The echo patterns on ultrasono-cardiotomogram were evaluated in relation to the histological changes of the myocardium. The ultrasono-cardiotomographic data were collected from 9 consecutive patients with transmural infarction (3 patients with antero-septal, 5 with postero-inferior, 1 with antero-lateral infarction) and also from 11 dogs with experimental myocardial infarction. Analyses of data obtained led to the following conclusion.
1) A decrement of the thickness and deformity of the wall echo: They were detected by a series of azimuthal angle and level ultrasono-cardiotomograms which were obtained by changing the direction and level of the ultrasonic beam through the heart along the long axis of the left ventricle.
2) An increment of echo-intensity of infarcted area: The intensity of abnormal echo of the infarcted area, when evaluated by using the intensity of the echo of normal pericardium as a reference of OdB, was +10 to +15dB more intense than that of the normal myocardium.
3) The study of the echo patterns in comparison with the histology of myocardium indicated that the echoes related to scar could be classified into 4 types: cord-like echo, scattered large nodular echoes, narrow band-like echo, and scattered small nodular echoes.
Types and indicated the formation of a transmural scar. Thus a possibility was suggested that histological characteristics of myocardial tissue could be estimated by a non-invasive method.

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The movements of the left ventricular wall in cases of myocardial infarction were studied by ultrasono-cardiotomography and M-mode echocardiography.
Ultrasono-cardiotomographic and echocardiographic data were collected from 15 consecutive patients with transmural myocardial infarction ranging in age from 28 to 60 years (4 with antero-septal infarction, 5 with postero-inferior infarction, and 6 with infarction of other areas) and also from healthy control subjects.
In myocardial infarction, a delay in timing and a decrement in amplitude of the excursion of the infarcted area were observed. As the result, compensatory movement occurred in the non-infarcted area. This compensatory movement was a major contributing factor for the maintenance of the function of the left ventricle.
In antero-septal infarction, the pump function was compensated for by the movement of the left ventricular posterior wall (LVPW) and by that of the non-infarcted area of the interventricular septum (IVS). On the other hand, in postero-inferior infarction, the pump function was mainly compensated for by an increment in movement of IVS.
This compensatory movement, which was very strong in the acute stage of myocardial infarction, decreased with time after infarction. On the other hand, in the hypokinetic infarcted area, there was a gradual increment of the amplitude of excursion with time after infarction.
These findings reflected the degree of the development of collateral circulation. It was found that the degree of asynergy could be determined by the evaluation of the delay in timing and amplitude of the excursion, and of mVCF at basal, middle, and apical portions of the left ventricle.

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The pre-ejection period (PEP) of systole is a widely used, non-invasive index of ventricular performance. For precise measurements, simultaneous recordings are required from which the Q-wave on the electrocardiogram, second heart sound on the phonocardiogram, and upstroke and incisura of the carotid pulse contour are discretely identifiable and temporally accurate. This is frequently difficult to accomplish. We, therefore, have compared 2 other noninvasive indices of ventricular performance for correlation with PEP in 17 female and 18 male subjects while supine and during head-up tilt. We also examined similarity of these indices to PEP in correlations with heart rate and blood pressure and compared them for ease in monitoring and precision in measurement. The ratio of the peak amplitude of the carotid pulse contour derivative to its total amplitude (DAR) is easier to monitor and more reliably measured than PEP; however, it is poorly correlated with PEP. Time from electrocardiographic Q-wave to peak dD/dt (Q-MAX) is also easier to monitor and somewhat more reliably measured than PEP. Although correlations of PEP and Q-MAX with subject age are dissimilar, Q-MAX is correlated with PEP in supine and tilted subjects; the 2 variables are similarly correlated with heart rate and arterial pressure; and in 6 subjects both variables were prolonged after intravenous administration of propranolol-hydrochloride. We, therefore, propose Q-MAX as an alternative measure of ventricular performance.

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The changes of left ventricular anatomy and function following treatment with antihypertensive agents for 1 to 2 years were studied by echocardiography in 34 patients with hypertension whose blood pressures and electrocardiographic voltages (SV₁+RV₅) were significantly decreased (p<0.001 and 0.01, respectively). The drugs administered or used were trichlormethiazide, β-blockers, α-methyldopa, clonidine hydrochloride, and guanethidine. Most patients received 2 or more of the above drugs.
The interventricular septal thickness, the left ventricular posterior wall thickness, the calculated left ventricular mass, the atrial dimensions, all decreased following treatment of hypertension for 1 to 2 years (p<0.001-0.05), and the ejection fraction improved (p<0.001). It is concluded that cardiac hypertrophy is not irreversible in patients with hypertension if their blood pressure is adequately controlled.

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The purpose of this study was to evaluate the reliability of two noninvasive techniques (STI and echocardiography) in assessing cardiovascular response during exercise.
STI were obtained using a new carotid pulse transducer (thermistor pulse) proved to be reliable in exercise recording. The study population included 12 male rowers (age 15-20 years), who performed supine bicycle exercise; STI and echocardiographic recording of left ventricle were simultaneously obtained at rest and continuously throughout the exercise period. A negative linear correlation (r=-0.782; p<0.001) was found between PEP (pre-ejection period) and %LVID (fractional shortening of left ventricle), reliable indexes of cardiac contractility measured by the two techniques. A lower, but significant correlation (r=0.643; p<0.001) was present between ETI (left ventricular ejection time corrected by heart rate) and SV (stroke volume) indexes of pump function.
The present study shows that STI measured with this new technique, can be employed in evaluating left ventricular function in those patients in whom a good echocardiogram is difficult to record during exercise.

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Conventional doctrine states that the QT interval is related to heart rate in an inverse exponential relationship, so that with increasing rate the QT interval shortens. This relationship has recently been studied in a group of patients undergoing physiological exercise stress tests, atrial pacing stress test, and in a further group of patients with complete heart block undergoing exercise at a fixed ventricular rate controlled by cardiac pacemaker. Examinations of recordings made during physiological exercise do show the expected shortening in QT interval, we believe that this shortening is only in part due to the intrinsic effect of increased rate as patients who were atrially paced to similar rates and within the same age group showed only a small decrease in measured QT interval and patients undergoing exercise at fixed ventricular rate showed shortening in QT interval which was related to the independent atrial rate. It appears, therefore, that the QT interval is governed mainly by extrinsic factors and not intrinsically rate related.
The physiological control of QT interval is being used now to construct a cardiac pacemaker which senses the interval between the delivered stimulus and the evoked T wave so that the stimulus-evoked T wave interval could be used to set the subsequent escape interval and subsequently the overall pacing rate. Physiological control of cardiac pacing rate using conventional unipolar lead systems and independent of atrial activity is possible and currently being investigated.

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Seven cases of excised left atrial myxoma are described. These are compared with organizing and organized thrombi. The tumors occurred at ages ranging from 13 to 48 years with male preponderance. There were distinct histological and histochemical differences between myxomas and thrombi. Myxomas were lobulated, soft and gelatinous. The cells were arranged singly, in syncytium, or in gland like manner and around blood vessels. Scant to abundant acid mucopolysaccharide rich stroma with strong metachromasia was present. The cells on histochemical staining revealed a wide range of differentiation and contained small amounts of neutral mucopolysaccharides. Thrombi, on the other hand, were firm, laminated, and the cells were arranged in several stratified layers. Metachromasia was absent. Neutral polysaccharides were absent within the cells of thrombi, These features support the concept that cardiac myxoma is a neoplasm and arises possibly from multipotential mesenchvmal cells.

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Changes of the activation sequence and vectorcardiogram (VCG) resulting from experimental block of specific sites of the left bundle branch were studied to determine the functional significance of the septal Purkinje network.
Discrete block of the septal Purkinje network (11 dogs) resulted in slight delay of epicardial activation in the apical area. In lead Z of McFee system of VCG, the antero-posterior ratio was increased from 1.4 to 2.6, and the QRS loop tended to be displaced anteriorly, Discrete block of the left posterior division (9 dogs) resulted in slight delay of activation in the posterior basal area.
Block of the left posterior division plus the septal Purkinje network (11 dogs) resulted in marked delay in activation of a wider area extending from the posterior basal area to the apical area. In lead X, the S wave became evident and the direction of the maximum QRS vector in the frontal plane showed significant right axis deviation.
Discrete block of the left posterior division did not change the epicardial activation sequence or the direction of the maximum QRS vector, because there is extensive interconnection of the left ventricular conduction system.
These results suggest that block of the septal Purkinje network itself may produce an electrocardiographic change and that this network may also be important in left anterior and posterior hemiblocks producing axis changes in the frontal plane of VCG.

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In order to evaluate the role of carnitine on fatty acid metabolism in subepicardial (Epi) and subendocardial (Endo) regions in ischemic heart, tissue levels of carnitine, free fatty acids (FFA), and adenosine triphosphate (ATP) were determined in ischemic, non-ischemic and border areas in dog hearts with acute regional ischemia. Acute regional ischemia was induced by ligation of the left anterior descending coronary artery for 15min.
In normal hearts, tissue carnitine levels were lower in Endo than in Epi. On the other hand, FFA levels were higher in Endo than in Epi. In ATP levels, no significant differences were observed between Endo and Epi. In acute regional ischemia, tissue carnitine levels decreased not only in ischemic and border areas but also in nonischemic area. And the levels were lower in Endo than in Epi in all areas. Tissue ATP levels were also lower in Endo than in Epi in all areas. From nonischemic area toward the center of ischemic area, the difference in ATP levels between Endo and Epi became more prominent. Tissue FFA levels increased in ischemic and border areas, while no significant differences were observed between Endo and Epi.
These results confirmed that Endo was metabolically more anaerobic than Epi even in normal heart and it became more prominent in the heart with acute regional ischemia.

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The most remarkable finding in SHRSP with cardiac death under specific pathogen-free system was idiopathic diffuse fatty degeneration of the myocardium.
Besides fatty degeneration, diffuse myocardial fibrosis and scattered infarction were observed. In male rats the incidence of cardiac death increased with each generation. Therefore, this myocardial degeneration seemed to be hereditary disorder. The SHRSP with cardiac death seemed to be a new type of SHR, namely Heart-Prone SHR (SHRHP). SHRHP may be a kind of animal model for congestive cardiomyopathy (COCM) in human beings.

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Effects of pulsatile venous flow upon the microcirculation were investigated in conditions with different venous pressures by using regional perfusion in dog's hind legs. In animals with venous pressure of -18cm H₂O (collapsed stage), venous pulsation brought about a significant increase in mean oxygen consumption ratio and suppressed a rise of mean resistance ratio significantly.
In animals with venous pressure of +2cm H₂O (normal venous pressure stage), the venous pulsation was effective in a rise of mean oxygen consumption ratio but was not effective in suppression of mean resistance ratio. In animals with venous pressure of +10cm H₂O (congestive stage), no effect of venous pulsation was recognized.
We suppose that the intermittent elevation of venous pressure by venous pulsation is effective for opening some capillaries in animals with venous pressure below +2cm H₂O.

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The hemodynamic changes induced by coronary occlusion were investigated in anesthetized dogs. Coronary occlusion elicited an immediate but transient increase in the systemic blood pressure and in the vascular resistance of the hind limb perfused at constant flow. Thereafter, systemic hypotension and vasodilatation in the perfused region were observed. Vagotomy abolished the initial increase of the systemic and perfusion pressure and reduced significantly the late vasodilator response both systemically and in the perfused hind limb. After the subsequent administration of hexamethonium the vasodilatation in the hind limb was no longer manifest but the fall in blood pressure was unmodified.
These results seem to suggest that multiple mechanisms are involved in the hemodynamic response to coronary occlusion.

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Effects of trapidil on ergonovine-induced contractions of isolated dog coronary arteries were investigated in vitro. Ergonovine produced dosedependent contractions of helical strips cut from the left circumflex branches of coronary arteries. Trapidil significantly depressed thesecontractions. 5-HT also produced dose-dependent contractions of the strips, which were depressed by trapidil. In isolated rabbit femoral arterial preparations, norepinephrine dose-dependently contracted the strips. Phentolamine significantly depressed these contractions, and trapidil depressed them when relatively high doses were applied previously. Results indicate that trapidil has a depressant effect on coronary arterial contractions induced by ergonovine, partly through antagonism to 5-HT receptor and/or adrenergic alpha receptor.

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A hypothesis was proposed for a fundamental principle of adaptation of normal hearts to pressure and volume loads: The end-systolic active stress (F) and shortening fraction (S) of myocardium in the ventricular wall were hypothesized to be preserved near normal levels by the adaptation regardless of heart size and animal species. F and S were mathematically related to ventricular wall volume (M) and end-diastolic chamber volume (D) both normalized to stroke volume with afterload pressure (P) as a parameter. The deduced M-P and D-P relationships were compared with corresponding data documented in literature, The actual data from normal hearts including pressure and volume overloaded but compensated hearts of different animal species from rats to horses including human children and adults distributed near the theoretical curves for S=0.1-0.2 and F=60-160Gm/cm² despite the 2×10³ times difference in heart size and weight. However, data from failing and abnormal hearts significantly deviated from those curves. These results seem to support the present hypothesis as a fundamental principle of the adaptation of normal hearts to loads.

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A flow probe for direct measurement of blood flow of the mitral valve was devised. It was useful for acute experiment, particulary concerning pathophysiology of the mitral valve function. Insertion of the probe into the left atrium and fixation to the left atrial wall and thus to the mitral orifice were readily and satisfactorily performed without disturbance of blood flow and valvular function. It must also be emphasized that support with cardiopulmonary bypass was not necessary at the time of insertion of the probe. Effectiveness of the procedure has been confirmed through simultaneous observation of echocardiogram and mitral blood flow of the dog's heart with ruptured chordae tendineae.

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Acute myocardial infarction occurred in a 26-year-old woman with normal coronary arteriogram and primary thrombocythemia (500, 000-1, 500, 000/mm³).
Hyperaggregability of platelets was also demonstrated by stimulation with adenosine diphosphate, collagen, and epinephrine administration. A stillbirth at the 8th month of gestation in her past history was referred to the complication of primary thrombocythemia, too. Since discharge, the patient has been on 750mg of aspirin and then free of any thromboembolic symptoms and signs, even during pregnancy and labour.

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Two previously healthy young individuals died suddenly and unexpectedly, and in both of them there was gangloitis in the heart, especially near the sinus node. Electron microscopic examination demonstrated virus-like particles in the vicinity of the ganglionitis of both hearts. Viral cardioneuropathy may play a role in the pathogenesis of sudden unexpected deaths and deserves further investigation.

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Spontaneous hypertensive rats produced a natural thymocytotoxic autoantibody (NTA) which was cytotoxic for the thymocytes of the various strains of rats tested. More than a 60% incidence of NTA in the SHR occurred from 1 month of age and was observed throughout their life span. The titers of the autoantibody varied among individual rats and progressively increased with age. The NTA was cytotoxic for thymocytes but weak or negative for spleen, lymph node and bone marrow cells. However, absorption test indicated that NTA-reactive antigens were distributed in the thymus, spleen, lymph nodes, and brain of adult rats. The NTA in SHR was an IgM-globulin as determined by sensitivity to 2-ME treatment and by Sephadex G-200 column chromatography. These results suggest that the NTA is responsible for the selective suppression of T-cell functions in SHR.

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1) Feeding 1.5% salt to pregnant SHRSP led to IUGR of the fetus. The incidence of SFD became 50%. 2) In view of the above-mentioned results, pregnant SHRSP can be regarded as the model animal of SFD.

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Hypertension was augmented by Na-loading and attenuated by K-loading in SHRSP. These findings indicate that not only Na-restriction but also K-loading more actively reduces high blood pressure and may be effective in preventing hypertensive diseases. The attenuation of severe hypertension by K-loading was more marked in salt-sensitive SHRSP than in less salt-sensitive SHRSR. These experimental findings support our epidemiological study indicating that blood pressure is significantly correlated with urinary Na/K ratio in 1120 inhabitants of "one rural community" in Japan. Our experimental clinical attempts to reduce Na/K ratio by using low salt soy sauce (9% NaCl) or low salt soy sauce containing KCl (at NaCl to KCl ratio of 65 to 25) and table salt containing KCl (25%) in 12 healthy volunteers under strict medical observation for 3 weeks have confirmed that the reduction of Na/K ratio is effective in lowering systolic blood pressure significantly.

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Because 2, 3DPG is one of the main factors which are concerned with the affinity of Hb for oxygen and 3PG is the degrading metabolite of 2, 3DPG, there are three following possibilities in SHRSP: 1) in pulmonary tissues the diffusion of oxygen may be interfered to some extent (cf. results 1 & 2), 2) in peripheral tissues the less releasing of oxygen from Hb may cause oxygen deficiency (cf. results 3 & 4) and therefore, these findings may be the underlying factors which cause hypertension (cf. result 6), and 3) the inability of producing 2, 3DPG may result in the decreased tolerance under oxygen deficiency, and the process of production or degradation of 2, 3DPG in SHRSP must have some defects.

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Destructive changes in the wall of mesenteric artery were more predominant in SHRSP than in WKY. Remarkable differences in staining characteristics of elastic fiber were found even between SHRSP and WKY at 30 days of age.

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Hydralazine and α-methyldopa administered per os, did not significantly lowered the blood pressure of SHRSP rats, in the 8, 16 and 24 week-old SHRSP in the doses used in this study.
In group of 40 week-old SHRSP, both of the drugs did not lowered the blood pressure. However, the narrowing of the retinal arterioles was less progressive in the treated groups of SHRSP than in the untreated SHRSP.
These findings may suggest that sclerotic alterations of the retinal arteriolar wall caused by long duration of hypertension are prevented by vasodilative agents such as hydralazine and α-methyldopa.

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Experimental results demonstrate that allogeneic thymus graft completely restored the immune functions in the T-cell depressed SHR as detected by a rosette forming test, plaque forming assay and blastogenesis, and lowered titers of NTA in the serum of SHR. Injection of TS had less effects to immune functions and NTA titers. The relationship between T-cell depression and hypertension of SHR is not clear yet. However, allogeneic thymus grafts significantly suppressed hypertension of SHR from 2 weeks after grafts. Injections of TS prevented the development of hypertension in SHR. These results suggest that immunological abnormality may be related to development of hypertension in SHR.

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