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dine, procainamide, and disopyramide.6 Torsades de pointes was not observed in our patient, although it might be potentially manifested in the presence of significant flecainide-induced QT, prolongation. In our current controlled study of 14 patients with ventricular ectopy taking flecainide versus quinidine, four patients randomized to quinidine had clinical side efl’ects such as diarrhea, causing them to discontinue treatment. It appears that flecainide results in less frequency of similar side effects and possesses potent suppression (> 85 % ) of VPCs. While the single patient presented herein manifeste,d the unusual response of VT with flecainide, a number of studies including our own L* have shown no other or similar adverse effects. F’lecainide remains a promising new antiarrhythmic agent that warrants further clinical investigation.

We studied the relationships among collateral flow, regional myocardial shortening and the grade of coronary stenosis during ameroid-induced chronic coronary constriction in 22 conscious dogs. A radiolucent ameroid, a Doppler flow probe and a cuff occluder were placed on the left circumflex coronary artery (LCx). Regional myocardial shortening and regional myocardial blood flow were assessed simultaneously using ultrasonic dimension gauges and the tracer microsphere technique, respectively, during temporary occlusion of the LCx. Regional hypokinesia and ischemia were attenuated as a function of time during progressive coronary stenosis. Fifty percent recovery and full recovery of regional shortening during occlusion were observed 19 +/- 3 and 25 +/- 4 days after instrumentation, respectively, when the endocardial blood flow recovered from 0.42 +/- 0.07 ml/min/g at 7 days to 0.56 +/- 0.07 and 0.80 +/- 0.05 ml/min/g, respectively. Greater than 75% coronary stenosis coincided with collateral development, as estimated from regional shortening rate and the appearance of angiographically opacified collaterals. Our study confirms that the development of collateral vessels reduces regional ischemia and hypokinesia induced during abrupt coronary occlusion in a canine model.

Serial recordings of ST segment mapping were performed in 15 patients with acute anterior myocardial infarction. Reelevation of ST segment was observed in all cases between 12 hours and one week after infarction without clinical evidence of reinfarction. There was significant correlation between the magnitude of the sum of ST reelevation (sigma ST) and time to the peak of ST reelevation. The higher was sigma ST at the peak, the later was the appearance of the peak of ST reelevation. sigma ST recorded between 24 and 72 hours after infarction correlated with the extent of abnormal Q (NQ) in the precordial mapping as well as the percent of abnormally contracting segment (%ACS) on left ventricular angiography examined after 4 weeks following infarction. However, there was no correlation between sigma ST recorded at 12 hours after infarction and NQ studied at 4 weeks after infarction. The results indicate that the magnitude of sigma ST changes in time during the course after infarction and that the time of recording is important when sigma ST is used for the estimation of infant size. Reelevation of ST segment should be considered in the study of therapeutic intervention in acute myocardial infarction.

A 60-year-old woman with multiple coronary aneurysms, complicated with acute infero-posterior myocardial infarction is presented. The cine-coronary arteriogram disclosed a diffuse dilatation of epicardial coronary arteries associated with multiple aneurysms, fusiform ones in the right coronary and the left circumflex coronary arteries and saccular ones in the left anterior descending coronary artery. Distal run-off was poor. Ventriculography revealed a decrease in the ejection fraction (36%) and segmental abnormal wall motion at the apical and infero-posterior regions. The cause of the aneurysms appeared to be atherosclerotic. We suggested that coronary embolization was the cause of acute myocardial infarction in this case.

The effect of graded coronary stenosis on resting regional myocardial flow and left ventricular (LV) wall motion was studied in 18 anesthetized dogs. The left circumflex coronaary artery (LC) was constricted. The degree of LC stenosis and the changes in LV wall motion were determined by cineangiography of the coronary artery and LV. Regional myocardial flow was determined by tracer microspheres (TM), labeled with two different isotopes, Sr85, Sc46 or Ce141. The first TM1 and the second TM2 were infused after LC stenosis, and during a temporary complete LC occlusion respectively. Resting flow in areas with 70% stenosis was reduced, with a greater reduction of subendocardium and posterior papillary muscle, but minimum impairment of LV wall motion. No ST elevation was found. Animals with 80--90% stenosis showed a marked reduction of flow and wall motion, a significant ST-elevation and a delayed antegrade run-off in coronary arteriography.

The diagnosis of the ball thrombus in the left atrium has been very difficult by conventional clinical techniques. In the present case, two-dimensional echocardiography successfully demonstrated a spherical tumor moving in unpredictable directions in the left atrium. M-mode echocardiography did not clearly identify the tumor because of the limited visual width and spatial orientation of the technique; however, simultaneous recordings of the M-mode echocardiogram with phonocardiogram, carotid pulse wave, and electrocardiogram provided some diagnostic clues to the occlusive left atrial tumor. In the absence mitral valve occlusion by the tumor, a logarithmic correlation between the ejection time and the preceding R-R interval, and a negative linear correlation between Q to the first sound interval and the preceding R-R interval were found. In the beat following the appearance of the tumor in the mitral orifice, the sudden shortening of the ejection time and the prolongation of Q to the first sound interval were noted. Both of these findings are indirect evidence of decreased left ventricular filling associated with an elevated left atrial pressure resulting from the sudden mitral orifice obstruction by the tumor. Detailed analysis of the data obtained by the conventional noninvasive techniques could provide critical clues for the diagnosis of the occlusive left atrial tumor.

The clinical importance of triggered activity as a cause of arrhythmias is uncertain. We assumed that ventricular premature contractions (VPCs) caused by triggered activity could be increased at higher heart rates and be suppressed by calcium channel blockers and beta-adrenoceptor blocker. Thus, we evaluated VPC frequency as a function of underlying heart rate and examined the efficacy of diltiazem and atenolol on VPCs, using 24 hour ECG recording. Plots of VPC frequency vs. heart rate were made at 1-beat/min intervals for all heart rates recorded for at least 5 min during 24 hours. Diltiazem (90-180 mg/day) and atenolol (50 mg/day) were given orally for 4 weeks, respectively in 36 and 16 patients with VPCs of more than 2000/day. Patterns of relationship between VPC frequency and heart rate observed before diltiazem therapy included: an increase of VPCs at higher heart rates (positive correlation) in 16 patients, an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in 13 patients, an increase at low heart rates and flat curve at high heart rates (positive-flat correlation) in 5 patients, a linear decrease (negative correlation) in 1 patient, and flat curve (flat correlation) in 1 patient. The patterns of correlation in patients treated with atenolol were positive in 6, bidirectional in 7, positive-flat in 2 and negative in 1. Both drugs significantly reduced the VPC frequency per 24 hours for patients with a positive correlation (P group), but induced no significant change for those with the other patterns of correlation (NP group). At the 70% VPC suppression level, diltiazem was effective in 9 of 16 patients of P group and only 1 of 20 patients of NP group (p less than 0.01); atenolol was effective in 5 of 6 patients of P group and only 1 of 10 patients of NP group (p less than 0.05). Both drugs reduced the slope of a positive correlation. These results suggest that: VPCs which increase at higher heart rates may be related to triggered activity, and an evaluation of VPC frequency as a function of heart rate predicts the response of VPCs to diltiazem and atenolol, and probably to other calcium antagonists and beta blockers.

The purpose of this study was to develop a technique measuring the perfusion area of the coronary artery preocclusively and to study the relationship between the perfusion area and infarct size. 125I tracer microspheres were selectively injected into the left circumflex coronary artery (LCX) preocclusively, and then the LCX was ligated. 48 hours later the heart was removed, rapidly frozen, and 50-mu transverse sections were obtained from base, middle and apex of the canine left ventricle, and used for autoradiography to measure perfusion area and for tetrazolium staining to measure infarct size. Dogs were divided into 2 groups: group 1 in which the main trunk of the LCX was occluded to produce large infarct (n = 10) and group 2 in which the distal branch of the LCX was occluded to produce small infarct (n = 10). There was a linear correlation between the perfused and infarcted area regardless of a size or location of the perfusion area involved. These results indicate that the extent of infarction is directly proportional to the perfusion area and is not altered by the location in the ventricle.

The relationship between peak isovolumic developed pressure (Pmax) and end-diastolic volume can indicate ventricular contractility. Therefore, we propose a practical method to estimate Pmax from the pressure curve of an ejecting contraction of left ventricle. For the estimation, we first considered the left ventricle a linear time varying hydromotive pressure source (HMP(t)) coupled in series with an internal impedance. To formulate the HMP(t) we Fourier analyzed isovolumic pressure curves obtained under various conditions in six dogs. Since the higher order harmonics were found to be very small, HMP(t) could be described simply as where Pd = end-diastolic pressure and w = 2/T in which T is duration of contraction. Finally, HMP(t) for ejecting contraction was estimated by fitting the equation to the isovolumic portions of the pressure curve of ejecting contractions. The estimated Pmax values correlated well with actually observed Pmax values (r = 0.951, N = 24). We conclude that the proposed technique can be used to estimate Pmax from a single ejecting beat.

The diameter of the coronary artery was measured in dogs in situ by an ultrasonic dimension gauge using 10-MHz piezoelectric crystals. Underestimation in measurements due to crystal rotation was limited to < 1% by adding a convex lens to the crystal. A pair of small 10- and 5-MHz crystals were sutured to the adventitia of the left circumflex coronary artery (LCX) and the descending aorta (Ao), respectively. Using cuff occluders for vessel constriction of the inferior vena cava (IVC) or the Ao, curvilinear relationships between pressure and diameters were obtained. Phasic changes of the aortic as well as coronary diameter were grossly similar to changes in the pressure wave. After intravenous administration of dipyridamole, aortic pressure (AP) decreased by 17% along with 3% decline of the Ao and LCX diameter, however, after nitroglycerin given by the same route, LCX diameter increased by 5% (P < 0.05) despite 16% and 2.3% reductions in AP and Ao diameter, respectively. This ultrasonic technique, which allows continuous measurement of the diameter of small vessels, should provide a new tool for the study of coronary circulation.

Concentrations of various lipids and glycosaminoglycans (GAG) in the intima of the grossly normal and atherosclerotic cerebral arteries were compared with those of the aorta and coronary arteries. The lowest percentage of esterified cholesterol (EC) in total cholesterol, and of chondroitin sulfate-4/6 (CS-4/6) in total glycosaminoglycans and the highest percentage of heparin sulfate (HS) in total GAG are the characteristic features of the normal intima of normal cerebral arteries when compared with those in the aorta and coronary artery. In the cerebral arterial intimas, but not in the aorta or coronary arteries, there was a significant positive correlation between contents of EC and percentage and total content of CS-4/6. Atherogenesis in cerebral arteries is discussed in comparison to that of the aorta and coronary vessels.

In order to evaluate chemically the macroscopic scoring methods for severity of arteriosclerosis in the cerebral arteries, concentrations of total lipids, esterified and free cholesterol and lipid phosphorus were compared to the macroscopic severity of lesions in the cerebral arteries obtained from 376 Japanese persons after unexpected death. An increase of cholesterol content was correlated significantly with an increase of Baker's score and/or Gore's atherosclerotic index. The correlation coefficient between Baker's score and total or esterified cholesterol was the highest among the tested correlations (r = 0.82, n = 376).

Effects of alpha adrenergic stimulation on diameter change of the epicardial coronary artery were studied in in-situ canine heart. The diameter of the left circumflex coronary artery (LCX) was continuously measured by 10 MHz PZT crystals applied to the external wall of the LCX. Aortic pressure was measured using high fidelity catheter-tip manometer. Enhanced activity of alpha adrenergic receptor by humoral and/or somatic nerve stimulations caused a reduction of the LCX diameter despite of the systemic pressure rise.

Autoregulatory escape and post-escape hyperaemia were studied in a passive hydrodynamic model of the capillaron (ie, one or more soft-walled permeable capillaries enclosed together with extracapillary filtrate in a compliant capsule). Constriction was simulated in the model by reduction of the calibre of an orifice in the arteriole through which flow entered the ‘vascular bed’ of the capillaron. Constriction lowered the intracapillary pressure, and the capillary collapsed partially, with a resultant decrease in flow rate. The rate of filtration across the capillary wall into the extracapillary space of the capsule also declined. The falling extracapillary pressure increased the transmural pressure and reopened the capillary, returning flow to preconstriction values (autoregulatory escape). Reopening of the arterial constrition increased intravascular pressure, distending the capillary, with a transient increase in flow above the control value (post-escape hyperaemia). The time rate of constriction of the arterioles determined the magnitude of the fall in flow. The rate of removal of the arterial constriction determined the magnitude of the post-escape hyperaemia. These results show that the phenomena of autoregulatory escape and of post-escape hyperaemia resemble effects generated by passive changes in transmural capillary pressure. Such passive changes are affected by the rates of change of arteriolar constriction or relaxation. The effects of downstream capillary permeability and of capsular compliance on these phenomena were also examined.

Four hundred twenty-three intracranial cerebral arteries (males and females) were obtained from the medicolegal autopsy cases. Special attention was given to the three sites and the circumferential distribution of lesions in order to investigate the effects of hydrodynamics on the development of cerebral atherosclerosis. The severest lesions were primarily found at the inner curvature at the terminal portion of the internal carotid artery, the medial portion at the origin of the anterior cerebral artery, and the posterior portion at the origin of the posterior cerebral artery. The present results obviously demonstrated the relationship between the predilection sites of atherosclerotic lesions and the shape of the cerebral arterial tree.

Little attention had been paid to J renin in clinical renal infarction until recently when we found a transient elevation of plasma renin activity (PRA) after attacks in three patients. 1 We have had two additional experiences with renal infarction in a patient with a mitral prosthetic valve. The case is significant because (1) an isozyme analysis, which is generally thought to be most useful in organ diagnosis, did not help because of the multiple sources of an increased level of serum lactic dehydrogenase (SLDH) possibly involved. Here, the determination of PRA was useful and thus proved to be superior as a diagnostic aid in renal infarction. (2) This case provided an opportunity to observe the time course of the elevation of PRA along with that of the other serum enzymes, and offered a clue to the mechanism of renin release in this condition. Patient Summary A 21-year-old woman has

We report herein a case with multiple coronary arterioventricular fistulas, in which exercise-induced myocardial ischemia was demonstrated by stress thallium scintigraphy, illustrating the coronary “steal” phenomenon. A 52-year-old Japanese man complained of exertional chest pain for 1 year. The chest pain was relieved by rest but not by sublingual nitroglycerin or oral isosorbide dinitrate. His past medical history and family history were not contributory. Physical examination revealed blood pressure or 100/60 mm Hg and regular heart rate of 80lmin. There was no heart murmur. The chest x-ray examination showed slight cardiac dilation with cardiothoracic ratio of 52 % . The ECG showed T wave inversion in leads II, III, aVr, and V,.,. He complained of chest pain at peak treadmill exercise, along with pseudonormalization of T waves in leads II, III, aVr, and V,.,. Thallium-201 emission computed myocardial tomography at rest showed a mild perfusion defect of the inferoposterior to lateral wall of the left ventricle (LV) and posterior half of the septum, where severe perfusion defect was induced by peak ergometer exercise, with chest pain and pseudonormalization of T waves in leads II, III, aVr, and V,, (Fig. 1). Cardiac catheterization showed normal right and left heart pressures and no evidence of an intracardiac shunt. Left ventriculography revealed normal cavity size and no wall motion abnormality. Selective coronary arteriography showed no stenotic lesions and multiple fistulas from all three major coronary arteries (Fig. 2). The coronary venous drainage was normal. Propranolol therapy was started at oral doses of 90 mg/day and the frequency of exertional angina decreased. Although coronary artery fistula is an unusual congenital anomaly, clinical experiences have accumulated along with the evidence of selective coronary arteriography. However, the majority of coronary artery fistulas drain into the right heart chamber from a single coronary artery. Multiple coronary artery fistulas communicating with the LV involving all three major coronary arteries are extremely rare, and only five cases have been reported in the world literature.‘-5