To examine the clinical significance of scintigraphic transient perfusion defects preceding the occurrence of anginal pain and ischemic ST depression, we performed both maximal and light exercise thallium-201 emission computed tomography in 13 patients with effort angina pectoris. The target heart rate in the light test was set at 80% of the peak heart rate in the maximal test. The scintigraphic transient perfusion defect was observed in all cases in both tests, while the incidence of anginal pain and/or ischemic ST depression was lower in the light test (5/13 cases) comparing to the maximal test (13/13 cases). However, the number of defect segments in the light test was smaller than that in the maximal test (13 vs 19 segments). In the former 13 segments, the initial relative activity in the maximal test was not significantly different from that in the light test (69.4 ± 9.3 vs 70.1 ± 10.0%). These results suggest that the light test can precipitate a transient perfusion defect preceding anginal pain and/or ischemic ST depression, therefore the light test is useful to detect coronary artery disease in patients who cannot perform the maximal test.

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Platelet function in the aortic blood in 39 patients who underwent intracoronary thrombolysis with urokinase was evaluated in the acute stage of myocardial infarction and after 4 weeks. The patients were classified into 2 groups according to the patency of the infarct vessel shown by coronary arteriography before urokinase administration. In the acute stage, 26 patinets with completely occluded infarct vessel (group 1) showed a decreased level of platelet aggregation induced by adenosine diphosphate or arachidonic acid as compared with 13 patients with patent infarct vessel (group 2). The platelet aggregation in group 1 increased 4 weeks later and both groups showed similarly enhanced platelet aggregation levels as compared with normal controls. Like platelet aggregation, serum thromboxane B₂ production in group 1 was lower than that in group 2 in the acute stage. Plasma thromboxane B₂ levels in the aorta in both groups were significantly elevated in the acute stage, and were normalized after 4 weeks. This elevation of thromboxane B₂ seems to be due to its washout from the infarct vessel, because plasma thromboxane B₂ levels were significantly higher in the great cardiac vein than those in the aorta after successful reperfusion in group 1 or group 2. In conclusion, despite a significant elevation in plasma thromboxane B₂ levels, platelet aggregation and serum thromboxane B₂ production relatively decrease in patients with totally occluded infarct vessel. The patency of the infarct vessels should be taken into account when evaluating platelet function in acute myocardial infarcion.

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Right heart catheterization was performed in 8 patients with progressive muscular dystrophy of the Duchenne type (DMD) at the advanced stage. A mean pulmonary arterial pressure in excess of 20 mmHg was observed in all cases. Five of them showed severe pulmonary hypertension with a mean pressure above 40 mmHg. Since pulmonary hypertension was relieved by correction of hypoxemia, this represented a precapillary pulmonary hypertension caused by constriction of the pulmonary artery. Furthermore, elevation of the mean right atrial pressure above 5 mmHg was observed in 6 of the 8 cases, indicating the possible presence of right ventricular failure. Despite the presence of left ventricular dysfunction as assessed by echocardiogram, no manifestations of left ventricular failure, such as dyspnea and pulmonary rales, were noted in any of the patients. In conclusion, it can be said that even in the terminal stage of DMD, the left ventricular function may, in fact, still remain not markedly involved, and that respiratory failure, as well as right ventricular failure caused by precapillary pulmonary hypertension, will tend to occur frequently and may play a determinant role in prognosis of the advanced DMD patient.

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The distribution and progression of coronary arterial and aortic lesions were examined in 40 conventional Watanabe Heritable Hyperlipidemic (WHHL) rabbits. They were classified according to age into stage I (3-5 months old, 14 rabbits), stage II (6-12 months old; 12 rabbits) and stage III (14-28 months old; 14 rabbits). Fifteen normal Japanese rabbits served as controls. The findings obtained from serial and trasverse sections of each of the extramural coronary arteries (ECA) and trasverse section of each of 4 to 5 equal pieces of whole ventricle for intramural coronary arteries (ICA) were quantified by an image analyzer. Atherosclerosis with positive Sudan III stain was seen in aorta, ECA and ICA over 200μ in diameter. Atherosclerotic lesions were noted in the aortic arch in stage I rabbits and in the whole aorta in stages II and III rabbits. In ECA, stenosis due to atherosclerosis was noted in 14, 33 and 93% of stages I, II and III rabbits, respectively. Stenosis of over 75% in the orifices of the left and right coronary arteries was noted frequently (71%), while mural thrombi, hemorrhage, intimal rupture and recanalization were seen rarely. Striking features were non-atherosclerotic stenosis with negative Sudan III, seen in the ICA less than 200 in diameter of almost all the hearts of stages II and III rabbits. Acute and old myocardial infarction appeared in 5 of the 14 hearts of the stage III rabbits and the infarct-related ECA showed severe stenosis of over 90%. In conclusion, to detect coronary atherosclerosis, serial and transverse sections of ECA are needed. In conventional WHHL rabbits, the incidence of stenosis in ECA is very high, compared with that of the previous reports, and myocardial infarction is due to severe stenosis in ECA. Non-atherosclerotic lesions in ICA occur before the appearance of the atherosclerotic lesions in ECA.

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To ascertain whether or not left ventricular geometry changes during preload reduction and afterload increment, the shortening characteristics of small segments in the left ventricular free wall were examined using 4 pairs of ultrasonic crystals in 10 dogs. Three pairs of ultrasonic crystals were circumferentially implanted in the basal, the midventricular and the apical portion of the left ventricle. Another pair of crystals were longitudinally placed in the midventricle. In the control state, the shortening at the apex was largest of all segments. During preload reduction, the end-diastolic length decreased significantly in each segment. The percent shortening decreased significantly at the apical and the longitudinal segment, but it remained unchanged at the midventricular and the basal segment. During afterload increment, the enddiastolic length increased significantly, but the percent shortening remained unchanged in each segment. We concluded that left ventricular geometry was altered during preload reduction and that the apical part is more responsive to preload change than the other portion.

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Exercise-induced changes in P maps were investigated in normal subjects (n = 20) in order to clarify the basic changes in P maps caused by exercise in patients with ischemic heart disease or by exercise-induced dysfunction of the left ventricle in patients with various heart diseases. Maps were obtained using an 87 lead-point system (HPM-6500, Chunichi-Denshi Corporation) and were recorded at rest and at heart rates up to 140/min in 20/min steps under graded bicycle ergometric exercise. P waves were divided into 3 phases (initial, middle and terminal) by locating the maximum. Maps were characterized by the distribution pattern of the positive and negative potentials in each frame. Peak voltages increased proportionally to the increase in heart rate. We observed a decrease in P wave duration concomitant with the increase in heart rate. Time from P onset to peak voltage increased slightly. We believe these findings to be due to the acceleration of sympathetic nerve tone accompanying exercise. We observed 2 patterns: type A showed the relatively short middle and terminal phases, and type B a prolongation of the middle phase and a shortening of the terminal phase. We consider the differences between types A and B to be partly due to individual differences in the degree of increase in pulmonary air volume and sympathetic nerve tone influence on the atria. In evaluating the exercise-induced P map changes, special consideration should be paid to the changes due to increase in heart rate.

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The changes in activation sequences in and around the epicardial reentrant circuit were analyzed during rapid pacing against ventricular tachycardia by using a canine infarction model. In 13 episodes of sustained ventricular tachycardia induced by a premature stimulation technique in eight dogs, reentry circuits were located in the superficial subepicardial myocardium in eight. Pacing stimuli were clearly demonstrated to enter the reentrant circuit in two directions: one wavefront collided with the orthodromic reentrant wavefront and the other entered prematurely into the reentrant circuit to reset the tachycardia (resetting phenomenon). With a faster pacing rate, stimuli failed to reset the tachycardia due to slower entry into the circuit despite the fact that most epicardial recording sites were activated by pacing wavefronts (concealed perpetuation). Termination of tachycardia was achieved by a local conduction block in the center of the reentrant circuit. A pacing impulse which encountered the local block was also shown to reinitiate the tachycardia using a different reentrant pathway. These different phenomena could be observed in consecutive pacing beats. These epicardial mapping data provided a direct electrophysiological basis for the mechanisms of reentrant ventricular tachycardia and the mode of its termination.

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The ability of hyperosmolar mannitol to salvage evolving myocardial infarction was studied in 50 open-chest dogs subjected to 3 hours occlusion of the left anterior descending coronary artery. In 28 dogs, 20% hyperosmolar mannitol was infused in to the distal half of the infarcted portion after commencement of reperfusion, leaving the proximal half mannitol free. In the other 22 dogs, physiological saline was infused instead of mannitol. The wall thickness at the distal half of the infarcted portion was increased 2 hours after reperfusion in both the saline and the mannitol groups. After 2 hours reperfusion the chest was closed. Thirteen out of 28 dogs in the mannitol group and 12 out of 22 dogs in the saline group died over one week. Seven days later, myocardial samples was measured for myocardial water content and creatine phosphokinase activity (CPK). Myocardial water content was increased in the infarcted portion in both the saline and the mannitol groups. In the saline group, myocardial CPK was reduced markedly in the proximal half (54.8 7.8% at the inner layer and 53.1 4.7% at the outer layer). These depletions were even more marked in the distal half (47.9 5.8 and 48.3 3.3%). In the mannitol groups, although the CPK was similarly depressed in the proximal half (44.8 5.8 and 41.1 5.4%), the CPK depletion in the distal half was less (44.8 6.1 and 58.1 6.7%) than the proximal half, suggesting mannitol preserved CPK depletion in the infarcted portion. It was concluded that intracoronary infusion of mannitol after reperfusion may salvage the infarcted myocardium.

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The purpose of this study was to characterize the regulatory mechanisms of atrial muscle contraction. Natural actomyosin (NAM) and tropomyosin troponin (TM-TN) complex were prepared from atrial and ventricular muscle of the same bovine heart. The results were as follows: (1) Atrial NAM was more sensitive to Ca²⁺ than was ventricular NAM: the pCa required for 50% ATPase activation was 5.96 ± 0.10 vs. 5.63 ± 0.07, (mean ± SE; n = 6; p < 0.01); (2) reconstitution of desensitized actomyosin of rabbit skeletal muscle plus atrial or ventricular TM-TN complex produced higher Ca²⁺ sensitivity in atrial muscle than in ventricular muscle: the pCa required for 50% ATPase activation was 6.48 ± 0.10 vs. 6.23 ± 0.15 (n = 3; p < 0.05); (3) the amount of inorganic phosphate covalentkly bound to atrial NAM was equivalent to that bound to ventricular NAM; (4) SDS-polyacrylamide gel electrophoresis of the two NAMs revealed several protein bands of different mobility from 16, 000 to 30, 000 daltons; and (5) the superprecipitation response of atrial NAM was characterized by a stepwise change in turbidity after the addition of MgATP, in contrast to the biphasic pattern of ventricular NAM. These data suggest that the free Ca ion concentration required for atrial muscle contraction is lower than that required for ventricular muscle contraction and that the difference is attributable to differences in atrial and ventricular regulatory proteins.

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A 22-year-old female patient was diagnosed as having systemic sarcoidosis with pulmonary, skin and ocular lesions, and ventricular tachycardia in resting ECG. Although cardiac sarcoidosis was strongly suspected at diagnosis, no clinical symptom such as palpitation or syncope developed during the three year observation period. Cardiac silhouette was unchanged in chest X-ray and ²⁰¹ thallium myocardial scintigraphy revealed no abnormality. Ventricular complex was suppressed by exercise or tachycardia. Two-dimensional echocardiogram showed abnormal fascicular bands attached from the mid-septum to the apex (false tendon). Therefore, it was concluded that this benign form of ventricular tachycardia might be due to the false tendon, rather than to the cardiac involvement of sarcoidosis. The cause of arrhythmia is important when evaluating the prognosis of a patient with a systemic disease.

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