To elucidate the role of right ventricular asynergy and tricuspid regurgitation (TR) in hemodynamic alterations occurring during right ventricular infarction, left and right ventriculography with pressure meas-urements were performed in 22 patients with acute inferior myocardial infarction. Twelve patients with a proximal right coronary artery (RCA) occlusion (Group I) had elevated right atrial pressure (16±4 vs 8±5mmHg, p<0.01), low cardiac output (2.5±0.7 vs 3.5±0.6l/min/m2, p<0.05) and a greater degree of TR, compared with 10 patients with a distal RCA occlusion (Group II). Inferoposterior wall asynergy of the right and left ventricles was similar in Groups I and II. In Group I, there was an additional asynergy of the anterolateral free wall of the right ventricle. Cardiac output in those patients was not related to the left ventricular ejection fraction (EF) but to the right ventricular EF. A greater degree of TR was found in association with a lower right ventric-ular EF. The decrease in cardiac output was closely related to the extent of TR. These results indicate that right ventricular asynergy and TR due to proximal RCA occlusion may play important roles as causes of hemodynamic alterations seen during the acute phase of inferior my-ocardial infarction.

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We studied the hemodynamic effect of a single dose of the new directacting vasodilator, flosequinan, in 25 patients with severe acute-onset heart failure complicating acute myocardial infarction, which was resistant to high doses of diuretics, nitrates and dobutamine given intravenously. Flosequinan was added to conventional therapy within 3.7± 0.8 days of the infarction in the form of a single oral dose of 100mg. Hemodynamic monitoring was performed every hour for 4 hours after the administration, without any other drug being added. Flosequinan produced hemodynamic improvement in all patients. The effect peaked at 1 to 2 hours and remained at this level at 4 hours. Pulmonary capillary wedge pressure decreased from 28.4±4.5 to 17.8±5.7mmHg and cardiac output increased from 3.5±0.3 to 4.0±0.4L/min (p<0.05 for both). Pulmonary arterial and pulmonary vascular resistances were also significantly reduced. Heart rate was not significantly altered. Mean systemic arterial pressure was slightly but not significantly reduced. Administration of flosequinan was not associated with symptomatic hypotension, cardiac arrhythmias or other adverse events and the hemodynamic effect was not related to the pre-treatment serum sodium concentration. We conclude that flosequinan is effective in producing acute hemodynamic improvement in patients with heart failure complicating acute myocardial infarction which is resistant to conventional therapy. Flosequinan is well tolerated in this group of patients and therefore further studies to determine the duration of action of the drug in this condition are appropriate.

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The incidence and risk factors for cerebral infarction in Japanese patients with acute myocardial infarction were evaluated. Seven (5.0%) of 140 patients with acute myocardial infarction suffered from cerebral infarction during their initial hospitalization. The incidence was slightly higher than those reported in Western countries. Anterior wall myocardial infarction and a past history of cerebrovascular disease were considered to be probable risk factors for the complication. A beneficial effect of anticoagulant therapy in preventing cerebral infarction in cases of acute myocardial infarction with those risk factors is suggested.

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Although there are many reports on sudden cardiac arrest occurring outside the hospital, little is known about the precise prognostic factors that determine the outcome after cardiopulmonary resuscitation. Clinical information before and immediately after sudden cardiac arrest is frequently incomplete because the event occurs outside the hospital. We studied 90 consecutive patients with sudden and unexpected cardiac arrest who were resuscitated in the general ward of our hospital. Twenty-five (28%) were discharged from the hospital. Multivariate analysis revealed that the promptness of initiation of CPR, age, severity of cardiac dysfunction, time and the type of arrhythmia are of significance in relation to survival. To evaluate long-term survival after hospital cardiac arrest, we analyzed long-term follow-up data accumulated during a 16 year period. In the group of 25 patients in our study, there have been a total of 10 deaths (40%). Five of the 10 deaths resulted from recurrent cardiac arrest and 1 was a noncardiac death. There was a high rate of recurrence of cardiac arrest in the first year following resuscitation, especially among the cardiomyopathy patients.

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The difficulty in making an accurate diagnosis of acute pulmonary embolism is well known. To clarify the role of echocardiography, including Doppler echocardiography, in acute pulmonary embolism, we examined hemodynamic and echocardiographic parameters in 9 patients with acute pulmonary embolism just before and after treatment with urokinase. As hemodynamic parameters normalized after treatment, echocardiographic parameters such as deformity index of the left ventricle (LV-DI), end-diastolic dimension of the right ventricle (RVDd), the left ventricle (LVDd), the inferior vena cava, and RVDd/LVDd all significantly changed toward normal. Highly significant correlations were found between the echocardiographic and hemodynamic parameters, the best of which was between the LV-DI and systolic pulmonary artery pressure (r=-0.885, p<0.001). Doppler echocardiography quantitatively evaluated the grade of tricuspid regurgitation, and accurately estimated systolic pulmonary artery pressure.
We conclude that echocardiography, including Doppler echocardio-graphy, sensitively reflects the right ventricular pressure and volume overload of acute pulmonary embolism, is quite useful for its diagnosis which is often difficult, and is suitable for noninvasive follow up of these patients.

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A new method for the calculation of left ventricular volumes called the "semi-geometric" method, was reported by Nichols et al in 1984. This method, however, still had certain limitations for practical use. This paper describes a modified semi-geometric method in which the left ventricular volume was obtained from conventional left ventricular ejection fraction measurement data collected from the modified left anterior oblique position with a caudal tilt of 10 degrees or more and a left posterior oblique blood pool image. The left ventricular end-diastolic volumes obtained by this method were compared with those calculated by combining the thermodilution cardiac output and the left ventricular ejection fraction. The correlation coefficient was r=0.93 (n=20). In the phantom experiment, the true volumes and those obtained by this method showed an excellent correlation (r=0.99). This method is considered accurate and practical.

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An 80 year old diabetic male with evidence of peripheral and autonomic neuropathy was admitted with chest pain. He was found to have atrial flutter at a ventricular rate of 70/min which slowed down to 30-40/min when nifedipine (60mg) in 3 divided doses, during which he was paced at a rate of 70/min. This is inconsistent with the well-established finding that nifedipine induces tachycardia in normally innervated hearts. However, in hearts deprived of compensatory sympathetic drive, it may lead to bradycardia.

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Between 1974 and April, 1988, 9 patients with congenital coronary artery fistulas underwent surgical repair. Of these, 4 were female and 5 male, ranging in age from 6 to 50 years (mean 28.2±18.9). Seven patients were symptomatic (congestive heart failure and/or angina), whereas in 2 patients the diagnosis was established through the investigation of an asymptomatic continuous murmur. The origin of the fistula was the left main coronary artery in 1, left anterior descending artery (LAD) in 2, circumflex artery (Cx) in 3, Cx+LAD in 2 and LAD+right coronary artery in 1 patient. The sites of termination of the fistulous tract were the pulmonary artery in 6, the right atrium in 1, the right ventricle in 1 and the left ventricle in 1 patient. In 2 cases the fistulous tracts were ligated without utilizing cardiopulmonary bypass (CPB). In 7 cases CPB was instituted and in 6 of these the fistulous communications were closed from within the termination chamber, in 1 patient the fistula was closed through a coronary arteriotomy during elective ventricular fibrillation. There was no operative mortality and long term follow-up was uneventful after a mean follow-up of 5.4±5.2 years, with 8 patients still completely asymptomatic.
Surgical therapy is recommended for patients having coronary artery fistulas in order to prevent fistula-related complications. In those cases requiring CPB, closure of the fistula from the involved chamber only is suggested.

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The effect of a varying period of ischemia on the development of myocardial infarction was investigated in the rabbit. Radiomicrosphere measurements confirmed that the collateral blood flow is almost zero (0.02±0.01ml/min/g) and without a significant transmural gradient in the rabbit heart (n=15). A coronary branch of the left circumflex artery was occluded for 5, 10, 15, 30 or 60min and then reperfused. The coronary branch was occluded permanently in another group of rabbits. Three days after the coronary occlusion, the infarct size was determined by hematoxylin-eosin and Mallory's staining and the ischemic zone size was determined by fluorescent particles. The results showed that the percentage of the ischemic zone infarcted (% infarction) vs the log of duration of ischemia yielded a sigmoid curve which could be linearized by probit analysis: Probits of % infarction=3.05×log (ischemic duration in minutes)+0.33, r=0.83, p<0.01. The regression equation indicated that 50% of the ischemic myocytes necrotized after 34min of coronary artery occlusion. Unlike in the dog heart, the infarct of the rabbit heart first appears in the midmyocardium and then progresses towards both the endocardium and epicardium.

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The ineffectiveness of β-adrenergic blockade in abolishing adenosineinduced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flowdependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16μg•kg^-1•min^-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5mg•kg^-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary β-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heat emission. However, both types of effects were moderate, and only the hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30μg•kg^-1•min^-1 infused into the left heart), the flowreducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventional β-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.

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Thrombolytic therapy with plasminogen activators, urokinase (UK) and streptokinase (SK), can produce serious complications such as systemic bleeding. We have developed an autologous plasmin (AP) solution as a new potential thrombolytic agent and evaluated its efficacy in animal experiments. The AP solution was prepared by the addition of UK to autologous plasma separated by centrifugation (4°C, 3, 000rpm, 10min). The plasmin activity in the AP solution was measured by the plasminogen-free fibrin plate method and spectrophotometric assay with the chromogenic substrate S-2251. In animal experiments, the femoral artery of anesthetized mongrel dogs (n=20) was constricted by ligation (1mm in diameter) and a fibrin clot was embolized into this site. Either AP solution (n=8), UK solution (n=6) or saline (n=6) was selectively infused for 3min. Prior to the infusion, a temporary flow obstruction was made by inflation of a balloon tip catheter located proximal to the embolized site. The thrombolytic effect was sequentially observed with an ultrasound flow meter for up to 60min. The total dose of UK was 120, 000IU in both AP and UK solutions. The results showed that the plasmin activity of AP solution was maintained up to 90min at 22°C with an additional dose of more than 6, 000IU/ml of UK. In animal experiments, a restoration of the flow was observed more frequently with the AP solution than the UK solution within 15min of the infusion (p<0.01). Thus, a high thrombolytic efficacy was observed with a selective infusion of rich, activated plasmin (AP) solution. This treatment could be applied as a new approach for arterial thrombolysis.

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The efficacy of N-acetylcysteine in reversing nitrate tolerance has been controversial. This study examined whether continuous administration of N-acetylcysteine, a sulfhydryl compound, can prevent the development of tolerance to nitroglycerin; its acute effects on developed tolerance were also assessed. Rats were treated with subcutaneous injections of 1) 100mg/kg nitroglycerin, 2) 100mg/kg nitroglycerin and 700mg/kg N-acetylcysteine, 3 times a day for 3 days. The sensitivity to nitroglycerin was studied in aortic preparations. The degree of developed tolerance to nitroglycerin was partially inhibited by simultaneous injection of N-acetylcysteine. Subsequent in vitro preincubation of aortic strips with nitroglycerin (10^-5M) reduced the subsequent nitroglycerin sensitivity of vessels from rats treated with nitroglycerin and N-acetylcysteine; sensitivity returned to the initial control level after in vitro preincubation with N-acetylcysteine. The nitroglycerin sensitivity of vessels from rats treated only with nitroglycerin, though, was not affected by in vitro preincubation with N-acetylcysteine. In conclusion, N-acetylcysteine is not effective in reversing the high degree of tolerance developed to nitroglycerin. However, continuous administration of Nacetylcysteine is effective in preventing the development of nitroglycerin tolerance.

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The cardiac effects of mildronate were studied in isolated and blood-perfused atrial and ventricular preparations from mongrel dogs. Mildronate (10^-9-10^-6mol) did not induce any chronotropic or inotropic responses in spontaneously beating isolated right atria at 37°C. However, it produced negative chronotropic and inotropic effects at large doses (10^-5-10^-4mol). Mildronate-induced responses were not significantly inhibited by treatment with atropine, suggesting that they do not involve muscarinic mechanisms. Mildronate produced only a slight negative inotropic effect in electrically paced, isolated left ventricular preparations at extremely large doses. Intravenous injections of 10-4mol/kg mildronate to the support (donor) dog induced a slight, non-significant, depressor effect, and did not significantly influence either atrial pacemaker activity or atrial developed tension. From these results, it is concluded that a therapeutic dose of mildronate has no direct influence on SA nodal pacemaker activity and atrial contractility, but that it has a slight cardiac depressant property at large doses.

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In the present study, we report a case of pheochromocytoma whose high blood pressure was well controlled by single-agent therapy with longacting nifedipine, in spite of the failure of the combination of labetalol and prazosin in lowering blood pressure satisfactorily. A 48 year old female was first noted to have hypertension (160/100mmHg) at 45 years of age. Hypertension was not controlled by conventional antihypertensive drugs. She was admitted to Fukui Prefectural Hospital in September, 1985. Her blood pressure on admission was 210/110mmHg. Extraction of the left adrenal gland containing a pheochromocytoma (30×37×10mm) was performed in November, 1985. Her hypertension and abnormally high plasma noradrenaline (NA) concentration (1, 760pg/ml, normal value 40-350pg/ml) were sustained even after operation. Combination therapy with labetalol (400mg/day) and prazosin (6mg/day) was unsatisfactory, and the addition of long-acting nifedipine (40mg/day) produced a marked decrease in blood pressure. Furthermore, single therapy with longacting nifedipine was effective. No reduction of urinary NA excretion was observed in our patient during long-acting nifedipine therapy, suggesting that the decrease in blood pressure was not caused by suppression of NA release from pheochromocytoma tissue.

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Unilateral total anomalous pulmonary venous connection from a unilateral lung is extremely rare. A 6-year-old patient with anomalous pulmonary venous connection from the entire left lung to the left innominate vein, with an intact atrial septum, diagnosed by two-dimensional and Doppler echocardiography is reported. The combination of two-dimen-sional and Doppler echocardiography is very useful not only for anatomical diagnosis, but also for evaluation of its hemodynamics, despite the wide anatomical variability of the pulmonary venous connection. This is the first report of a case of left total anomalous pulmonary venous connection diagnosed noninvasively.

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