We investigated the coronary angiography (CAG) of 1, 022 patients to clarify the clinical significance of myocardial squeezing and obtained the following results.
1) Of 1, 022 patients undergoing CAG, 164 patients (16.0%) had myocardial squeezing of the left anterior descending artery (LAD) and 16 patients (1.6%) had only the first septal perforating branches producing a squeezing of the artery during systole. The association of myocardial squeezing of the LAD with different diagnosis was anterior chest pain syndrome (26.6%), arrhythmia (23.6%), cardiomyopathy (21.7%), angina pectoris (15.8%) and myocardial infarction (6.9%).
2) The degree of narrowing of the LAD was classified into 4 grades; 25-49%: 36 patients (22.0%), 50-74%: 82 patients (50.0%), 75-89%: 35 patients (21.3%) and greater than 90%: 11 patients (6.7%).
3) The morphology of the vessel subjected to myocardial squeezing was classified into 4 patterns on CAG. Type A is localized narrowing. Type B is bead-like narrowing. Type C is diffuse narrowing. Type D is tapering and obstructive narrowing. All type D patients had the septal perforating branches.
4) We investigated whether only myocardial squeezing has ischemic ST-T segment changes in the ECG. Fifty-five of 87 patients (63.2%) with myocardial squeezing of greater than 75% and organic stenosis of less than 50% of the LAD had ischemic changes in the ECG during exercise or pacing-induced tachycardia.
5) There was no special feature between myocardial squeezing and subjective symptoms.

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The correlation between R wave voltage variations (ΔR) and the angiographic severity of coronary artery disease (CAD) at progressively increasing heart rate (HR) steps was evaluated in 51 patients (pts) without CAD (OV), in 42 pts with single (SVD), in 43 with double (DVD) and in 59 pts with triple vessel disease (TVD).
At the end of stress the sensitivity of ΔR was higher in DVD and TVD pts than in SVD pts. There was no clear correlation between exercise-induced R wave changes and the angiographic severity of CAD, since the qualitative and quantitative ΔR evaluation during effort showed similar changes in ΔR for a wide range of HR's in the entire study population.
Since different degrees of exercise tolerance were found in pts with SVD, DVD and TVD, we hypothesize that the correlation between ΔR and the severity of CAD at the end of stress testing may be artifactual.

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Body surface mapping was used to study the effects of diltiazem on exercise-induced QRS amplitude changes in 7 patients with stable effort angina pectoris. Body surface areas showing R or S amplitude changes (>0.2mV) after treadmill exercise were calculated. After the administration of 90mg of diltiazem, the R increased area was significantly smaller than that without diltiazem (p<0.02), although the same workload was performed. It was suggested that diltiazem diminished the exercise-induced myocardial ischemia and this improvement of ischemia resulted in the reduction of the R increased area after exercise.

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We have investigated the use of M-mode echocardiography for the quantification of aortic valve stenosis through the application of a hydraulic orifice equation using only noninvasively determined hemodynamic variables. The new equation is A=(2/5)SV/(t^3/2dP^1/4HR), where A is the effective aortic valve area in cm², SV is the stroke volume in ml, t is the systolic ejection period in seconds, dP is the echographically estimated aortic valve gradient and HR is the heart rate. The predicted valve areas correspond with those derived by conventional cardiac catheterization studies at a level of r=0.84, SE=0.14cm², N=10. The results suggest that M-mode echocardiography may have application to the quantitative diagnosis of aortic stenosis.

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To evaluate the significance of left ventricular (LV) hypertrophy in dilated cardiomyopathy (DCM), 50 patients seen between 1976 and 1983 were studied echocardiographically. Patients were classified into 4 groups according to the degree of LV dilatation and LV hypertrophy. Group I consisted of 17 patients who had mild to moderate LV dilatation without LV hypertrophy (LV end-systolic dimension: Ds<60mm, LV wall thickness at end-systole: WTs<15mm). Group II consisted of 12 patients who had mild to moderate LV dilatation with LV hypertrophy (Ds<60mm, WTs≥15mm). Group III consisted of 8 patients who had marked LV dilatation with LV hypertrophy (Ds≥60mm, WTs≥15mm). Group IV consisted of 13 patients who had marked LV dilatation without LV hypertrophy (Ds≥60mm, WTs<15mm). Twenty patients had LV hypertrophy and 30 patients were without LV hypertrophy at the beginning of this study. New York Heart Association functional classes, cardiothoracic ratio and ECG findings during the first study did not show statistically significant difference among 4 groups.
During a follow-up period averaging 2.7 years, 8 patients died of congestive heart failure (CHF), including 5 of Group IV patients and 3 of Group I patients who had progressive LV dilatation. Three patients without signs of CHF expired suddenly; they were in Groups I, II and III during the initial study. Ambulatory ECG studies showed complex ventricular arrhythmias in all 32 patients studied.
In conclusion, LV wall hypertrophy in DCM may be an important factor to predict their prognosis regarding CHF death. Sudden and unexpected death could occur in any patient with DCM and intensive antiarrhythmic therapy is important.

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The results of echocardiographic examination of 23 diabetics are presented.
Significantly increased left ventricular posterior wall thickness and mass and elevated ratio of wall thickness to chamber radius were found in the group of diabetic patients without coronary artery disease and hypertension. The interventricular septum thickness was significantly increased only in the diabetics with hypertension. The possible causes of these findings may be the presence of microangiopathy at the periphery of the coronary circulation or the presence of PAS-positive substances with resulting interstitial fibrosis.

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The computed tomography (CT) number within the region of interest (ROI) was used as a parameter to assess lung density in patients with congestive heart failure. Thirty-eight patients with valvular heart disease (VHD) and 34 patients with ischemic heart disease (IHD) were studied. Based on the New York Heart Association (NYHA) classification, 24 VHD patients were in class I or II (VHD I-II) and the other 14 were in NYHA class III or IV (VHD III-IV). Eighteen patients with IHD were in NYHA class I or II (IHD I-II) and 16 were in class III or IV (IHD III-IV). The CT number was measured bilaterally at the upper, middle and lower levels of the chest and compared with the corresponding values in 21 normal subjects (Group N). In a preliminary study on Group N, the CT numbers were insensitive to the size of the ROI, but were closely related to its location.
In clinical applications, the mean values of the CT numbers in all six lung fields increased in the order of IHD I-II, to VHD I-II, IHD III-IV and VHD III-IV. Except for patients in IHD I-II, they were significantly larger than in Group N. The relationship between the CT number and the systolic and mean pulmonary arterial pressures and the pulmonary capillary wedge pressure were evaluated in 36 patients. Significant correlations were obtained in all six lung fields (r=0.65-0.78, p<0.001). The results suggest that measurement of lung density by CT is useful for the quantitative evaluation of the severity of disease in patients with congestive heart failure.

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Total body hyperthermia (TBHT) was induced in patients with terminal cancer, using a femoral arterio-venous shunt as an extracorporeal circuit incorporating a heat exchanger. A total of 31 systemic hyperthermic treatments lasting 3 to 4 hours at 41.5°C to 42°C (rectal temperature) were performed on 11 patients; chemotherapy had previously been unsuccessful in all of these cases. The effect of TBHT on cardiovascular function was explored in these patients. The heart rate and cardiac output were always markedly increased during hyperthermia, however, the peripheral arterial, central venous, pulmonary arterial and pulmonary wedge pressures were little affected and no progressive metabolic acidosis occurred. TBHT was generally well tolerated and there was no instance in which this treatment had to be terminated because of severe cardiovascular failure during hyperthermia.

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Plasma concentrations of 6-keto-prostaglandin F_1α (6-keto-PGF_1α) and thromboxane B₂ (TXB₂), the stable nonenzymatic metabolites of prostacyclin and TXA₂, respectively, were assayed in 26 patients with essential hypertension and 25 normotensive subjects to investigate the pathophysiological role of prostacyclin and thromboxane A₂ (TXA₂) in essential hypertension. A tourniquet test was also performed on the upper limb of each subject to study the reactivity in peripheral vessels. In addition, platelet aggregation was investigated.
There were significantly increased plasma TXB₂ concentrations and platelet aggregation and significantly decreased plasma 6-keto-PGF_1α concentrations in patients with essential hypertension as compared with normotensive subjects. The responses to tourniquet tests were also different. There were significantly increased plasma concentrations of 6-keto-PGF_1α and TXB₂ and platelet aggregation in normotensive subjects, but no significant changes with essential hypertension as compared to resting values.
These results indicate that the reduction of plasma prostacyclin and increase of plasma TXA₂ may contribute to the maintenance of blood pressure elevation in patients with essential hypertension. In addition, it is also suggested that increased prostacyclin generation in normotensive subjects during the tourniquet test is a protective mechanism. In patients with essential hypertension, the protective activity is reduced.

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Sitting or orthostatic positions and trinitrine-like drugs reduce venous return. We focused on the non-invasive assessment of postural-induced cardiovascular stress and isosorbide dinitrate (IDN) induced changes in 8 male patients with coronary artery disease (CAD), using polygraphic recordings by means of a Thermistor Pulse Transducer.
The pre-ejection period (PEP) is sensitive to reduced preload and to the positive inotropic state of the myocardium. In addition, the % diastole (RR interval-electromechanical systole / RR interval) has been recently demonstrated to be correlated to coronary perfusion in CAD patients.
We observed that IDN in clinostatism and the sitting position reduced preload (longer PEP) with increased heart rate (HR) and did not affect % diastole. In orthostatism, while controls showed an increased HR and prolonged PEP, the HR was higher after IDN, with a fall in PEP and a significant decrease in % diastole.
We ascribed this change to adrenergic stimulation by the hypotensive actions of IDN (lowered mean blood pressure) in orthostatism and with a fall in coronary perfusion. Caution should be taken in CAD patients when postural stress could occur during IDN treatment. Moreover, polygraphic studies can be useful to detect individual responses to nitrates and serial recordings could be employed to assess late responses to chronic management with IDN.

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Respiratory responses during exercise were observed to determine whether improvement of oxygen availability in working skeletal muscle is attributable to increased aerobic capacity after administration of nitrate in patients with effort angina. After isosorbide dinitrate (ISDN) administration, the aerobic capacity increased 3.3ml/min/Kg (20%) as compared with the control test (p<0.001), but the anaerobic threshold (AT), a good indicator of oxygen availability, was unchanged, and the respiratory quotient at the peak of exercise was elevated. These findings suggest that oxygen availability in skeletal muscle was not altered after ISDN, and increased exercise load accompanied increased anaerobic glycolysis. It was concluded that the nitrate-induced increase in aerobic capacity was not dependent upon the change in oxygen availability in skeletal muscle but rather upon the elevated anginal threshold.

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For clarifying the onset mechanism of essential hypertension, the hemodynamics in 9 mildly hypertensive men, mean age of 39.8±10.7 (mean±SD), was compared with 7 normotensive men, mean age of 39.8±10.7, by means of exercise echocardiography, and the effects of indenolol (administered 30 mg/day for 7 days orally to both groups) were studied.
The interventricular septum and the left ventricular posterior wall were thickened in the mild hypertensives. No significant differences between the both groups were shown in the cardiac performance at rest and the cardiac index during exercise. The total peripheral vascular resistance was higher in the mild hypertensives than the normotensives during exercise. However, during exercise, the normotensives showed significant increases in the left ventricular end-diastolic dimension (LVDd) and the stroke index (SI); these changes were not significant in the mild hypertensives. After administration of indenolol, the significant increases in LVDd and SI during exercise were observed in the mild hypertensives.
This study suggests that mild hypertensives with cardiac hypertrophy display a diminished Frank-Starling effect during exercise which may be attributed to the decreased left ventricular compliance due to cardiac hypertrophy and elevated afterload. Indenolol improved the Frank-Starling effect, which decreased in the mild hypertensives.

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In this study, the loss of a diffusible indicator in the pulmonary vascular circuit was quantitated by comparing cardiac output values obtained by measuring paired dilution curves, one from the pulmonary artery (PA) and the other from the aorta, resulting from the injection of a few ml of 5% saline in the right atrium. Cardiac outputs were calculated from the PA and aortic dilution curves from the same indicator injection in 10 anesthetized dogs. From 43 paired trials, the cardiac output values derived from the aortic dilution curves exceeded those obtained from the PA, indicating loss of this diffusible indicator in the pulmonary vascular circuit.

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The usefulness of the thermodilution method for measuring cardiac output (CO) was evaluated in awake rats by comparison with electromagnetic flowmetry. CO was measured in 3- and 6-month-old conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The correlation coefficient between CO obtained by the two methods was 0.66 (p< 0.01). Although CO values obtained by the thermodilution technique tended to be overestimated in comparison with those determined by electromagnetic flowmetry, this method was shown to be useful for measuring CO in unanesthetized rats because of its technical simplicity. Left ventricular mass (LVM) and the ratio of CO to LVM were significantly greater in SHR than in WKY at both ages and CO/LVM increased with increasing age in SHR. The ratio of heart work (HW) to body weight (HW/BW) was increased only in 3-month-old SHR compared with WKY and there was no difference in HW/LVM in 3- and 6-month-old SHR compared with age-matched WKY. The present results suggest that the development of cardiac hypertrophy in SHR is an adaptation to the increased HW due to high afterload.

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The following results were obtained.
A) During brief ligation of the coronary artery, a change in the cardiac wall motion appeared as the first abnormality of the CMG. Succeedingly, epicardial ECG changes were recognized, and lastly, changes of dP/dt appeared.
B) After reperfusion of the coronary artery, dP/dt was quickly normalized, followed by restoration of ST elevation. Cardiac motion, measured by CMG, was the last abnormality to improve.

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Pulmonary changes in acute cerebral ischemia were studied in anesthetized Mongolian gerbils, in which both carotid arteries were occluded simultaneously. Lactate, pyruvate and adenosine triphosphate (ATP) in the brain were measured as indicators of the severity of cerebral ischemia. Microscopic changes in the lung were arbitrarily scored from 0 (normal) to 3 points (severely affected) by the grade and the extent of lesions. Mean arterial pressure (MAP) was also measured through the cannulated femoral artery before and after carotid artery occlusion in a separate group of animals.
Cerebral lactate was increased while ATP decreased in ischemic animals in which pulmonary changes such as intra-alveolar hemorrhages were prominent and frequent. The lung pathology score averaged 1.3 in animals with severe ischemia (lactate≥10 mM/Kg), 0.7 in moderate ischemia (5-10 mM/Kg) and 0.3 in mild or no ischemia (<5 mM/Kg), respectively, suggesting that severe brain ischemia may cause fulminant pulmonary changes. The mechanism of pulmonary lesions in acute cerebral ischemia is discussed.

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The effect of nifedipine on the ejection flow pattern in the left ventricular outflow tract was observed using pulsed Doppler echocardiography in 6 patients with hypertrophic cardiomyopathy. After sublingual administration of nifedipine (10 mg) to 1 patient, the turbulent ejection flow pattern became more marked and increased in duration compared with the initial state. An increase in turbulence in the left ventricular outflow tract may increase the pressure gradient between the left ventricle and the aorta. Nifedipine appeared to have the potential of adverse action on left ventricular outflow obstruction.

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Successful vasodilator therapy of a 27-year-old woman with primary pulmonary hypertension is described. Prazosin 2 mg, orally in combination with isosorbide dinitrate 10 mg, sublingually caused a marked fall in pulmonary vascular resistance. Pulmonary hemodynamics reevaluated after 3 months of combination therapy with prazosin 1 mg qid and isosorbide dinitrate 5 mg qid showed sustained improvement. Therefore, in selected patients with primary pulmonary hypertension, this combination therapy can be used.

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