Considerations of the physical basis of cardiac contraction and sound generation explain the mechanism of the first sound. Older theories examining this sound as the result of valve closure or stiffening are refuted. It has been demonstrated that the normal first sound originates in the left ventricle alone and that accelerations and decelerations, "timed" by mitral and aortic valves events, are its cause. Three components have been recognized in the first sound: a occurs when the left ventricular wall and septum have reached a certain tension; b when the aortic valve opens; c when the peak of the aortic pulse has been reached. The ventricular septum is an integral and essential part of the left ventricle. In left bundle branch block, abnormal activation of the septum transforms this into a passive structure resulting in a slower rise of left ventricular pressure and a longer isovolumic period. This causes a small and delayed first sound, whose components, however, are still separated by normal intervals. In right bundle branch block, the first sound has a normal amplitude and its components are separated by normal intervals. If there is a larger late component, it is a c component, similar to that of normal elderly subjects. A larger c component may also be found in atrial septal defect. The cannon sound of AV block is caused by more rapid deceleration due to higher atrial pressure at the onset of ventricular contraction resulting in intense vibrations. The first sound of arrhythmias varies in the different conditions and even in different subjects, due to the effect of several variable factors. Elevated left atrial pressure, stiffening of the mitral valve in mitral stenosis, causes a slow onset and a more rapid rise of LV pressure. This results in a delayed, but larger, first sound. The action of catecholamines on the myocardium dramatically increases the first sound. The latter can be considered as an index of contractility and may be of great interest during stress tests.

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Susceptibility of unipolar AAI pacemakers to myopotential inhibition (MPI) was assessed in 10 patients by provocative maneuvers and 24-hour Holter monitoring, and compared to that of unipolar VVI pacemakers in 12 patients. Five maneuvers were performed for each of four different sensitivity levels, and an MPI score of from 0-4 points was given according to the lowest sensitivity level at which MPI was provoked. The MPI score in patients with AAI pacemakers was significantly lower than that in patients with VVI pacemakers, 1.60±1.26 vs 2.83±1.03 (p<0.05). On Holter monitoring, no MPI was detected in any of the patients with AAI pacemakers, whereas myopotential inhibition was detected in 5/12 patients (42%) with VVI pacemakers. Intracardiac electrograms were of lower amplitudes for AAI pacing than for VVI pacing, 3.13±1.83mV vs 11.20±5.95mV (p<0.01). Although the amplitude of atrial signals was lower than that of ventricular signals, the AAI pacemakers were less susceptible to MPI than were the VVI pacemakers. However, when MPI occurs in AAI pacing, it may be more difficult to correct without undersensing because of the lower amplitude of the intracardiac signals.

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QRST isointegral maps were constructed from 87-lead ECGs in 37 patients with abnormal ventricular activation, such as ventricular premature beats, WPW syndrome, left bundle branch block and right bundle branch block. Patients were divided into 2 groups, the old myocardial infarction (OMI) group (n=18) and the non-infarction group (n=19). In the latter group, QRST isointegral maps showed smooth bipolar surface distributions, with positive values located over the precordium and negative values over the right upper anterior chest and the back, independent of the ventricular activation sequence. In the OMI group, for individual patients, the distribution patterns of QRST isointegral maps were similar between normal sinus rhythm and VPB or WPW conduction. Including the patients with BBB, a decrease of the time-integral value was consistently found in leads which corresponded to an asynergic site indicated by left ventriculography. To evaluate the abnormalities of QRST isointegral maps, particular attention was given to the area where the QRST time-integral value was less than the lower limit determined by 40 normal subjects; this area was designated as the negative departure area. Characteristic distribution patterns of the negative departure area seem to indicate the asynergic site, independent of the activation sequence. Thus, the QRST isointegral map may be useful for identifying the asynergic site in patients with abnormal ventricular activation sequence, that is hardly detected with conventional electrocardiograms.

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The effects of treadmill exercise on platelet function, blood coagulability and fibrinolytic activity were evaluated in 20 patients with lone atrial fibrillation (AF) and 15 age-matched normal controls (normals). Multistage treadmill exercise up to 85% of the predicted maximal heart rate was performed, and blood for measurements was obtained pre-exercise, and immediately and 6 min post-exercise. There was an increase in the platelet sensitivity to ADP-aggregation after exercise in both groups. Preexercise plasma β-thromboglobulin (β-TG) levels were higher in AF than in normals. Beta-TG increased after exercise in both groups (immediate post-exercise; 35.1ng/ml for normals and 62.8ng/ml for AF), and the increase was greater in AF than in normals. PT and APTT shortened, and plasma fibrinogen levels increased after exercise in both groups. Pre-exercise levels of plasma ATIII and protein C were lower in AF than in normals. These two proteins increased after exercise in both groups. However, the increase was greater in normals. Plasma α₂-PI increased after exercise in both groups; the level was lower in AF than in normals at each exercise stage. In conclusion, enhanced platelet activity, and lower levels of anticoagulant and antifibrinolytic activity were observed in AF not only at rest but also after treadmill exercise. These changes might reflect the hypercoagulable state in patients with AF. It is speculated that the risk of thromboembolic complications may be enhanced with exercise in AF patients.

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The correlations between blood pressure, left ventricular hypertrophy and left atrial enlargement were examined in 2, 010 autopsied cases. The cases were classified into 3 groups: 972 (48.2%) normotension cases, 313 cases (15.5%) of systolic hypertension and 725 cases (36.1%) of diastolic hypertension. The incidence of left ventricular hypertrophy (LVH) was significantly higher in systolic and diastolic hypertensive cases than in normotensives (p<0.05), but no significant difference in LVH incidence was found between the 2 hypertensive groups. The incidence of an enlarged left atrium was also significantly higher in both hypertensive groups than in the normotensive group (p<0.05). The incidence of congestive heart failure and a large CTR were also higher in both hypertensive groups. However, there were no intergroup differences in atrial fibrillation incidence, despite significant differences in atrial size.
Finally, the incidence of moderate to severe coronary artery stenosis was significantly higher in both hypertensive groups, but no difference was found between the 2 types of hypertension. We concluded that both systolic and diastolic hypertension contributed to the genesis of left ventricular hypertrophy, left atrial dilatation, coronary sclerosis and congestive heart failure.

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This paper describes clinical features of high renin hypertension in the elderly. Peripheral plasma renin activity ranged from 0 to 20.1ng/ml/hr in 59 hypertensive in-patients aged 70 to 86. The patients were divided into 2 groups: 9 cases with plasma renin activity greater than or equal to 3.0ng/ml/hr (high renin group) and the remaining 50 with plasma renin activity less than 3.0ng/ml/hr (control group). The development of hypertension differed between the 2 groups. Six of the high renin group (66.7%) had a history of acceleration of previously mild hypertension, while only 3 of the control group (6.0%) had this history (p<0.01). The frequencies of high diastolic blood pressure (greater than or equal to 120mmHg), massive proteinuria (at least 3.0g/day), hypokalemia (serum potassium less than or equal to 3.0mEq/L) and high serum cholesterol (greater than or equal to 250mg/100ml) were significantly greater in the high renin group than in the control group (p<0.01, respectively). Renovascular hypertension was suspected in 6 patients from the high renin group (66.7%), as compared with 1 of the control group (2.0%) (p<0.001). There was massive proteinuria in 3 of 6 patients with renovascular hypertension in the high renin group and 2 showed nephrotic syndrome. Thus, two-thirds of the elderly patients with high renin hypertension had probable renovascular hypertension with a history of rapid progression of hypertension.

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Changes in plasma levels of atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were studied in 8 patients during a 30 min period of induced supraventricular tachycardia (SVT). The mean plasma ANP concentration increased immediately after the onset of SVT, peaked at 30 min and gradually returned to the control level. The mean plasma AVP concentration, on the other hand, was suppressed during SVT and rebounded above the control level in the post-SVT period. In 4 patients, SVT was associated with polyuric and natriuresis. The mean urine volume in these patients increased to 580% of the control and the mean urinary sodium excretion to 278% of the control, respectively. It was concluded that both a stimulation of ANP secretion and an inhibition of AVP release, elicited by an increase in atrial pressure, may be responsible for polyuria and natriuresis associated with SVT.

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We evaluated the dipsogenic effects of angiotensin II (Ang II) in relation to the steady-state level of the endogenous reninangiotensin system (RAS) by measuring water intake in 22 trained dogs during three 20 min intravenous (i.v.) infusions of [Ile⁵] Ang II (10, 15 and 50ng/kg/min). Measurements obtained in normally hydrated (NHyd) dogs were compared with those obtained in dogs pretreated as follows: 1) 24hr water deprivation (WD); 2) WD combined with chronic blockade of the RAS (300mg/day×3 days of SQ 14225) (WD+SQ); and 3) 48hr after bilateral nephrectomy (BNX). Both WD and WD+SQ were given water before Ang II infusion. Plasma renin activity (PRA) and serum and CSF electrolytes (cisterna magna catheter) were measured. All treatments caused a significant (p<0.05) increase in CSF sodium (Na⁺) that was not paralleled by hypernatremia in BNX dogs (142±1 vs 144±1mEq/L in NHyd). WD and WD+SQ caused a 2- and 12-fold increase in PRA, respectively; PRA was not detectable in BNX. Suppression of blood Ang II by WD+SQ produced a reduced latency and significant enhancement of the thirst behavior elicited by Ang II at all doses; however, i.v. Ang II did not elicit drinking in the WD state. Furthermore, in BNX, the same phenomenon as in WD+SQ was observed. These data are compatible with the concept that endogenous levels of Ang II play a key role in regulating drinking behavior. However, these findings do not negate the possibility that Ang II acts synergistically with CSF Na⁺, but not plasma Na⁺, to modulate drinking behavior.

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The effects of synthetic atrial natriuretic peptide (ANP) on the renal hemodynamics, glomerular filtration rate (GFR), fluid and electrolyte excretion and renin release were studied in the isolated perfused rat kidney (IPK). When 10^-9mol of ANP was administered in 75ml of perfusate, the renal vascular resistance (RVR) was transiently decreased for 3 to 5min, thereafter increased for 30min and then tended to return to the control level. ANP increased the GFR (0.55±0.08 to 0.71±0.07ml/min), urine flow (UV) (0.018±0.002 to 0.194±0.028ml/min), absolute Na excretion (UNaV) (1.83±0.03 to 17.93±2.71μEq/min) and absolute K excretion (UKV) (0.67±0.13 to 2.33±0.18μEq/min). The addition of indomethacin or mefenamic acid to the perfusate before the administration of ANP exerted no influence on any of the effects of ANP. Renin release was inhibited by approximately 50% compared to the ANP-free control group. With the administration of ANP, UV and UNaV reached a peak 15-20min after the GFR reached a peak and remained elevated after the GFR fell below the control level. These findings suggest that 10^-9mol of ANP causes natriuresis and renin suppression in the IPK, and that the natriuresis is prostaglandin-independent and cannot be explained only by an increase in GFR.

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The effects of coronary collaterals on regional myocardial function during temporary ischemia and hypoxia were studied in 12 open-chest dogs. Using an ultrasonic dimension gauge, systolic segment shortening in the left anterior descending coronary artery (LAD) area was measured at 1min after the following three experimental conditions: LAD occlusion and LAD hypoxic perfusion with nonoxygenated solutions at two different pressures (60mmHg and 120mmHg). Collateral function was assessed by both LAD diastolic retrograde pressure and the percentage of increase in left circumflex coronary flow at 1min after LAD occlusion. Systolic segment shortening decreased less with hypoxic perfusion than with occlusion, however, this beneficial effect on regional contraction was greater at a perfusion pressure of 60mmHg than at one of 120mmHg. The magnitude of decrease of systolic shortening was variable among individual dogs but correlated linearly with each of the two collateral function indexes, not only during occlusion but also during hypoxic perfusion.
In conclusion, the preventive effect of hypoxic coronary perfusion on the early decline of regional myocardial function, in comparison to the changes seen during ischemia, may depend on coronary collaterals in addition to its washout effect on metabolites. In order to maintain myocardial function, perfusion pressure should be at an optimal level.

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To evaluate the protective effects of L-carnitine on the ischemic myocardium, the effects of its administration on tissue levels of high energy phosphate and phospholipids were studied in ischemic dog hearts. Myocardial ischemia was induced by the ligation of the left anterior descending coronary artery for 40min. In the experiment, L-carnitine (300mg/kg) was administered intravenously prior to coronary artery ligation. Mitochondrial phospholipids were extracted from nonischemic and ischemic regions of the myocardium and subsequently analyzed. In ischemic myocardial tissues, levels of adenosine 5'-triphosphate (ATP) were reduced. The decrease was significantly elevated by L-carnitine pretreatment. The mitochondrial fractions obtained from ischemic myocardia had significantly lower levels of phospholipids than those obtained from nonischemic tissues. Moreover, the amounts of phosphatidyl-choline, phosphatidylinositol and phosphatidylethanolamine were significantly decreased in ischemic myocardial tissues. L-carnitine-pretreatment prevented the reduction of these phospholipids. Lysophosphatidylethanolamine and sphingomyelin did not show statistically significant decreases. This may explain why the administration of carnitine has beneficial effects on ischemic myocardium.

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The cardiovascular effects of ZSY-39 [4-methyl-5-(4-pyridinyl)-thiazole-2-carboxyamide] were investigated in isolated and blood-perfused atrial and ventricular muscles perfused with donor's arterial blood. When ZSY-39 was given i.v. to the intact donor dog, hypotension with a slight tachycardia was induced at a dose range of 30-1, 000μg/kg. At the same time, slight positive chronotropic and inotropic responses appeared in isolated, perfused atria at i.v. doses of 300 and 1, 000μg/kg ZSY-39, indicating a relatively dominant inotropic action.
Direct injection of ZSY-39 into the cannulated sinus node artery of the isolated atrium produced positive chronotropic and inotropic responses in a dose-related manner (1 to 300μg). ZSY-39 also induced a dose-dependent increase in developed tension in the isolated ventricle. The positive chronotropic and inotropic effects of ZSY-39 were not modified by an adequate dose of propranolol which completely blocked norepinephrine-induced positive chronotropic and inotropic responses. From these results, it is concluded that ZSY-39 has mild cardiotonic properties, showing relatively selective positive inotropic activity.

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A newly developed phenoxyalkylamine derivative, 2-isopropyl-5-[3-(2-methoxyphenoxy)propylamino]-2-(3, 4, 5-trimethoxyphenyl)-valeronitrile fumarate (HV-525), was investigated in intact dogs and in isolated dog atria perfused with anesthetized donor dog's arterial blood. When 0.3mg/kg of HV-525 was intravenously administered to the donor dog, a depressor effect without significant changes in heart rate was observed in donor dogs and a decrease in developed tension was observed in the isolated atrium. At 1mg/kg, HV-525 caused a depressor response in donor dogs and decreases in developed tension and atrial rate in isolated atria. The decrease in systemic blood pressure seen following 1mg/kg of HV-525 was between 15-40mmHg. These effects continued for about 60min. When HV-525 was administered into the cannulated sinus node artery of the isolated atrium, dose related negative inotropic and chronotropic actions were observed. Occasionally, HV-525 induced slight, brief positive chronotropic and inotropic effects followed by long-lasting negative effects. The threshold dose for inducing the negative chronotropic effect was approximately 3μg while the negative inotropic one was approximately 1μg. A large dose of 100μg of HV-525 caused a profound deceleration but not atrial arrest. The order of potencies for inducing a negative chronotropic effect in dog atria was verapamil>propranolol>HV-525_??_lidocaine_??_quinidine>phenytoin>disopyramide>procainamide, and that for inducing a negative inotropic effect was verapamil_??_propranolol>HV-525>lidocaine>phenytoin>disopyramide>procainamide_??_quinidine. HV-525 did not induce a significant effect on sinoatrial conduction time. HV-525 at the doses studied, uniformly suppressed the frequency-force relationship, while verapamil, one of the phenoxyalkylamine derivatives, caused a marked depression of high frequency-induced contraction. Thus, it is concluded that HV-525 has mild depressant properties on the cardiovascular system and may have characteristics different from those of verapamil.

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The mode of antiarrhythmic actions of the newly developed antiarrhythmic drugs, tocainide, mexiletine and SUN1165, which bear the N-2, 6-dimethylbenzene ring as a common structural unit, were examined by comparing the use-dependent blocking actions on the maximum rate of rise of action potentials (Vmax) in guinea pig ventricular muscle. The time course of the use-dependent reduction of Vmax after stimulation and its recovery after cessation of stimulation were fitted by double exponential curves to avoid the effects of the rapid stimulation (2Hz) on the level of the membrane diastolic potential.
The onset rates constants of the use-dependent block were 0.29±0.07 per action potential for tocainide (10^-4M), 0.07±0.02 (mean±SE, n=5) per action potential for SUN1165 (10^-5M) and were too rapid to be accurately fitted for mexiletine (10^-5M). The time constants of the Vmax recovery from the use-dependent block were prolonged to 0.67±0.32, 0.27±0.13 and 96±11 (mean±SE, n=5) sec in the presence of tocainide, mexiletine and SUN1165, respectively. These data indicate that tocainide and mexiletine should be classified as lidocaine-like drugs, while SUN1165 may be a quinidine-like drug which interacts with Na⁺ channels and has slower kinetics than lidocaine-like drugs.

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Cardiac tamponade complicated by classic rheumatoid arthritis was markedly alleviated by pericardiocentesis and intrapericardial administration of steroid. For the following 2 years, no recurrence of cardiac tamponade or constrictive pericarditis was observed. According to the literature, only one other patient with cardiac tamponade complicating rheumatoid arthritis (RA) had been successfully treated patient by intrapericardial steroid administration.

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