Echocardiographic study was performed on 21 cases with hypertrophic cardiomyopathy (HCM), 10 obstructive and 11 nonobstructive.
Asymmetric septal hypertrophy was demonstrated in both obstructive and nonobstructive HCM. In all cases of HCM studied, the thickness of the interventricular septum was 1.4cm or more (1.4-3.7cm) and the ratio of septal to left ventricular posterior wall thickness was 1.4 or more (1.4-3.2). A systolic anterior movement of the mitral valve (SAM) was observed in obstructive cases only and characterized by a large backward component in late systole and an extreme approximation to the interventricular septum at its peak.
Patients with HCM also showed abnormal echocardiographic indices of the left ventricular diastolic properties, such as the rate of diastolic descent of the mitral valve (DDR), mean diastolic posterior wall velocity (mPWVd), D/S ratio and mean rapid filling rate (mRFR). DDR correlated well with the ratio of rapid filling to total filling volume, rapid filling fraction, (r=0.79, p<0.001), suggesting that reduced DDR in HCM was related with an abnormal left atrio-ventricular flow pattern.
A significant correlation was also observed between mRFR and negative maximum dp/dt derived from the first derivative curve of the left ventricular pressure (r=0.68, p<0.005). Thus echocardiography was proved to be a valuable means for investigation of the left ventricular properties during early diastole.

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The sinus node function was evaluated by rapid atrial pacing in 35 aged patients (mean age 78.2 years) including 10 aged controls, 12 cases with various degrees of AV block, 6 with bradycardia-tachycardia syndrome (BTS), and 7 with sinus bradyarrhythmia (SB). AV block was further divided into A-H block (7 cases) and H-V block (5 cases) by His bundle electrogram which was simultaneously recorded with 3 leads of surface electrocardiogram.
Sinus node recovery time (SRT) was measured and its maximum value (SRTmax) was selected from SRTs obtained after pacing with various rates and durations in each patient. SRTmax was also expressed as percentage of the control P-P interval (%SRTmax).
For patients in whom the study was repeated 3 to 8 months later, %SRTmax was reproducible in 9 of 14 instances. Prolongation of SRT was not always observed as the rate and/or duration of pacing was increased. SRTmax and %SRTmax were 1, 363±188msec and 147±19% (mean±SD), respectively, for aged controls, 1, 597±442msec and 156±31% for patients with AV block, 2, 087±1, 315msec and 203±132% for those with BTS, and 3, 069±1, 287msec and 247±115% for those with SB. SRTmax exceeding the range for aged controls was noted in 4 of 7 cases (57%) with A-H block, 2 of 6 (33%) with BTS, and 5 of 7 (71%) with SB; normal SRT was not infrequently observed in patients with sick sinus syndrome, especially in those with BTS.
Analysis of 10 consecutive atrial cycles following cessation of pacing revealed that in 8 cases the first P-P interval (SRT) was followed by longer ones in some occasions (secondary suppression). It was observed almost exclusively in patients with sick sinus syndrome. The possibility of this phenomenon to reflect another feature of sinus node abnormality was discussed.

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For confirming the configuration of the QRS loop in left anterior hemiblock, 82 cases with the frontal QRS vector above minus 30 degrees were collected and classified by the configuration of the horizontal QRS loop. Thereafter, a comparison has been made between the configuration of the QRS loop in clinical cases and that in the authors' construction method, and the following findings for criteria of left anterior hemiblock are obtained.
1) The afferent limb of the frontal QRS loop is dislocated to the left and more superiorly.
2) The efferent and afferent limbs of the horizontal QRS loop are located left posteriorly. The configuration of the horizontal QRS loop is long and narrow and the direction of inscription is clockwise, a figure of 8 or counterclockwise.
3) Cases with the right posterosuperior dislocation of the afferent limb of the QRS loop is excluded from left anterior hemiblock.

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The presence of supernormal excitation was confirmed repeatedly in all 10 cases following cardiac surgery.
By the stimulation of minimum subthreshold impulses capable of originating ventricular responses, the supernormal excitation was limited only at the descending limb of T wave. The duration lasted only 0.02 sec at the minimum subthreshold stimuli.
But the higher subthreshold stimuli produced the longer duration of supernormal excitation phase. The duration of the excitation phase prolonged towards the following R wave, hardly extending towards the preceding R wave, with the increase of subthreshold stimuli.

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Twenty-eight goats with an artificial heart (AH) were studied pathologically. Being continued from the previous report, the liver, gastrointestinal tract, and kidneys were taken up in this paper and finally, general discussion was done to get our ideas in shape concerning the pathophysiological status of the goat.
Central necrosis of the liver was always observed in the goats which survived for over 140 hours. This finding seemed to be caused mainly by circulatory insufficiency of the portal vein at the latter half of the survival time.
Microscopic findings of degeneration, necrosis and edema were commonly observed at the walls of gastrointestinal tracts, when goats showed poor appetite, mucous feces and constipation. But these problems have been improved by application of a new control method to regulate the output of AH system within a goat's physiological range since October 1974.
The lesions seen in the kidneys are classified into 5 groups. The most important findings of them are lower nephron nephrosis and cortical necrosis, both of which indicate the occurrence of long standing vasoconstriction of proximal renal arteries. By means of microangiographic method and others, thrombi were detected frequently in the kidneys. The vascular walls, where thrombi were attached to, were often damaged. Therefore, these thrombi were thought to be formed in the local vessels in situ through renal circulatory insufficiency. The renal pathological lesions have been also improved and severe renal failure from which the previous goats could not escape, has been lessened since the application of a new AH control method.
As a whole, the main pathophysiological status of the animals replaced by the AH are thought conclusively to be peripheral circulatory insufficiency. This would be caused by abnormal hemodynamics, so that, the essential clinical etiology is thought to be AH function itself.

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Regional blood flow at the frontal cortex, which was fed by recurrent branches from anterior cerebral artery, was markedly decreased in SHRSP with severe hypertension over 200mmHg at the age of 5 and 10 months. SHRSP, treated with antihypertensive agent, with blood pressure lower than 200, did not show such a marked decrease in rCBF, although rCBF was less than the control level. These data indicate that the impairment of rCBF is intensified at the cerebral region corresponding to "locus minoris" in cerebral circulation, especially when systemic blood pressure surpasses 200mmHg, and such an impairment of rCBF is supposed to be involved in the basic process for the development of cerebrovascular lesions in SHRSP with severe hypertension.

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SHR were clearly vulnerable to hypoxia induced by simultaneous carotid ligation; all SHRSP and 80% of SHRSR died in 35 and 32 hours in average after ligation, while all WK survived. The predilection sites of lesions in these SHR were consistent with those observed in SHR after natural death. However, the incidence of lesions in basal ganglia, especially in its anteromedial and anterolateral parts, were markedly increased by the acute induction of lesions in comparison with spontaneous lesions observed in SHRSP at autopsy. These findings confirmed that cerebral lesions were acceleratedly induced by simultaneous bilateral carotid ligation even in young SHRSP and SHRSR, and that these lesions developed at the "minor loci" of cerebral circulation fed by "recurrent" branches, especially at the basal ganglia fed by lateral lenticulostriate arteries and Heubner's arteries which branched off with a sharp angle from middle and anterior cerebral arteries, respectively. The preponderant occurrence of the lesions in basal ganglia and the increased incidence of cerebral hemorrhage indicate that the acute induction of the lesions by simultaneous bilateral carotid ligation makes SHRSP and SHRSR better models with very similar lesions to those in man.

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SHRSP with signs and symptoms of cerebral stroke showed marked abnormalities in cortical EEG and during drowsiness; laterality in EEG was manifested more remarkably.
Especially, lateralities in spindle-like activity (lazy activity), which were frequently observed in SHRSP over 8-month-old (during wakefulness, they often showed diffuse slow α or diffuse θ pattern EEG), were defected in 5-month-old SHRSP with blood pressure of over 200-220mmHg.
These findings suggested that any functional change in the brain prior to increased cerebrovascular permeability might occur, and that there are the possibilities for further electroencephalographical studies to throw light on the predictive detection of cerebrovascular involvement in hypertension.

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Female SHRSP from 3 months of age, treated with androgen after gonadectomy for 2 months, became gradually masculinized in their distribution of blood pressure, vulnerability to hypoxia, and the brittleness of the aorta. As the sex difference in the incidence of stroke might be related to these characteristics, it seems to be possible that alteration of hormonal environment can be used for the regulation of pathogenetic mechanism of stroke.

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1) In male SHRSP fed on a diet containing 50% white fish meal by weight from 5 or 6 weeks of age, the blood pressure showed significantly slower incremental increases and maintained levels under 230mmHg for a longer time. Cerebrovascular lesions (stroke) have not yet been observed in this group (after 1 year or more). This effect was weaker in those rats which were fed on a diet containing 30% white fish meal and was not noticeable in those which were fed on 50% white fish meal by weight from 15 weeks of age.
2) In male SHRSP fed on a diet containing 50% casein from 5 or 6 weeks of age, the blood pressure first showed initial incremental increases similar to that of the control group but afterwards displayed slower increases. The incidence of stroke in this group was obviously low.
3) In female SHRSP fed on a diet containing 50% white fish meal or 50% casein from 5 or 6 weeks of age, the blood pressure and the incidence of stroke showed a similarity to those of male SHRSP fed on a diet containing 50% casein as described in 2) above.
4) Effects of dried bean-curd, dried laver, dried "Wakame", or gelatin diets upon the incidence of stroke were not noticeable, at least under present feeding methods.
These findings probably contribute to the interpretation of the difference of the incidence of stroke between the Japanese and the Occidental. They may also contribute to the prevention of stroke.

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Pituitary weights were already increased in SHR at the young stage (8weeks of age) compared with WK. The weights of anterior lobes were also increased at the age of 4 months. This increase in weight appeared to have a functional significance as proved by the increased ³H-lysine incorporation into the pituitary. As the prevention of the development of hypertension by apresoline treatment or by splanchnicotomy had no effect on the increased lysine-incorporation, the acceleration of such a metabolism did not seem to be the secondary phenomenon to hypertension, but was supposed to be a primary alteration in SHR. ACTH content in the pituitary was increased in pretreatment of dexamethasone, ACTH content was rather decreased in SHR. 4-month-old SHRSP compared with the age-matched WK. After the acute pretreatment of dexamethasone, ACTH content was rather decreased in SHR. This finding suggested one possibility that dexamethasone did not efficiently block ACTH secretion from the pituitary in SHR.

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PRA and BP were measured after administration of NE and FA to evaluate the relationship between plasma NE and renin-angiotensin system in SHR.
(1) PRA increased after drip infusion of NE.
(2) BP decreased in proportion to the dose of FA administered and this effect was more prominent in the group with higher blood pressure before administration.
(3) PRA increased after intraperitoneal administration of FA, whose vasodilating effect could play a role as a renin releasing factor. During oral administration, BP decreased but PRA showed no change, and this discrepancy could be due to the time needed to achieve proper BP and its final level.

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In this report, the development of false aneurysm of the ascending aorta 8 years following the repair of congenital aortic stenosis is described.
A 14-year-old male patient was found to have congenital aortic stenosis in 1966 after medical check-up and subsequently operated upon. In the postoperative period, he was complicated by remittent fever of 1 month's duration, which was finally controlled by antibiotics. Arterial blood cultures taken on a few occasions were negative. Eight years and 5 months after surgery, he was noticed to have a mediastinal mass around the base of the heart and the presence of false aneurysm was confirmed by aortography. Aneurysmectomy was carried out almost 9 years after the previous operation, and it was found that aneurysm was arising from the suture line of the aortotomy with communication to the aorta at the bottom of the aneurysm. Postoperatively, patient's recovery was uneventful and was discharged on the 23rd postoperative day.
Etiology, timing of operation and techniques utilizing hypothermia and/or circulatory arrest are discussed.

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A 18-year-old female with unusual type of parchment-like right ventricle died of intractable congestive heart failure was reported. A catheter study revealed the absence of systolic contraction of the right ventricle. The pressure tracing curve in the right ventricle was virtually the same as in the right atrium. At autopsy, there was an extensive myocardial fibrosis of the left ventricle in addition to the almost total absence of the myocardium of the right ventricle. The case was considered to be a unique type of idiopathic cardiomyopathy.

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