Shimon A. Reisner

Superiority of visual versus computerized echocardiographic estimation of radionuclide left ventricular ejection fraction

An optimal method for determining left ventricular ejection fraction (LVEF) by echocardiography should be rapid, reliable, and widely applicable in order to be utilized routinely in a busy clinical laboratory. Most methods reported in the literature are reliable in selected, high-quality echocardiograms. Most require off-line computer analysis and are time-consuming and poorly suited to the routine of a busy laboratory. We compared in a blinded manner several echocardiographic methods of LVEF determination with the ejection fraction obtained by equilibrium radionuclide angiography (ERNA) in 44 patients unselected for image quality. Echocardiographic methods included: [1] cubed M-mode formula; [2] Teichholz M-mode formula; [3] subjective estimation of LVEF from two-dimensional echocardiographic videotape; [4] area-length method in one four-chamber view; [5] average of area-length method in three four-chamber views; [6] average of area-length method in four-chamber and two-chamber views (one beat each); [7] subjective estimation from stored videoloop of four-chamber and two-chamber view. In 30 cases M-mode tracings were available for analysis. In only 23 of the 44 patients were the apical views suitable for quantitative analysis. The ERNA ejection fraction was 44 +/- 17% (mean +/- 1 SD). The best echocardiographic correlation with ERNA ejection fraction in each patient subgroup studied was obtained by method 3. We concluded that subjective analysis of the videotaped study by an experienced cardiologist/echocardiographer provided the best estimation of ERNA ejection fraction. More time-consuming and costly computer techniques yielded a worse estimate.

Functional Tricuspid Regurgitation in Patients With Pulmonary Hypertension: Is Pulmonary Artery Pressure the Only Determinant of Regurgitation Severity?

BACKGROUND Pulmonary hypertension is a common cause of functional tricuspid regurgitation (TR), but other factors play a role in determining TR severity. The objectives of our study were to determine the distribution of TR severity in relation to pulmonary artery systolic pressure (PASP) and to define the determinants of TR severity. METHODS The echocardiographic reports and selected echocardiographic studies of patients with echocardiographic estimation of PASP were reviewed. Patients with organic tricuspid valve (TV) disease were excluded from the analysis. RESULTS Among 2,139 patients, the frequency of moderate or severe TR was progressively greater in patients with higher PASP. Nevertheless, TR was only mild in a substantial proportion of patients with high PASP (mild TR in 65.4% of patients with PASP 50-69 mm Hg and in 45.6% of patients with PASP >or= 70 mm Hg). By multivariate analysis, age, female gender, PASP (odds ratio, 2.26 per 10-mm Hg increase; 95% confidence interval, 1.95 to 2.61), pacemaker lead, right atrial (RA) and right ventricular enlargement, left atrial enlargement, and organic mitral valve disease were independently associated with greater degrees of TR. In patients with PASP >or= 70 mm Hg, RA size, tricuspid annular diameter, and TV tethering area were greater in patients with greater degrees of TR. CONCLUSIONS PASP is a strong determinant of TR severity, but many patients with pulmonary hypertension do not exhibit significant TR. In addition to PASP, demographic characteristics, mechanical factors, remodeling of the right heart cavities, and other factors (possibly reflecting the presence of atrial fibrillation or occult organic TV disease) are predictive of TR severity.

Cardiac involvement in patients with primary antiphospholipid syndrome

To evaluate cardiac involvement in primary antiphospholipid syndrome, two-dimensional and Doppler echocardiographic studies were performed in 34 consecutive patients with this syndrome. All patients had an increased level of serum anticardiolipin antibodies with no evidence of malignancy or systemic lupus erythematosus. The clinical manifestations of primary antiphospholipid syndrome were arterial thrombosis in 14 patients, venous thrombosis in 6 and recurrent fetal loss in 14. Valvular lesions were observed on two-dimensional echocardiography in 11 patients (32%) (9 women and 2 men), aged 24 to 57 years (mean +/- 1 SD 36 +/- 10). Abnormal echocardiographic findings were observed in 9 (64%) of 14 patients with arterial thrombosis versus 1 (17%) of 6 patients with venous thrombosis and 1 (7%) of 14 patients with recurrent fetal loss. The most common echocardiographic abnormality was mitral leaflet thickening, found in five patients; this was associated with mitral regurgitation in three and with combined mild mitral stenosis and regurgitation in one patient. Localized subvalvular mitral thickening was observed in one patient and calcification of the anulus in another. Aortic valve thickening was observed in two patients, one of whom also had a moderate degree of aortic regurgitation. Vegetation-like lesions on the mitral or aortic valve were found in two patients. It is concluded that valvular lesions are commonly found in primary antiphospholipid syndrome, particularly when the syndrome is manifested by peripheral arterial thrombosis. The location and appearance of valvular lesions in this syndrome are heterogeneous. Most patients have no clinically significant valvular disease. Two-dimensional and Doppler echocardiographic studies are often informative in these patients.

Intravenous contrast echocardiography with use of sonicated albumin in humans: Systolic disappearance of left ventricular contrast after transpulmonary transmission☆

The transmission of echocardiographic contrast medium and the cyclic changes in left ventricular videodensity during transpulmonary contrast echocardiography were investigated in nine adult volunteers with the use of intravenous injections of sonicated albumin (microbubble size 5.2 +/- 2.6 microns). Right and left ventricular and myocardial contrast were quantitated by videodensitometric analysis. The injections caused no symptoms, and no hemodynamic or electrocardiographic changes were observed. All injections resulted in right ventricular contrast. Mean peak right ventricular videodensity was 75 +/- 48 at end-diastole and 61 +/- 36 gray scale U/pixel at end-systole (p less than 0.05). Seventy-eight percent of injections resulted in left ventricular contrast with a mean peak videodensity of 21 +/- 33 gray scale U/pixel. Early systole was associated with a rapid decrease in left ventricular contrast intensity with near total disappearance of contrast by end-systole (from 23 +/- 33 and 17 +/- 23 U/pixel at end-diastole to 6 +/- 10 and 3 +/- 2 at end-systole at the left ventricular base and apex, respectively; p less than 0.05). None of the injections resulted in myocardial contrast enhancement by visual or quantitative analysis. Thus, left ventricular contrast echocardiography can be achieved after intravenous injections of sonicated albumin. Transpulmonary left ventricular contrast echocardiography is associated with near total disappearance of contrast during systole. This may be secondary to the destruction of microbubbles by the high left ventricular systolic pressure. These findings may help explain the limited success of this technique thus far for myocardial perfusion imaging.

Myocardial perfusion imaging by contrast echocardiography with use of intracoronary sonicated albumin in humans.

Sonicated albumin has been proposed as a near ideal echocardiographic contrast agent with little myocardial toxicity or hemodynamic effect. Its use has not yet been reported in humans, partly because of difficulties in preparation. With use of the newly modified sonication method, 10 ml of 5% albumin was sonicated for 75 s with a 5.0 ml slow infusion of air. This resulted in microbubbles with a mean diameter (+/- SD) of 5 +/- microns). Fourteen patients undergoing routine coronary angiography were studied. One patient had normal coronary arteries; the other 13 had significant coronary artery disease. In a subgroup of nine patients, sonicated albumin and sonicated diatrizoate meglumine sodium (microbubble diameter 9 +/- 3 microns) were injected several minutes apart, using the same technique. Videodensity-time curves were obtained from a region of interest in the myocardium. Corrected peak contrast intensity (baseline contrast intensity subtracted from peak contrast intensity, gray scale U/pixel) for sonicated albumin and for sonicated diatrizoate meglumine sodium was 51 +/- 26 and 52 +/- 19, respectively (p = 0.89). Washout half-time (T1/2) for the two agents was 5.5 +/- 4.5 and 16.0 +/- 12.2 s, respectively (p = 0.01). One patient with unstable angina experienced transient chest pain after repeated albumin injections. No electrocardiographic changes, blood pressure changes or wall motion abnormalities were observed. Administered by intracoronary injection, sonicated 5% albumin is a safe and effective echocardiographic contrast agent for myocardial perfusion imaging, yielding excellent myocardial contrast with physiologic washout time.

Electroanatomic mapping of arrhythmogenic right ventricular dysplasia

OBJECTIVES We tested the hypothesis that spatial association of low-amplitude intracardiac electrograms can identify the presence, location and extent of dysplastic regions in arrhythmogenic right ventricular dysplasia (ARVD). BACKGROUND Arrhythmogenic right ventricular dysplasia is a right ventricular (RV) cardiomyopathy characterized pathologically by fibrofatty infiltration and clinically by a spectrum of arrhythmias, sudden cardiac death and RV failure. Diagnosis of ARVD still remains a clinical challenge. METHODS A three-dimensional electroanatomic mapping technique was used to map the RV of two groups of patients: 1) those with ARVD presenting with typical clinical, electrocardiographic and echocardiographic or magnetic resonance imaging (MRI) findings; and 2) those with structurally normal ventricles. RESULTS The dysfunctional RV area could be identified only in the first group and was characterized by the presence of discrete areas of abnormally low-amplitude electrograms. Hence, the normal voltage values observed in the control group (unipolar: 11.9 +/- 0.3 mV; bipolar: 4.6 +/- 0.2 mV [mean +/- SEM]) and in the nonaffected zones in the ARVD group (unipolar: 10.4 +/- 0.2 mV; bipolar: 4.6 +/- 0.2 mV) were reduced significantly (p < 0.05) in the dysplastic areas (unipolar: 3.3 +/- 0.1 mV; bipolar: 0.5 +/- 0.1 mV). The pathologic process mainly involved the RV anterolateral free wall, apex and inflow and outflow tracts and ranged from patchy areas to uniform and extensive involvement. Concordance between electroanatomic findings and MRI or echocardiographic findings was noted in all patients. CONCLUSIONS The pathologic substrate in ARVD can be identified by spatial association of low-amplitude endocardial electrograms, reflecting replaced myocardial tissue. The ability to accurately identify the presence, location and extent of the pathologic substrate may have important diagnostic, prognostic and therapeutic implications.

Pulmonary hypertension is an independent predictor of mortality in hemodialysis patients

Pulmonary hypertension in patients with end-stage renal disease on hemodialysis is a newly described entity. To determine its impact, we measured selected clinical variables in the survival of 127 hemodialysis patients. Overall, pulmonary hypertension was found in 37 of these patients; it was already prevalent in 17 of them before initiation of dialysis and was associated with severe cardiac dysfunction. In the other 20 it developed after dialysis began, without obvious cause. These two subgroups of patients had similar survival curves, which were significantly worse in comparison to those without pulmonary hypertension. Following the initiation of hemodialysis, 20 patients with otherwise matched clinical variables survived significantly longer than the 20 who developed pulmonary hypertension after dialysis began. With univariate analysis, significant hazard ratios were found for age at onset of hemodialysis therapy (1.7), valvular diseases (1.8), pulmonary hypertension prevalence before hemodialysis (3.6) and incident after hemodialysis (2.4) for predicting mortality. In a multivariable Cox proportional hazard model, the development of pulmonary hypertension both before and after initiation of hemodialysis had significantly increased odds ratios and remained an independent predictor of mortality. Our study shows the incidence of pulmonary hypertension, after initiation of hemodialysis therapy, is a strong independent predictor of mortality nearly equal to that associated with long-standing severe cardiac abnormalities.

Relation of Myocardial Mechanics in Severe Aortic Stenosis to Left Ventricular Ejection Fraction and Response to Aortic Valve Replacement

Decreased left ventricular (LV) longitudinal strain and increased circumferential LV strain have been demonstrated in patients with severe aortic stenosis (AS) and normal LV ejection fraction (LVEF). Biplane myocardial mechanics normalize after aortic valve replacement (AVR). This study objective was to examine LV mechanics before and soon after AVR in patients with AS and LV systolic dysfunction. Paired echocardiographic studies before and soon (7 ± 3 days) after AVR were analyzed in 64 patients with severe AS: 32 with normal LVEF (≥ 50%), 16 with mild to moderate LV dysfunction (LVEF <36% to 50%), and 16 with severe LV dysfunction (LVEF ≤ 35%). Longitudinal myocardial function was assessed from 3 apical views (average of 18 segments) and circumferential function was assessed at mid-LV and apical levels (average of 6 segments per view). Strain, strain rate, and mid-LV and apical rotations were measured using 2-dimensional velocity vector imaging. Before AVR (1) longitudinal strain was low in all patients and correlated with LVEF (ρ = 0.74, p <0.001), (2) mid-LV circumferential strain was supranormal in patients with normal LVEF and low in patients with low LVEF (ρ = 0.88, p <0.001), and (3) apical rotation was highest in patients with mild to moderate LV dysfunction. After AVR, LVEF increased in patients with LV dysfunction and myocardial mechanics partly normalized. In conclusion, compensatory mechanisms (high circumferential strain in patients with preserved LVEF and increased apical rotation in patients with mild to moderate LV dysfunction) were observed in patients with severe AS. Compensatory mechanics were lost in patients with severe LV dysfunction. AVR partly reversed these changes in patients with LV dysfunction.

Pulmonary Hypertension in Hemodialysis Patients: An Unrecognized Threat

Pulmonary hypertension (PH) is a progressive, fatal pulmonary circulatory disease that accompanies many conditions (including left to right side shunt) with compensatory elevated cardiac output. PH also complicates chronic hemodialysis (HD) therapy immediately after the creation of an arteriovenous (AV) access, even before starting HD therapy. It tends to regress after temporary AV access closure and after successful kidney transplantation. Affected patients have significantly higher cardiac output. This syndrome is associated with a statistically significant survival disadvantage. The laboratory hallmark of this syndrome is reduced basal and stimulatory nitric oxide (NO) levels. It appears that patients with end‐stage renal disease (ESRD) acquire endothelial dysfunction that reduces the ability of their pulmonary vessels to accommodate the AV access‐mediated elevated cardiac output, exacerbating the PH. Doppler echocardiographic screening of ESRD patients scheduled for HD therapy for the occurrence of PH is indicated. Early diagnosis enables timely intervention, currently limited to changing dialysis modality or referring for kidney transplantation.

Pulmonary hypertension in chronic dialysis patients with arteriovenous fistula: pathogenesis and therapeutic prospective

Purpose of reviewEnd-stage renal disease patients receiving chronic haemodialysis via arteriovenous access often develop various cardiovascular complications, including vascular calcification, cardiac-vascular calcification and atherosclerotic coronary disease. This review describes recently published studies that demonstrate a high incidence of pulmonary hypertension among patients with end-stage renal disease receiving long-term haemodialysis via a surgical arteriovenous fistula. Both end-stage renal disease and long-term haemodialysis via arteriovenous fistula may be involved in the pathogenesis of pulmonary hypertension by affecting pulmonary vascular resistance and cardiac output. Recent findingsMorbidity and mortality from cardiovascular disease are greatly increased in patients on maintenance haemodialysis therapy. Using Doppler echocardiography, we found a significant increase in cardiac output in 40% of chronic haemodialysis patients, probably related to the large arteriovenous access or altered vascular resistance as a result of the local vascular tone and function expressed by the imbalance between vasodilators such as nitric oxide, and vasoconstrictors such as endothelin-1. SummaryWe propose different potential mechanisms as explanations for the development of pulmonary hypertension. Hormonal and metabolic derangement associated with end-stage renal disease might lead to pulmonary arterial vasoconstriction and an increase in pulmonary vascular resistance. Pulmonary arterial pressure may be further increased by high cardiac output resulting from the arteriole–venous access itself, worsened by commonly occurring anaemia and fluid overload.