This study examined mainly the adverse effects of ²⁰¹T1 myocardial scintigraphy with dipyridamole (D-T1) in 73 elderly patients over 70 years old in comparison with those in 65 younger patients. Fifty-five of 73 elderly patients (75%) and 49 of 65 younger patients (75%) had a persistent or dipyridamole-induced perfusion defect on D-T1. The hemodynamic changes induced by dipyridamole as well as the incidence of cardiac and noncardiac adverse effects were similar in both groups and no serious adverse effect occurred in either group. Secondly, we examined the procedure's usefulness for detecting ischemic heart disease in elderly and younger patients. Dipyridamole induced perfusion defect was noted in 21 elderly patients and in 24 younger patients (N.S.). Among the patients in whom coronary angiography was performed, significant coronary artery stenosis was found in 5 of 8 elderly patients and 17 of 20 young patients (N.S.). In patients with one or two-vessel disease, the area with dipyridamole induced ischemia was concordant with the stenotic area seen on coronary angiography in 3 of 3 elderly patients and 12 of 13 younger patients (N.S.). Thus, the safety and usefulness of D-T1 for detecting myocardial ischemia were comparable in elderly and young patients.

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We analyzed the site of VT origin and the induction mode of VT in 9 patients who showed new VT morphologies with different bundle branch block patterns after administering antiarrhythmic drug(s). In all patients, VT exhibiting the clinical morphology was induced in the drug free state. (1) VT origin: In 6 patients, VTs showing LBBB pattern had a site of origin at the right ventricular free wall, and VTs with RBBB pattern originated from the left ventricular free wall. VT from the intraventricular septum of the right ventricle showed RBBB pattern in two patients and VT with LBBB pattern arose from the posteroseptum of the left ventricle in one patient. (2) VTs with new morphologies: After administering drug(s), VTs with new morphologies were induced in 18 studies and the mean cycle length of these VTs was not different from that in the control study. Among them, the induction mode was less aggressive in 4 of 7 drug studies and more aggressive in 1 study. (3) VTs with the same morphology: VTs with morphologies identical to those of the clinical VTs were induced in 15 studies. However, the drugs' effect was evident. The mean cycle length of these VTs was significantly prolonged, and VTs were induced by less aggressive modes or at longer coupling intervals. In conclusion: (1) After administering drug(s), different electrophysiologic characteristics were observed between the VTs with new morphologies and the VTs with the same morphology. (2) If a new VT was induced by less aggressive modes after administering drug(s), the drug(s) might act to facilitate inducibility: proarrhythmic effect.

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To determine the clinical significance of ST-segment depression observed in paroxysmal supraventricular tachycardia (PSVT), we evaluated the 12-lead electrocardiogram (ECG) during spontaneous PSVT in 54 patients (27 men and 27 women: mean age±SD; 47±18 years), who came to our clinic for the treatment of PSVT. Coronary angiography was performed in 16 patients (16 to 74 years; mean=50±18) and treadmill exercise testing was performed in 21 patients. A cardiac electrophysiological study was carried out in 24 patients. During PSVT, ST-segment score was calculated as the sum of the ST-segment depression in 12 leads. The correlations between the ST-segment score, PSVT rate and age of the patient were analyzed as follows: The most significant positive correlation was observed between the ST-segment score and the PSVT rate (r=0.615, p<0.000001). The next most significant correlation was found between the PSVT rate and the age of the patient (r=-0.500, p=0.00011). A negative correlation was also observed between the ST-segment score and the age of the patient (r=-0.429, p=0.0012). In 13 of 16 patients, coronary angiography did not reveal any significant (≥75% in area) stenosis. Exercise testing induced significant ST-segment depression in 3 patients, of whom two had significant coronary artery lesions.PSVT was due to atrioventricular reentry via an overt (n=3) or concealed accessory pathway (n=15), atrioventricular nodal reentry (n=5) and sinus node reentry (n=1). In conclusion, patients with a faster PSVT rate revealed more pronounced ST-segment depression than did those with a slower PSVT rate, possibly reflecting the modified repolarization process instead of coronary artery involvement.

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We studied the relationship between physical activity and ambulatory blood pressure (BP) in young and older shiftworkers by simultaneous recordings of activity, blood pressure and pulse rate (PR). Activity was assessed using Activetracer, a self-contained microcomputer with an acceleration sensor, attached to a waist belt. Ambulatory BP was monitored every 30 minutes for 48 hours with a TM2421.
Three types of hemodynamic responses were noted in relation to the physical activity. The balance type, in which both BP and PR increase with physical activity, was observed in 5 of 10 young cases (50%) but only in 1 of 7 older cases (14.3%). The BP response type, in which the BP increases with no change in the PR, was observed in 6 of the 7 older workers (86%) but only in 3 cases in the young group (30%). The PR response type, in which only the PR increase correlated with activity, was observed in 2 cases in the young group (20%) and none in the older group.
The difference in systolic BP between periods of activity and rest in the older shiftworker was significantly larger than that in the young group (15.9±6.4 vs. 5.9±6.6mmHg, p<.01), although no significant difference was observed in diastolic BP. In contrast, the increase in pulse rate after movement was significantly higher in the young group (4.4±4.0 vs. 9.0±4.8bpm, p<.05). Thus, the fluctuation of the systolic BP was more dependent on physical activity in the older group, whereas PR variations correlated with the physical activity in the young group.

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The purpose of this study was to clarify the role of calcium flux in the pathogenesis of transient overshoot in regional myocardial contractile function after brief ischemia (post-ischemic hypercontraction). Six open-chest anesthetized dogs were examined. The left anterior descending coronary artery (LAD) was cannulated with a bypass system from the left carotid artery. Two minutes of total coronary occlusion of the LAD resulted in a post-ischemic hypercontraction 1 minute after reperfusion. Post-ischemic hypercontraction was abolished after reperfusion following 2 minutes of perfusion with anoxic Krebs-Henseleit solution containing 2.5mM calcium. Post-ischemic hypercontraction occurred after calcium-free anoxic perfusion. The regional myocardial contractile function remained depressed 1 minute after reperfusion following anoxic perfusion with 5.0mM calcium solution. Thus, post-ischemic hypercontraction was modified by the calcium concentration during anoxia. Alteration in transsarcolemmal calcium influx during reperfusion, which was modified by alterations in the calcium environment during anoxia, could be responsible for this phenomenon.

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The effects of pilsicainide, a new class Ic antiarrhythmic agent, on the atrial fibrillation threshold (AFT), the atrial effective refractory period (ERP), and the interatrial conduction time (ACT) in Langendorff-perfused guinea pig hearts were investigated. These effects were compared with those of disopyramide, lidocaine and flecainide. Whole guinea pig heart was perfused with Tyrode's solution containing acetylcholine (3×10^-7M). Three indices were measured before and after the administration of the test drugs using right atrial extrastimulus and high frequency stimulation. Pilsicainide, disopyramide and flecainide (≥10^-6M) all significantly increased the AFT. Both pilsicainide and flecainide (≥3×10^-6M) significantly prolonged the ERP, but this prolongation was less pronounced than that observed with disopyramide. The ACT was significantly prolonged with pilsicainide (≥10^-6M), and this prolongation was greater than that observed with disopyramide but less than that with flecainide. Lidocaine had no effects on any of the indices measured. In conclusion, pilsicainide had a preventive effect on the atrial fibrillation induced by a combination of acetylcholine and high frequency stimulation in guinea pig hearts, by increasing the atrial ERP and slowing the interatrial conduction. These effects may explain, in part, the clinical effectiveness of this drug on paroxysmal atrial fibrillation.

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Cardiac energy metabolism of pressure-overloaded rat hearts was examined under in vivo and in vitro conditions. Two, 4 and 6 weeks after constriction of the abdominal artery, the hemodynamic and metabolic profiles of hearts in vivo and of perfused hearts were determined. Significant increases in left ventricular weight/body weight (30 to 45% increase relative to the sham group), systolic and diastolic blood pressure (22 to 33% increase) and pressure-rate product (31 to 33% increase) were observed 2, 4 and 6 weeks after the operation, and a slight but significant decrease in heart rate was observed at 2 weeks after the operation. Tissue hydroxyproline content increased (17 to 93%) with time after pressure-overload. These findings are indicators of pressure-over-loaded cardiac hypertrophy. The total high-energy phosphates of the in vivo rat myocardium under artificial respiration were lower than those of sham-operated rat myocardium 2 (23%) and 4 weeks (21%), but not 6 weeks after aortic constriction. The maximal oxygen consumption rates of mitochondria, when determined in the skinned cardiac fibers, also decreased 2 (47%) and 4 weeks (36%), but reversed 6 weeks after pressure-overload. However, the myocardial ATP, a utilizing form of high-energy phosphate, of pressure-overloaded rat myocardium remained normal at all times after cardiac hypertrophy. This suggests that alterations in hemodynamic variables of in vivo pressure-over-loaded rats may not be attributable to a reduction in the myocardial energy production. In the perfused hearts isolated from pressure-overloaded rats, tissue ATP levels were similar to those of sham-operated rats, although the tissue creatine phosphate tended to be reduced in the pressure-overloaded animals at all stages of cardiac hypertrophy examined. Only a marginal decrease in the tissue high-energy phosphate (13%) was observed 4 weeks after the operation relative to that of sham-operated rats. In contrast, the developed tension of the perfused pressure-overloaded rat hearts was consistently lower (27 to 36%) than that of the sham-operated rat hearts. The results suggest that the high-energy phosphate levels of pressure-overloaded rat myocardium in vitro are unlikely to account for the observed decline in cardiac contractile function. The reduction of myocardial high-energy phosphates of pressure overloaded rats may be due to an adaptative change rather than a causal event.

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To determine whether clonidine can improve the central alteration of the baroreflex in SHR, the centrally cut end of the aortic depressor nerve was electrically stimulated in SHR with intravenously administered clonidine. Aortic depressor nerve (ADN) stimulation elicited depressor and sympatho-inhibitory responses in a frequency-dependent manner in WKY and SHR. These responses were significantly smaller in SHR than in WKY. The attenuated depressor and sympatho-inhibitory responses to ADN stimulation in SHR were restored following i.v. injections of clonidine, although the drug did not affect the responses to ADN stimulations in WKY.
These findings suggest that clonidine can improve central attenuation of the baroreflex in hypertension.

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Vasoreactivity of laser-treated vessels was investigated in two different experimental conditions. The canine left circumflex coronary artery (LCx) was lased under perfusion with Krebs-bicarbonate buffer by means of a thermal laser (hottip probe, HT) at 7W for 6 seconds and an argon laser beam through a 300μm optical fiber at 3W (tip power) for 1 second at 12 spots. A nontreated segment of the LCx served as a control. Two 3-mm long segments were obtained from the treated segment: one to measure the results of potassium (K) induced contraction, and another 3, 4 diaminopyridine (DAP; K channel inhibitor) induced contraction. In 11 instances, coronary angiography of the perfused artery showed less than 50% stenosis after laser treatment. The segments were then mounted isometrically with 1g tension in Krebs-bicarbonate buffer. Contraction was induced either with 30mM KCI or 10^-2M DAP and expressed as developed tension (gram; g). KCI induced vasocontraction of 4.15±0.93g in the control, 0.33±0.71g in laser irradiated segments (P<0.0001vs control), and 0.02±0.06g in thermally-treated segments (P<0.0001 vs control). DAP induced vasocontraction of 5.21±1.32g in the control, 0.39±0.83g in laser irradiated segments (P<0.0001 vs control), and 0.07±0.13g in thermally treated segments (P<0.0001 vs control). In 4 instances, more than 5O% stenosis remained and additional balloon dilatation reduced the stenosis to less than 50%. The lesions also showed reduced vasoreactivity. In vivo thermal angioplasty resulted in reduced vasoreactivity compared to control in 4 anesthetized dogs. Thus, laser and thermal angioplasty reduced vasoreactivity induced by either KCI or 3, 4 DAP. Neither acetylcholine at 10^-6M nor papaverine at 10^-4M was able to induce relaxation of treated segments. In conclusion, 1) the lased coronary artery loses its vasoreactivity to either a constrictive or relaxing agent, 2) although stenosis may be produced by laser energy, additional balloon dilatation can reduce residual stenosis, and 3) laser thermal or argon laser angioplasty may prevent severe coronary spasm.

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Hypocalcemia is a relatively uncommon but reversible cause of left ventricular dysfunction in infants and children. A 30-day-old boy with idiopathic hypocalcema presented with congestive heart failure and convulsive seizures. He had no evidence of underlying cardiac disease. The cardiac failure responded to calcium therapy. It is suggested that hypocalcemia should be considered as a possible cause of left ventricular dysfunction in infants.

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A 25-year-old female developed high-grade atrioventricular block and markedly elevated central venous pressure after sustaining a crushing injury to the chest while driving a car. An echocardiographic examination with color Doppler revealed severe tricuspid regurgitation due to a torn papillary muscle. An extensive review of the literature showed the following: 1) correct diagnosis is often delayed because of coexisting multisystem involvement and the subtleness of abnormal physical signs, 2) identification of abnormally elevated right atrial pressure with a prominent "v" wave, and characteristic electrocardiogram appeared to be the key to early diagnosis, and 3) the final diagnosis may be confirmed by echocardiography with Doppler and/or cardiac catheterization. The role of echocardiographic examination with color Doppler technique deserves special emphasis because the final diagnosis can be easily reached during the acute phase at the bedside noninvasively.

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A 68-year-old man with aortic aneurysm who had repeated episodes of obstructive bronchopneumonia is reported. Serial chest X-rays revealed infiltrative shadows in the left lower lung field. A thoracic computed tomogram demonstrated a dissecting descending aorta compressing the left lower bronchi and abnormal shadows, probably inflammatory, distal to the obstructions. Because of signs of impending rupture of the dissected aorta, surgical repair was performed and there has been no recurrence of respiratory infection since.

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