Serum guanase activity was measured by a new method using direct colorimetric determination of ammonia in 25 patients with acute myocardial infarction, 21 dogs with experimental myocardial infarction and 6 CCl₄-treated dogs, and compared with serum GOT and GPT activity. We found normal serum guanase activity in patients with acute myocardial infarction and in dogs with experimental myocardial infarction without liver damage, even when the serum GOT and GPT activities increased. On the other hand, serum guanase and transaminase activities were elevated significantly in the patients with acute myocardial infarction who had prominent symptoms of cardiac failure and congestion of the liver and CCl₄-treated dogs. These findings suggested that the serum guanase activity was more specific than serum GOT and GPT activity as an indicator of liver damage and determination of serum guanase activity in the patients with acute myocardial infarction might be useful in assessing the presence of liver impairment.

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Abnormal ventricular activation in Wolff-Parkinson-White Syndrome (WPW) can be identified by echocardiography, but the effects of premature ventricular contractions have not been demonstrated. We examined motion of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) by surface echocardiography in 12 awake dogs using a method developed and validated in our laboratory. Premature ventricular contractions (PVCs) were induced by right (RV) and left ventricular (LV) pacing (6 dogs), injection of dopamine (2 dogs) and phenylephrine (2 dogs), and posterior myocardial infarction (MI) caused by embolization of the circumflex coronary artery (2 dogs), and posterior myocardial infarction (MI) caused by embolization of the circumflex coronary artery (2 dogs). PVCs induced by RV and LV septal pacing showed early IVS systolic posterior motion beginning 40.0 msec (range 26-48 msec) after the pacing impulse, while LVPW showed normal motion beginning 78.8 msec (range 63-116 msec) after the pacing impulse and accompanied by decreased posterior IVS motion. PVCs induced by LVPW pacing demonstrated early LVPW systolic anterior motion beginning 43.3 msec (range 31 -68 msec) after the pacing impulse, while IVS showed a normal motion which began 97.3 msec (range 76-130 msec) after the pacing impulse and was accompanied by reduced anterior motion of the LVPW. PVCs induced by dopamine and phenylephrine showed a similar echocardiographic pattern to RV and LV septal pacing, while PVCs induced by MI exhibited a pattern similar to LVPW pacing. This study demonstrates that early IVS or LVPW contraction can be demonstrated by echocardiogram, and also indicates where the site of early excitation after PVCs is.

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Rabbits and Wistar rats developed myocarditis after intracardiac inoculation with Cryptococcus neoformans. Myocardial lesions were observed on the 1st, 2nd, 3rd and 4th weeks after this inoculation in all animals. The cardiac lesions consisted of focal necrosis with mononuclear inflammatory cells infiltration in the myocardium. Cryptococcus neoformans itself was found by PAS stain and indirect immunofiuorescence stain by the 2nd week afte the inoculation. Maximal cardiac lesions were observed in the 2nd week and thereafter, the lesions showed progressive scarring. In the 9th week, there were fibrotic lesions and we were not able to demonstrate cryptococcal antigens in these lesions. Fungemia and antibody for Cryptococcus neoformans were not found over the entire period. Cryptococcal meningeal lesions were observed in all animals. In the animals given an intracardiac administration of saline, Pseudomonas aeruginosa, and Serratia marcescens, there were no myocardial lesions. The relationship of this experimental fungal myocarditis and fungal endocarditis in human is discussed.

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Development of tension in aortic helical strips was studied using the male Kyoto Wistar normotensive (KNR) and age-, sex-matched spontaneously hypertensive rats (SHR) (8 to 10 weeks), to clarify the contractile response of vascular smooth muscle in SHR. In Ca²⁺-containing solution, noradrenaline-induced tension was smaller in SHR than in KNR. After washing the strips with Ca²⁺-free EGTA solution, the tension that developed by the addition of Ca²⁺ was greater in SHR than in KNR. Tension induced by the combination of Ca²⁺ and noradrenaline was the same between the KNR and SHR. It is assumed that these differences between the KNR and SHR aortic strips may be attributed to the abnormal contractility of the vascular smooth muscle in SHR.

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The effects of L-carnitine on ventricular arrhythmias were evaluated in dogs with acute myocardial ischemia and a supplement of excess free fatty acids (FFA). Acute myocardial ischemia was induced by ligation of left anterior descending coronary artery. After 80 minutes of coronary occlusion, high plasma FFA was induced by intravenous injection of heparin 200 u/kg and Intralipid^(R) 5 ml/kg as a bolus. After additional 60 minutes, beating hearts were removed from animals and tissue levels of free carnitine, short and long chain acyl carnitine, FFA and adenosine triphosphate (ATP) were determined. L-carnitine 100 mg/kg was administered intravenously 5 minutes before coronary artery ligation. Electrocardiograms were recorded continuously by a Holter electrocardiographic recorder during the experiment and ventricular arrhythmias were quantified by an arbitrary scoring system. In ischemic and excess FFA supplemented myocardium, free carnitine and ATP decreased, whereas long chain acyl carnitine and FFA increased. And these metabolic changes tended to be reduced by L-carnitine. Pretreatment of L-carnitine also reduced the grade of ventricular arrhythmias induced both by acute myocardial ischemia and by supplement of excess FFA. These results suggest that the administration of L-carnitine may be beneficial to prevent serious arrhythmias in ischemic heart disease, presumably by restoring the impaired FFA oxidation.

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Serial recordings of ST segmen_t mapping were performed in 15 patients with acute anterior myocardial infarction. Reelevation of ST segment was observed in all cases between 12 hours and one week after infarction without clinical evidence of reinfarction. There was significant correlation between the magnitude of the sum of ST reelevation (ΣST) and time to the peak of ST reelevation. The higher was ΣST at the peak, the later was the appearance of the peak of ST reelevation. ΣST recorded between 24 and 72 hours after infarction correlated with the extent of abnormal Q (NQ) in the precordial mapping as well as the percent of abnormally contracting segment (%ACS) on left ventricular angiography examined after 4 weeks following infarction. However, there was no correlation between ΣST recorded at 12 hours after infarction and NQ studied at 4 weeks after infarction. The results indicate that the magnitude of ΣST changes in time during the course after infarction and that the time of recording is important when ΣST is used for the estimation of infarct size. Reelevation of ST segment should be considered in the study of therapeutic intervention in acute myocardial infarction.

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Hemodynamic and clinical evaluation of 50 patients with acute myocardial infarction were performed. A majority of patients had depressed left ventricular function, but the level of depression was not uniform and a wide spectrum existed. Left ventricular function curves appeared to demonstrate a peak or plateau with a pulmonary arterial end-diastolic pressure (PAEDP) from 17 to 19 mmHg. There was negative correlation between stroke volume index and total peripheral vascular resistance (TPRI). Mean arterial blood pressure (MABP), TPRI, PAEDP were decreased significantly and cardiac index (CI) was markedly increased after administration of nifedipine. Seventeen patients had congestive heart failure. These patients showed a marked increase in PAEDP and a wide degree of valiability in CI and left ventricular stroke work index (LVSWI). Sixteen of 17 patients with congestive heart failure showed a PAEDP greater than 18 mmHg. Six patients developed cardiogenic shock. In these patients CI and LVSWI were markedly reduced. Two patients showed normal PAEDP. Three patients with septic shock showed a marked increase in CI and a decrease in TPRI. Hemodynamic subsets established by a PAEDP of 18 mmHg and a mean right atrial pressure (MRAP) of 100 mmH₂O was beneficial to evaluate the right ventricular function. Four patients with the findings of elevated MRAP out of proportion to PAEDP were diagnosed as right ventricular infarction. Three of them showed normal PAEDP. Two patients who showed hypotension and low CI died with shock. It is concluded that hemodynamic evaluation of patients with acute myocardial infarction is useful in understanding the extent of altered cardiac function, classifying the severity of the clinical state, measuring the response to various treatments and predicting the prognosis of the patient.

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Radionuclide imaging was useful for noninvasively visualizing a location and size of infarction in two patients with acute myocardial infarction. In one patient, inferior subendocardial myocardial infarction was detected by ^99mTc-PYP myocardial scintigraphy and then inferior transmural infarction was observed as more intense radioactivity with a larger size. In the other patient with acute extensive anterior myocardial infarction, akinesis of the left ventricular wall and left ventricular aneurysm were confirmed by first-pass radionuclide angiocardiography and multigated equilibrium cardiac pool scan.

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The results of treatment of 400 patients with established acute myocardial infarction in a hospital at different periods with changing care systems are described. Significant reduction of death from arrhythmias could be obtained only when an organization with immediate availability of well-trained medical personnel and reliable actual continuous monitoring of electrocardiograms had been established. Components of delay in the pre-hospital phase of acute myocardial infarction were also studied. There were two significant factors in delay: one was delay due to ignorance of patients about the disease, second was the delay after consultation of family doctors until arrival at the CCU. Time is consumed in the latter factor mainly in making of definite diagnosis. The implication of these data in the management of patients with a diagnosis of acute myocardial infarction are discussed.

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One hundred and nineteen patients with acute myocardial infarction (AMI) were examined to establish the correlation between clinical and hemodynamic status. Patients were divided into 5 groups: uncomplicated AMI (Group A, 34 cases), congestive heart failure (Group B, 56 cases), cardiogenic shock (Group C, 14 cases), right ventricular dysfunction in cases with acute inferior infarction (Group D, 7 cases), and rupture of the interventricular septum (Group E, 8 cases). Hemodynamic classification of the first three groups with 18 mmHg for pulmonary arterial diastolic pressure (PADP) or pulmonary capillary pressure (PCW), 2.0 L/min/m² for cardiac index (CI), and 20 g·m/beat/m² for left ventricular stroke work index (LVSWI) correlated well with our clinical classification. In addition to hemodynamic measurements, monitoring of the temperature difference between the core and the periphery of the body reflects both cardiac function and clinical status of peripheral circulation and has been useful in selecting the appropriate therapy for AMI. Mortality rates were similar in the clinical and hemodynamic subset classifications, averaging 2.9% in Group A, 7.1% in Group B, 57.1% in Group C, 42.9% in Group D, and 62.5% in Group E. The hemodynamic effects of intravenous nitroglycerin (TNG), TNG ointment, and molsidomine were studied in 54 patients. All three vasodilators significantly reduced PADP or PCW and systemic vascular resistance (SVR), and increased CI in patients with elevated PADP or PCW. Also, TNG was effective in decreasing PADP or PCW, SVR, and left-to-right shunt ratio, and increasing forward cardiac output in Group E. However, in cases with severe pump failure in which CI was less than 2.1 L/min/m², LVSWI was less than 20 g·m/beat/m² and PADP or PCW was more than 18 mmHg, dopamine and a combination of dopamine and phentolamine produced beneficial hemodynamic responses. The overall early mortality rate of the AMI at our CCU decreased from 22.9% during 1974 to 1976, when no such therapy was applied, to 15.9% after therapy. A marked reduction in the mortality rate due to left ventricular failure from 33.3% to 13.5% was observed. Both hemodynamic and clinical data indicate that a new therapy employing vasodilators and a combination of vasodilators and catecholamines can be applied effectively in patients with pump failure following AMI.

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(1) In Tokyo metropolitan area, CCU network including 17 hospitals has been established. Its aim is saving the lives of patients with acute myocardial infarction by facilitating their admission to CCU as promptly as possible. The task of hospitals cooperating in the CCU network is 1) to admit without fail patients suspected of myocardial infarction, 2) to transmit ECG by telephone lines and 3) to perform telephonic consultation. ECG telephone line transmission is a system in which an ambulance having equipment to transmit a patient's ECG on a telephone line goes to the actual site where the patient is located and transmits the patient's ECG on an ordinary telephone line to the CCU staff installed in the CCU if myocardial infarction is suspected. The CCU staff interprets the transmitted ECG and advises the ambulance staff on what action should be taken. If an emergency does not permit such time to be taken, only telephone consultation without transmission of standard 12-1ead ECG will be used by the ambulance staff. By this method, about 10 minutes of time can be saved as compared with ECG telephone line transmission, and the objective achieved within a shorter period. (2) In 19 cases of cardiogenic shock due to acute myocardial infarction, the clinical results obtained by intra-aortic balloon pumping (IABP) alone and in combination with the use of isosorbide dinitrate (ISDN), and the therapeutic results have been discussed. At 48 hours after the start of IABP, the maximal effect could be obtained with significant decrease in heart rate, pulmonary capillary wedge pressure (PCWP), central venous pressure and systemic vascular resistance and significant increase in systolic and diastolic blood pressure, cardiac index (CI), stroke volume index and transmyocardial pressure gradient. A comparison of the left ventricular function curves of survivors (6 cases) and non-survivors ( 13 cases) revealed that in the former group the curve shifted toward the upper left area, commencing at 12 hours after the start of IABP and continuing up until after completion of IABP, while in the latter group the curve shifted toward the right upper area from 48 to 60 hours after the start of IABP, followed by a shift toward the lower right area thereafter, with a more aggravating tendency after completion of IABP. When IABP was combined with ISDN, a remarkable improvement could be obtained in cardiac function 15 minutes after sublingual administration of ISDN. Among 19 cases in which IABP was applied, this treatment could be successfully discontinued in 13 cases (68%), with 6 of them surviving for prolonged periods of more than 6 months. It is concluded that IABP is effective in improving the hemodynamics of cardiogenic shock due to acute myocardial infarction. Maximum response is noted between 24 and 48 hours.

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