Circadian rhythms of atrioventricular conduction properties in chronic atrial fibrillation with and without heart failure.

OBJECTIVES: We examined the circadian variations in atrioventricular (AV) conduction properties during atrial fibrillation (AF) by a technique based on the Lorenz plot of successive ventricular response (VR) intervals and analyzed their relations with clinical features. BACKGROUND: The VR interval in chronic AF shows circadian variation, which is attenuated in patients with an increased risk of death. Although the VR interval is determined by the dynamic processes in the AV node randomly stimulated by rapid atrial activity, the circadian variations of the AV conduction properties related to this mechanism are unknown. METHODS: In 48 patients with chronic AF, Lorenz plots were generated on overlapping sequential segments of 512 VR intervals in 24-h ambulatory electrocardiograms. For each scatter plot, the 1.0-s intercept of the lower envelope (LE1.0) of the plot and the degree of scatter above the envelope (root mean square difference from the envelope [scattering index]) were measured for estimating AV node refractoriness and concealed AV conduction, respectively. RESULTS: In all patients, a significant circadian rhythm was observed for the average VR interval, LE1.0 and scattering index, with an acrophase occurring at night. The mesor, amplitude and acrophase of LE1.0 and the scattering index closely and independently correlated with the corresponding rhythm variables of the average VR interval (partial r2 0.98, 0.86 and 0.68 for LE1.0 and 0.98, 0.92 and 0.92 for scattering index). The amplitudes of these measures were lower in patients with congestive heart failure (CHF) even after adjustment for the effects of age, duration of AF, medications, left atrial diameter and blood pressure (p < 0.01 for all). CONCLUSIONS: These results suggest that 1) both AV node refractoriness and the degree of concealed AV conduction during AF may show a circadian rhythm; 2) the circadian rhythms of these properties may independently contribute to the circadian variation of the VR interval; and 3) these circadian rhythms may be attenuated in patients with CHF.

Changes of HDL subfraction concentration and particle size by intralipid in vivo.

The effects of the artificial triglyceride-phospholipid emulsion (10% intralipid) on HDL subfraction were studied in vivo. After a 14-h fast, subjects received intralipid via a 4-h infusion. Serum lipoproteins were analyzed before and at 4 and 6 h after the start of the infusion. At 4-h the following acute changes by infusion were observed. Triglyceride, phospholipid, free cholesterol, and esterified cholesterol in chylomicrons and VLDL increased. HDL2 as well as triglyceride, phospholipid, free cholesterol and protein within the HDL2 increased, while HDL3 decreased. An increase in HDL3 triglyceride was observed. The masses of apo A-I and A-II in the HDL2 density interval rose while these parameters fell in HDL3. There were decreases of apo C-II and C-III in the HDL subfractions and elevations in chylomicrons and VLDL. The particle size of the HDL subfractions increased. However, most of these acute changes at 4 h tended to disappear by 6 h. These results suggest that there is exchange of lipids and reversible transfer of apo C-II and C-III between HDL subfractions and intralipid, and conversion of HDL3 to HDL2 followed by the reverse conversion of HDL2 to HDL3 as the synthetic emulsion is cleared from the plasma.

Clinical significance of reverse redistribution on 24-hour delayed imaging of exercise thallium-201 myocardial SPECT: comparison with myocardial fluorine-18-FDG-PET imaging and left ventricular wall motion.

UNLABELLED: Clinical significance of reverse redistribution on 24-hr delayed images after exercise 201Tl myocardial SPECT was investigated in 16 patients with recent myocardial infarction. METHODS: Findings of 24-hr delayed 201Tl SPECT imaging were compared with those of glucose-loaded 18F-fluorodeoxyglucose (FDG) imaging by myocardial PET and with left ventricular wall motion obtained by bi-plane contrast left ventriculography. In each patient, transaxial thallium images and corresponding 18F-FDG images were divided into five ROIs. RESULTS: Reverse redistribution was found in 15 of 80 regions. The mean FDG activity score in regions with reverse redistribution was significantly lower than that in regions having normal or slightly decreased thallium activity on 24-hr delayed imaging; it was significantly higher than that in regions having severely decreased or no thallium activity on 24-hr delayed imaging. The mean wall motion score in regions with reverse redistribution was significantly lower than in regions with normal or slightly decreased thallium activity, however, it was significantly higher than that in regions with moderately or more decreased thallium activity. CONCLUSION: These findings demonstrate that in regions showing reverse redistribution on 24-hr delayed 201Tl imaging, myocardial exogenous glucose utilization and left ventricular wall motion had deteriorated, but were not on a level with the scar.

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.

Short- and long-term effects of cigarette smoking on heart rate variability.

The short- and long-term effects of cigarette smoking on autonomic cardiac regulation were investigated by power spectral analysis of heart rate variability under controlled respiration (15/min). The short-term effects were examined in 9 smokers without evidence of cardiopulmonary disorders after an overnight abstinence from smoking. The heart rate spectral component reflecting the respiratory sinus arrhythmia (0.25 Hz), a quantitative index of vagal cardiac control, decreased 3 minutes after smoking 1 cigarette (p = 0.0061) and the component reflecting Mayer wave sinus arrhythmia (0.04 to 0.15 Hz), which includes sympathetically mediated activity, increased after 10 to 17 minutes (p = 0.0124). The long-term effects were examined in 81 normal subjects comprising 25 nonsmokers, 31 moderate (1 to 24 cigarettes/day) smokers and 25 heavy (greater than 25 cigarettes/day) smokers after an overnight abstinence. Although the magnitude of the Mayer wave component was unaffected by the smoking status, the respiratory component in the supine position was smaller in the young (less than or equal to 30 years) heavy smokers than in the young nonsmokers or moderate smokers (p = 0.0078). Also, postural changes in the components, a decrease in the respiratory component and an increase in the Mayer wave component with standing, were observed in the nonsmokers but not in the heavy smokers. These results suggest that smoking causes an acute and transient decrease in vagal cardiac control, and that heavy smoking causes long-term reduction in vagal cardiac control in young people and blunted postural responses in autonomic cardiac regulation.

Accuracy of assessment of cardiac vagal tone by heart rate variability in normal subjects.

The correlations of 11 indexes of heart rate variability were examined with pharmacologically determined cardiac vagal tone in 15 normal subjects at supine rest. After sympathetic influences by intravenous propranolol were eliminated, RR interval variability was measured for 10 minutes under controlled respiration (0.25 Hz), and cardiac vagal tone was determined as the decrease in mean RR interval following complete vagal blockade with atropine. Time domain indexes (standard deviation, coefficient of variance and mean successive difference) correlated strongly with vagal tone (r = 0.87, 0.81 and 0.92, respectively; p less than 0.001 for all). The same was true for frequency domain indexes for the high-frequency (0.25 Hz) component calculated both by autoregressive spectrum analysis (square root of power and coefficient of component variance) and by fast Fourier transform (mean amplitude) (r = 0.91, 0.85 and 0.86, respectively; p less than 0.0001 for all). However, frequency domain indexes for the low-frequency spectral component (0.03 to 0.15 Hz) correlated less strongly (r = 0.69, 0.55 and 0.70, respectively), and the fraction of power [power/(total power greater than 0.03 Hz)] of both components showed no correlation. Principal component analysis showed that the first 6 indexes with strong correlations contained solely the first principal component closely related to vagal tone, whereas the remaining 5 indexes also contained the second component unrelated to vagal tone. These results indicate that most of the time and frequency domain analyses in use provides an accurate and common measure of cardiac vagal tone at rest.

Selectivity and contribution of lecithin: cholesterol acyltransferase to plasma cholesterol ester formation.

Selectivity factors (Vm/Km) for human and rat lecithin: cholesterol acyltransferases (LCAT) for the transfer of various acyl groups from the 2-position of phosphatidylcholine were determined. By multiplying these values by the proportions of acyl groups at the 2-position of phosphatidylcholine, one can predict the proportions of molecular species of cholesterol ester which will be synthesized by LCAT. In human subjects fasted overnight, the molecular composition of plasma cholesterol ester was found to reflect the LCAT selectivity relatively accurately. This result supports the concepts that hepatic acyl-CoA:cholesterol acyltransferase (ACAT) does not contribute significantly to the synthesis of plasma cholesterol ester and that removal of cholesterol ester from plasma is not selective with respect to molecular species under these conditions. In contrast to the results with humans, the molecular composition of plasma cholesterol ester formed in spontaneously hypertensive rats fed a high-cholesterol diet and then fasted overnight differs from that which is predicted from LCAT selectivity and the proportion of various fatty acids at the 2-position of phosphatidylcholine: these results suggest that cholesterol ester is formed mainly via the ACAT reaction.

Assessment of frequency shifts in R-R interval variability and respiration with complex demodulation.

A complex demodulation (CDM) method for continuous assessment of frequency shifts and time-dependent changes in amplitude in the rhythmic components existing in predefined frequency bands was proposed and applied to the analysis of high-frequency (HF) and low-frequency (LF) components of the R-R interval and to the analysis of respiration via impedance spirogram. Simulation studies revealed that this CDM technique furnishes mathematical features well suited to the investigation of non-stationary R-R interval signals and can delineate time-dependent fluctuations in both amplitude and frequency, accurately differentiating between HF and LF components. Analysis of data during paced breathing at different respiratory frequencies revealed that the estimated frequency of the HF component and respiration faithfully reflected the frequency of paced breathing. Analysis of data during dynamic exercise with increasing workload (20 W/min) showed that the frequency of the HF component was elevated with exercise and that both HF and LF amplitudes were reduced progressively with advancing load. CDM-derived frequency and amplitude of respiration were highly correlated to direct breath-by-breath respiratory frequency and tidal volume measurements. We conclude that this method could provide a powerful means for continuously assessing time-dependent changes in both cardiovascular and respiratory variations.

Effect of nifedipine on oxygen delivery in patients with angina pectoris: relation between blood viscosity and hematocrit.

The effect of nifedipine on blood viscosity and hematocrit was investigated. Blood was sampled from eight patients with angina pectoris (mean age: 59 +/- 8 yr) treated with nifedipine (20-30 mg/day) for 5 months. Using a cone-plate type viscometer, blood viscosity was determined at the shear rates of 37.5 and 375 sec-1 at 37 degrees C. Hematocrit was also measured at the same time. Since the ratio of hematocrit to blood viscosity at a shear rate of 375 sec-1 can be considered to reflect oxygen delivery, this ratio (oxygen delivery index) was also calculated. Blood viscosity at a shear rate of 37.5 sec-1 was significantly (P less than .05) decreased by nifedipine treatment, but hematocrit and the blood viscosity at a shear rate of 375 sec-1 were not changed. The oxygen delivery index, however, was significantly (P less than .01) increased after the administration of nifedipine. These results suggest that oxygen delivery increased by the treatment with nifedipine and inhibited erythrocyte aggregation by decreasing blood viscosity at low shear rate.

Block of Na+ channel by moricizine hydrochloride in isolated feline ventricular myocytes.

The effect of moricizine hydrochloride, a potent class I antiarrhythmic agent, on Na+ current (INa) of single feline ventricular myocytes were studied using whole cell patch clamp techniques. Moricizine inhibited INa in a concentration-dependent manner without altering the current-voltage relationship for INa. INa inhibition was expressed by the Hill equation with a Hill coefficient of 1.3 and dissociation constant of 105 microM in the resting state (holding potential = -140 mV). Moricizine 30 microM shifted the steady state inactivation curve for INa toward more negative potentials by 7.3 +/- 2.4 mV without causing significant changes in the slope factor. Recovery of INa from inactivation was retarded (time constant = 8 s) at a holding potential of -140 mV in the presence of 30 microM moricizine. When the start of INa block was studied in experiments using a double pulse protocol, moricizine reduced INa by only 4% after a 4-ms prepulse, but strongly inhibited it after prepulses longer than 200 ms. Intracellular application of 100 microM moricizine did not produce significant resting or use-dependent INa block. These results suggest that (1) moricizine blocks INa by binding to the Na+ channel with a 1:1 stoichiometry, (2) the drug has a higher affinity to the inactivated state than to the activated and resting states of the Na+ channel, (3) recovery kinetics of moricizine from Na+ channel inactivation, or drug dissociation observed during the transition from inactivated to resting state was relatively slow, (4) the drug binding site appeared to be located on the external side of the membrane.

HDL3 exerts more powerful anti-oxidative, protective effects against copper-catalyzed LDL oxidation than HDL2.

OBJECTIVE: To evaluate which HDL subfraction, HDL2 or HDL3 exerts the greater preventive effect on the Cu(2+)-induced LDL oxidation. METHODS: LDL was incubated for 6 h with 2.5 microM Cu2+ in phosphate-buffered saline alone, or in the presence of HDL2 or HDL3 at various protein concentrations. Each sample was subjected to agarose gel electrophoresis, and the amount of lipid hydroperoxide in each sample of LDL was measured. RESULTS: There was no significant difference in the levels of LPO between the LDL and LDL + HDL2 cases, whereas a significant reduction was apparent with LDL + HDL3. Both HDL2 and HDL3 significantly inhibited oxidative modification of LDL, as assessed by electrophoretic mobility, in a concentration dependent manner, but this effect was much more pronounced with HDL3. CONCLUSION: HDL3 may play an important role in the prevention of atherosclerosis in vivo, more effectively inhibiting oxidation of LDL than HDL2.

Left ventricular isovolumic relaxation flow and left ventricular systolic performance.

We investigated isovolumic relaxation flow in patients with coronary artery disease (CAD) and evaluated the relationship between its velocity and left ventricular performance in 23 patients with atypical chest pain, 30 patients with CAD without prior myocardial infarction (MI), and 57 patients with prior MI, in whom cardiac catheterization was performed. The isovolumic relaxation flow velocity was measured at the basal portion of the left ventricle with pulsed Doppler echocardiography. The isovolumic relaxation flow ( > 15 cm/sec) was detected in 98 of 110 patients. The isovolumic relaxation flow velocity was significantly lower in patients with prior MI than in patients with atypical chest pain (p < 0.001) and in those with CAD without prior MI (P < 0.05). It was significantly lower in patients with CAD without prior MI than in those with atypical chest pain (p < 0.05). The isovolumic relaxation flow velocity showed a significant positive correlation with left ventricular ejection fraction. It also showed a significant negative correlation with left ventricular end-systolic volume index. These findings suggest that the isovolumic relaxation flow velocity is decreased in patients with CAD and is influenced by left ventricular systolic performance. Isovolumic relaxation flow may be a clinical manifestation of elastic recoil of the left ventricle.

Effects of trimebutine maleate on gastric motility in patients with gastric ulcer.

The effects of trimebutine maleate (TM), a prokinetic drug, on gastrointestinal motility in patients with gastric ulcer were investigated. Twenty patients with active gastric ulcers were allocated to two groups; 10 patients received a proton pump inhibitor alone (PPI group), given orally, and 10 patients received oral TM in combination with a PPI (PPI + TM group), each for a period of 8 weeks. Electrogastrography (EGG) and gastric emptying were measured before and after the treatment period. During the active ulcer stage, tachygastria (more than 0.06 Hz) or bradygastria (less than 0.04 Hz) in the EGG frequency were observed in 9 patients either before or after meals. During the healed ulcer stage, tachygastria or bradygastria was observed in 4 of 10 patients in the PPI group, while in the PPI + TM group, 1 patient had tachygastria and none had bradygastria. Postprandial dip (PD) was observed in 3 of the 20 patients during the active stage, while after treatment, PD was observed in 3 patients in the PPI group and in 6 patients in the PPI + TM group, respectively. Gastric emptying in the PPI group did not show any change between before and after treatment, while that in the PPI + TM group improved significantly after treatment. These results suggest that TM may have an ameliorative effect on abnormal gastric motility in patients with gastric ulcer.

Fractional removal rate of fat emulsion (K2) remains to be low in APOE3/3 phenotype subjects with serum triglyceride level above 180mg/dl.

The relation between fractional catabolic rate (K2) of an intravenously injected fat emulsion, Intralipid, and the level of serum triglyceride (TG) was evaluated to cast light on TG-rich lipoprotein metabolism in 182 subjects who were homozygotes for the most common form of apoE3/3. Both normolipidemic individuals and primary hyperlipidemic patients were included. To assess the influence of variation in the apoE phenotype on fat emulsion metabolism, 25 subjects with the apoE 4/3 phenotype and 21 with apoE 3/2 phenotype were also evaluated. In the apoE 3/3 subjects, K2 decreased with increasing TG level up to 180mg/dl, but above 180mg/dl, K2 remained at a constant level. This TG value was therefore concluded to be a cut off beyond which the TG-dependent decrease in K2 disappeared. No apparent correlation between K2 and serum TG was observed in subjects with apoE 4/3 or 3/2 phenotypes. In subjects with TG above 180mg/dl, presumably both accelerated synthesis and limited removal are involved in the development of their hypertriglyceridemia. Since K2 demonstrated little change with increase of TG over 180mg/dl in apoE 3/3 subjects, we concluded that the capacity to catabolize fat emulsion reaches a kinetic saturation. The TG value of 180mg/dl may be a physiological significance. The relation between K2 and TG was specific in apoE 3/3, as it was not observed in subjects having apoE 4/3 or 3/2 phenotypes.

Effects of dehydroepiandrosterone on proliferation of human aortic smooth muscle cells.

Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) have been shown to be associated with the progression of coronary atherosclerosis in clinical and in vivo studies. However, the mechanisms responsible for the association have not been determined. In the present study, we found that DHEA influences the in vitro growth of vascular smooth muscle cells obtained from the human aorta (hASMC). The concentrations of DHEA ranging from 10(-8) M to 10(-6) M significantly stimulated the mitogenesis of hASMC in serum-free culture. On the other hand, 4 hrs of pretreatment with DHEA attenuated the fetal calf serum induced proliferative effect in a dose-dependent manner. However, the in vitro effects of DHEA on the mitogenesis observed in hASMC were not seen in rat-derived aortic smooth muscle cell lines (A10 cells). With respect to DHEAS, the hormone, at concentrations up to 10(-5) M did not affect the growth of either hASMC or A10 cells in vitro. The growth response of hASMC to DHEA in vitro was markedly affected by the culture conditions. The differential proliferative effects of DHEA on smooth muscle cells between rat and human are of interest. We conclude that the effects of DHEA on mitogenesis of hASMC may, at least in part, explain the association between DHEA and atherosclerosis.

Effect of ascorbic acid on pituitary prolactin secretion in the non-ascorbate synthesizing Osteogenic Disorder Shionogi (ODS) rat.

We examined the secretion of prolactin (PRL) in the hereditary scurvy-prone Osteogenic Disorder Shionogi (ODS) rat to investigate the role of ascorbic acid (AsA) in pituitary lactotroph and hypothalamic function. Plasma PRL concentrations of conscious AsA-deficient or control ODS rats were measured before and after the administration of metoclopramide (MCP), 5-hydroxy-L-tryptophan (5-HTP) or saline. The basal plasma PRL levels did not differ between the two groups. However, the AsA-deficient rats exhibited significantly larger changes in plasma prolactin concentration in response to MCP or 5-HTP than the control ODS rats. Thus, AsA deficiency enhanced the stimulated, but not the basal, secretion of PRL in ODS rats. Our findings suggest that AsA may have an inhibitory effect on PRL secretion.

Excretion of urinary epidermal growth factor in non-insulin dependent diabetes mellitus.

Morning urine samples were assayed for human EGF (hEGF) in 137 non-insulin dependent diabetic patients with normal serum creatinine and beta 2-microglobulin levels. Serving as controls, 80 age- and sex-matched healthy subjects were also examined. A significant positive correlation between hEGF excretion and the level of hemoglobin A1C (HbA1c) was present in those patients with a HbA1c value exceeding 8% (r = 0.37; p = 0.003) but not in the overall patients. The urinary hEGF level did not correlate with the concentration of glucose in urine or plasma. The mean urinary hEGF level of diabetic patients was significantly lower than that of healthy subjects. The mean urinary hEGF level was significantly lower in the patients with a diabetic history that exceeded five years as compared with those with a history below five years. The mean urinary hEGF level was significantly lower in the patients with retinopathy vs. those without retinopathy. In the patients with HbA1c value below 8%, the mean urinary hEGF level was lower in the patients whose urinary albumin level exceeded 1.7 mg/mmol.creatinine as compared with those whose urinary albumin excretion was below 1.7 mg/mmol.creatinine. These findings suggest that urinary hEGF excretion may decrease with the progression of diabetic complications in the patients with well-controlled glycemia, and that inadequate glycemic control may lead to an increased excretion of urinary hEGF in the early disease stage.

Effects of fructose ingestion on sorbitol and fructose 3-phosphate contents of erythrocytes from healthy men.

To investigate the effect of fructose ingestion on sorbitol and fructose 3-phosphate (F3P) in erythrocytes, we administered 50 g fructose with and without treatment with an aldose reductase inhibitor, epalrestat, to seven healthy, normal-glucose-tolerant, male volunteers aged 20-43 years. The same subjects were given 50 g glucose on another day. The sorbitol and F3P contents in their erythrocytes increased significantly, reaching peak levels at 60 min and 180 min, respectively, following fructose in gestion. On the other hand, glucose ingestion did not cause any statistically significant change in sorbitol content in their erythrocytes, although it significantly elevated their F3P content. Treatment with epalrestat had no significant effect on incremental changes in erythrocyte sorbitol and F3P content following fructose ingestion. This suggests that oral fructose may be converted directly to sorbitol and F3P in erythrocytes instead of being converted via glucose. Thus, the dietary intake of fructose may affect the concentrations of sorbitol and F3P in erythrocytes in normal men.

Detection of impaired left ventricular function in coronary artery disease with acceleration index in the first derivative of the transthoracic impedance change.

In order to detect impaired left ventricular (LV) function in coronary artery disease (CAD) patients using acceleration index (Ac) of impedance cardiography (ICG), exercise ICG was performed in 29 patients with chest pain but without CAD (Group 1) and 21 patients with CAD (Group 2), and their resting values were compared with 30 healthy controls (Group 3). The acceleration index, which reflects indirectly aortic blood flow acceleration, was calculated as the ratio of dZ/dtmax to its accelerating time (AT). At rest, the values for Ac in Groups 1, 2, and 3 were 23 +/- 10, 15 +/- 6, and 36 +/- 13 omega/s2, respectively. There were significant differences between Group 1 versus 3, 2 versus 3, and 1 versus 2 (all p less than 0.001). At maximal exercise, Ac showed the largest percent change among the various indices used in this study. An increase of 198% for Group 2 was markedly lower than that of 250% in Group 1 (40 +/- 14 vs. 68 +/- 24 omega/s2, p less than 0.001). With a value of less than or equal to 40 omega/s2, Ac can detect the CAD patients, with a sensitivity of 62% and specificity of 90%, superior to stress ECG using CM5 lead. It is concluded that: (1) Ac is the sole index capable of distinguishing not only between the normals and diseased groups, but also between CAD patients and suspected CAD cases at rest. (2) Ac is a remarkably sensitive index for detecting impaired LV function at maximal exercise. (3) Exercise ICG is useful for predicting CAD from the population predisposing to CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive evaluation of left ventricular performance by the shortest distance between mitral leaflets coaptation and interventricular septum at end-systole.

We attempted to evaluate left ventricular performance from the shortest distance between the mitral leaflets coaptation and the interventricular septum at end-systole (MVC-IVS distance). The subjects were 37 patients with coronary artery disease (CAD) with prior myocardial infarction (MI), 8 with CAD without prior MI, 22 with atypical chest pain, and 4 with aortic regurgitation. The MVC-IVS distance was measured on a two-dimensional echocardiogram obtained from the parasternal or apical long-axis view and frozen at end-systole. Left ventricular end-systolic volume and end-diastolic volume were obtained by left ventriculography, and the left ventricular ejection fraction was calculated. A significant positive correlation was observed between the MVC-IVS distance and the end-systolic volume (r = 0.83, p less than 0.001); a close correlation was observed between the MVC-IVS distance end-systolic volume and ejection fraction by monoexponential fitting (r = -0.91, p less than 0.001). Thus, a significant negative correlation was observed between the MVC-IVS distance and the left ventricular ejection fraction (LVEF) (r = -0.83, p less than 0.001). An MVC-IVS distance of greater than or equal to 30 mm suggests diagnosis of left ventricular dysfunction (LVEF less than 50%) with high sensitivity (94.4%) and specificity (90.6%), while a value less than 30 mm suggests that the left ventricular performance is likely to be normal. Thus one can easily evaluate the left ventricular performance noninvasively using this new index.