The transmitral flow (TMF) profile was studied in 18 patients with ischemic heart disease and in 4 patients with chest pain syndrome in order to clarify the dependency of preload alteration on the pattern of TMF. Pulsed Doppler echocardiography with simultaneous measurement of right-sided cardiac catheterization and M-mode echocardiography during lower body negative pressures (LBNP 0, -10 mmHg, -20 mmHg) and Dextran infusions (Dex 100 ml, 200 ml) were used in the study. After LBNP, peak velocities in rapid filling (peak R) (cm/sec) decreased (control; 68.3±13.9, LBNP -10 mmHg; 59.8±15.2, p<0.01, LBNP -20 mmHg; 55.2±11.0, p<0.01) and the integrals in the first half phase in rapid filling (IR₁) (cm) also decreased (control; 4.0±0.8, LBNP -10 mmHg; 3.4±0.9, LBNP -20 mmHg; 3.2±0.9, p<0.05). During Dextran infusion, peak R (cm/sec) increased (control; 53.5±7.5, Dex 100 ml; 57.8±10.0, p<0.05, Dex 200 ml; 60.4±10.6, p< 0.01) as did IR₁ (cm) (control; 3.2±1.1, Dex 100 ml; 3.8±1.0, p<0.01, Dex 200 ml; 4.2±1.3, p<0.01). In conclusion, changes in preload may alter the peak velocity and the first half integral in left ventricular rapid filling depending on the pattern of transmitral flow velocity.

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Thirty one patients with stable effort angina who had no prior myocardial infarctions underwent symptom-limited ergometer exercise test. Hemodynamic responses during exercise were assessed to determine whether or not the limiting symptoms were related to the severity of exercise-induced myocardial ischemia. Twenty-two subjects (Group I) were limited by angina and nine (Group II) were limited by other symptoms. There were no differences in age, sex distribution, prevalence of diabetes mellitus, and left ventricular ejection fraction between the two groups. Multivessel coronary artery diseases, however, were more frequent in group I (16/22 vs 3/9: p <0.05). Maximal work load (46.6±16.0 vs 62.5±13.4 W: p<0.05), exercise duration (4.7±2.0 vs 7.2±1.4 min: p<0.005), and maximal oxygen consumption (12.4±4.1 vs 19.3±3.3 ml/kg/min: p<0.005) were significantly lower in group I. The magnitude of ST depression was not different between the two groups (2.0±0.8 vs 1.8±0.7 mm:NS). At maximal exercise, heart rate, mean blood pressure, cardiac index, and stroke work index (SWI) were significantly lower in group I (p<0.05) and pulmonary capillary wedge pressure was significantly higher in group I (31.1±6.1 vs 25.1±5.6 mmHg: p<0.05). Stroke volume index and SWI increased significantly in group II (from 42.7±8.8 to 55.0±11.2 ml/m²: p<0.005, and from 56.8±12.7 to 80.0±12.0 g·m/m²: p<0.005, respectively), but not in group I (from 46.1±11.8 to 51.1±14.4 ml/m²: NS, and from 60.3±17.2 to 92.9±19.6 g·m/m²: NS, respectively). These results indicate that the anginal symptom during exercise test in patients with proven effort angina without myocardial infarction is suggestive of hemodynamically more significant myocardial ischmia.

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The development and reversal of tolerance to the hemodynamic and antianginal effects of isosorbide dinitrate in a sustained release from (ISDN-SR) were investigated in 11 male patients (mean age 58.9 y.o.) with stable effort angina. Treadmill exercise test, evaluation of hemodynamic parameters and measurement of plasma ISDN concentrations were performed during the control period on the 1st, 7th and 14th days of therapy with 40 mg of re-administered after a 72 h placebo period (17th day). Initially, exercise tolerance time (ETT) was prolonged significantly (p<0.001) by ISDN-SR from 257±50 sec in the control period to 434±55 sec on day 1. This prolongation was significantly reduced with sustained therapy and ETT was shortened to 332±69 sec on the 7th day (p<0.01 vs day 1) and 326±73 sec on the 14th day (p<0.01 vs day 1). The effects of ISDN-SR initially observed were restored after a 72 h placebo period and ETT was increased significantly (p<0.01 vs control) and systolic blood pressure was decreased (p<0.001 vs control) by ISDN-SR on day 1. These changes were also diminished significantly (p<0.01 vs day 1) with sustained therapy and were restore after a 72 h nitrate-free interval. The average plasma ISDN concentration was significantly higher during sustained than during acute therapy (p<0.01). It is concluded that partial tolerance to hemodynamic and antianginal effects developed during sustained (1 week) therapy with ISDN-SR and was reversed after a 72 h nitrate-free interval.

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The relation between heart function and the prognosis of patients with Duchenne muscular dystrophy (DMD) was analyzed in 27 non-survivors and 40 survivors by fractional shortening (FS) of the left ventricle from M-mode echocardiogram, and by the PEP/ET ratio from the systolic time interval. the patients were divided into 5 groups; (1) patients who died of congestive heart failure (group 1), (2) those who died of congestive heart failure and respiratory failure (group 2), (3) those who died of respiratory failure (group 3), (4) those who died suddenly of undefined etiology (group 4) and (5) survivors (group 5). Data from non-invasive cardiac function tests were analyzed retrospectively for 2 years and compared at 2 years, 1 year and about 3 months before their deaths in cases of group 1, 2, 3 and 4, and the data obtained at the same period were also compared with those of survivors (group 5). The age at death in group 1 (17.3±4.9 years) was significantly younger than that in group 2 (25.3±4.2 years), however, it did not statistically differ from group 3 (19.8±3.3 years old). The value of FS in group 1 were significantly lower than those in group 3, 4 and 5 at three examinations, whereas no difference in PEP/ET was observed among them. Cardiothoracic ratio (CTR) on chest X-ray in group 1 was not significantly different from other groups in each period, but the left ventricle dilated rapidly in the terminal stage of congestive heart failure which could be more precisely detected by the M-mode echocardiogram. These results indicate that in DMD, early development of congestive heart failure was associated with a poor prognosis. FS was a most sensitive noninvasive tool in predicting the prognosis. Significant reduction in FS was detectable 2 years before death. Progression in abnormality of left ventricular dimension as well as in FS may be another useful index for evaluating the prognosis of patients dying from congestive heart failure.

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The patient presented in this paper had been stable for 3 months after the induction of hemodialysis, when nausea, vomiting and hepatomegaly suddenly developed. A chest film revealed rush cardiomegaly, and massive pericardial effusion was demonstrated by echocardiography. One liter of hemorrhagic fluid was removed by pericardiocentesis and subsequent pericardial drainage under echocardiography. The patient received chemotherapy against pulmonary tuberculosis 30 years ago and calcification on chest film was apparent. Although sputum smear and pericardial effusion was negative for acid-fast organisms, combination therapy was initiated for suspected tuberculosis. The patient recovered completely and 2 months later it was demonstrated that cultures of sputum grew mycobacterium tuberculosis. Tuberculin skin test (PPD), which was negative 2 months previously, converted to positive. Tuberculosis must be considered as a potential cause of pericardial tamponade in patients on regular hemodialysis, and prompt therapy for both cardiac tamponade and the occult infection is warranted.

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Positron emission tomography enables us to measure, in-vivo, regional cerebral blood flow and metabolism. recently developed method of H₂¹⁵O bolus i.v. injection in our laboratory made it possible to quantitate regional cerebrovascular response rate from stimuli. High resolution tomographic images of regional cerebral blood flow, metabolism and regional brain activation by verbal stimulation are presented by using those methods. Features of cerebral circulation and metabolism on the control of regional cerebral blood flow are briefly described.

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To analyze the origin of the coronary artery inflow and the coronary vein outflow, we measured the intramyocardial artery flow and the epicardial small vein flow by means of a laser Doppler velocimeter with an optical fiber. The functional characteristics of the intramyocardial capacitance vessels were investigated by analyzing the responses of coronary vein flow after stepwise changes in coronary artery pressure during long diastole. Then the effect of the intramyocardial capacitance vessels on coronary artery inflow and vein outflow was evaluated. Intramyocardial artery flow was found to be almost exclusively diastolic with frequent systolic reverse flow, whereas peripheral coronary vein flow was almost systolic exclusively. The intramyocardial capacitance vessels have two functional components, unstressed volume and ordinary capacitance. When the unstressed volume was saturated, the intramyocardial displacable blood volume impeded the coronary artery inflow, but promoted vein outflow.

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To clarify the mechanical adaptation and interference of coronary vessels, we studied hemodynamics of coronary circulation in control and 4 different pacing rates (80, 100, 120, 150/min) in 5 patients with angina pectoris (AP) and in 5 patients with hypertrophic cardiomyopathy (HCM). Coronary sinus flow (CSF) was measured by a Webster's thermodilution catheter, and we applied ascorbic acid-platinum reaction for the mean transit time measurement in left coronary flow (t₀-t₂). Coronary vascular bed (CVB) was obtained by multiplying CSF and t₀-t₂. CSF in AP gradually increased from 104±21 ml/min at 72/min to 148±42 ml/min at 120/min, while CSF in HCM changed slightly from 91±25 ml/min at 64/min to 94 ml/min at 120/min. Average t₀-t₂ in HCM was 6.0±1.6 sec in control which was significantly lower than that in AP (7.8±0.7 sec). Calculated CVB in AP increased at any given heart rate up to 120/min (13.5±2.4, 15.8±1.7, 15.0±4.7, 15.1±4.3 ml), but CVB in HCM decreased from 9.1±2.3 ml at 64/min to 8.1±1.7 ml at 120/min. These data suggest that myocardial compression and suction at different heart rates and with different cardiac muscle structures play an important role for beat adjustment of coronary circulation in cardiac cycle.

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Since it is still controversial as to whether or not atrial natriuretic peptide (ANP) antagonizes norepinephrine (NE)-induced vasoconstriction, we examined the interactions of ANP and NE with respect to renal circulation. (I) Although ANP infusion at 25 ng/kg/min for 40 min caused a decrease in total peripheral resistance (-11%, p<0.01) in 34 patients with cardiovascular disease and 15 normotensives (NTs), renal vascular resistance (RVR) was not reduced consistently by ANP. However, there was a negative correlation between changes in RVR and the preinfusion plasma NE level (r=-0.51, p<0.001). (II) When NE infusion into 6 NTs at 100 ng/kg/min was followed by ANP infusion, urinary Na excretion was increased to a greater degree than that by ANP infusion alone (+234% vs +34%, p<, 0.01). Furthermore, ANP brought about a recovery in NE-induced falls in renal blood flow (+40%) and glomerular filtration rate (+38%, both p<0.05). these effects were attributed to both a decrease in calculated renal afferent resistance and an increase in efferent resistance (-43% and +17%, respectively, p<0.05). thus, increased sympathetic nervous activity seems to augment the renal effects of ANP, and the antagonistic effects of ANP to NE-induced pregllomerular vasoconstriction may counteract Na retention caused by excessive sympathetic tone.

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The total blood flow and microvessel blood flow in the mesentery and the intenstine anesthetized rabbits were measured while systemic hemodynamics were altered by baroreceptor stimulation and by noradrenaline injection. The percent change of the total peripheral resistance (Rt) was greater than the change in resistance in the intestinal vascular bed (Ri) during baroreceptor stimulation. The capillary blood flow in the intestinal muscle layer (Qs) and villus (Qv) increased slightly while the intestinal arterial flow (Qa) and the arteriolar flow in the mesentery (Qm) decreased. These data indicated that Qs and Qv were not controlled by the sympathetic vasoconstrictor system. The percent change of Ri was greater than that of Rt during noradrenaline injection. Noradrenaline decreased Qa, but Qs and Qv were decreased while Qm was increased. These results show that noradrenaline stimulates alpha-adrenoceptors on small arteries and arterioles in the intestine. The observed Qm changed was in response to the systemic hemodynamic change caused either by the baroreceptor input or by noradrenaline.

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