To determine changes in platelet activity, prostaglandin metabolism and catecholamine release along with changes in hemodynamics during exercise, we measured these parameters before and immediately after treadmill exercise. Measurements were made on peripheral arterial blood simultaneously with a direct aortic pressure recording in 30 patients with coronary artery disease (Group 1), in 20 patients without significant coronary disease (Group 2), and in 11 young healthy volunteers as controls. At the peak of the exercise regimen, the ST segment depression was found to be significantly lower in Group 1 than in Group 2, whereas the changes in the DPTI/TTI ratio in Group 2 and the controls decreased with the increase in the duration of exercise.
The increased serum lactate level at the intermediate level of exercise (420±20sec) was significantly lower in the controls than in the other 2 groups. Changes in β thromboglobulin, platelet factor 4, and plasma norepinephrine were similarly increased in all 3 groups by exercise. At the termination of exercise, however, 6 ketoprostaglandin F₁α, in Group 1 was insignificantly elevated, whereas it increased from 42.9±7pg/ml to 55.7±7.1 (p<0.05) in Group 2 and from 38.2±5.7pg/ml to 45.1±6.8 (p<0.01) in the controls.
These results suggest that decreased prostacyclin production in the vessel wall might be an indicator of myocardial ischemia, and that the administration of prostacyclin may modulate the coronary vascular tone exaggerated by exercise.

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Six patients with dtransposition of the great arteries and I patient with tricuspid atresia were diagnosed echocardiographically. Balloon atrial septostomy (BAS) was performed successfully in all cases with the aid of twodimensional echocardiography. Echocardiography may be superior to fluoroscopy during BAS because it permits easy detection of spontaneous passage of the inflated catheter into the left ventricle spontaneously through the mitral valve (like a left atrial myxoma). With the visualization of related cardiac structures during BAS, obstruction of the IVC with the balloon was also prevented. Using this method, bedside application of BAS is possible.

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Echocardiographic left ventricular (LV) dimensions in patients with complete transposition of the great arteries (TGA's) were measured before and after the Jatene procedure and/or pulmonary artery banding (PAB). The LV posterior wall thickness at enddiastole (LVPWTD) increased from 3.5±0.4 to 4.9±0.9mm (mean±1SD) (p<0.01) after PAB, but it did not show a significant change following the Jatene procedure (from 4.5±1.0 to 5.3±0.8mm). The LV enddiastolic internal dimension (LVIDD) increased from 17.7±4.0 to 22.6±6.5mm after PAB (p<0.01), but remained unchanged after the Jatene procedure (from 24.5±5.0 to 25.0±3.0mm). The LV shortening fraction (LVSF) decreased from 0.62±0.10 to 0.47±0.14 after PAB (p<0.01), but remained unchanged after the Jatene procedure (0.40±0.10 to 0.37±0.10). The a/b ratio at endsystole: (a/b)s, which indicates the flatness of the LV configuration, increased from 0.27±0.14 to 0.60±0.21 after PAB (p<0.01) and from 0.61±0.13 to 0.74±0.17 after the Jatene procedure (p<0.01). The data obtained became stable 1 month after operation. One patient died of low cardiac output with no evidence of myocardial infarction after the Jatene procedure. In this patient, LVPWTD was 5.7mm, LVIDD was 26mm, LVSF was 0.71 and the (a/b)s ratio was 0.55.
In conclusion, PAB effectively increases LV wall thickness 1 month after operation, and echocardiographic prerequisites for the Jatene procedure were LVPWTD>4.0mm, (a/b)s ratio>0.5, and LVSF between 0.2 and 0.56 in patients younger than 16 months.

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Hematocrit (Hct) changes during mental stress were studied in 21 patients with mild hypertension. A 10min arithmetic stress test increased blood pressure from 129±2/80±2mm Hg (mean±SEM) to 167±5/98±3mm Hg, and heart rate from 64±2 to 81±3 (p<0.001). Concomitantly, a significant (p<0.001) increase in Hct was observed (from 41.5±0.7% to 42.2±0.8%), and increments of Hct (-0.1% to 2.2%) were significantly (r=0.61, p<0.01) correlated with those of systolic blood pressure. Plasma levels of norepinephrine (NE), epinephrine (E) and atrial natriuretic peptide (ANP) also showed a significant increase after mental stress. All these changes disappeared after a 60min recovery period. The results suggest that mental stress increases Hct promptly, which may be due to concomitant increases in plasma NE, E and ANP levels. Hct elevation resulting from mental stress may be clinically relevant, at least, in hypertensive patients who are at risk of occlusive vascular diseases.

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To study the time course of spontaneous and induced ventricular arrhythmias after myocardial infarction (MI), 20 dogs underwent ligation of the left anterior descending coronary artery and temporary occlusion and reperfusion of the obtuse marginal branch. There were 5 early deaths (<24 hours) due to spontaneous ventricular fibrillation (VF). All 15 survivors exhibited spontaneous ventricular tachycardia (VT) up to day 3 with the shortest cycle length occurring at 17 hours after MI (232±11 msec: mean±SEM). The grade of arrhythmia complexity was decreased after day 4 compared to day 1 (p=0.049), and the number of ventricular premature complexes was reduced after day 6 (1700±1390/hour) compared to day 1 (9500±640/hour, p=0.042). Serial electrophysiologic studies were carried out on days 8, 15, 22, and 29 via an implanted antitachycardia pacemaker using 1 to 3 extrastimuli and rapid ventricular pacing (RVP). On day 8, VT was inducible in 7 dogs (46%), VF in 4 (27%), and 4 dogs (27%) exhibited a negative response. On day 15, 3 more dogs became negative, and all previously negative dogs displayed negative responses. From day 15, the inducibility of VT/VF remained "constant" using RVP. However, inducibility by triple extrastimuli declined week by week until day 29. Stepwise logistic regression analysis of 20 variables selected the mass of the MI as the only independent predictor of inducible VT/VF by multiple extrastimuli and RVP after day 15 (p=0.049). Thus significant timeand modedependent changes in inducibility of VT/VF occur during the early phase after MI.

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Fifteen week old male Wistar rats (n=7) were made diabetic by intravenous injection of streptozotocin (50mg/kg). Agematched, untreated male Wistar rats (n=9) served as controls. Hearts were removed after 5-6 weeks of diabetes, and the isometric developed tension (T) of isolated left ventricular papillary muscles and its first derivative (dT/dt) were measured at a frequency of 0.2Hz. During testing, the muscles were perfused with Tyrode's solution (Ca2⁺ concentration was half of normal Tyrode's solution, pH7.4, 32°, bubbled with 95% O² and 5% CO₂). In addition, the left ventricular isoenzyme pattern, which is related to myocardial energetics, was determined by pyrophosphate gel electrophoresis. There was no significant difference in isometric developed tension between diabetic and control rats (DM: 2.90±0.89 vs controls: 2.87±0.85g/mm², mean±SD), but in diabetic rats, dT/dtmax decreased significantly as compared with controls (DM: 23.5±4.2 vs controls: 31.9±7.9g/mm²•s, p<0.05). Myocardial mechanical responses to isoproterenol (10-⁷M) and dibutyryl cyclic AMP (10-⁵M) also decreased in diabetic rats. The left ventricular myosin isoenzyme pattern shifted toward VM-3 in diabetic rats (VM-3: DM: 74.9±10.7 vs controls: 9.5±4.1%, p<0.001). These results indicate that diabetes influences myocardial contractility and changes cardiac energetics. Postreceptor processes may play a role in myocardial mechanical responses to catecholamines in streptozotocindiabetic rats.

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This study used an isolated right atrial preparation, crossperfused with arterial blood from a support dog. We investigated the effects of dibutyryl cyclic AMP (DBcAMP) on heart rate and arterial blood pressure of the support dog and on the sinus rate and atrial contractile force of the isolated perfused atrium. DBcAMP was injected into the external jugular vein of the support dog or into the sinus node artery of the isolated atrium. DBcAMP to the support dog induced a small increase and/or decrease in arterial blood pressure at a dose of 3 or 10mg/Kg i.v. It produced a decrease, with or without an increase in blood pressure, at a dose of 30mg/Kg i.v., and a dosedependent increase in heart rate in the support dog. In the isolated atrium, positive chronotropic and inotropic effects were observed. Direct injection of DBcAMP (3-30mg) into the sinus node artery of the isolated atrium induced positive chronotropic and inotropic effects, after initial brief negative effects, in a dosedependent manner. DBcAMP did not change norepinephrineinduced positive chronotropic and inotropic effects in the isolated atrium. These results demonstrate that DBcAMP induces a decrease in systemic arterial blood pressure with increases in sinus rate and atrial contractile force, and acts additively with the norepinephrineinduced positive cardiac effects in the dog heart.

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The purpose of the present study was to investigate the mechanisms of the hypotensive actions of an angiotensin converting enzyme inhibitor (captopril) in hypertension. In perfused mesenteric vasculatures from spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, 10-13 weeks of age) and agematched normotensive Wistar Kyoto rats (WKY), the effects of captopril on vascular responsiveness and norepinephrine release from the adrenergic nerve endings were examined. The vasoconstrictor responses and norepinephrine release during the electrical nerve stimulation were significantly enhanced in SHR compared to those in agematched WKY. Captopril reduced both vasoconstrictor responses and norepinephrine release during the electrical nerve stimulation, dosedependently. These inhibitory effects of captopril were significantly greater in SHR than in WKY.
The results demonstrate that captopril affects presynaptic sites on the resistance vessels and causes a decrease in electricallystimulated norepinephrine release from the adrenergic nerve endings. The marked reduction of both pressor responses and norepinephrine release by captopril in SHR suggests an enhanced reninangiotensin system in the vascular walls of hypertension.

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Decreased oxygen supply rather than increased demand may be the primary pathogenic mechanism of myocardial ischemia in patients with unstable angina. Coronary artery spasm and in vivo platelet aggregation may play an important role in the mechanism by which the magnitude of fixed obstruction secondary to coronary atherosclerosis is transiently exacerbated.^{1), 2)}
In this case report, we describe a patient who developed chest pain accompanied by ischemic ECG changes during coronary arteriography, due to a transient thrombotic aggravation of a fixed, significant coronary stenosis. Percutaneous transluminal coronary angioplasty was performed with relief of the coronary stenosis and of the symptoms.

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An asymptomatic 48 year old man had transient Twave inversion in the anterolateral leads after nonpenetrating chest trauma. Both the patient and his 6 year old son showed the typical skin hyperelasticity and joint hyperextensibility of the Ehlers-Danlos syndrome, suggesting autosomal dominant inheritance. The coexisting cardiac abnormalities of the patient included multiple coronary aneurysms, mitral valve prolapse with slight regurgitation, fusiform dilatation of the ascending aorta with moderate insufficiency and left anterior hemiblock. A routine noninvasive cardiovascular evaluation should be performed in all patients with Ehlers-Danlos syndrome in order to exclude valvular heart disease and dilatation of the aortic root or of other vessels, including the coronary arteries.

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Serum apolipoprotein (apo) B concentration in SHRSP showed considerably low value in comparison with that in WKY at all ages examined, and the agerelated change was relatively similar to that in serum apo A-IV concentration. The ratio of apo B to apo AI in SHRSP was not significantly different from that in WKY except 48 weeks of age when renal failure might cause the marked increase of serum apo AI concentration in SHRSP. This suggested that there might be no distinct difference in atherogenesity (tendency toward atherosclerosis) between SHRSP and WKY when the rats were fed a normal diet.

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