To investigate the effects of verapamil on indicators of atrial vulnerability, we examined 30 patients with paroxysmal supraventricular tachycardia who received intravenous verapamil during an electrophysiologic study. Single atrial extrastimuli were given before and after intravenous administration of verapamil to induce repetitive atrial firing (RAF) or atrial fibrillation, and to examine the maximum A₂/A₁, which was defined as the maximum ratio of the duration of the atrial electrogram resulting from premature stimulation (A₂) to that resulting from the basic drive beat (A₁). The maximum A₂/A₁ increased from 145±20% to 154±25% (p<0.02) after verapamil administration. The maximum A₂/A₁ in patients in whom neither RAF nor atrial fibrillation were induced both before and after verapamil were smaller than those in patients in whom RAF was induced only after verapamil (before; 138±20% vs 165±15%, p<0.02. after; 144±22% vs 172±17%, p<0.05). RAF or atrial fibrillation was induced only after verapamil in 6 patients, who showed a maximum A₂/A₁ before verapamil of 150% or more. These data suggest that verapamil may induce repetitive atrial firing and possibly atrial fibrillation in some predisposed patients, especially in those that have a greater maximum A₂/A₁, which may be an indicator of local intraatrial conduction delay before drug infusion.

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Comparative study of Takayasu arteritis in 3 Asian countries (India, Korea and Japan) has revealed some significant differences. In angiographic findings, Japanese patients more frequently have lesions at the aortic arch and/or its branches (99% of 96 cases), while most lesions in Korean (76% of 109 cases) and Indian patients (92% of 50 cases) are at the abdominal aorea. The presence of HLA-Bw52 or B5 is closely associated with Takayasu arteritis in all 3 Asian countries. The complications in 108 Japanese, 101 Korean and 50 Indian patients were also compared. The most frequent complications were aortic regurgitation in Japan and hypertension in the other 2 countries. Death occurred most frequently due to congestive heart failure or sudden death resulting from aortic regurgitation in Japan, but resulting from hypertension in Korea and India.

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To assess the perfusion reserve of coronary collateral circulation, we analyzed exercise-stress tomographic thallium-201 myocardial images in 12 patients who had total occlusion in the right coronary artery (RCA) or left circumflex coronary artery (LCX) with well-developed collateral circulation and 90% stenosis in the left anterior descending coronary artery (LAD). In 6 of the 12 patients, the collateral circulation was non-jeopardized (group A). In the remaining 6 patients, the collateral circulation was jeopardized (group B). All 6 of the patients in group A had an exercise-induced decrease in thallium uptake in the segments supplied by the occluded RCA or LCX with collateral circulation, and 3 (50%) of these 6 also showed a decrease in thallium uptake in the segments supplied by the LAD. All 6 of the patients in group B also had an exercise-induced decrease in thallium uptake in the segments supplied by the occluded RCA or LCX with collateral circulation, but none showed a decrease in thallium uptake in the segments supplied by the LAD. In conclusion, the perfusion reserve of collateral circulation is equal to or less than 90% stenosis and myocardial ischemia occurs first in the collateralized segments during exercise in patients with jeopardized collateral circulation.

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The effects of exercise and isoproterenol infusion on the antegrade effective refractory period of the accessory pathway (ERP-AP) were compared in 10 patients with Wolff-Parkinson-White (WPW) syndrome. During an electrophysiologic study, the ERP-AP (paced cycle length: 400 msec) was measured before and during isoproterenol infusion at a rate of 1μg/min. On the next day, a symptom-limited ergometer exercise test was performed and the ERP-AP (paced cycle length: 400 msec) was measured before and during the test using an indwelling atrial electrode catheter. Isoproterenol infusion and the exercise test increased the heart rate from 84±24 to 122±17 beats/min and from 85±25 to 128±25 beats/min, respectively (p=NS isoproterenol versus exercise). The ERP-AP was shortened from 268±34 to 230± 19 msec with isoproterenol infusion (p<0.001) and from 273±42 to 237±31msec with the exercise test (p<0.001). There was no significant difference between the effects of isoproterenol and exercise. The percent change in the ERP-AP with exercise (Y) was significantly correlated to that with isoproterenol infusion (X) (Y=-3.04+0.70X, r=0.92, p<0.001). In conclusion, isoproterenol infusion at the present dose shortens the ERP-AP to the same degree as exercise, and thus is useful for predicting the exercise-induced shortening of the ERP of the accessory pathway in patients with WPW syndrome.

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To assess the vasodilator reserve in microcirculation, post-occlusive reactive hyperemia was examined in 21 chronic cigarette smokers (mean age; 50±7 years) and 21 non-smokers (mean age; 51±6 years), who were all healthy males. Reactive hyperemia was induced by occluding the digital artery at the base of the middle finger, and the increase in skin blood flow (Δflow) was analyzed with a laser Doppler flowmeter. Occlusion time was increased in a stepwise manner from 30 sec up to 300 sec. Baseline skin blood flow was similar in both groups (smoker, 27±9ml/min/100 g; non-smoker, 25±10ml/min/100 g, NS). The Δflow in smokers was significantly less (23%-59%) than that in non-smokers. Furthermore, the reduced Δflow in smokers was inversely correlated with Brinkmann's smoking index (r=0.567, p<0.01). These results indicate that chronic cigarette smoking impairs the microvascular response to transient ischemia, and that this impairment correlates with the intensity of the smoking habit.

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To clarify how angiotensin converting enzyme inhibition affects left ventricular function through ventricular unloading, ventricular wall stress, ventricular volumes, and other cardiac indices and exercise tolerance were evaluated in 17 patients with mild to moderate chronic congestive heart failure before and after 3 months of treatment with enalapril. Echocardiographic examination revealed that treatment with this angiotensin converting enzyme inhibitor resulted in significant reductions in end-systolic wall stress (117±25 to 89±28 g/cm², p<0.01) and left ventricular volume indices (end-diastolic: 163±56 to 143±60; end-systolic 99±51 to 77±57 ml/m² p<0.01). Ejection fraction (42±11 to 48±13%, p<0.01) and systolic blood pressure/end-systolic volume (SBP/ESV; 1.06±0.30 to 1.33±0.48 mmHg/ml, p<0.01) were both increased. By radionuclide ventriculography, ejection fraction and peak ejection rate (2.30±0.74 to 2.80±0.76 EDV/sec, p<0.01) were increased, while time to peak ejection, time to peak filling, and peak filling rate were unchanged. Heart rate and double product at exercise were decreased and ΔEF was significantly increased (-1.4±4.1 to 1.6±4.4%, p<0.02). The decrease in end-systolic wall stress was consistently related to both the increase in ejection fraction and SBP/ESV, while the decrease in end-diastolic volume was related only to SBP/ESV and not to ejection fraction. Furthermore, there was a direct relationship between the decrease in systolic wall stress and the decrease in end-diastolic volume. These results suggest that the improvement of left ventricular contractility due to angiotensin converting enzyme inhibition was produced through a parallel reduction of both afterload and preload. Afterload reduction had a greater effect on the improvement of left ventricular ejection fraction than preload reduction.

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Although the prognosis of patients with chest pain and normal coronary arteries is reportedly good in the Western literature, it is unclear in Japan. The purpose of this study was to examine the natural history of 274 consecutive patients with chest pain and normal or nearly normal coronary arteries, and to determine whether the possibility of minor coronary artery disease has clinical implications as a prodromal factor of other heart diseases. Six of the patients died during the mean observation period of 6 years (74.5±35.4 months): 2 cancer, 3 cerebro-vascular accident, and 1 renal failure death. Three additional patients suffered from nonfatal cerebro-vascular accidents. Eleven patients were readmitted for evaluation of chest pain, and 4 of these were diagnosed as having vasospastic angina. Progression of significant coronary artery disease was not detected in these 11 patients with repeated coronary angiography. None of the patients in this study developed fatal or nonfatal myocardial infarction. A small number of patients (36/240, 15.0%) continued to suffer from chest pain, None of the patients developed cardiomyopathies or valvular heart diseases. Our observations indicate that the prognosis of chest pain with normal or nearly normal coronary arteries is better than that presented in the Western reports.

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To investigate the clinical applicability of automatic analysis of wall thickness in two-dimensional echocardiography, computer-assisted and conventional manual methods were compared in 26 cases. An echo threshold was automatically set in short-axis echo images through a discriminatory variance analysis of the signal-to-noise ratio. A fixed standard was determined inside the left ventricle using the circle window method, which we developed previously. Two abrupt echo reflections were selected as candidate points for the borders, and an outward search was conducted in all directions from a fixed standard to separately delineate the endocardial and epicardial interfaces. Interpolation using a spline function was applied to these points to complete the border lines. Differentiation was also used to eliminate the anterior and posterior papillary muscles. Significant correlations of r=0.98 were found between the computer and manual assessments of the epicardial and endocardial intraluminal ventricular areas (p<0.01). A correlation of r=0.87 was also obtained for myocardial wall thickness as determined by the 2 methods (p<0.01). Variability of the reproducibility using the computer method was 0.22% for the epicardial area and 0.64% for the endocardial area. These results confirm that computer-aided automatic measurement of wall thickness is clinically applicable to two-dimensional echocardiography .

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This study was designed to clarify whether changes in transmitral flow velocity patterns in left ventricular (LV) dysfunction are determined primarily by changes in left atrial (LA) pressure and LV relaxation, and, if not, to determine the contribution of changes in other parameters. Two levels of acute LV dysfunction were produced in 11 dogs by coronary microembolization, and pulsed Doppler transmitral flow velocity patterns and hemodynamic parameters were recorded. The mean ratio of peak early diastolic filling velocity (E) to peak late diastolic filling velocity decreased with mild LV dysfunction (LV end-diastolic pressure of between 12 and 17 mmHg), and redistribution of diastolic filling to early diastole was observed with severe LV dysfunction (LV end-diastolic pressure of &ge;18 mmHg). Changes in E correlated best with those in the LA-LV pressure gradient integral. Multiple linear regression analysis of the changes in possible determinants of the pressure gradient integral, i.e.. LA to LV crossover pressure, LV time constant, LV minimum pressure, and LA and LV chamber compliance, yielded a highly significant correlation with the changes in E. However, analysis of only the changes in the crossover pressure and the time constant showed a very poor correlation. Thus, changes in chamber compliance and LV minimum pressure, in addition to the changes in LA pressure and LV relaxation, may significantly affect the changes in E that are associated with LV dysfunction.

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Low doses (&le;100 pmol/kg) of endothelin-1 (ET-1) and endothelin-3 (ET-3) elicited a fall in mean arterial pressure (MAP) and a dose-related reduction in hindquarter vascular resistance in anesthetized rats. The depressor response to low doses of ET-1 or ET-3 was short-lived (about 10 sec) and reversible. High doses (&ge;200 pmol/kg) of ET-1 and ET-3 elicited a biphasic response; an initial fall in MAP followed by a gradual increase in MAP. The pressor response to large doses of ET-3 was less than that to large doses of ET-1. On the other hand, the depressor response to low doses of ET-3 was similar to that to low doses of ET-1. Both ET-1 and ET-3 at low doses exhibited primarily a vasodilatory activity. Pretreatment with N^G-monomethyl-L-arginine (L-NMMA), a compound that inhibits nitric oxide (NO) production by endothelial cells, attenuated the hypotensive and hindquarter vasodilating effects of low doses of these isopeptides, indicating that the hindquarter vasodilating responses to these peptides depend upon the release of NO from endothelial cells. On the other hand, pretreatment with either aspirin or indomethacin did not alter the hypotensive or the hindquarter vasodilating effects of either ET-1 or ET-3, indicating that cycloxygenase products may not be involved in the vasodepressive mechanisms of these peptides. L-NMMA attenuated the vasodilating effects of these peptides, but did not completely inhibit the response, suggesting that NO production by endothelial cells plays only a partial role in the vasodilation of ET in vivo. Although endothelin per se is a potent vasoconstrictor, this peptide also has vasodilatory activity in vivo due to the interaction between endothelium derived relaxing faetor and other vasoactive substances to regulate vascular tone in regional criculation.

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Surgical treatment of a right atrial myxoma with a right-to-left shunt and coronary artery disease was successfully performed in a 61-year-old man. The interatrial shunt occurred through a patent foramen ovale and was the result of a high central venous pressure due to tricuspid stenosis and regurgitation. Instead of right heart catheterization and cardioangiography, we chose an intraoperative blood-gas study to diagnose the intracardiac shunt. Preoperative polycythemia and hypoxemia were improved after removal of the tumor and closure of the patent foramen ovale.

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