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Background Several reports have suggested a possible link between bronchial asthma and coronary spasm, but the possibility of a relationship in coronary spastic angina (CSA) has not been clarified. Methods and Results Airway responsiveness to methacholine and coronary spasticity to acetylcholine were examined in 42 patients with CSA and 36 patients with chest pain syndrome (CP). Furthermore, 18 control subjects were examined and their airway responsiveness compared with that of the CSA and CP patients. The incidence of airway hyperresponsiveness was significantly higher in the CSA group (74%) than in the CP (19%) and control (17%) groups (p

Nisoldipine, a newly developed coronary vasodilating agent, was administered to 12 patients with variant angina to assess its efficacy in this condition. A placebo was administered during an observation period of ⩾2 days, after which nisoldipine 10 mg/day was administered as a single daily dose during a 3- to 4-day treatment period. The number of angina attacks significantly decreased from 5.4 ± 1.4 times/day/patient during the observation period to 1.1 ± 0.4 times/day/patient during the treatment period ( P P

Hemodynamic effects of flosequinan (BTS 49 465), a new vasodilator, were studied in 29 patients with severe heart failure. During right heart catheterization by Swan-Ganz catheter, a single 100mg dose of flosequinan was orally administered, and pertinent hemodynamic parameters were obtained serially for 24hr after administration. Flosequinan produced significant increases in cardiac index and stroke index (16% and 12%, respectively, P

The efficacy and safety of intravenous infusion of human tissue-type plasminogen activator (rt-PA), developed in Japan (TD-2061), were investigated in 205 patients (154 men and 51 women) with evolving myocardial infarction (EMI). TD-2061 was given at a rate of 3.2 to 50 mg over 1 h after angiographic documentation of complete or subtotal (99%) occlusion. Nineteen patients were excluded as they did not meet the inclusion criteria. A total of 186 patients were divided into 6 groups according to the total dose given: Group I, 3.2 mg, 10 patients (pts); Group II, 6.4 mg, 15 pts; Group III, 12.8 mg, 15 pts; Group IV, 25.6 mg, 38 pts; Group V, 33.3 mg, 70 pts; Group VI, 50.0 mg, 38 pts. Ages ranged from 30 to 70 years (mean 60 +/- 1). Coronary angiography was done at 30 min and 1 h. In patients with TIMI grades 0 and 1, reperfusion was accomplished after 1 h in 22% of Group I, 50% of Group II, 64% of Group III, 70% of Group IV, 67% of Group V, and 74% of Group VI patients. Complications were hypotension, nausea and vomiting, bradycardia and bleeding at the puncture site. These findings suggest that clot-selective coronary thrombolysis can be induced in patients with EMI by means of human tissue-type plasminogen activator without concomitant induction of a severe systemic lytic state. The optimal dose for Japanese patients is considered to be 33.3-50.0 mg from the standpoint of reperfusion.

Several reports have suggested a possible link between bronchial asthma and coronary spasm, but the possibility of a relationship in coronary spastic angina (CSA) has not been clarified.Airway responsiveness to methacholine and coronary spasticity to acetylcholine were examined in 42 patients with CSA and 36 patients with chest pain syndrome (CP). Furthermore, 18 control subjects were examined and their airway responsiveness compared with that of the CSA and CP patients. The incidence of airway hyperresponsiveness was significantly higher in the CSA group (74%) than in the CP (19%) and control (17%) groups (p0.0001). The geometric mean of the log minimum dose (Dmin), defined as the cumulative dose at the point at which respiratory conductance began to decrease, was significantly lower in the CSA group (0.75 log units) than in the CP (1.20 log units) and control (1.38 log units) groups (p=0.004).These results demonstrate that acetylcholine-induced coronary spasticity is significantly related to methacholine-induced airway responsiveness in patients with CSA. A generalized hyperresponsiveness of the vascular and nonvascular smooth muscles, including that through cholinergic mechanisms, may exist in patients with CSA.

Intravenous administrations of 2000 x 10(4)IU (33 mg) (rt-PA2) and 3000 x 10(4)IU (50 mg) (rt-PA3) of a new recombinant tissue plasminogen activator (rt-PA:TD-2061) derived from uterine endothelial cells and urokinase (UK) 96 x 10(4)IU were compared in a double blind, randomized trial of 198 patients with evolving myocardial infarction. All patients entered the trial within 6 h of the onset of symptoms and underwent baseline coronary angiography of the infarct-related coronary artery before thrombolytic therapy was instituted. Sixty minutes following thrombolytic therapy occluded infarct-related arteries were successfully reperfused in 41.5% of 66 patients in the UK, 76.4% of 72 patients in the rt-PA2, and 74.6% of 59 patients in the rt-PA3 group. Statistically significant differences were observed between the UK and rt-PA groups (p less than 0.01). Serum fibrinogen levels declined in all 3 groups at 60 min post-therapy by averages of 35.9 +/- 3.1% in the UK, 16.8 +/- 4.8% in the rt-PA2 and 17.5 +/- 4.5% in the rt-PA3 group. The difference between the UK and the rt-PA groups was statistically significant (p less than 0.01). Plasma plasminogen and alpha 2-plasmin inhibitor levels showed the same tendencies. Bleeding was the most commonly observed complication and was most commonly seen at the catheterization site. There was no difference in the incidence among the 3 groups. Hospital deaths occurred in 5.3%, 6.3%, and 4.7% of the cases in the UK, rt-PA2 and rt-PA3 groups, respectively. We conclude, therefore, that rt-PA achieves a significantly higher rate of recanalization with less extensive systemic fibrinogenolysis at the dose employed than does UK. The optimum intravenous dose of rt-PA for Japanese patients is considered to be 2000 x 10(4)IU (33 mg).

Two patients who had previously experienced old myocardial infarction and who died suddenly after an attack of chest pain were examined and discussed. In both cases two of the three main coronary arteries showed severe stenosis with canalization. Ruptured atheromatous plaque was found in the unblocked coronary artery. Fibrin was already formed and surrounded the fractured intimal collagen fiber, foam cells, and cholesterin clefts, but a luminal thrombi had not yet been formed. Fresh occluding thrombi were formed at the site of the ruptured atheromatous plaque. Coronary thrombi containing abscess components such as foam cells, cholesterin clefts, and the fractured intimal collagen fiber were found in our preliminary study 1 . These views support the supposition that this fracture between the lumen and the plaque might precede and be responsible for the formation of the thrombus and the onset of acute myocardial infarction. It was confirmed that the attack of preinfarction angina occurred at the time of the rupture of the atheromatous plaque. The rupture of the atheromatous plaque plays an important part as an initiating factor of peinfarction angina and myocardial infarction. Thus, it is necessary to examine coronary arteries by serial histopathological section method.

A comparative study of right ventricular histopathologic findings and clinical profiles in 174 cases with hypertrophic cardiomyopathy (HCM), 145 cases with dilated cardiomyopathy (DCM), and 241 cases with idiopathic arrhythmia and/or conduction disturbance with significant myocardial pathology [Electric disturbance type of cardiomyopathy (ECM)], totaling 560 cases, was made in order to clarify the role of viral myocarditis in these conditions. Postmyocarditis change (PMC) was defined by assessing serial biopsy findings in nine cases with acute myocarditis. The PMC was observed in three cases with HCM (1.7%), 22 with DCM (15%), and 21 with ECM (8.7%). The incidence of PMC was significantly higher in DCM and ECM than in HCM (P less than 0.001). The typical pattern of onset of acute myocarditis, i.e., high fever, upper respiratory infection, and gastrointestinal symptoms preceding cardiac symptoms within 10 days, was recognized in one case with HCM, eight with DCM, and 6 of 123 cases with ECM. The incidence was higher in DCM and ECM than in HCM (P less than 0.05). Of 46 cases with PMC, 12 (26%) showed this pattern, on the other hand only 3 of 377 cases (0.8%) without PMC did so (P less than 0.0001). Familial occurrence was not found in any of the 46 cases with PMC but was found in 38 of the 377 cases without PMC (P less than 0.01). This study indicates that viral myocarditis may often be the causative agent of idiopathic cardiomyopathy, especially DCM and ECM. It is also noticed that familial occurrence of the cases with PMC was never seen.

Fourteen cases of heart disease with hypereosinophilia were analyzed employing conventional cardiologic methods, including echocardiography, cardiac catheterization, and endomycoardial biopsy. The cases were divided into four types: (1) Acute carditic (endocarditis, myocarditis, pericarditis; five cases); (2) ventricular dilation (three cases); (3) restrictive (three cases); (4) electric disturbance (three cases). Biopsy revealed significant changes in all cases. In one case of the ventricular dilation type, endomyocardial fibrosis with myocardial degeneration was seen, and in another case mural thrombus formation was shown to be present. In three cases of the restrictive type, endomyocardial fibrosis (EMF) was observed. In two cases of the electric disturbance type, minor right ventricular myocardial degeneration was observed. In two of the three cases of the carditic type and in three of eight cases in other categories, postmyocarditic changes were observed. The course of the disease compared with the type of disorder revealed a short course in the carditic type and a longer course, ranging from 2 to 24 years, with one exception, in the other types. It is also confirmed that the various histopathologic changes can be related to particular clinical presentations. We have shown that the basic changes in eosinophilic heart disease are not restricted to the endomyocardium and that they occur in various parts of the heart causing more widespread manifestations. The more comprehensive term “eosinophilic heart diease” is a preferable description.

The effect of ticlopidine (fig. 1), a new platelet aggregation inhibitor, was studied in 15 patients with Bjork-Shiley prosthetic heart valves (6 aortic, 6 mitral, 3 aortic and mitral). The patients were 9 men and 6 women, aged 22 to 55 years old, who had had valve prostheses placed 2 to 43 months (mean 23.7 months) prior to entry into the study. They received 200mg of ticlopidine, divided into two oral doses, daily, and were followed up for more than 3 months. Platelet adhesiveness and aggregation were examined 1, 2, and 4 weeks, and 3 months after the treatment, and the values were compared to those obtained before the treatment. Platelet adhesiveness was determined by a modified technique of Salzman. A Sienco dual sample aggregation meter was used to measure changes of platelet aggregation through light transmission of citrated platelet-rich plasma to which adenosine diphosphate (ADP) had been added. The platelet count of the plasma sample was adjusted to a range of 250-350, 000/mm3. Student's paired t-test was used for statistical significance.Platelet adhesiveness decreased significantly at 1 week, 2 weeks, and 3 months after the treatment, but no significant change was found at 4 weeks (fig. 2).In every patient, platelet aggregation induced by 4μM ADP (final concentration) showed an obvious reduction one week after the treatment, and this effect continued for more than 3 months (fig. 3). A similar reduction in the aggregation caused by 20μM ADP (final concentration) was observed. In many cases, the aggregation caused by 20μM ADP, which showed the second phase of aggregation, changed after the treatment to show only the first phase of aggregation (fig. 4). Ticlopidine inhibited both the first and the second phase of ADP-induced aggregation. This dosage seemed to cause a reduction in platelet aggregation about 3 days after the start of the treatment.We did not observe any interaction between ticlopidine and warfarin in this study.None of the patients had clinical symptoms or side effects due to ticlopidine and no episodes of thromboembolism occurred during the examination period. Bleeding time increased slightly at 4 weeks after the treatment. No abnormal alteration was observed in the white blood cell counts, coagulation time, fibrinogen level, fasting blood sugar, serum electrolites, total protein, hepatic and renal function tests at 4 weeks and 3 months after the treatment.Ticlopidine seems to be a useful platelet function suppressing drug for patients with prosthetic heart valves.

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.

In a patient with patent ductus arteriosus, a pulmonary regurgitant murmur developed after the treatment of endocarditis. M-mode echocardiograms showed abnormal echo mass, characterized by fine diastolic fluttering, in the right ventricular outflow tract during diastole which were continuous with anterior pulmonary leaflet and thick pedunculated lesions attached to the anterior pulmonary leaflet were seen to be moving freely by cross-sectional echocardiography. At autopsy the destruction of the pulmonary valve was confirmed.This study suggests that diagnosis of flail pulmonary valve is feasible by M-mode and cross-sectional echocardiography.

In a normal man sitting upright, pulmonary perfusion is several times greater in the lower lung zone than in the upper zone. This pattern may sometimes be reversed in patients with cardiac disease. Tc99m-macro-aggregated albumin pulmonary perfusion images were computerized to isocounts area images (digital perfusion images; DPI). DPI were applied to various types of cardiac disease and patterns of DPI were divided into 4 classes according to amount of nonperfused pulmonary vascular bed. C-0; normal perfusion. C-1; decrease of nonperfused pulmonary vascular bed. C-2; disappearance of nonperfused pulmonary vascular bed. C-3; decrease of pulmonary vascular bed. In 71 patients with mitral stenosis relationships between pulmonary hemodynamics during exercise and distribution of pulmonary perfusion were studied, i.e. at rest (n = 71, mean pulmonary arterial pressure; 23 mmHg-cardiac index; 2.4 L/m) and during exercise C-0 (n = 13, 41 mmHg-5.4 L/m), C-1 (n = 17, 52 mmHg-5.2 L/m), C-2 (n = 27, 52 mmHg-4.5 L/m) and C-3 (n = 14, 65 mmHg-3.6 L/m) respectively. In patients with congestive heart failure cardiac status was classified to 4 classes according to ejection fraction and DPI. Patients with EF less than 30% and DPI more than C-2 showed high morbidity and mortality (two years mortality 47%; 27/40). Pulmonary venous pressure increases to maintain the cardiac index (Starling's law) in cases of decline in cardiac function or mitral stenosis. It was shown that increases in pulmonary venous pressure cause changes in distribution of pulmonary perfusion, which in turn works to depress the cardiac index. A decline in cardiac function and changes in the distribution of pulmonary perfusion coexist, mediated by pulmonary venous pressure and cardiac index. The distribution of pulmonary perfusion reflects the severity of cardiac failure itself, so by using DPI the severity of cardiac failure can be easily evaluated.

In 96 cases of paroxysmal tachycardia, results of chronic pharmacological assessment (CPA) were compared with acute electrophysiological-pharmacologic assessments (EPA) to evaluate the usefulness of EPA. I. Patients with sustained VT (31 cases): Sustained VT and repetitive ventricular response (RVR) could be induced in 61% and 23% respectively. More than one effective drug was found by EPA for 23 of 24 subjects. Of the 22 followed by CPA, the effectiveness of medication was excellent for 14 (64%), moderate for 1, slight for 4, and ineffective for 3 (14%). II. Patients with non-sustained VT (23 cases): RVR could be induced in 52%. Effective medication was identified by EPA for 8 of 10 patients. Of the 7 followed by CPA, the effectiveness of medication was excellent for 2(28.5%) moderate for 2, and ineffective for 3. III. Patients with PSVT (42 cases): PSVT could be induced in 90% of cases. Effective medication was found for all 31 cases which underwent EPA. Of the 23 cases followed by CPA, the chronic efficacy of drugs was excellent for 7 (30%), moderate for 5 (22%), slight for 7 (30%), and noneffective for 4 (18%). Therefore, we conclude that the usefulness of EPA differs according to the type of tachycardia. EPA is most useful in predicting chronic results for patients with sustained VT, especially when the sustained VT is readily reproducible by electrical stimulation. It is less useful for nonsustained VT and PSVT. With nonsustained VT, EPA is limited by difficulty in repeatedly inducing RVR, and by difficulty in predicting the appropriate medication for chronic oral therapy. With PSVT, even though the PSVT can be induced with greater success, EPA is limited by variations in pharmacologic effects over time, which create discrepancies between EPA and CPA.

We investigated the platelet volume and other blood coagulation parameters in early postoperative periods in patients who underwent cardiac surgery. They were 11 (coronary artery bypass grafting, 5; prosthetic valve replacement, 6) in total numbers, and their mean age was 52.3 (41-61).We tested their blood for platelet numbers, and mean platelet volume (MPV) as well as plasma levels of beta-thromboglobulin (β-TG), fibrinogen (Fbg), antithrombin III (ATIII) and plasminogen (Plg). The tests were done on the preoperative day, immediately after the operation, 1d, 2d, 5d, 1w, 2w, 3w and 4w after the operation.The platelet number fell from 21.2±5.7×104 (M±SD)/μl to 7.9±2.1×104/μl immediately after the operation and showed its lowest value (5.3±3.1×104/μl) two days after the operation. Then it showed dramatic increase through 1st and 2nd weeks and reached its maximum value of 39.3±7.1×104/μl two weeks postoperatively. Plasma β-TG reached its highest value of 107.6±35.3ng/ml immediately after the operation. MPV changed from preoperative values of 8.96±0.73μm3 to 8.11±0.5μm3 immediately after the operation. MPV changed from preoperative values of 8.96±0.73μm3 to 8.11±0.5μm3 immediately after the operation and then gradually increased. The value reached its maximum value of 9.27±0.63μm3 on the fifth postoperative day. Fibrinogen levels increased mono-exponentially after the surgery and returned to its preoperative value very slowly.These results suggested the destruction and consumption of the platelet within extracorporeal circulation circuit during cardiac surgery. Rapid rebound increase in platelet numbers and changes in coagulation parameters may explain the hypercoagulable state in the early postoperative period following cardiac surgery.

In a 48-year-old woman, the diagnosis of a right coronary arteriovenous fistula communicating with the coronary sinus was made noninvasively using two-dimensional, pulsed and color Doppler echocardiography. These noninvasive techniques were superior to angiography in delineating the cardiac chamber into which the fistula emptied.

In order to determine the characteristics of the interstitial fibrotic change of the myocardium in cases with viral or idiopathic myocarditis, right ventricular endomyocardial biopsy findings in 9 cases where serial endomyocardial biopsy had been performed at the acute (5-10 days after the onset of the disease), subacute (11-21 days) and convalescent stages (22-167 days) and in 1 case at the acute stage were analyzed. They were then compared with right ventricular endomyocardial biopsy findings from 58 cases with chronic right ventricular overloading and which were of various kinds of congenital and valvular heart diseases. The following results were obtained: 1)Interstitial fibrosis was seen at the acute stage along with an increase in fibroblasts, macrophages and lymphocytes. 2) An analysis of the interstitial changes revealed that, at the acute stage, thin collagenous fibers were prominent as well as interstitial edema and at the convalescent stage, the edema became less prominent and instead, thick collagenous fibers increased. 3) comparison with the 58 cases with chronic right ventricular overloading revealed that diffuse and/or subendocardial fibrosis and endocardial thickening were more frequent and statistically more significant in cases with myocarditis.

We administered tissue-type plasminogen activator (t-PA) intravenously to 10 patients with acute myocardial infarction (AMI) within 6 hours after onset of symptoms, and then examined the state of reperfusion by coronary arteriography (CAG) and observed changes in blood coagulation and fibrinolytic activity to evaluate their effects. AK-124 (by Asahi Chemical Industry and Kowa Co., Ltd. in collaboration), a t-PA produced by tissue culture of normal human lung cells, was given in dosage of 48, 000-576, 000 A. K. units by intravenous infusion over 30-45 minutes. In 7 patients who received t-PA reflow or improved flow was detected on CAG. In t-PA treated patients, euglobulin lysis activity clearly increased, euglobulin lysis time clearly shortened, and D-dimer increased. Levels of circulating fibrinogen and α2-plasmin inhibitor decreased after treatment with t-PA by an average of 12%, 14% of baseline values respectively, but plasminogen showed no detectable change. A hematoma at the site of the catheter insertion was observed in one patient. These observations suggest that t-PA has a higher specificity for fibrin bound plasminogen than for plasminogen and prduces coronary thrombolysis without causing systemic fibrinolysis at least with the present dosage.

Recently, we experienced a case of hepatic injury in a patient who had undergone mitral valve replacement and was taking warfarin to prevent the thromboembolism.After starting warfarin treatment, it took approximately two weeks for the hepatic injury to appear. And the increase in the ratio of the eosinophilic leucocytes was roughly parallel to the deterioration of the liver function and the lymphocytes' blastoid transformation was positive. These findings suggest hepatitis due to a delayed hypersensitivity to warfarin.On the other hand, the clinical course (Fig. 1) seems to show the hepatic injury having a dose dependent factor to warfarin.This discrepancy between the laboratory data and the clinical course is very interesting and fully suggestive, and the etiology of this hepatic injury must be further studied.

Our recent survey of the Japanese literature, actual case experience, and previous studies revealed the following results. Fifty-three cases were reported in which the main cause of death in sarcoidosis was congestive heart failure (11 of 17 cases, 64.7%) and not sudden death as was previously believed. ECG analysis revealed that third degree AV block, bundle branch block, and ventricular arrhythmias were the most frequent findings indicating the presence of cardiac sarcoidosis. It was recognized that in the Japanese population fatal myocardial sarcoidosis or clinical diagnosed cardiac sarcoidosis occurred most frequently in females over the age of 40 years. It is suggested that myocardial changes progress independently of granulomatous changes. This is due to the detection of a high incidence of basal lamina layering of myocardial capillaries (14 of 18 cases, 77.8%) and is considered to play a significant role in the progression of this disease. Radionuclide studies showed that thallium scintigraphy or technetium ventriculography were positive in those cases where ECG abnormalities are prominent, indicating the presence of myocardial disease. Previous therapeutic studies of cardiac sarcoidosis have shown a decrease in the incidence of sudden death; death due to congestive heart failure occurred more frequently despite pacemaker implantation. Control of congestive heart failure is thus regarded as the most important aspect of improved treatment and prognosis.

Summary The echocardiographic features of annuloaortic ectasia were studied in 12 patients. Eleven of them exhibited skeletal and/or ophthalmic findings of Marfan's syndrome and one was considered as having forme fruste . Echocardiograms revealed not only marked dilatation of the aortic root but also unique motion of the aortic wall and aortic valve. Posterior motion of the posterior aortic wall during early to middle ejection period, i.e. "paradoxical" motion, was noted in eight cases, and premature systolic partial closure of the aortic valve was seen in all cases.

Summary A standard echocardiographic technique was proposed for an analysis of the intracardiac anatomy of endocardial cushion defect (ECD). It consisted of two beam directions, mitral and tricuspid, and two M-mode scans, between the mitral and tricuspid valves and between the mitral and aortic valves. Using this technique, echocardiopgraphic studies were performed on 13 patients with ECD, including 10 patients with the incomplete form and three patients with the freefloating form. In patients with the incomplete form, an M-mode scan between the mitral and tricuspid valves showed the specific features of the interaction between the mitral valve, the interventricular septum, and the tricuspid valve, termed the “mitral-interventricular septal-tricuspid (MVT) connection.” The systolic multiple echoes and the diastolic echoes of the so-called posterior leaflet of the mitral valve were constant findings in the mitral direction. The tricuspid valve, although less continuous, was recorded simultaneously with the mitral valve in the same direction. Anterior displacement of the anterior mitral leaflet was shown on an M-mode scan between the mitral and aortic valves, giving an echocardiographic representation of the angiocardiographic “goose-neck” sign. Evidence showing the presence of right ventricular volume overload was also found. In patients with the free-floating form, an anterior common A-V valve with a large excursion was recorded on an M-mode scan between the mitral and tricuspid valves. The valve was located posterior to the interventricular septum in the mitral direction and anterior to the septum in the tricuspid direction. There was no finding to show the interaction between the valve and the septum. The posterior common A-V valve was registered only in the mitral direction. Our technique made it possible to diagnose ECD, using a noninvasive echocardiographic method, and discriminate the free-floating form from other forms of ECD.

Thirty nine cases, in which sudden cardiac death (SCD) was suspected, were studied to evaluate the mechanism and the prediction of SCD in arrhythmia-patients using electrophysiological studies (EPS). The 39 cases (28 male and 11 female) were located by surveying 2098 patients who underwent EPS for the evaluation of arrhythmias. Age at time of EPS ranged from 4 to 86 years, average 50.5 years. Time from EPS to death was 2 to 163 months, average 27.9 months. Underlying heart disease was: dilated cardiomyopathy in 11, old myocardial infarction in 5, ischemic heart disease in 5, hypertensive heart disease in 5, valvular heart disease in 3, hypertrophic cardiomyopathy in 2, arrhythmogenic right ventricular dysplasia in 1, myocarditis in 1, sarcoidosis in 1, cor pulmonale in 1, and no obvious heart disease in 4. Fifteen had a permanent pacemaker implanted. SCD in cases without a permanent pacemaker (24 cases): 2 had chronic complete A-V block (one BH block, one HV block), 1 had advanced A-V block (HV block), 3 had bundle branch block with first degree HV block, 9 had ventricular tachycardia (VT), 3 had sick sinus syndrome (SSS), 3 had paroxysmal atrial flutter, 1 had WPW syndrome and paroxysmal atrial fibrillation, 1 had paroxysmal atrial tachycardia, and 3 had premature ventricular beats and first degree HV block. SCD in cases with permanent pacemaker (15 cases): 5 had SSS, and 10 had A-V block. In 3 of the 5 with SSS and 7 of the 10 with A-V block, VT was found before pacemaker implantation. In our study, brady and tachyarrhythmias coexisted in 25 cases (64%).(ABSTRACT TRUNCATED AT 250 WORDS)

The postoperative course of 294 patients with rheumatic mitral valve disease, who underwent mitral valve surgery during a period form July, 1978 to June, 1981, was studied by comparing the influences of the following clinical parameters: a low left ventricular ejection fraction (LVEF), a high pulmonary arterial systolic pressure (PASP), a high pulmonary vascular resistance (PVR), tricuspid regurgitation (TR), a high right ventricular end-diastolic pressure (RVEDP) and a giant left atrium (GLA). The patients with a functional capacity of class II or IV according to the New York Heart Association were classified into 3 groups (improved, unimproved and died), and from this data we calculated the improvement ratio and the mortality rate. The improvement ratios were 73% in patients with a low LVEF, 70% with a high RASP, 78% with a high PVR, 66% with TR, 11% with a high RVEDP and 77% with a GLA; the mortality rates were 19, 14, 17, 24, 78 and 19%, respectively. As compared with the case of deteriorated left ventricular performance and pulmonary hypertension, deteriorated right ventricular performance, especially high RVEDP, was accompanied by a comparatively poorer surgical prognosis. It is concluded that mitral valve surgery should be performed during the period in which the right ventricular function is still preserved.

We studied the clinical and echocardiographic features of eight patients with infective pulmonary valve endocarditis. In two patients, the vegetation was limited to the pulmonary valve; in the six other patients, infective lesions were also present on the mitral or aortic valves. None of the patients were addicted to narcotics. Seven of the eight patients had underlying congenital heart disease. In six patients the organism responsible for the infective endocarditis was Streptococcus viridans. Two-dimensional echocardiography performed using a wide-angle sector scanner was more useful than M-mode echocardiography for evaluating patients with pulmonary valve endocarditis.

Thromboembolism continues to be a major complication occurring after prosthetic heart valve replacement. It is thought that thrombus formation on prosthetic surfaces may be primarily related to the adherence of platelets with subsequent platelet aggregates and the deposition of fibrin.Platelet adhesiveness was examined in 40 patients with Bjork-Shiley prosthetic heart valves; 28 of them were receiving 1500-2250mg of clofibrate, 5 receiving 300mg of dipyridamole, and the remaining 7 receiving warfarin alone. None of the patients had a history of thromboembolism. Platelet adhesiveness in a glass bead column was determined by a modified technique of Salzman. It is known that by this method not only platelet adhesiveness was detected but also platelet aggregation induced by ADP which was released from erythrocytes hemolysing on the glass surface owing to the blood flow. Student's t-test was used to compare the means for statistical significance.The mean platelet adhesiveness in patients with prostheses was decreased, and differed significantly (p

Left ventricular performance was assessed in ten patients with acute myocarditis during the acute stage (within the first 3 days after the onset of cardiac symptoms) and during the convalescent phase (3–5 weeks later). In nine, the diagnosis was confirmed by endomyocardial biopsy during the acute stage, when left ventricular function was markedly reduced, i.e., cardiac index 1.53±0.33 1/min/m2 (mean ±SD), left ventricular stroke work index 14.1±3.9 g/beat/m2, pulmonary capillary pressure 25.9±4.3 mm Hg, and systemic vascular resistance 27.9±9.4 R units. During convalescence, seven patients improved clinically with normal cardiac function and in three it remained impaired. Cardiovascular response to nitroglycerin ointment in three patients and a combination of dopamine and nitroglycerin ointment in five were compared. Nitroglycerin ointment reduced pulmonary capillary pressure by an average of 28.5% (P

In a series of studies with endomyocardial biopsy, 7 adult cases with cardiac disease and eosinophilia were studied clinically and electromicroscopically. Degranulation of the eosinophils in the peripheral blood was observed ultrastructurally in 3 of the cases studied. The clinical expression of the 7 patients were, restrictive cardiomyopathy in 2, dilated cardiomyopathy in 2 and sick sinus syndrome in 1 and others in 2. Endocardial thickening was observed in 5 cases, one of whom showed a marked cellular infiltration with macrophages, plasma, cells, lymphocytes and mast cells. One other case showed cell debris of degranulated eosinophils. Degeneration of the myocytes was manifested by an increase in Z-bands of the myofibrils as well as streaming (1 case), disarrangement of the myofibrils, and mitochondrial change (1 case) which was characterized by giant mitochondria (1 case) as well as by a numerical increase in mitochondria. Increase of atrial granules and mitochondria in a right atrial biopsy of a case with sick sinus syndrome was noteworthy. Basal lamina layering of the capillaries of the myocardium and pyknosis of an edothelian cell cytoplasm were also noted in each case. These observations may reveal that various disease processes are taking place in the endocardium and adjacent myocardium.

In order to observe the characteristics of interstitial cellular proliferation in cases with myocarditis of possible viral origin, a systematic ultrastructural analysis of the cell components in the interstitium was made employing endomyocardial biopsy at the acute (0-10 days after onset), subacute (11-25 days), and convalescent stages (26-167 days) of the disease in ten cases. For comparison, myocardial specimens from cases with myocardial infarction were taken from early autopsy cases or from tissue obtained during surgery. The dominant interstitial cells observed in the acute stage of myocarditis were fibroblasts (38.3% +/- 17.5%, mean +/- SD), macrophages (23.3% +/- 12.1%), and lymphocytes (18.0% +/- 18.1%); at the convalescent stage, fibrocytes (44.6% +/- 20.2%) and fibroblasts (22.5% +/- 8.0%) were commonly seen. In myocardial infarction, the dominant cells were macrophages (35.0% +/- 16.0%) and neutrophils (26.0% +/- 13.9%) at the acute stage, and lymphocytes (30.0% +/- 17.8%), plasma cells (27.1% +/- 20.0%), and macrophages (26.4% +/- 11.4%) at the late stage. Thus, some differences between the two diseases could be recognized.

One hundred and thirty patients at our Heart Institute with infectious endocarditis during the past 5 years were reviewed to provide an overview of the spectrum of infective endocarditis and to assess the accuracy of echocardiography in detecting the infective valvular and endocardial lesions. Of the 130 patients, 36 (28%) had the previous cardiovascular surgery. The mean age of the patients was 34 years, and only 11% of the patients were over 50 years of age. Of the 94 patients who had no cardiovascular surgery before developing infective endocarditis, 6 underwent urgent surgery, 49 had elective surgery and the remaining 39 were followed up with medical treatment. The mortality rate of the 55 patients who were operated on was 5.5% as against 18.0% in 39 without surgery. Half of the 36 patients who had been operated on before developing endocarditis had prosthetic valves inserted. Of the 5 patients with bioprosthetic valve endocarditis, only one survived as a result of prompt medical and surgical treatment. Streptococci were still commonly found, about 75% in the group without surgery and 50% in the group with surgery. Gram-negative bacilli and fungi were found in patients with prosthetic valve endocarditis. In 61 patients, morphologic abnormalities confirmed at surgery or necropsy were compared with the preoperative echocardiograms. Vegetations were identified preoperatively in 50 (95%) of the 53 valves involved, and valve destruction was correctly predicted in all 23 cases. Mycotic aneurysm was detected preoperatively in only 3 of the 12 patients in whom it occurred. Thirteen patients, in whom vegetation was recorded, were treated successfully with antibiotics alone and they needed no surgical intervention during the 2-year follow up period. The presence of a vegetation in an echocardiography does not necessarily require surgical intervention in itself or predict the ultimate course.

A new hydroxybenzyl alcohol derivative TA-064 exerts a positive inotropic action in experimental preparations. To assess the acute effects in man, we made a cardiac catheterization study of the hemodynamic responses to TA-064 (20 mg and/or 40 mg given orally) in eleven patients with refractory heart failure due to cardiomyopathy (nine patients with dilated cardiomyopathy and one with amyloidosis). All patients were already receiving full digitalis and diuretics therapy. The following statistically significant (P less than 0.05-0.01) effects were noted: Upon administration of 20 mg of the drug, the cardiac index (CI) increased from a mean +/- 1 SD of 1.6 +/- 0.4 to 2.1 +/- 0.6 l/min/m2; pulmonary capillary wedge pressure (PCW) fell from 25 +/- 5 to 21 +/- 5 mm Hg; right atrial pressure (RA) fell from 12 +/- 3 to 10 +/- 4 mm Hg. In contrast, when 40 mg TA-064 were administered orally, the CI increased from 1.7 +/- 0.4 to 2.4 +/- 0.9 l/min/m2; PCW fell from 25 +/- 8 to 20 +/- 6 mm Hg; pulmonary arterial mean pressure fell from 35 +/- 11 to 29 +/- 9 mm Hg. Neither systemic arterial mean pressure nor heart rate increased. No toxicity was observed. The plasma concentration of TA-064 increased dose-dependently and reached a peak value 0.5-1.5 h after oral administration. Plasma catecholamine levels revealed no significant changes before and after use of the drug; therefore, the mechanism of action may not have been mediated by catecholamine.

To clarify the production mechanism of atrial natriuretic peptide (ANP) in right (RA) and left atria (LA) in mitral valve disease, histopathological and immunohistocytochemical analyses were performed and ANP levels were investigated by radioimmunoassay (RIA) in 28 patients. Atrial tissues were obtained during mitral valve replacement. ANP-like immunoreactivity of the myocytes applied by the avidin-biotin peroxidase complex method was observed around the nuclei of the atrial myocytes. Electronmicroscopically, immunoreactivity was observed in atrial specific granules. Light-microscopically determined intensity of the immunoreactivity was classified into 4 grades and the intensity in 100 myocytes was expressed by adding the scores of each myocyte. Mean right atrial pressure was positively correlated with the activity score in RA (r = 0.80). Pulmonary capillary wedge pressure was not correlated with the score in LA. The score in RA was significantly higher than that in LA. The ANP level in RA investigated by RIA was also higher than that in LA. Histopathological findings such as myocyte hypertrophy, degeneration and interstitial fibrosis were more severe in LA than in RA. In conclusion, longstanding atrial overloading, especially in LA, caused severe pathological damage, resulting in a smaller production of ANP. Much more ANP may be produced from RA in long-standing mitral valve disease.

Ninety-one patients with true and dissecting aortic aneurysm were reviewed. They ranged in age from 65 to 87 years (mean 71 years). Forty-eight patients were diagnosed with abdominal aortic aneurysm, 21 patients with thoracic aortic aneurysm and 22 patients with dissecting aortic aneurysm. They were divided into 2 categories, surgical group and non-surgical, and the prognoses of the 2 groups were compared. The average age of surgically treated cases was significantly younger than that of non-surgical cases. This study suggests that elective operation should be considered for abdominal aortic aneurysms because of the high risk of late rupture. In older patients with thoracic aortic aneurysm, the prognosis was better in surgically treated patients than in those not treated. However, the surgical mortality rate of elective operation was high. The surgical mortality rate of older patients with dissecting aortic aneurysm was not satisfactory, and medical treatment which decreases blood pressure should be considered first. All patients classified as Stanford type A should be operated on if possible.

A 20-year-old male was admitted because of palpitation and dyspnea. A routine echocardiography revealed an abnormal echo in the left atrial outflow tract and was thought to have originated from the anomalo septum, and subsequently it was confirmed by operation.

When the incidence of thromboembolism (TE) as a complication was investigated in 171 patients with prosthetic heart valves using pyrolytic carbon, 10 cases were identified in a mean follow-up period of 2.43 years. Of these 10, two patients had died. The incidence of TE as a percentage per patient--year was 2.41 on the whole, 2.15 in patients with aortic valve replacement (AVR), 2.48 in patients with mitral valve replacement (MVR) and 2.52 in patients with double valve replacement (DVR). It is evident that TE is still an important complication following prosthetic heart valve surgery and the patient's return to society. TE tended to occur somewhat more often in cases of MVR and DVR than in those of AVR. TE was apt to appear early in the postoperative period, often within a year, and was often seen in the brain. To prevent TE, it is necessary to carefully control blood coagulation by the administration of anticoagulants.

We performed serial electrophysiological-pharmacological studies on 21 patients with recurrent sustained or non-sustained ventricular tachycardia (VT). In 8 of 11 patients with recurrent sustained VT, VT could be induced repeatedly by programmed electrical stimulation and terminated by ventricular burst pacing. In 13 of the 21 patients, repetitive ventricular response (RVR) was successfully induced. In the 8 patients with induced VT, the efficacy of several antiarrhythmic drugs intravenously administered was assessed. Procainamide prevented the initiation of VT in 57%, disopyramide in 50% and mexiletine in 40%. However, lidocaine, propranolol and verapamil could not prevent VT in any of 5, 3 and 6 patients, respectively. Verapamil in combination with quinidine prevented the initiation of VT in one case. Each of disopyramide, propranolol and verapamil increased the VT zone in 2 patients. The drugs belonging to the same group classified by their electrophysiological properties were not interchangeable in 2 patients. Their ability to terminate induced VT did not always correlate with that to prevent its initiation in 2 patients. The effects of specific drugs were rather variable and unpredictable in each patients, and especially those of combination regimens using more than 2 antiarrhythmic drugs were more unpredictable. In all patients, the induced VT was morphologically identical to the spontaneously occurring VT and its rate was ranged within 13% of that of the spontaneously VT. In 10 of 13 patients with RVR, QRS configuration of RVR was not similar to the spontaneously occurring arrhythmia. The pharmacological suppression of RVR as an index for prevention against spontaneous VT remains controversial. This study concludes that the serial electrophysiological-pharmacological study provides a rapid prediction of effectiveness of a particular regimen and combination and a rapid identification of the deleterious effects of certain drugs in patients with recurrent sustained VT.

Ten patients with previous myocarditis were evaluated to determine cardiac conditions by T1-201 myocardial perfusion imaging and stress radionuclide ventriculography during the follow-up of 18-102 (average 56) months; the results were compared with those from ten sex- and age-matched controls. Exercise capacity by supine bicycle ergometer was reduced in patients with myocarditis. Their resting left ventricular ejection fraction (LVEF) was 57.5% +/- 3.9%, similar to that of controls. LVEF response to stress in myocarditis was abnormal with an increment of end-systolic volume, while in the controls LVEF increased significantly during stress. Seven of the eight patients with an abnormal ejection fraction response had constant T1-201 perfusion defects. This study indicates that latent left ventricular dysfunction is present in patients with prior myocarditis and that nuclear study is useful for long-term follow-up.

Fifteen cases of idiopathic VT responsive to verapamil were studied to examine its clinical, electrocardiographic and electrophysiologic features. All patients were male, aged 15-49, average age 28. Initial onset of VT occurred at ages 9-48 (average 21). Time from onset of VT to first admission was 1-20 years (average 8.2 years), and patients had been followed for 17-40 months (average 27 months). 13 cases had palpitations, 5 had faintness, 1 had syncope, but no deaths were reported. ECG's at time of VT exhibited CRBBB + LAD pattern in 12 cases, CRBBB + RAD pattern in 1, and LBBB in 2. VT rate was 130-200 bpm (average 163 bpm), with QRS width of 0.11 - 0.16 sec (average 0.14 sec). ECG's during sinus rhythm revealed no ST/T abnormalities, although in 6 cases they were found post-VT. 5 cases had recognizable H waves during VT, and HV intervals were shorter than that during sinus rhythm. VT could be induced by programmed electrical stimulation in 14 cases. VT or RVR could be induced by atrial pacing in 6 of 14, single RV extra-stimuli in 12 of 14, paired pulses in 5 of 12, RV overdrive pacing in 7 of 14, and burst pacing in 6 of 14 cases. VT could be terminated by RV burst pacing in 14 of the 15 cases, while single RV stimuli were effective in 5 out of 12 cases. Among the 12 cases in which VT could be induced by single RV extra-stimuli, the relationship between changes in premature interval for the induction of VT and the echo interval of VT (extrastimulus to first VT complex) was examined. 8 showed an inverse relationship, 3 showed a concordant relationship and 1 case could not be assessed. An inverse relationship was found between changes in paced cycle length and echo interval for the 2 cases in which VT could be induced by rapid pacing. Verapamil terminated sustained VT in 12 out of 13 cases, and in another case had a pronounced decelerating effect. Prior to termination, VT rate was drastically reduced (from 163 +/- 29 bpm to 128 +/- 29 bpm). Verapamil was able to prevent the induction of VT in 6 out of 14 cases, while in 6 cases the VT zone was expanded and in 2 cases the VT zone was narrowed.(ABSTRACT TRUNCATED AT 400 WORDS)