Ventriculo-atrial (VA) conduction was studied in 133 patients with various kinds of arrhythmias using intracardiac electrograms and programmed stimulation. One-to-one V A conduction was observed during RV pacing at the rate just above the sinus rate in 6 of 31 patients (19.4%) with advanced AV block, in 7 of 26 patients (26.9%) with impaired AV nodal conduction, in 25 of 71 patients (35.2%) with normal AV nodal conduction and 3 of 5 patients (60%) with enhanced AV nodal conduction. However, the differences between these groups were not significant. There was no significant difference in either the AH block rate during RA pacing or the antegrade functional refractory period (FRP) of the AV node in patients with or without VA conduction, and the VA block rate during RV pacing was not significantly correlated with the AH block rate or the FRP of the AV node. VA conduction time (S-HRA) also showed no significant differences between these groups. The mean. VA conduction time during RV pacing at rates of 60 to 80 bpm was 208±87 msec, ranging from 100 to 395 msec. In conclusion, AV conduction disturbances may influence VA conduction, but VA conduction cannot be predicted from antegrade conductivity.

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To evaluate the role of the autonomic nervous system in vasospastic angina, plasma catecholamine and cyclic nucleotide levels were measured and the pilocarpine test was performed in 19 patients with vasospastic angina, 14 patients with nonvasospastic angina and 7 control subjects who were hospitalized patients without heart disease. Diurnal and nocturnal levels of plasma catecholamines were significantly higher in patients with angina pectoris, especially in patients with vasospastic angina, as compared with those of controls. In addition, an increase in plasma catecholamines preceded the onset of spontaneous and pilocarpine induced anginal attacks associated with significant increases in plasma catecholamines in patients with vasospastic angina. On the other hand, while nifedipine significantly suppressed both spontaneous and pilocarpine induced anginal attacks, the increase in plasma catecholamines remained.
These results indicate that increased activity and responsiveness of the sympathetic nervous system may possibly contribute to the development of vasospastic angina on the basis of parasympathetic hyperactivity.

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To study the role of catecholamines in the pathogenesis of hypertrophic cardiomyopathy (HCM), hemodynamic responses to low and high dose infusions of epinephrine (0.037 and 0.074μg/Kg/min) were compared between 21 patients with nonobstructive HCM and 21 healthy controls, matched for age and sex. During low dose infusion, patients with HCM showed significantly greater responses (p<0.05) than controls in echocardiographic left ventricular (LV) end-systolic dimension (-8±1% vs -4±1%, mean±SEM), fractional shortening (12±2% vs 7±1%) and peak systolic velocity of the LV posterior wall (32±5% vs 15±4%), but the differences disappeared during high dose infusion. Thus, patients with HCM started to respond to epinephrine earlier than controls and seemed to have an increased sensitivity of β-adrenergic receptors in the cardiovascular system. As the augmented responses were more evident in younger patients (<35 years) who manifested frequent familial occurrences of HCM, the increased sensitivity to catecholamine was postulated to be genetically determined and to be related to the abnormal myocardial hypertrophy of HCM.

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In 32 adult patients with a secundum type atrial septal defect (ASD) and normal pulmonary vascular resistance, the posterior aortic wall excursion (AoE) was measured using M-mode echocardiography, before, 16.2±4.5 days after, and 2.4±1.1 years after operative repair of the ASD. This parameter was also measured in 50 control subjects. The AoE index (AoE corrected for body surface area) in patients with ASD was significantly greater than in disease-free subjects (0.81 vs 0.59cm, p<0.01). When the AoE index was plotted against the pulmonary to systemic blood flow ratio (Qp/Qs) obtained by the Fick method, a single linear relationship was evident (r=0.65, p<0.01). The index normalized within 1 month after the operation; left ventricular dimension index became normal only 1 year after the operation. The right ventricular dimension index remained enhanced even 1 year after the operation. We suggest that exaggerated AoE might be another echocardiographic feature of ASD with normal pulmonary vascular resistance.

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The quantitative use of palm temperature changes during a fixed-load treadmill exercise was evaluated in normal subjects and patients with various degrees of cardiac disability. Treadmill exercise revealed different temperature patterns between subject groups. Normal subjects showed an initial transient decrease to a plateau phase, followed by a prompt return to the control level after cessation of exercise. Cardiac patients with severe disabilities showed a progressive decrease during and even after exercise, and the return to the control level was delayed. Patients with less severe cardiac disabilities showed an intermediate pattern. A significant correlation was observed between the temperature pattern and the plasma catecholamine concentration. The simultaneous measurement of forearm and hand blood flow, and palm temperature during a supine ergometer exercise showed that the temperature change reflected the blood flow changes. In conclusion, palm temperature monitoring during treadmill exercise is a simple and useful method for assessment of the vasoconstrictor response to exercise and, therefore, the pattern of temperature changes indicates indirectly the exercise capacity in heart disease.

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Left ventricular filling pressure (LVFP) as reflected by pulmonary capillary wedge pressure (PCWP) was measured in 40 adult cases of chronic severe anemia (CSA) before and after transfusion of 1 unit of whole citrated blood, using Swan-Ganz monitoring catheters. The cases were randomized into 4 groups of 10 each. Blood was transfused at a rate of 2ml, 5ml and 10ml/min in groups A, B and C, respectively. In group D, blood transfusion (BT) was given at 5ml/min but this group received, in addition, 40mg furosemide intravenously just prior to the transfusion.
Pretransfusion PCWP was normal in all the cases. Following BT the "wedge" pressure increased significantly in the first 3 groups, the rise being proportionately greater with faster transfusions (15.8, 20.9 and 32.2% in groups A, B and C, respectively). In group D, however, PCWP actually decreased by 21.7% (P<0.001).
As far as we know, this is the first study in which a definite and significant rise in PCWP has been documented following transfusion of blood even at conventional speed (group A). The implications of such an increase in "wedge" pressure as well as the observation that it can be completely blocked by furosemide are discussed. On the basis of these observations it is recommended that intravenous furosemide should be administered routinely before any BT in cases of CSA. Such practice will also permit blood to be transfused at a comparatively faster speed, without jeopardizing patient safety.

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Myocardial involvement in progressive muscular dystrophy of the Duchenne type was evaluated in 19 patients using thallium-201 myocardial perfusion imaging. A qualitative analysis was performed from five projection images by three experienced physicians. Distinct perfusion defects were shown in 13 patients, especially in the LV posterolateral or posterior wall (11 patients). There was no significant relationship between the presence of perfusion defects and the skeletal muscle involvements or thoracic deformities assessed by transmission computed tomography. Extensive perfusion defects were shown in 2 patients who died of congestive heart failure 1 to 2 years after the scintigraphic study.Progression of the myocardial scintigraphic abnormalities were considered to be minimal in 7 of 9 patients who underwent two serial scintigraphic studies over 2 to 3 years. It was concluded that thallium myocardial perfusion imaging is a useful clinical technique to assess myocardial involvement in Duchenne's progressive muscular dystrophy.

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The pneumocardiogram (PNCG) is a record of the pulsatile flow of air in the trachea coincident with each heart beat. In 5 anesthetized mongrel dogs, the cardiogenic air flow through an endotracheal tube was measured with a research pneumotachograph. The correlation between the pneumocardiographic volume of air, obtained by integrating the PNCG over the period of ventricular ejection, and stroke volume (SV), measured lay the saline-dilution method, was determined for a physiologic range of SV. Although the pneumocardiographic volume tracked measured SV, the former was always less. The range of correlation coefficients was 0.60 to 0.91. The results suggest that the PNCG may be suitable for continuous tracking of changes in SV on a noninvasive, beat-by-beat basis. The technique is ideally applicable to intubated human subjects, particularly those undergoing closed-chest surgical procedures.

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The extent of capacitive effects on coronary diastolic pressureflow relationships was investigated by proposing a theoretical model and by actually measuring the time constants of the coronary and systemic circulation. The dynamic pressure-flow relationship obtained by an aortic declining pressure perfusion and the static pressure-flow relationship obtained by constant pressure reservoir perfusion were compared to support the theoretical model, which revealed that the capacitive effects could be quantified by the α value, i.e. the ratio of the time constants of the coronary and systemic circulations. In 10 anesthetized dogs, the two independent methods disclosed that capacitive effects are limited and diastolic outflow pressure in the coronary circulation is the static zero-flow pressure intercept determined by the vascular tonus and intramyocardial pressure.

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Both bethanechol and physostigmine produced dose-dependent negative chrono-, dromo- and inotropic effects in the dog isolated atrial preparation. Within a relatively small dose of bethanechol and physostigmine, negative inotropic effect was clearly induced but no significant chrono- and dromotropic changes were observed. With a relatively large dose, the two cholinomimetics caused negative chrono-, dromo- and inotropic effects. The order of the negative actions of the drugs in % changes was inotropism >dromotropism≥chronotropism. These results indicate that pacemaker activity, sinoatrial conductivity and atrial contractility may be differentially sensitive to actions of cholinomimetics.

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We studied the effect of thymectomy on the development of hypertension in spontaneously hypertensive rats (SHR). There were no significant differences between thymectomized and sham thymectomized SHR during either the initial or chronic phase of spontaneous hypertension. Similarly, administration of anti-Thyl. 1 or anti-T sera did not influence the blood pressure in SHR during the chronic phase. The results suggest that the thymus does not play a direct role in the development and maintenance of blood pressure in SHR.

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Using a Langendorff rat heart preparation, we examined effects of nicardipine, a calcium channel blocker, on different stages of ischemic damage, characterized by a development of contracture and leakage of intracellular enzymes. Maximum recoveries of heart rate (HR) and peak left ventricular pressure-HR product, after 20min ischemia were attenuated by about 25% compared with those before ischemia. When nicardipine (0.1μmol) was added to the perfusate 5min prior to ischemia, this mechanical failure recovered completely to the pre-ischemic level. Although a significant increase in left ventricular end-diastolic pressure was observed in hearts exposed to 30min ischemia, the amount of creatine kinase (CK) released during re-flow after 30min ischemia was not enhanced by contracture but was proportional to the duration of ischemia (compared with that of 20min ischemia). Nicardipine reduced CK leakage by 25% after 30min ischemia but did not alter either ATP levels or coronary flow. The beneficial effects of nicardipine on ischemic damage are probably related to inhibition of calcium influx (Terai et al: Biochem Pharmacol 30: 375, 1981), which may accompany reperfusion of ischemic myocardium.

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The distribution of ³H-diltiazem in myocardial cell organelles was studied using an electronmicroscopic autoradiographic technique. At 3, 5 and 10min after ³H-diltiazem injection, silver grains, which indicate the existence of diltiazem, were detected in plasma membranes and intracellular organelles. Silver grains in Tsystems were observed more frequently at 3min than at 5 and 10min. In contrast, silver grains in sarcoplasmic reticula and mitochondria apparently increased with the passage of time. These findings suggest that diltiazem is transported through the T system and may accumulate within the sarcoplasmic reticula and mitochondria. Furthermore, our study revealed morphologically for the first time that the intracellular sites of action where diltiazem was directed were possibily the mitochondria.

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BIO 14.6 Syrian hamsters and diabetic KK mice have been reported to develop hereditary cardiomyopathy spontaneously. In order to investigate the pathophysiological role of carnitine metabolism in hereditary cardiomyopathy, tissue levels of carnitine derivatives and the histology of the heart, liver and skeletal muscles from BIO 14.6 hamsters and KK mice were studied.
Free carnitine levels in the heart of the BIO 14.6 hamsters (287.0±27.0n mole/g wet tissue) were significantly lower than in the control group (348.8±83.8, p<0.05). Short chain acylcarnitine (197.0±56.0n mole/g wet tissue) and total carnitine (667.6±136.4n mole/g wet tissue) in the hearts of the BIO 14.6 hamsters were significantly lower than in the control group (short: 425.2±54.8, total: 1023.6±81.4, p<0.001). There was no significant difference in the levels of various carnitine derivatives of the liver and skeletal muscles from the BIO 14.6 hamsters and control hamsters. On the other hand, carnitine derivatives in KK mice did not change significantly compared with those in the heart, liver and skeletal muscles of the control mice.
Histological findings showed that heart muscle degeneration and necrosis were found in both cardiomyopathic animals. Coagulative necrosis was found in both animals, whereas myocytolytic necrosis was found only in the BIO 14.6 hamsters. In KK mice, the right ventricle, especially tissue under the epicardium, was severely affected compared with the left ventricle. In the BIO 14.6 hamsters, however, lesions were scattered over both ventricles with a predilection for the left ventricle.

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In patients with pheochromocytoma, blood pressure was monitored continuously for 2 days using direct measurement techniques. Systolic blood pressure sometimes increased to more than 300mmHg. These sudden elevations of blood pressure were associated with increased levels of plasma catecholamines. Preoperative prazosin and propranolol therapy lowered mean systolic and diastolic blood pressure throughout the 2 day observation periods and was associated with decreased hematocrit levels. However, these agents did not prevent the rapid elevation of blood pressure.

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A 61 year old male with left main coronary artery disease died suddenly during ambulatory Holter monitoring. The monitoring documented ST depression followed by ST elevation, followed by junctional and ventricular escape rhythms with no measurable blood pressure by cuff methods. The mechanism of sudden death in patients with left main coronary artery disease is thought to be a combination of ventricular fibrillation or bradyarrhythmia and electromechanical dissociation secondary to a sudden onset of severe pump failure.

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We report on a 15 year old patient with Duchenne's progressive muscular dystrophy who demonstrated a narrowing of the left ventricular inflow and outflow tracts due to compression by a highly deformed thoracic spine. A systolic murmur (4/6) with thrill and a diastolic murmur (2/6) were heard, with these murmurs being louder in the expiratory phase as compared with the inspiratory phase. The second heart sound showed a paradoxical splitting. Echocardiograms revealed a compressed and narrowed left ventricle and a prolapsed mitral valve. The intensities of the heart murmurs changed synchronously with the chamber's narrowing due to respiration. A narrowed left ventricle occurring as a result of the compression by the deformed thoracic spine is thought to be the cause of these cardiac findings.

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An autopsy case of an advanced form of hypertrophic cardiomyopathy (HCM) showing marked fibrosis with intramural small arterial abnormalities is presented in this report.
A 52-year-old woman, who had a positive family history of HCM, was admitted because of palpitations. The chest roentgenogram showed a mildly enlarged cardiac silhouette and the electrocardiogram revealed abnormal Q waves and R wave and T wave abnormalities. The echocardiogram revealed hypokinesis with thinning of the interventricular septum and the anterior wall of the left ventricle. Percutaneous right ventricular endomyocardial biopsies demonstrated moderate interstitial fibrosis with small arterial thickening. At necropsy, the anterior and posterior walls of the left ventricle and the interventricular septum were markedly thinned and showed a massive transmural fibrosis. Moreover, the intramural small arteries, 50-300 microns in diameter, showed marked intimal and medial hypertrophy with proliferation of elastic fibers and smooth muscle cells.
From these findings, it is suggested that this was originally a case of HCM which progressed to a decompensated stage because of the abnormal intramural small arteries. The significance of small arterial lesions in HCM is discussed.

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An acute, intermittent sticking of a Björk-Shiley valve placed in the mitral position is described. It occurred shortly after the valve replacement, but 9 hours later, this 10-year-old female patient recovered from the accident without reoperation. Fluid infusion, left atrial compression, a sharp precordial blow or atrioventricular sequential pacing were effective for unlocking or prevention of the stuck valve. The mechanism was suspected to be impingement of remnant chordae tendinea.

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