiazide but no reduction with isradipine. At 6 months of treatment, diastolic blood pressure (BP) by design was equally reduced in both treatment groups. At 3 months, systolic BP was reduced by 17 +/- 15 mm Hg with isradipine and by 26 +/- 15 and 25 +/- 17 mm Hg at 3 and 6 months, respectively, with hydrochlorothiazide (p = 0.003, between-group comparison). However, on stepwise multivariable regression analysis, treatment selection (partial r2 = 0.082, p = 0.001), change in average 24-h systolic BP (partial r2 = 0.032, p = 0.029) and change in average sitting systolic BP (partial r2 = 0.017, p = 0.096) were predictive of LV mass reduction. CONCLUSIONS: Despite an equivalent reduction of diastolic BP, 6 months of therapy with hydrochlorothiazide is associated with a substantial reduction of LV mass, greater than that with isradipine. The superior efficacy of hydrochlorothiazide for LV mass reduction is associated with a greater reduction of systolic BP as well as drug selection itself. These data may have important therapeutic implications.     

Symmetric and asymmetric left ventricular hypertrophy in patients with end-stage renal failure on long-term hemodialysis

BACKGROUND: Patients with end-stage renal disease on regular hemodialysis have an increased prevalence of left ventricular (LV) hypertrophy that is associated with morbidity and mortality. Asymmetric septal hypertrophy and impairment of LV outflow can occur in these patients and may contribute to adverse outcomes. More insight into the prevalence, extent, geometry, and promoting factors of LV hypertrophy is important. METHODS: An unselected group of 62 patients (31 women), aged 55 +/- 14 years, on maintenance hemodialysis was investigated by Doppler echocardiography. Eight patients with valvular heart disease were excluded from further analysis. We assessed prevalence of LV hypertrophy and asymmetric septal hypertrophy, as well as parameters of LV geometry and LV filling and outflow dynamics. RESULTS: Prevalence of LV hypertrophy was 65%. Patients were analyzed according to LV mass and geometry. Mean LV mass index was normal (105 +/- 17 g/m2) in Group 1 without LV hypertrophy (n = 19); it was markedly elevated in Group 2 (symmetric hypertrophy, n = 22) and Group 3 (asymmetric hypertrophy with systolic anterior movement of mitral valve, n = 7), and highest (191 +/- 54 g/m2) in Group 4 (asymmetric hypertrophy without systolic anterior movement of mitral valve, n = 6, p < 0.001). Age, body mass index, and duration of hypertension were associated with LV hypertrophy and asymmetric septal hypertrophy (p = 0.01). Group 3 with systolic anterior motion of mitral valve had the smallest end-diastolic LV diameters (p = 0.02); increased heart rates, and increased ejection velocities in the LV outflow tract (p = 0.03, and p = 0.005, respectively, vs. Groups 1, 2, and 4) which pointed to an impairment of LV outflow. CONCLUSIONS: Symmetric LV hypertrophy and asymmetric septal hypertrophy are frequent in patients on maintenance hemodialysis. Predictors for LV hypertrophy were age and body mass index, and, particularly for asymmetric septal hypertrophy, age and hypertension duration. Volume withdrawal during hemodialysis may lead to symptomatic hypotension due to dynamic obstruction in some patients with severe asymmetric septal hypertrophy.