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Neurohumoral factors, which is divided to two groups, are activated in patients with congestive heart failure(CHF). One is cardiotoxic biochemical markers such as nor-epinephrine, angiotensin II, endothelin-1, and vasopressin, the other is cardioprotective biochemical markers such as atrial natriuretic peptide, and brain natriuretic peptide (BNP). Among various neurohumoral factors, plasma level of BNP is the most useful marker to diagnose and evaluate the severity and prognosis of CHF patients. The reason why the usefulness of plasma BNP is 1) BNP is of ventricular origin, 2) BNP reflects hemodynamic abnormalities(high left ventricular end-diastolic pressure and/or low left ventricular ejection fraction), 3) Attenuation of biological compensation of beneficial effects of BNP(vasodilation, diuresis) in advanced-staged CHF.

Regionally reduced 123I-BMIPP uptake in the interventricular septum (SEP) is observed in some patients with chronic right ventricular (RV) pressure overload. We studied the significance of this finding by comparing it with mean pulmonary arterial pressure (mPAP). 123I-BMIPP SPECT imaging was carried out in 21 patients with pulmonary hypertension (PH; 51(+)-14 years; 11 men and 10 women; 7 with primary pulmonary hypertension, 11 with pulmonary thromboembolism, and 3 with atrial septal defect). mPAP ranged from 25 to 81 mmHg (49 +/- 16 mmHg). Using a midventricular horizontal long-axis plane, regional BMIPP distributions in the RV free wall and SEP were estimated by referring to those in the LV free wall. Count ratios of the RV free wall and SEP to the LV free wall (RV/LV, SEP/LV) were determined by ROI analysis. RV/LV showed a linear correlation with mPAP (r = 0.42). However, SEP/LV was inversely correlated with mPAP (r = -0.49). When SEP/RV was compared among three regions of SEP in each patient, basal SEP/RV was most sensitively decreased in response to increased mPAP (r = -0.70). These results suggest that the assessment of septal tracer uptake in 123I-BMIPP SPECT imaging is useful for evaluating the severity of RV pressure overload in patients with PH.

Using transesophageal echocardiography (TEE) we assessed left ventricular end-systolic elastance (Ees) during the pre- and post-cardiopulmonary bypass (CPB) periods in 10 patients undergoing an elective coronary artery bypass graft surgery. The end systolic volume of the left ventricle was obtained by TEE, and the end systolic pressure was obtained by the femoral artery pressure wave form. LVSWI decreased at post-CPB compared to the value at pre-CPB. There were no significant differences in cardiac output, ejection fraction and Ees between pre-CPB and post-CPB period. Intraoperative end-systolic pressure-volume relationship may be clinically useful to assess left ventricular function and also useful to confirm anesthetic management in patients who has undergone an coronary artery bypass graft surgery.

This study estimates the perioperative left ventricular function of VSD and TOF by using Pressure-Volume (PV) loop. The most characteristic hemodynamic change of VSD is a decreased volume load. Although ejection fraction significantly decreased after the operation, this change did not mean a deteriorated left ventricular contractility. Emax, which is an index of left ventricular contractility on PV loop, improved and pressure-volume area (PVA) which is correlated with 02 consumption of left ventricule was reduced. Mechanical efficiency of left ventricular energetic state did not significantly change. Left ventricular volume and ejection fraction in TOF slightly increased after the operation. Increased ejection fraction reflected a compensation to volume overload after surgery. Emax slightly decreased and PVA increased. Meanwhile mechanical efficiency increased after the operation indicating well preserved ventricular contractility. In particular, the shape of PV loop of both VSD and TOF eventually became usual square after operation due to recover of the isovolumic contraction and relaxation phase. These characteristics had better to be concerned for improvement of surgical techniques as in conotruncal repair, particularly in TOF in the setting of better quality of life with low atrial pressure.

Myocardial contractility independent on the loads of the heart was examined during progressive hypoxemia in nine pigs. left ventricular pressure-volume relation (LVPVR) was analyzed to obtain end-systolic elastance (Ees) and ventriculoarterial coupling (Ea/Ees), concomitantly with the measurements of cardiac output (CO), systemic oxygen delivery (DO2) and other indicators of systemic oxygen metabolism. Hypoxemia was induced by reducing inspired oxygen fraction (FIO2), and the measurement was performed at an FIO2 levels of 0.21, 0.18, 0.15, 0.13, 0.11 and 0.10. During progressive hypoxemia, a maximal increase in CO was observed at FIO2 of 0.11 (P < 0.05, vs FIO2 0.21), while, Ees reached the maximum at FIO2 of 0.13 (P < 0.05, vs FIO2 0.21), then it decreased below FIO2 of 0.11. Ea/Ees showed the best ventriculoarterial coupling at FIO2 of 0.13, and the coupling worsened below FIO2 of 0.11. It is concluded that load-independent myocardial contractility started to decline even when CO was still increasing to compensate the reduction of DO2 during progressive hypoxemia.

A left ventricular pressure volume loop (PV loop) is useful not only in evaluating cardiac function, but also in predicting the postoperative hemodynamic state. There are two methods available for the intraoperative measurement of a PV loop: a conductance catheter and two-dimensional echocardiography. Although the accuracy of conductance catheter is well established for the measurement of ventricular volume, however, the accuracy of echocardiography remains controversy. This paper describes the relationship of parameters including volumes and Emax calculated with each method. Six patients who underwent open heart surgery were included in this study. Comparison of the absolute volumes at four points at the corners of the PV loop showed a Pearson's correlation coefficient of 0.62 (p-value < 0.01). In comparison with the relative volumes at four points which reflect the preoperative to postoperative change ratio, the correlation coefficient was 0.74 (p < 0.01). The correlation coefficients were 0.76 (p = 0.16) and 0.63 (p = 0.29) for the ratio of the end-diastolic and end-systolic volume respectively. Each preload-varying "Emax: out" (r = 0.84, p < 0.01) were highly correlated. As a predictor of cardiac oxygen consumption, each PVA (r = 0.84, p < 0.01) was highly correlated. We conclude that the measurement of left ventricular volume using two-dimensional echocardiography is as reliable as the conductance catheter.

Preconditioning with repetitive brief periods of ischemic (IPC) is known to induce myocardial protection against a subsequent more prolonged period of ischemia. We investigated whether IPC can offer similar beneficial effects on myocardial function after cardioplegic preservation in isolated and crystalloid-perfused rat hearts. IPC was produced by 5 periods of 1 min ischemia followed by 5 min reperfusion before 25 min of unmodified ischemia or 40 min of cardioplegia. IPC had no significant effect on the time to contractile arrest (control: 211 +/- 27 sec, IPC: 240 +/- 32 sec) after unmodified ischemia, while the time to electrical asystole was significantly (p < 0.05) shortened by IPC (676 +/- 107 sec) compared to control (1021 +/- 197 sec). However, rapid contractile arrest concomitant with electrical asystole was induced by infusion of St. Thomas' Hospital solution in control as well as in IPC-treated hearts without a significant intergroup difference (control: 33 +/- 7 sec, IPC 39 +/- 9 sec). Although myocardial ATP was significantly reduced by IPC, IPC-treated hearts showed a significantly higher ATP level after 25 min of unprotected ischemia. Accumulation of myocardial lactate after 25 min of unprotected ischemia was significantly (p < 0.05) inhibited by IPC. However, the levels of myocardial ATP and lactate after 40 min of cardioplegia were comparable between control and IPC-treated hearts. Left ventricular developed pressure (LVDP) at 30 min reperfusion after unprotected ischemia was significantly improved by IPC, while the recovery of LVDP at 30 min reperfusion after cardioplegia was comparable between control and IPC-treated hearts. The onset of ischemic contracture, i.e., a rise of left ventricular end-diastolic pressure (LVEDP), was significantly accelerated and its magnitude was significantly greater in IPC-treated hearts during unprotected ischemia and also during cardioplegia. However, a significant decrease of LVEDP during reperfusion compared to control hearts was observed only after unprotected ischemia. The amounts of creatine kinase (CK) released during 30 min reperfusion after unprotected ischemia was significantly greater in control than in IPC-treated hearts, but there was no significant difference in CK release between control and IPC-treated hearts during reperfusion after cardioplegia. These results suggest that IPC-induced cardioprotection may be induced via inhibition of anaerobic energy metabolism through a negative chronotropic effect during unprotected ischemia, but such a beneficial effect is dissipated with cardioplegia by which rapid electrical asystole is induced. It is, therefore, concluded that IPC may not provide additional myocardial protection over conventional hyperkalemic cardioplegia.

We compared the results of 19 mm SJM aortic valve replacements with those of 23 mm SJM aortic valve replacements conducted the same period. [Material & Method] The subjects were 21 patients who underwent valve replacement with a 19 mm SJM prosthesis (the SJM19A group). The age ranged among 16 and 65-year-old, mean of 51. The body surface area was 1.24 to 1.76 m2, mean of 1.48 m2. The post-operative follow-up period was 156 months at maximum and 44 months on average. We compared the SJM19A group with the SJM23A group by chest X-ray and echocardiography. [Results] Two patients in the SJM19A group died soon after surgery. Of the other patient, 19 were categorized NYHA I and one in NYHA II classification in their late phase. Arrhythmia of Lown IVa developed in one patient. The cardio-thoracic ratio decreased from preoperative 60% in the late phase after surgery (p < 0.002) in the SJM19A group, although there was no significant difference with that in the SJM23A group. Echocardiographic improvement in left ventricular hypertrophy was considerable between before and late after surgery in the SJM19A group, while it was not significantly different between the SJM19A and SJM23A group. The mean value of aorta-left ventricle pressure difference in the late stage was 32 mmHg in the SJM19A group and significantly different from the value in the SJM23A group (p < 0.001). This pressure difference tended to be greater as the follow-up period was progressed, while the percentage decrease in the myocardial mass of the left ventricle tended to decreased with longer follow-up period. This data suggests that an increasing level of aorta-left ventricle pressure difference should raise little problem in the mid-term late stage after surgery but possibly cause a serious problem in the long term. Clinical observation should be continued over a long period of time after surgery.

The prognostic value of left ventricular inflow velocities by the pulsed Doppler method was studied in 32 patients with congestive heart failure including 18 with old myocardial infarction, 9 with dilated cardiomyopathy, and 5 with hypertensive heart disease, who initially revealed pseudonormalized left ventricular inflow pattern. Pulsed Doppler echocardiography, apexcardiography, and phonocardiography were performed at 3- to 9-month intervals. The prognosis was evaluated for two groups of patients with persistent or transient pseudonormalized inflow patterns. Survival rates at 6 months and 2 years in the total patient population were 78% and 47%, respectively. Twenty-one patients had the pseudonormalized left ventricular inflow pattern (persistent group), while the other 11 patients had a changed pattern (transient group). The survival rate at 2 years was 37% for the persistent group, and 82% for the transient group. Significant differences in patient profiles and the initial data between the two patient groups were the presence of cardiogenic shock (10/21 in persistent group vs 1/11 in transient group; p < 0.001) and the value of left ventricular end-diastolic wall stress (159 +/- 62 g/cm2 in persistent group vs 135 +/- 42 g/cm2 in transient group; p < 0.05). There were no significant differences in NYHA class, the values of left ventricular end-diastolic pressure, left ventricular ejection fraction. A/E ratio, or deceleration half time of left ventricular inflow velocities. Left ventricular end-diastolic wall stress in patients with persistent pseudonormalized left ventricular inflow pattern was significantly increased, and may be related to decreased preload reserve. Atrial fibrillation and atrioventricular dissociation were recorded prior to the development of ventricular fibrillation in two patients with sudden cardiac death. Abrupt loss of atrial contribution as well as ventricular arrhythmias may be a trigger of sudden death. Evaluation and follow-up of the pseudonormalized left ventricular inflow pattern is a sensitive indicator for the management of patients with congestive heart failure.

The purpose of this study was to clarify the clinical significance of 123I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy in patients with left ventricular pressure-overload diseases. MIBG scintigraphy was applied to 10 pts with aortic valve stenosis (AS group), 11 pts with hypertrophic obstructive cardiomyopathy (HOCM group), 17 pts with hypertrophic non-obstructive cardiomyopathy (HCM group) and 6 control cases (C group). Mean pressure gradient in AS and HOCM groups was 62 +/- 21 mmHg and 38 +/- 18 mmHg, respectively. Initial myocardial uptake of MIBG (MU) was higher in the AS (1.92 +/- 0.46%) and HOCM (2.27 +/- 0.47%) groups than those in the HCM (1.61 +/- 0.29%) and C (1.50 +/- 0.23) groups. Myocardial clearance of MIBG (MC) was higher in the AS (39 +/- 11%), HOCM (37 +/- 19%) and HCM (28 +/- 17%) groups than that in the C (14 +/- 6%) groups. Heart/mediastinum count ratio (H/M) of AS, HOCM, HCM and C groups was 1.87 +/- 0.29, 2.09 +/- 0.19, 1.98 +/- 0.26, and 2.20 +/- 0.10, respectively. In the cases of AS, positive correlation was observed between mean pressure gradient and MU (r = 0.618, p < 0.05). In conclusion, MU was increased in the case of left ventricular pressure-overload state (AS and HOCM).

Body surface isopotential T map was analyzed to detect right ventricular volume and pressure overloads in 25 patients with secundum atrial septal defect. Three patterns were distinguished: the T map resembling normal (type A, n = 9); that with isolated negative area in positive area (type B, n = 11); and that with rightward movement of maximum (type C, n = 5). Right ventricular end-diastolic volumes in type B (161 +/- 19% of normal; %N) and C (175 +/- 40% N) were significantly (p < 0.01) greater than those in control (100 +/- 9% N) and type A (113 +/- 18% N). Right ventricular systolic pressure in type C (48 +/- 11 mmHg) was significantly (p < 0.01) higher than those in control (30 +/- 5 mmHg), type A (31 +/- 4 mmHg) and type B (34 +/- 5 mmHg). These results suggest that the cases with type B have right ventricular volume overload, and those with type C have both volume and pressure overloads.

We studied QRS and QRST isointegral maps, and isochrone map for the diagnosis of right ventricular hypertrophy and its severity in atrial septal defects and primary pulmonary hypertensions. The discriminant analysis in QRS isointegral map showed better results for differential diagnosis between atrial septal defects and both normal subjects and incomplete right bundle branch block patients than these in QRST isointegral map and isochrone map. Three parameters (Qp/Qs, systolic right ventricular pressure, right ventricular ejection fraction) for right ventricular overload showed significant correlation with QRS isointegral map and QRS isopotential map. Thus body surface map was an useful method for the evaluation of right ventricular hypertrophy.

A time constant (T) of the left ventricular isovolumic relaxation, which expresses the relaxation rate of the left ventricle, may be affected by change of the heart rate. There are few clinical reports concerning the relationship between T and heart rate. We studied the relationship between T and heart rate in 10 patients with normal coronary arteries and left ventricular function. Left ventricular pressure was measured using a catheter-tip manometer during right atrial pacing, which was performed at the rate of 10, 20, 40 beats/min in addition to the baseline rate, and finished at 140 or 150 beats/min. Two measurements were made for T.1) Tw from the slope of In (pressure) against time, and 2) Tb by exponential analysis which also estimated the asymptote. As the heart rate increased, both Tw and Tb gradually shortened (Tw: from 38.5 +/- 4.9 msec at the control heart rate to 28.9 +/- 5.6 msec at 140 or 150 beats/min; Tb: from 54.7 +/- 11.4 msec at the control heart rate to 34.9 +/- 5.7 msec at 140 or 150 beats/min). These findings suggest that left ventricular isovolumic relaxation is strongly affected by change of the heart rate in man.

In this study, the clinical usefulness of the conductance catheter technique was assessed. The end-systolic pressure-volume relations (ESPVR) measured with the increase and decrease in the preload were also compared. Fourteen patients with various heart diseases who underwent diagnostic cardiac catheterization were studied. Using a right atrial pacing catheter, 8 electrical stimuli delivered at a fixed rate of 800 msec were followed by a single early stimulus of 500 msec coupling interval, resulting in premature atrial contraction and post-extrasystolic potentiation (PESP). Left ventricular (LV) volume was measured by 2 methods; namely, the conductance catheter technique and single-plane left ventriculography (LVG). ESPVR was obtained either with the inferior vena cava occlusion induced by balloon inflation, or with the rapid transfusion of saline with electrical resistance identical to the blood volume in the right atrium. The LV volume obtained with the conductance catheter technique (VCON) was correlated with the LV volume as obtained by LVG (VLVG) (end-diastolic volume, VCON = 1.09VLVG - 4.66, r = 0.95; end-systolic volume, VCON = 1.42VLVG - 18.2, r = 0.89). There was correlation of the change in LV volume (delta V) induced by PESP between the 2 methods (end-diastolic volume, delta VCON = 0.52 delta VLVG + 0.94, r = 0.76; end-systolic volume, delta VCON = 0.42 delta VLVG - 4.78, r = 0.72), suggesting that the change in LV volume estimated by the conductance catheter technique was smaller than that estimated by LVG. The LV volume curves were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

The diagnostic value of preoperative echocardiography was assessed in 51 patients with aortic stenosis. We measured 1) left ventricular-aortic pressure gradient (LV-Ao PG), 2) aortic valve area (AVA), 3) grade of LV hypertrophy and function, and 4) aortic annulus diameter for determining the availability and size of a prosthesis. The maximal instantaneous PG (max-PG) by continuous-wave (cw) Doppler echocardiography correlated well with the peak-to-peak PG by cardiac catheterization (cath), and their correlation equation was y = 1.49 x -48.3 with a correlation coefficient of 0.90. Excellent correlations were also found between cw-max PG and cath-max PG (r = 0.84), and between cw-mean systolic PG and cath-mean systolic PG (r = 0.80). The AVA of the echocardiogram, which was derived from the stroke volume using Gibson's M-mode echocardiographic formula and the cw-Doppler echocardiographic mean gradient, correlated well with the AVA of the cardiac catheterization using Gorlin's formula (y = 1.33 x -0.61, r = 0.79). Preoperative LV pump function, which was obtained from the M-mode echocardiogram, correlated inversely with end-systolic wall stress, and a depressed LV pump function was observed in patients with inadequate hypertrophy. In such patients, however, depressed function was alleviated after surgical treatment. Thus, we considered that cardiac catheterization for further examination is unnecessary, even in such patients. To determine the available size of the prosthesis, measurement of the inner diameter of the aortic annulus on the long-axis cross-sections was the most useful.(ABSTRACT TRUNCATED AT 250 WORDS)