Effects of left ventricular asynchrony on time constant and extrapolated pressure of left ventricular pressure decay in coronary artery disease.

To elucidate the effects of ventricular asynchrony with or without myocardial ischemia on the time constant of left ventricular pressure decay and asymptote, that is, the level to which pressure would decrease if isovolumic pressure decrease continued infinitely, left ventriculography and pressure measurements were investigated in 14 normal subjects and 25 patients with coronary artery disease. Ventricular asynchrony was quantitated by the segmental area-time curve. This study consisted of two parts. 1) After a right atrial pacing stress test, the time constant and asymptote remained unchanged in eight normal subjects. In 18 patients with coronary artery disease and pacing-induced angina, asynchrony increased, the time constant was prolonged (64 +/- 13 to 94 +/- 17 ms, p less than 0.01) and the asymptote decreased (-22 +/- 10 to -46 +/- 20 mm Hg, p less than 0.01) after the pacing. 2) During right ventricular pacing at 80, 100 and 120 beats/min in the patients, asynchrony increased and the time constant was prolonged (55 +/- 7 versus 70 +/- 10, 47 +/- 11 versus 66 +/- 19, 36 +/- 7 versus 53 +/- 13 ms, respectively, p less than 0.01 versus right atrial pacing), whereas the asymptote was unchanged in six normal subjects compared with the value during right atrial pacing at each pacing rate. In seven patients with coronary artery disease, right ventricular pacing at 80, 100 and 120 beats/min also produced an increase in the time constant, while the asymptote was unchanged. Thus, prolongation of the time constant of left ventricular pressure decay may result from ventricular asynchrony even in the absence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of digoxin on congestive heart failure in old myocardial infarction, dilated cardiomyopathy, acute myocardial infarction and mitral stenosis.

The hemodynamic effects of digoxin (0.01 mg/Kg) on congestive heart failure were compared in 32 patients with old myocardial infarction (OMI) (n = 9), dilated cardiomyopathy (DCM) (n = 10), acute myocardial infarction (AMI) (n = 5) and mitral stenosis (MS) (n = 8). The responses of heart rate (HR) and pulmonary capillary pressure (PCP) to digoxin in OMI, DCM and MS were marked but different in each of these groups and no significant changes were found in patients with AMI. The responses of cardiac index (CI) to digoxin in patients with OMI and DCM in whom left ventricular myocardial contractile force was impaired were divided into 2 groups (Group 1: CI increased more than 15% and Group 2: less than 15%). In Group 1, both CI and percent fractional shortening (%FS) before digoxin administration were lower than in Group 2, i.e., 1.97 +/- 0.27 vs 2.80 +/- 0.48 L/min/m2 (p less than 0.001) and 10.9 +/- 8.0 vs 19.5 +/- 11.9% (p less than 0.05), respectively. In MS, CI increased after digoxin administration only in the 2 patients with low CI and rapid HR in the control state. These results indicate that the mode of hemodynamic response to digoxin is considerably different in various diseases. They further suggest that digoxin should not be used in the early phase of AMI, although digoxin was of great clinical benefit in patients with OMI and DCM through such mechanisms as its positive inotropic and negative chronotropic effects and lowering of PCP.

Assessment of left ventricular function in ischemic heart disease. The relation between pressure decay during the isovolumic relaxation phase and regional wall motion abnormality.

We examine whether regional wall motion abnormality (RWMA) could contribute to the slowed relaxation rate of the left ventricle (LV) in patients with coronary artery disease (CADpts). Simultaneous observations were made on the time constant (Tc) of the isovolumic pressure decay and left ventriculography at the control period and after right atrial pacing. Subsequently, the subjects investigated were divided into 3 groups, i.e. normal subjects (Group I, n = 8), CADpts with normal wall motion during the control period (Group II, n = 21), and CADpts with RWMA during the control period (Group III, n = 28). The latter two groups were further divided into two subgroups according to the presence (Group IIa and IIIa) or absence (Group IIb and IIIb) of pacing-induced RWMA. We measured Tc by a method of exponential analysis that could estimate the asymptote. During the control period, Tc was significantly prolonged in Group III (82 +/- 26 msec) than that in Group I (60 +/- 6 msec) and Group II (63 +/- 12 msec). Tc was prolonged in proportion to the extent of RWMA during the control period. Immediately after right atrial pacing, Tc was markedly prolonged in Group IIa (from 61 +/- 12 to 90 +/- 20 msec, p less than 0.001) and in Group IIIa (from 73 +/- 26 to 95 +/- 34 msec, p less than 0.001). The post-pacing prolongation of Tc was closely correlated with the extent of post-pacing RWMA. From these results, it is postulated that RWMA may play an important role as a causes of the altered LV relaxation in CADpts.

Asymptomatic cor triatrium in an elderly patient--observation by biplanar transesophageal Doppler echocardiography.

We present a case of asymptomatic cor triatrium in a 78-year-old man, in whom the condition was diagnosed and the severity of the lesion was accurately assessed by biplanar transesophageal echocardiography. To our knowledge, our patient is the oldest living person with cor triatrium.

A comparison of two exponential models of the time constant during left ventricular isovolumic pressure decay in coronary artery disease.

To make a comparison of two exponential models of the time constant (Tw: Weiss's method, Tc: exponential analysis with a variable asymptote) during left ventricular (LV) isovolumic relaxation, we assessed LV pressure decay in 104 patients with coronary artery disease (CADpts) and 21 normal subjects at rest and after pacing, and investigated the hemodynamic determinants of these two models using forward-backward stepwise multiple regression analysis. At rest, Tw was prolonged as the left ventricular minimal pressure (LVPmin), the left ventricular end-diastolic pressure (LVEDP) and the end-systolic volume (ESV) increased (multiple regression coefficient: R = 0.87), whereas Tc was prolonged as ESV and regional wall motion abnormality (RWMA) increased (R = 0.72). Pacing-induced changes in Tw were augmented as LVPmin and RWMA increased (R = 0.75), whereas changes in Tc were augmented as RWMA increased (R = 0.63). Thus, the changes in Tw may be due to an increase in LVPmin rather than to any direct effect of ischemia on the relaxation rate. The relaxation rate can be evaluated more reliably by Tc than by Tw, irrespective of associated pressure changes during ischemia in CADpts.

Effects of diltiazem and nitroglycerin on left ventricular diastolic properties in patients with coronary artery disease.

To determine the effects of diltiazem (DTZ) and nitroglycerin (NTG) on left ventricular (LV) diastolic relaxation and filling in patients with cornary artery disease (CADpts), LV graphy and time constant (Tc) of LV isovolumic pressure decay were studied before and 5 min after intravenous DTZ (10 mg) in 16 CADpts and sublingual NTG (0.3 mg) in 11 CADpts. Diastolic regional ventricular filling dynamics were quantitated by segmental area-time curves during early-, mid- and late-filling periods. After NTG, LV systolic pressure (LVSP), end-diastolic pressure (EDP) and end-diastolic volume (EDV) decreased. Early-filling rate (EFR) decreased (165 +/- 82 to 122 +/- 61 ml/sec/m2) due to a decrease in the regional early-filling rate in the normokinetic area and late-filling rate (LFR) increased (95 +/- 38 to 145 +/- 45 ml/sec/m2), while LV peak positive dp/dt, peak LVSP/end-systolic volume (ESV) ratio, Tc and mid-filling rate (MFR) were unchanged. After DTZ, LVSP decreased and EDV increased. EFR increased. EFR increased (127 +/- 54 to 166 +/- 60 ml/sec/m2) due to an enhanced regional early-filling rate in the mildly hypokinetic area, while EDP, LV peak positive dp/dt, peak LVSP/ESV ratio, Tc, MFR and LFR were unchanged. From these results, it was postulated that NTG caused a decrease in LV early filling and an increase in LV late filling, probably due to LV preload reduction. In contrast, DTZ caused significant improvement of LV early filling particularly in the mild hypokinetic area. Thus, DTZ but not NTG was able to relieve local myocardial dysfunction secondary to a stenosed coronary artery during the filling period, resulting in clinical improvement in CADpts.

[Intracardiac flow pattern in dilated cardiomyopathy studied with pulsed Doppler echocardiography].

Left ventricular (LV) flow dynamics were analyzed by pulsed Doppler echocardiography in patients (pts) with dilated cardiomyopathy (DCM). Subjects consisted of five normal controls, 27 pts with DCM, five with myocardial infarction and five with valvular heart disease. The equipment used was a two-dimensional echocardiograph ( Toshiba SSH- 11A ) coupled with a pulsed Doppler flowmeter ( Toshiba SDS-10A). The long-axis plane through the left ventricle was obtained from an apical transducer position and Doppler flow signals were recorded at the apex (point A), the middle portion (point B), the inflow portion (point C), the portion near the mid-IVS (point D) and the outflow portion (point E) of the left ventricle, respectively. Left ventriculography was performed in all subjects, and ejection fraction (EF), the ratio of the short-axis to long-axis distance in end-diastole, percent shortening of the long axis and percent shortening of the short axis of the left ventricle were measured. Doppler signals of an ejection flow were recorded at points A, B, D and E in the normal controls, while in 27 pts with DCM Doppler signals of an ejection flow were detected only in two pts (7%) at the point A, in three pts (11%) at the point B, 16 pts (59%) at the point D and 27 pts (100%) at the point E. Twelve pts (44%) had abnormal Doppler signals with wide-band spectral pattern at the point C in systole. Toward flow signals in early diastole were recorded at the points A, B, C and D in the normal controls, while in pts with DCM the signals were visualized in only three pts (11%) at the point A, in 27 pts (100%) at the points B and C, and 10 pts (37%) at the point D. EF in pts with DCM was lower than that of the normal controls (36 +/- 11 vs 65 +/- 5%, p less than 0.005). The ratio of the short-axis to long-axis distance of the left ventricle was higher in pts with DCM compared with that of the normal controls (0.82 +/- 0.09 vs 0.60 +/- 0.02, p less than 0.005). Percent shortening of the long axis and the short axis was depressed in pts with DCM compared with the normal controls (11 +/- 5 vs 21 +/- 4%, p less than 0.02 and 15 +/- 6 vs 34 +/- 3%, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

[Two-dimensional echocardiographic findings in a case of arrhythmogenic right ventricular dysplasia].

Two-dimensional echocardiographic findings in a patient with arrhythmogenic right ventricular dysplasia ( ARVD ) were described. A 38-year-old male was admitted to our hospital on January 1982 because of palpitation and dyspnea caused by ventricular tachycardia. A cardiothoracic ratio was 45% and electrocardiogram revealed right axis deviation and T wave inversion in right precordial leads. A QRS configuration during ventricular tachycardia showed left bundle branch block pattern. The right ventriculogram showed dilatation and diffuse hypokinesis of the right ventricle, although the left ventriculogram and the coronary angiogram were normal. Histological findings of both right and left ventricular tissues obtained by endomyocardial biopsy revealed myocytolysis, scarcity of myofibrils and proliferation of collagen fibers, and the final diagnosis of ARVD was established. Echocardiographic examination disclosed right ventricular and right atrial dilatations, hypokinesis of the right ventricular anterior wall and abnormal motion of the interventricular septum. These seemed to be diagnostic of this condition, if right ventricular volume overload including atrial septal defect, endocardial cushion defect, Ebstein's anomaly, tricuspid regurgitation and pulmonary regurgitation was clinically excluded.

[Regional myocardial contraction in ischemic heart disease: evaluation of regional myocardial thickening by two-dimensional echocardiography].

There were many studies concerning the evaluation of regional wall motion in ischemic heart disease by left ventriculography (LVG) and two-dimensional echocardiography (2DE), but only a few observations on the regional myocardial thickening have been reported. In a survey of 48 cases of old myocardial infarction, we selected 21 cases with adequate 2DE images for the evaluation of regional wall motion and thickening. In all cases the 2DE examinations were performed within seven days before or after LVG examinations. The left ventricular wall on 2DE was divided into 11 segments and wall motion and thickening in each segment were graded to three classes, i.e. none, reduced and normal. The results on 2DE were then compared with the grade of wall motion of the corresponding segment on LVG. The sensitivity and specificity of 2DE wall motion were 50% and 89% in none, 59% and 48% in reduced, and 89% and 84% in normal, respectively. The sensitivity and specificity of 2DE myocardial thickening were 81% and 93% in none, 82% and 70% in reduced, and 92% in normal, respectively. These results indicated that the regional myocardial thickening by 2DE has a higher sensitivity and specificity. Therefore, observation of both myocardial thickening and wall motion will be necessary for the proper evaluation of regional myocardial contraction in ischemic heart disease.