Histological gap between ablation lesions detected by phased array intracardiac echocardiography.
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BACKGROUND: The recent introduction of the automated cardiac flow measurement (ACM) method, using spatiotemporal integration of the Doppler velocity profile, provides a quick and accurate automated calculation of cardiac output. OBJECTIVE: To evaluate the ACM method against oximetry during cardiac catheterisation for estimating the Qp/Qs (pulmonary to systemic flow) ratio in patients with an atrial septal defect. METHODS: Left and right ventricular stroke volume (LVSV, RVSV) were calculated by ACM in 22 patients with an atrial septal defect who underwent cardiac catheterisation and in 11 patients without heart disease (control group). With ACM, the Qp/Qs ratio was estimated from RVSV divided by LVSV. In the patients with an atrial septal defect, the Qp/Qs ratio was assessed by oximetry at the time of cardiac catheterisation. RESULTS: There was a good correlation between LVSV and RVSV obtained by ACM in the control group (r = 0.98, y = 0.97x + 0.25, SEE = 2.9 ml). The mean difference between LVSV and RVSV by ACM was -1.25 (2.76) ml. The Qp/Qs ratio obtained by ACM in the control group was 0.98 (0.06). The Qp/Qs ratio in patients with an atrial septal defect was significantly higher than in the control group (3.11 (1.20), p < 0.001). ACM determination of the Qp/Qs ratio correlated well with oximetry determination (r = 0.86, y = 0.75x + 0.55, SEE = 0.64). The mean difference between ACM and oximetry for the measurement of the Qp/Qs ratio was -0.28 (0.69). CONCLUSIONS: The newly developed ACM method is clinically useful for non-invasive automated estimations of the Qp/Qs ratio in patients with an atrial septal defect.
OBJECTIVE: To explore the application of a new 10 French intracardiac echocardiography (ICE) catheter with phased array and Doppler capable transducer for the assessment of epicardial and intramyocardial coronary blood flow. METHODS: The coronary arteries were detected by cross sectional imaging in seven closed chest dogs, and coronary blood flow visualised by colour Doppler. Blood flow velocities were recorded by pulsed Doppler at baseline for reproducibility of repeated measurements, and during hyperaemia for coronary flow reserve measurements. Comparisons were made with Doppler guide wire data obtained simultaneously. Intramyocardial coronary artery blood flow was assessed by colour flow mapping, and the blood flow velocities recorded using pulsed Doppler at baseline and during hyperaemia. RESULTS: Seven left main, six left anterior descending, seven left circumflex, and five right coronary arteries were visualised in the seven animals by cross sectional or colour Doppler imaging. Repeated measurements of coronary flow velocity showed a good correlation (mean diastolic velocity, r = 0.93, n = 22, p < 0.0001; peak diastolic velocity, r = 0.96, n = 22, p < 0.0001, respectively). Intraobserver/interobserver variability was satisfactorily low. Coronary flow reserve from ICE correlated highly with the value obtained from the Doppler guide wire (r = 0.90, n = 26, p < 0.0001). Intramyocardial coronary blood flow was identified in all seven dogs, and flow velocities were recorded at baseline and during hyperaemia in four animals. CONCLUSIONS: This new ICE catheter provides high quality diagnostic resolution. It is useful for coronary blood flow assessment.
BACKGROUND: The production of peroxynitrite, an extremely potent oxidant, is increased in inflammatory lung disease. It is therefore important to measure antioxidant activity against peroxynitrite in epithelial lining fluid to examine the physiological effects of peroxynitrite in the airways of patients with asthma. This study was designed to determine whether peroxynitrite inhibitory activity in induced sputum is correlated with clinical characteristics and airway inflammatory indices in asthmatic patients. METHODS: Inflammatory indices were measured in induced sputum from 25 patients with asthma and 12 normal control subjects. Peroxynitrite inhibitory activity was also measured by monitoring rhodamine formation in sputum samples. RESULTS: Peroxynitrite inhibitory activity in induced sputum was significantly lower in asthmatic patients (52.4 (24.5)%) than in normal control subjects (92.1 (3.9)%, p<0.0001). Its activity was significantly correlated with forced expiratory volume in 1 second (FEV(1)) % predicted (r=0.774, p<0.0001) and bronchial hyperreactivity to methacholine (r=0.464, p=0.023). There was a significant negative correlation between peroxynitrite inhibitory activity and the degree of eosinophilic airway inflammation (% eosinophils, r=-0.758, p<0.0001; eosinophil cationic protein, r=-0.780, p<0.0001). CONCLUSIONS: Decreased peroxynitrite inhibitory activity occurs in induced sputum of asthmatic patients. Since even in patients with stable asthma the airway lining fluid lacks peroxynitrite inhibitory activity, large amounts of peroxynitrite, which are further increased during an acute asthma attack, would not be completely inactivated and asthmatic airways might have markedly increased susceptibility to peroxynitrite induced airway injury.
CONTEXT: Recent studies have shown that passive smoking is a risk factor for ischemic heart disease and may be associated with vascular endothelial dysfunction. The acute effects of passive smoking on coronary circulation in nonsmokers are not known. OBJECTIVE: To determine the acute effects of passive smoking on coronary circulation using coronary flow velocity reserve (CFVR), assessed by noninvasive transthoracic Doppler echocardiography. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional study conducted from September 2000 to November 2000 among 30 Japanese men (mean age, 27 years; 15 healthy nonsmokers and 15 asymptomatic active smokers) without history of hypertension, diabetes mellitus, or hyperlipidemia. MAIN OUTCOME MEASURES: Coronary flow velocity reserve, calculated as the ratio of hyperemic to basal coronary flow velocity induced by intravenous infusion of adenosine triphosphate and measured in each participant before and after a 30-minute exposure to environmental tobacco smoke. RESULTS: Heart rate and blood pressure responses to adenosine triphosphate infusion were not affected by passive smoking exposure in either group. Passive smoking exposure had no effect on basal coronary flow velocity in either group. Mean (SD) CFVR in nonsmokers was significantly higher than that in active smokers before passive smoking exposure (4.4 [0.91] vs 3.6 [0.88], respectively; P =.02), while CFVR after passive smoking exposure did not differ between groups (P =.83). Passive smoking exposure significantly reduced mean (SD) CFVR in nonsmokers (4.4 [0.91] vs 3.4 [0.73], respectively; P<.001). CONCLUSIONS: Passive smoking substantially reduced CFVR in healthy nonsmokers. This finding provides direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.
Coronary flow velocity can be measured by transthoracic Doppler echocardiography (TTDE). The purpose of this study was to detect severe coronary stenosis using the diastolic-to-systolic flow velocity ratio (DSVR) determined by TTDE at rest. We prospectively examined 190 consecutive patients with angina pectoris for whom coronary angiography was planned. Doppler spectral tracings of flow velocity in the distal left anterior descending artery were recorded by TTDE at rest. The mean and peak DSVR values were computed using mean and peak coronary flow velocities. DSVR measurement by TTDE at rest was performed within 24 hours before angiography, and in patients who underwent coronary intervention it was performed again within 48 hours after the intervention. The success rate for DSVR measurement by TTDE was 83.7%. There were significant differences in peak DSVR and mean DSVR between the patients with severe stenosis (percent diameter stenosis >85%) and those without severe stenosis (1.3 +/- 0.4 vs 1.9 +/- 0.50 and 1.2 +/- 0.4 vs 1.8 +/- 0.5, respectively; p <0.0001). In the 17 patients with successful intervention, DSVR was significantly increased after the procedure (mean 1.2 +/- 0.1 vs 2.0 +/- 0.2; peak 1.2 +/- 0.2 vs 2.0 +/- 0.3, respectively; p <0.0001). For percent diameter stenosis >85%, the best cut-off points were 1.6 for peak DSVR (sensitivity 79.0%, specificity 75.7%) and 1.5 for mean DSVR (sensitivity 77.0%, specificity 77.9%). Thus, DSVR measurement by TTDE is a simple, noninvasive method for detection of severe coronary stenosis at rest.
BACKGROUND: There is accumulating data that acute coronary syndromes relate to recent onset activation of inflammation affecting atherosclerotic plaques. Increased blood levels of oxidized low density lipoprotein (ox-LDL) could play a role in these circumstances. METHODS AND RESULTS: Ox-LDL levels were measured in 135 patients with acute myocardial infarction (AMI; n=45), unstable angina pectoris (UAP; n=45), and stable angina pectoris (SAP; n=45) and in 46 control subjects using a sandwich ELISA method. In addition, 33 atherectomy specimens obtained from a different cohort of patients with SAP (n=10) and UAP (n=23) were studied immunohistochemically for ox-LDL. In AMI patients, ox-LDL levels were significantly higher than in patients with UAP (P<0.0005) or SAP (P<0.0001) or in controls (P<0.0001) (AMI, 1.95+/-1.42 ng/5 microgram LDL protein; UAP, 1.19+/-0.74 ng/5 microgram LDL protein; SAP, 0.89+/-0.48 ng/5 microgram LDL protein; control, 0.58+/-0.23 ng/5 microgram LDL protein). Serum levels of total, HDL, and LDL cholesterol did not differ among these patient groups. In the atherectomy specimens, the surface area containing ox-LDL-positive macrophages was significantly higher in patients with UAP than in those with SAP (P<0.0001). CONCLUSIONS: This study demonstrates that ox-LDL levels show a significant positive correlation with the severity of acute coronary syndromes and that the more severe lesions also contain a significantly higher percentage of ox-LDL-positive macrophages. These observations suggest that increased levels of ox-LDL relate to plaque instability in human coronary atherosclerotic lesions.
Percutaneous transluminal coronary angioplasty (PTCA) is routinely performed using the femoral approach. However, recent reports suggest the usefulness of the brachial approaches for patients for whom the femoral approach is impossible due to peripheral vessel disease or to shortened postoperative rest times. However, some reports have revealed that the incidence of vascular complications undergoing brachial-approach PTCA may be higher than those with the femoral approach, possibly due to relatively higher dose of heparin. Accordingly, in this study we evaluated the efficacy and safety of PTCA using the brachial approach and low-dose heparin, hypothesizing that lowering the heparin dose might result in reduced vascular complications. The study population of patients admitted for angina pectoris consisted of 217 subjects (221 lesions) who underwent brachial-approach PTCA and 102 subjects (115 lesions) who underwent PTCA via the femoral approach. Both groups were monitored for complications. There were no significant differences in patient or lesion characteristics between the groups. Incidence of vascular complications tended to be lower in the brachial group than in the femoral group (1.8% vs. 3.5%), although the difference did not reach statistical significance. Use of anodynes was also significantly lower in the brachial group (3.6% vs. 33%). PTCA from the brachial approach with low-dose heparin is as safe and effective a strategy as compared with the femoral approach with standard dose of heparin.
Recent studies have shown that oxidative stress plays an important role in cardiovascular diseases. NADPH oxidase is one of the major sources of superoxide anions and a candidate for the initiation and development of atherosclerosis, which involves the remodeling of vasculature. However, the relevance of NADPH oxidase in ventricular remodeling has not been well-characterized. This is the first report showing that the expression of p22-phox and gp91-phox, essential components of NADPH oxidase, are increased in the infarcted sites after myocardial infarction. The levels of thiobarbituric acid reactive substance, which indicates the lipid peroxidation level, and nuclear factor-kappaB (NF-kappaB) DNA binding activity are also increased in infarcted sites. Our results suggest that the increased expression of NADPH oxidase may have an effect on left ventricular remodeling by increasing the redox-sensitive NF-kappaB DNA binding activity as well as the lipid peroxidation level.
There have been many studies concerning the hemodynamics and physiological mechanisms in ischemic heart disease, little is known about molecular mechanisms during myocardial ischemia in in vivo study. As the signal transduction pathway responsible for myocardial hypertrophy and apoptosis, janus kinase (JAK) and signal transducers and activators of transcription (STAT) are suggested to play an important role. However, whether in vivo activation of JAK-STAT pathway occurs during myocardial ischemia is still unknown. The purpose of this study was to determine whether myocardial JAK or STAT is activated in ischemic heart, and to evaluate the angiotensin blockade on the pathway. Myocardial infarction was produced by ligation of the coronary artery in Wistar rats. After myocardial ischemia, we analysed both activated levels and total amounts of JAK1, JAK2, STAT1 and STAT3 by Western blot analyses at 0, 5, 15, 30, 60, 120 and 240 min. Compared with JAK activities at 0 min, JAK1 activities were significantly increased at 60 and 120 min (3.0- and 3.7-fold, respectively, P<0.01). JAK2 and STAT1 activities of ischemic myocardium were unchanged through the time course. STAT3 activities were increased at 5 min (3.3-fold, P<0.01) and markedly enhanced at 30, 60 and 120 min (4.6-, 7.7- and 8.7-fold, respectively, P<0.01). Pretreatment with imidapril (ACE inhibitor) and candesartan cilexitil (AT1 receptor antagonist) significantly prevented the increase in the phosphorylation of JAK1 at 120 min and STAT3 at 30 and 120 min. Sis-inducing factor (SIF) DNA complex was supershifted by specific anti-STAT3 antibody, indicating that increased SIF complex at least contained activated STAT3 proteins in ischemic myocardium. Imidapril and candesartan cilexitil inhibited the activation of SIF DNA binding at 1 day after coronary ligation. In conclusion, we showed that JAK1 and STAT3 were activated by ischemia from the basal activities in in vivo rat myocardial ischemia model. Imidapril and candesartan cilexitil prevented the increase in phosphorylated JAK1 and STAT3, thereby suggesting that angiotensin II, especially angiotensin II type I receptor, partially mediates activation of myocardial JAK-STAT pathway in acute myocardial ischemia.
Inhibition of the renin-angiotensin system has been shown to prevent left ventricular remodeling after myocardial infarction. However, the effect of angiotensin on the signal transduction pathway of left ventricular remodeling after myocardial infarction is as yet unknown. The purpose of this study was to measure myocardial MAPKs and AP-1, NF- kappa B, and Sp-1 DNA-binding activities after myocardial infarction. Moreover, we evaluated the effects of angiotensin converting enzyme (ACE) inhibitor and angiotensin receptor blocker (ARB) on signal transduction pathway. Myocardial infarction was produced by ligation of the coronary artery in Wistar rats. Temocapril (ACE inhibitor) (3 and 30 mg/kg/day) and candesartan cilexitil (ARB) (1 and 10 mg/kg/day) were orally administered once a day. After ligation of the left descending coronary artery, JNKs (p46JNK and p55JNK) increased to 2.0- (P<0.01) and 2.8-fold (P<0.01) at 7 days, respectively. ERKs (p44ERK and p42ERK) and p38 activities did not increase significantly. AP-1 and NF- kappa B binding activities increased at 5 days, reached their peak 2.2- and 2.0-fold at 7 days. Sp-1 did not change. ACE inhibitor and ARB inhibited JNKs, NF- kappa B and AP-1 activities. Increased JNKs, AP-1, NF- kappa B, and Sp-1 DNA-binding activities were suppressed by both drugs in the infarcted region. Doppler-echocardiography showed that ACE inhibitor and ARB prevented the dilatation of left ventricular cavity at 14 days and improved diastolic filling pattern. JNKs, AP-1 and NF- kappa B activation in myocardial infarcted rats could be responsible for left ventricular remodeling after myocardial infarction and angiotensin may be related to the activation of these signals.
Our aim was to investigate the usefulness of helical CT during selective angiography (CT arteriography) in pretreatment assessment of unruptured intracranial aneurysms. We studied 47 unruptured aneurysms in 34 prospectively recruited patients for whom endovascular embolisation was initially considered. As pretreatment assessment, we performed rotational digital subtraction angiography (DSA) followed by CT arteriography. The findings on axial source images (axial images) and reconstructed three-dimensional CT angiography (3D-CTA) of CT arteriography were compared to those of rotational DSA, with particular attention to the neck of the aneurysm and arterial branches adjacent to it. Information provided by CT arteriography was more useful than that of rotational DSA as regards the neck in 25 (53%) of 47 cases and as regards branches in 18 (49%) of 37 aneurysms. On axial images, small arteries such as the anterior choroidal artery were seen in some cases. CT arteriography can provide valuable additional information about unruptured aneurysms, which cannot be obtained by rotational DSA alone. This technique is useful for obtaining anatomical information about aneurysm anatomy and for deciding the therapeutic strategy.
OBJECTIVES: We evaluated the value of coronary flow reserve (CFR), as determined by transthoracic Doppler echocardiography (TTDE), for physiologic assessment of coronary artery stenosis severity, and we compared TTDE measurements with those obtained by exercise thallium-201 (Tl-201) single-photon emission computed tomography (SPECT). BACKGROUND: Coronary flow reserve measurements by TTDE have been reported to be useful for assessing angiographic left anterior descending coronary artery (LAD) stenosis. However, discrepancies exist between angiographic and physiologic estimates of coronary lesion severity. METHODS: We studied 36 patients suspected of having coronary artery disease. The flow velocity in the distal LAD was measured by TTDE both at rest and during intravenous infusion of adenosine. Coronary flow reserve was calculated as the ratio of hyperemic to basal peak (peak CFR) and mean (mean CFR) diastolic flow velocities. The CFR measurements by TTDE were compared with the results of Tl-201-SPECT. RESULTS: Complete TTDE data were acquired for 33 of 36 study patients. Of these 33 patients, Tl-201-SPECT confirmed reversible perfusion defects in the LAD territories in 12 patients (group A). Twenty-one patients had normal perfusion in the LAD territories (group B). Peak CFR and mean CFR (mean value +/- SD) were 1.5 +/- 0.6 and 1.5 +/- 0.7 in group A and 2.8 +/- 0.8 and 2.7 +/- 0.7 in group B, respectively. Both peak and mean CFR < or = 2.0 predicted reversible perfusion defects, with a sensitivity and specificity of 92% and 90%, respectively. CONCLUSIONS: Noninvasive measurement of CFR by TTDE provides data equivalent to those obtained by Tl-201-SPECT for physiologic estimation of the severity of LAD stenosis.
OBJECTIVES: The purpose of this study was to evaluate the feasibility of measuring coronary flow velocity (CFV) by transthoracic Doppler echocardiography (TTDE) in the left anterior descending coronary artery (LAD) during contrast-enhanced dobutamine stress echocardiography (DSE). We also assessed the value of TTDE for detecting stress-induced myocardial ischemia in the LAD territory. BACKGROUND: Noninvasive assessment of both CFV and wall motion during DSE would enhance the diagnostic accuracy of DSE. METHODS: One hundred forty-four consecutive patients underwent CFV recording in the distal LAD by TTDE during contrast-enhanced DSE. Regional wall motion score index (WMSI) in the LAD territory and CFV ratio at peak stress (CFV ratio peak), defined as a ratio of CFV at peak stress to basal CFV, were obtained. RESULTS: Coronary flow velocity was successfully recorded in 129 patients (90%) at baseline and during dobutamine infusion. Mean value of CFV ratio peak was 2.39 +/- 0.83 (range: 0.84 to 4.40). There was good correlation between WMSI at peak stress and CFV ratio peak (r = 0.62, p < 0.001). Coronary flow velocity ratio peak was significantly lower in patients who developed stress-induced wall motion abnormality (WMA) in the LAD territory than it was in those patients without WMA (1.51 +/- 0.51 vs. 2.76 +/- 0.65, p < 0.001). A CFV ratio peak <2.1 had a sensitivity of 92% and a specificity of 86% for detecting the presence of stress-induced WMA. CONCLUSIONS: Assessment of CFV in the distal LAD during DSE is feasible in the majority of cases and provides a CFV ratio for detecting stress-induced myocardial ischemia in the LAD territory.
OBJECTIVES: The purpose of this study was twofold: 1) to examine the relationship between menstrual cycle and coronary flow velocity reserve (CFVR) in young healthy women, and 2) to evaluate the effect of hormone replacement therapy by estrogen on CFVR in postmenopausal women, using transthoracic color Doppler echocardiography (TTCDE). BACKGROUND: Although the incidence of cardiovascular disease is lower in women before menopause compared with men, postmenopausal women have an incidence of coronary artery disease similar to that of men of the same age. This is mainly dependent upon estrogen deficiency. However, no clinical report has yet examined the effect of estrogen on CFVR, which is one index of coronary microcirculation. METHODS: We examined 15 male and both 15 premenopausal and 10 postmenopausal female healthy volunteers. We measured coronary flow velocity of the left anterior descending coronary artery at baseline and hyperemic conditions during adenosine triphosphate infusion by TTCDE and determined CFVR. Each premenopausal woman was studied two times (menstrual [M] and follicular [F] phases) in one menstrual cycle. Fifteen men were also studied at a time corresponding to women's menstrual cycle. The postmenopausal women were studied before and two hours after oral administration of conjugated estrogen (CE). RESULTS: Serum 17beta-estradiol level in premenopausal women increased in the F phase and decreased to the same levels as in men, as in the M phase and as in postmenopausal women (123 +/- 9 pg/ml vs. 28 +/- 6 pg/ml, 25 +/- 9 pg/ml and 19 +/- 11 pg/ml; p < 0.0001, respectively). The CFVR increased in the F phase compared with that in the M phase (4.8 +/- 0.4 vs. 3.7 +/- 0.8, p < 0.0001). We found that CFVR in men remained unchanged (3.7 +/- 0.6 vs. 3.8 +/- 0.5). After CE administration, CFVR increased compared with baseline in postmenopausal women (4.1 +/- 0.8 vs. 3.4 +/- 0.8, p < 0.005). CONCLUSIONS: In premenopausal women, CFVR determined by TTCDE varied during the menstrual cycle, and in postmenopausal women, CFVR increased after acute estrogen replacement.
BACKGROUND: Although it was reported that pulse pressure of the peripheral artery could differentiate patients with coronary heart disease (CHD) from those without CHD, it is not known whether pulsatility of the ascending aortic pressure waveform differentiates patients with CHD from those without CHD. The purpose of this study was to evaluate whether the pulsatility of ascending aortic pressure is associated with an increased risk of CHD. METHODS: For this study, we enrolled 293 subjects who had chest pain, normal contractions, no local asynergy, and no history of myocardial infarction. We measured the ascending aortic pressure using a fluid-filled system. To quantify the relative magnitude of the pulsatile to mean artery pressure, we normalized the pulse pressure to the mean pressure and referred to this value as the fractional pulse pressure (PPf). We investigated the association between the PPf and the risk of CHD. RESULTS: The PPf of the ascending aorta was associated with an increased risk of CHD. The multiple-adjusted odds ratio of CHD was 2.93 (95% CI, 1.44 to 5.94) for the middle tertile of the PPf level and was 3.93 (95% CI, 1.74 to 8.85) for the highest tertile compared with the lowest tertile. CONCLUSION: Ascending aortic pulsatility is related to an increased risk of CHD.
The purpose of this study was to examine the effect of diltiazem on cardiac function and neurohumoral factors (BNP, epinephrine, norepinephrine) after reperfused myocardial infarction without congestive heart failure (Killip class I). On the first day after myocardial infarction following reperfusion therapy patients were randomly assigned to diltiazem treatment (group 1, n=33) or no treatment (group 2, n=39). We then performed echocardiographic examinations on the patients and measured heart rate, mean blood pressure and neurohormones (BNP, epinephrine and norepinephrine). Follow-up evaluations of echocardiography were performed at 4 and 12 weeks and of neurohormones at 1 and 4 weeks after acute myocardial infarction. The highest peaks of plasma BNP, epinephrine, and norepinephrine levels were observed before treatment and decreased with time in both groups. After 4 weeks the level of plasma BNP in the diltiazem treatment group was lower than in the no treatment group [55+/-3 pg/mL vs 85+/-5 pg/mL (P < 0.05)]. Other neurohormones did not differ between groups. Fractional shortening (FS) and ejection fraction (EF)improved after myocardial infarction in both groups, but significantly more in the diltiazem group (P < 0.05) after 12 weeks of treatment. Changes in BNP correlated significantly with changes in left ventricular end systolic volumes, FS and EF. In this study, diltiazem significantly improved systolic function and reduced the level of plasma BNP after myocardial infarction, which suggest that diltiazem may have a beneficial effect on myocardial infarction without congestive heart failure.
Quantitative assessment of left ventricular ejection fraction is an essential component of cardiac evaluation. We performed real-time 3-dimensional echocardiography in 56 consecutive patients who underwent multigated radionuclide angiography. Thirteen patients were excluded for the following reasons: 5 for large size of left ventricle required for image acquisition, 5 for suboptimal image quality in real-time 3-dimensional echocardiography, and 3 for atrial fibrillation. Finally, we compared left ventricular ejection fraction assessed by real-time 3-dimensional echocardiography and conventional 2-dimensional echocardiography with that obtained by multigated radionuclide angiography in 43 patients. Left ventricular ejection fraction was determined by real-time 3-dimensional echocardiography with the use of parallel plane-disks and sector plane-disks summation methods. A good correlation was obtained between both real-time 3-dimensional echocardiography methods and multigated radionuclide angiography (r = 0.87 and 0.90, standard error of estimate = 3.7% and 4.2%), whereas the relation between the 2-dimensional echocardiography method and radionuclide angiography demonstrated a significant departure from the line of identity (P <.001). In addition, interobserver variability was significantly lower (P <.05) for the real-time 3-dimensional echocardiography methods than that by the 2-dimensional echocardiography method. Real-time 3-dimensional echocardiography may be used for quantification of left ventricular function as an alternative to conventional methods in patients with adequate image quality.