Forty-seven patients with coronary artery disease characterized by angina pectoris and/or old myocardial infarction underwent two maximal exercise tests, the supine ergometer test and the upright treadmill test, to study the relationship between exercise capacity and exercise hemodynamics. Subjects were divided into 3 groups: Group I (n=19) achieved 25 or 50 watts, Group II (n=15) achieved 75 watts and Group III (n=13) achieved 100 or 125 watts. During ergometer exercise, the mean pulmonary capillary pressure elevated by 25.3±8.3mmHg in Group I, 20.8±8.8mmHg in Group II and 12.0±8.4mmHg in Group III ; the Group III value was significantly smaller than the other groups. The stroke volume index decreased by 3.6±8.8ml/m2 in Group I, and increased by 10.9±.7ml/m² in Group II and 10.7±14.7ml/m² in Group III. Thus, the impaired exercise capacity correlated with the abnormal exercise hemodynamics and its severity. In addition, the exercise capacity in the treadmill test was comparable to that in the ergometer test. It was concluded that the impaired exercise capacity in the both supine and upright exercise tests was well related to the development of abnormal exercise hemodynamics in patients with coronary artery disease.

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The hemodynamic effects of digoxin (0.01mg/Kg) on congestive heart failure were compared in 32 patients with old myocardial infarction (OMI) (n=9), dilated cardiomyopathy (DCM) (n=10), acute myocardial infarction (AMI) (n=5) and mitral stenosis (MS) (n=8).
The responses of heart rate (HR) and pulmonary capillary pressure (PCP) to digoxin in OMI, DCM and MS were marked but different in each of these groups and no significant changes were found in patients with AMI. The responses of cardiac index (CI) to digoxin in patients with OMI and DCM in whom left ventricular myocardial contractile force was impaired were divided into 2 groups (Group 1: CI increased more than 15% and Group 2: less than 15%). In Group 1, both CI and percent fractional shortening (%FS) before digoxin administration were lower than in Group 2, i.e., 1.97±0.27 vs 2.80±0.48L/min/m² (p<0.001) and 10.9±8.0 vs 19.5±11.9% (p<0.05), respectively. In MS, CI increased after digoxin administration only in the 2 patients with low CI and rapid HR in the control state.
These results indicate that the mode of hemodynamic response to digoxin is considerably different in various diseases. They further suggest that digoxin should not be used in the early phase of AMT, although digoxin was of great clinical benefit in patients with OMI and DCM through such mechanisms as its positive inotropic and negative chronotropic effects and lowering of PCP.

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The common clinical electrocardiographic criteria for diagnosis of acute transmural myocardial infarction include ST segment elevation and tall, upright T waves, but do not include changes in QRS morphology. The purpose of this study was to show that development of a 50% or greater increase in R wave amplitude, the giant R wave, in patients with acute transmural myocardial infarction occurs, and also to characterize changes in QRS morphology which may aid the ECG diagnosis of acute transmural myocardial infarction. Over the past 6 years, 36 patients with an increase in R wave amplitude during acute transmural myocardial infarction were identified at the Strong Memorial Hospital Coronary Care Unit. A significant increase in R wave height (0.33±0.10 to 0.97±0.08mV, p<0.05), width (0.03±0.00 to 0.08±0.01, p<0.05) and area (0.01±0.00 to 0.05±0.01 mV-msec, p<0.05) appeared in the same ECG lead demonstrating ST segment elevation and tall T waves during the acute phase of transmural myocardial infarction. Patients with diaphragmatic myocardial infarction showed a significant (p<0.05) rightward QRS frontal plane axis shift and patients with anterior wall myocardial infarctions developed an anterior QRS axis shift in the horizontal plane during occurrence of the giant R wave.
We conclude from this preliminary study that the giant R wave may be observed during acute transmural myocardial infarction and may in part be caused by local intramyocardial conduction delay in acutely ischemic tissue as supported by an increase in the R wave width along with shifts in the frontal and horizontal plane QRS axis toward the area of acute ischemia. The giant R wave occurs in conjunction with ST segment elevation and tall T waves and may aid the ECG diagnosis of acute transmural myocardial infarction.

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In order to determine whether painless ST changes represent myocardial ischemia, we studied regional myocardial perfusion in patients with angina pectoris who showed painless ST-segment depression during a treadmill exercise test.
Twenty-one patients were evaluated by myocardial imaging using thallium-201 injected intravenously during exercise when painless ST-segment depression was evident. The same examination was repeated in 5 of the above patients when they showed ST-segment depression with chest pain. Myocardial images obtained during painless ST-segment depression revealed perfusion defects in 15 of 21 patients (71%). Images obtained during STsegment depression with chest pain showed perfusion defects in all 5 patients (100%) including 3 patients who demonstrated no defects during painless ST-segment depression. In these 5 patients, the ST-segment depression associated with pain was significantly greater than that without pain (3.4±1.1 vs 2.1±1.1mm, p<0.01).
These results suggest that the majority of episodes of painless ST-segment depression occurring during exercise are accompanied by regional myocardial perfusion abnormalities and that transient painless ST-segment depression in patients with angina pectoris might represent less severe myocardial ischemia.

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Despite a large number of papers concerning coronary spasm, its mechanism still remains unsolved. Several cases have been reported in which coronary spasm was triggered by allergy. Since histamine is one of the causative substances released in allergic reactions, we speculated on some involvement of an allergic mechanism in the pathogenesis of coronary spasm. We retrospectively examined by questionnaire the incidence of allergic history in patients with variant angina (n=47) and compared it with that in patients with non-ischemic heart diseases (n=83). We could not find any relationship between coronary spasm and allergy. Furthermore, we have not experienced any case in which myocardial ischemia was provoked by an allergic reaction. Accordingly, allergy could not be a major cause of coronary spasm in our present experience.

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Impedance cardiography was performed on 13 free-living subjects to determine the mechanism which ties modest sodium restriction to a reduction in blood pressure. During salt restriction intervention, significant decreases in systolic and diastolic blood pressure (6 and 7mmHg) were observed associated with mild reduction in urinary sodium excretion from 176 to 85mmol/day. The impedance cardiogram demonstrated a significant decrease in stroke volume (12ml), which was related to a fall in diastolic pressure (r=0.59, p<0.05). In the further analysis of individual parameters in Kubicek's formula calculating stroke volume, thoracic impedance (Zo/L) showed a significant increase during salt restriction and a change (Δ) in In L/Zo related significantly to Δln diastolic pressure in linear multiple regression analysis. As thoracic impedance has been reported to reflect intrathoracic fluid content, a decrease in extracellular fluid volume was suggested as a possible mechanism of the fall in blood pressure even with modest sodium restriction.

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To evaluate the effects of nitroglycerin on left ventricular function in 27 patients with ischemic heart disease, ejection fraction (EF) was measured every 1 to 5min by a nuclear stethoscope after sublingual administration of nitroglycerin (0.3mg).
(1) There was a good correlation between EF determined by the nuclear stethoscope and EF by left ventriculography (r=0.80, p<0.001). (2) EF showed a rise after sublingual nitroglycerin, which was most marked at 4 to 7 min and returned to the control level in 20 to 25min. (3) There were no significant differences in the maximum percent increase in EF among patients with. 0, 1, 2 and 3 vessel disease. The maximum percent increases in EF were 34.0±10.0% in the normal contraction group, 24.0±8.5% in the hypokinesis group (p<0.05 vs the normal contraction group) and 15.2±8.5% in the akinesis group (p<0.01 vs the normal contraction group, p<0.05 vs the hypokinesis group). (4) There was a weak correlation between the maximum percent increase in EF and the changes in heart rate (r=0.49, p<0.05) and there was an inverse correlation between the maximum percent increase in EF and the changes in systolic blood pressure (r=-0.65, p<0.01).
It was shown that the improvement in EF by sublingual nitroglycerin was greatest in the normal contraction group, somewhat less in the hypokinesis group and least in the akinesis group. The nuclear stethoscope is useful in monitoring changes in left ventricular function during intervention.

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The effects of slow-release nifedipine on blood pressure and cardiac workload have been studied during bicycle exercise testing in a randomized, double blind trial in 20 patients with mild to moderate hypertension.
After a fortnight's wash-out, patients were allocated to either slow-release nifedipine (20mg twice daily) or placebo for a 2-month period. At baseline and at the end of treatment blood pressure and heart rate were measured at rest and during ergometric exercise; cardiac workload was calculated as the product of systolic blood pressure by heart rate.
Significant decreases in blood pressure at rest and in cardiac workload on exercise were demonstrated at the end of nifedipine treatment. The reduction of cardiac workload was mainly due to the lower baseline values of resting blood pressure. Heart rate showed a reduction of its increase during ergometric exercise at the end of nifedipine treatment as compared to baseline, likely due to an improvement in stroke volume.

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Excised left atrial appendages were subjected to light and electron microscopy and histochemical analysis. Aschoff nodules (AN) showed strong acid phosphatase and nonspecific esterase activity. Ultrastructurally, the Aschoff cells had several features of fibroblasts and epithelioid cells. Rough endoplasmic reticulum (RER) was striking in most cells. Dilated cisterns of RER containing homogeneous material were also frequent. Mitochondria and ribosomes were present. AN thus seem to arise from mesenchymal tissues of the heart. It is likely that cross-reactivity between streptocococcal antigen and myocardial connective tissue causes the cardiac histocyte/macrophage to transform to cells having features of epithelioid cells and/or fibroblasts.

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This study examined the immunohistochemical findings in renal arterioles from biopsy specimens, and related the findings to those of light and electron microscopy. The renal biopsy specimens were obtained from 57 normotensive patients with primary glomerular diseases or idiopathic hematuria, 14 hypertensive patients with associated primary glomerular diseases, 4 patients with essential hypertension and 1 with primary aldosteronism. The tissue slices for the immunohistochemical study were processed with FITC-labelled rabbit antihuman immunoglobulin antisera. Deposits of IgM were detected on the renal arterioles in 16 of the hypertensive patients (84%), but in only 7 of the normotensive patients (12%). The difference in incidence was significant (p<0.005). C3 was almost always deposited in the renal arterioles regardless of whether the patient was hypertensive or normotensive. IgG, IgA or fibrinogen were demonstrated only in a few cases, and albumin in no cases. When sections stained with horseradish peroxidase-conjugated anti-IgM antibody were compared under a light microscope with the adjacent PAS-stained sections, it was demonstrated that IgM was deposited only in the portions of the arteriolar walls which showed hyalinotic changes. Electron microscopic examination demonstrated that electron-dense deposits in the subendothelial or intercellular spaces of arteriolar walls were more frequent in the hypertensive patients (11 of 14 cases, 79%) than in the normotensive patients (5 of 18 cases, 28%, p<0.05). The deposits appeared to be similar to those which are often found in the glomeruli of patients with glomerulonephritis and which are considered to be immune complexes. These findings suggest that some immunologic mechanism mediated by IgM antibody might be a factor in the development of hypertensive vascular lesions.

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The effects of coronary arterial perfusion with a perfluorochemical substance (perfluorotributylamine) on the segmental myocardium of the beating heart were studied in 12 open chest anesthetized dogs. Following 10min of left anterior descending coronary artery occlusion, perfusion of the coronary artery with the perfluorochemical returned myocardial function and metabolism toward control states, although myocardial diastolic properties as well as coronary venous PCO₂ and lactate were not restored completely within 7min after reperfusion. Perfluorochemicals may be of clinical importance in protecting the ischemic myocardium because of their oxygen carrying capacity together with favorable physicochemical properties for protection of the microcirculation.

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The effects of chronic instrumentation on regional myocardial performance and regional myocardial blood flow were studied in 8 mongrel dogs. Regional segment lengths were measured by an ultrasonic dimension gauge technique at two areas of the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX). Regional myocardial blood flow was measured by a tracer microsphere technique. These measurements were repeated while the animals were conscious on the 4th, 11th, 21st and 28th days after instrumentation. On the 4th day, the heart rate was rather high and regional shortening at both the LAD and LCX areas remained suppressed. After the 11th day, hemodynamic variables such as heart rate, left ventricular pressure and regional wall motion were fairly constant. Regional myocardial blood flow and its distribution were also constant throughout the experimental period. Fibrosis of the epicardium invariably induced by surgical procedures did not affect the distribution of regional blood flow as compared with that of the interventricular septum.
Thus, a stable hemodynamic state was recorded after the 11th day following surgical manipulation and the implantation of sensors and catheters did not affect the level of regional myocardial blood flow or its distribution at rest. Such long term reproducible measurements of regional wall motion and regional myocardial blood flow may facilitate chronic studies of cardiovascular physiology.

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To clarify the mechanism of mexiletine-induced changes in action potential duration (APD), we studied the effects of mexiletine (2μg/ml) on APD at 0mV (APD0mV) and 90% (APD_90%) repolarization and on restitution of premature responses in guinea pig ventricular muscle at three extracellular potassium concentrations ([K]0) and three stimulation rates using standard microelectrode techniques. The rates at which APD0mV and APD_90% were shortened by mexiletine (S-APD0mV and S-APD_90%) expressed as percent change from control were most pronounced at [K]0=5.4mM. The percent changes at the three concentrations were 5.0±2.1% at a [K]0 of 2.7mM, 6.0±3.2% at 5.4mM and 1.8±1.2% at 10.0mM for S-APD0mV and 2.0±1.9%, 4.7±2.0% and 1.3±1.5% for S-APD_90% at the same concentrations, respectively. SAPD0mV and S-APD_90% were more markedly affected when stimulated at a frequency of 1Hz than when stimulated at 0.2 or 0.5Hz. Mexiletine failed to produce any additional APD shortening beyond that produced by the introduction of tetrodotoxin (2.5×10-6M). Mexiletine and tetrodotoxin did not influence APD restitution that fitted a single exponential curve. We conclude that the shortening of APD by mexiletine results from inhibition of a tetrodotoxin-sensitive sodium current.

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Pantethine, which is known to be converted to coenzyme A, has been reported to have antiarrhythmic action on experimental cardiac arrhythmias. Using standard microelectrode techniques, the electrophysiological effects of pantethine under hypoxic (95% N₂+5% CO₂) perfusion were studied.
Hypoxia decreased resting membrane potential, action potential amplitude and maximum velocity of phase 0 and shortened action potential duration and effective refractory period. Application of pantethine 5×10-3Gm/ml under hypoxic perfusion prolonged action potential duration and effective refractory period significantly. Prolongation of action potential duration by pantethine might be caused by an increase in intracellular ATP.
The findings in this study could be an explanation of the possible antiarrhythmic effects of pantethine.

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Whether apical hypertrophic cardiomyopathy is a variant of classic hypertrophic cardiomyopathy or a separate entity is controversial. This is a case report of an apical hypertrophic cardiomyopathy. The patient was a 67-year-old man associated with giant negative T waves in electrocardiogram and asymmetric apical hypertrophy on echocardiogram. He died of liver cirrhosis and liver cell carcinoma. At necropsy the heart showed apical hypertrophy grossly and extensive disarray of myocardial fibers near the apex of the left ventricle histologically. The necropsy findings were indistinguishable from those of classic hypertrophic cardiomyopathy. This suggests that apical hypertrophic cardiomyopathy is a variant of hypertrophic cardiomyopathy.

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