Abstract: We evaluated whether heparin pretreatment accelerates the development of coronary collateral vessels induced by repeated, brief coronary occlusions. Sixteen dogs were instrumented for the measurement of subendocardial segment length in the area perfused by the left circumflex coronary artery (LCCA), LCCA flow and left ventricular pressure. An externally inflatable pneumatic occluder was placed around the LCCA. Two min coronary occlusions (CO) at rest were repeated hourly until there was no reduction in ischemic segment systolic shortening at the end of CO and negligible reactive hyperemia following the release of CO. Eight control dogs developed collaterals sufficient for resting myocardial oxygen requirements in the LCCA region by 129±45 (SD) CO. The remaining 8 dogs given heparin daily developed collaterals by 81±33 CO (p<0.05). Thus, in the presence of severe myocardial ischemia known to promote collateralization, heparin accelerated the development of coronary collaterals.

Abstract: Acute myocardial infarctions were produced in nine dogs by ligation of the left anterior descending coronary artery. Twenty-four hours after ligation, 0.5 mM/kg of gadolinium (Gd)-DTPA was injected intravenously, followed by cardiectomy 30 min later. Indium-111 antimyosin was administered intravenously 6 hr before cardiectomy to compare the infarct size with Gd-DTPA contrast enhancement. Areas of Gd-DTPA contrast enhancement were closely correlated with those of indium-111 antimyosin uptake (r = .86), although the former showed slightly greater than the latter. Partial and complete enhancements were observed in three and six dogs, respectively. In the T1 and T2 maps, T1 relaxation times of the infarcted area showed greater T1 shortening compared with normal myocardium, whereas T2 relaxation times were not different between infarcted and normal myocardium. Thus, Gd-DTPA showed significant contrast enhancement of the infarcted area because of greater T1 shortening and the extent of Gd-DTPA contrast enhancement expressed the infarct size precisely.

Abstract: 1. At the initial screening, 6.11% of elementary school children and 6.28% of junior high school students were picked up for the second secreening. At the second screening, 0.49% of elementary school children and 0.85% of junior high school students were referred to the final screening. The pick-up ratio was significantly higher in junior high school children .The ratio of children needing medical management was also significantly higher for junior high school students (2.96%) than for elementary school children (2.26%). 2. The reexamination system was useful for management of a group of children with minimal findings of ECG at minimal cost and effort and without giving rise to unnecessary anxiety for the children and their families. 3. In order to manage children from elementary school to junior high school without any risk, it is essential to establish more sophisticated systems of managing patient-records, such as computer managing systems. 4. In order to increase the reliability of questionnaires, it is necessary to explain the significance of the mass screening system for the prevention of cardiac accidents, to refine the questions and to give more easily understood instructions.

Abstract: The degradation of the sarcoplasmic reticulum (SR) in acute myocardial ischemia was studied with references to the regional irreversibility and to the mechanism of ischemic degradation by the measurements of Ca++-stimulated ATPase activity and composition of the major ATPase protein of the SR and activity of cathepsin B of the SR and lysosome (Ly) fractions. Ca++-stimulated ATPase activity decreased to 66% of that of the non-ischemic portion at 20 min after coronary ligation in the subendocardium (Endo) and to 44% at 30 min in the subepicardium (Epi). composition of the major ATPase protein decreased to 55 % and 73% at 30 min in Endo and Epi, respectively. In both SR and Ly fractions cathepsin B exhibited the maximal activity at 6.0-6.5, and pH dependent. And incubation of the SR at pH 6.0 induced the degradation of the ATPase protein quite similarly to that in vivo ischemia. These results suggest that the degradation of the SR membrane of ischemic myocardial cells begins earlier in Endo 20 to 30 min after the cease of the coronary blood flow, and extends to Epi later. Cathepsin B is strongly conceivable to play an initial role of necrotic process of the ischemic myocardial cells by activation inside of the SR in ischemic acidic state.

Abstract: The origin and the physiological role of an endogenous digitalis-like substance were investigated by measuring both the digoxin-like substance by a digoxin radioimmunoassay (RIA) and the inhibitory activity on the ouabain sensitive Na+,K+-ATPase in rats. The digitalis-like substance was in high concentration in the pituitary, and in decreasing concentration in the hypothalamus, adrenal and the other organs as measured by RIA using an antibody raised from a goat. However, the adrenal showed the highest content of digitalis-like substance as measured by the antibody raised from a rabbit. The plasma level markedly decreased during a 2-week sodium-loading, and the adrenal content decreased markedly on hypophysectomy as measured with the rabbit-antibody. Therefore, the substance measured with the rabbit-antibody must be one of ACTH-dependent adrenal steroids. The inhibitory activity on the Na+,K+-ATPase was high in the pituitary gland, and was decreased in order of the adrenal, hypothalamus and other organs. The 2-week sodium-loading increased both the content in the pituitary gland and the output in the urine, and decreased the hypothalamic content. Immunohistochemical staining of the hypothalamus with the antibody revealed that the immunoreactivity is restricted to the neurons of the paraventricular nucleus, supraoptic nucleus, magnocellular accessory nuclei and extended their fibers reaching to the inner layer of the median eminence. To determine the role of the substance in the brain, the crude extract dissolved in artificial cerebrospinal fluid was injected into the lateral ventricle; vasopressor responses, tachycardia and hyperactivity of the splanchnic nerve lasting for more than 30 min were recorded, which resembled the responses to ouabain injected similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract: We investigated the recognition of late potentials in patients with and without organic hear diseases and spontaneous ventricular arrhythmias. None of the normal subjects had late potentials and patients with ventricular arrhythmias but no organic heart diseases, also had no late potentials as well as patients with idiopathic ventricular tachycardias. Late potentials in patients with idiopathic cardiomyopathy were noted more frequently in the dilated type than in the hypertrophic type, especially in those with high grades of ventricular arrhythmias. Patients with old myocardial infarctions had a higher rate of late potentials recognition in cases of sudden death or ventricular tachycardias. On the other hand, we observed lower rates in patients during early stage of acute myocardial infarction in spite of the evidence of a higher rate of ventricular electrical instability. There was no association between ejection fractions, wall motion scores and late potentials. However, a higher recognition of late potentials was found in patients with inferior or posterior myocardial infarction and ventricular aneurysm. We concluded that the late potential must be evaluated in each of the different groups of organic heart diseases in order to estimate the clinical value of ventricular arrhythmias.

Abstract: Effects of dietary supplementation with highly purified EPA (1.8-2.7 g/day) for 16 weeks on platelet and red blood cell function and serum lipids concentration were investigated in patients with various thrombotic diseases. Decreases in platelet aggregation, thromboxane formation in platelets, platelet retention and whole blood viscosity, increased red blood cell deformation and prolongation of bleeding time were observed in the present study. In addition a reduction in serum cholesterol and triglyceride concentrations was noted in patients with hyperlipidemia after EPA ingestion. Some clinical improvements such as improvement of diabetic gangrene or peripheral vascular occlusive disease were observed. These results indicate that dietary supplementation of purified EPA may be beneficial for prevention and treatment of cerebro- and cardiovascular diseases.

Abstract: Nine patients with familial hypercholesterolemia (FH), 6 with homozygotes and 3 with heterozygotes, were treated with long term repetitive LDL-apheresis. The techniques are simple plasma exchange with human albumin solution, double membrane filtration, and selective LDL-adsorption by dextran sulfate-cellulose gel. The average term was 3.5 years except for the two homozygotes for whom the treatment was only initiated in our facility. Plasma total cholesterol levels were controlled between pretreating level, 320 to 500 mg/dl, and posttreating level, 100 to 160 mg/dl, by biweekly treatments. All patients showed remarkable improvement of cutaneous and tendinous xanthomas. One homozygous patient died at 31 years old of myocardial infarction after 2 years of treatment. A homozygous patient who has been treated since 5 years old for 6 years was reexamined by angiography and was shown to have atheromatous lesions regressed in the aortic valve region and in the left renal artery.

Abstract: Necropsy studies of coronary arteries were made in 14 patients who died after percutaneous transluminal coronary angioplasty (PTCA). Eight patients died shortly after PTCA, while the other six patients died some considerable time later. A total of 9, 920 serial step sections of necropsied coronary arteries at the site of PTCA were prepared and examined histopathologically by light microscope to determine the mechanism of luminal enlargement in PTCA, as well as the occurrence of restenosis. Of the eight patients who died shortly after PTCA, two had disruption of the intima and the media in the arterial wall located opposite the site that had atheroma, in spite of the fact that the former wall is more normal than the latter. Dissection of the media was camed out in four patients and intimal desquamation performed in six. All the patients revealed fresh thrombus formation. Of the six patients who survived for a longtime after PTCA was performed, two had disruption of the intima and the media located opposite the site with atheroma. In one, the media was dissected and in another, intimal desquamation was camed out. In one patient, release of atheroma into the lumen was suspected. Proliferation of intimal cells was revered in three patients indicating that restenosis had occurred. No compression of the atheroma was observed in any of the 14 patients. The above findings led to the conclusion that the mechanisms of luminal enlargement in PTCA are 1) intimal and medial disruption in the arterial wall located opposite the atheroma; 2) medial dissection; 3) intimal desquamation; 4) release of atheroma into the lumen; and 5) any combination of 1) - 4). With regard to restenosis, all patients in our study revealed fresh thrombus formation, which suggests the early occurrence of restenosis after PTCA. Three of the six patients who survived long after PTCA showed proliferation of intimal cells. This suggests the possibility that even if the stenosed artery were dilated by PTCA, stenosis may have again occurred as a result of excessive proliferation of intimal cells repairing arterial lesions.

Abstract: Right ventricular endomyocardial biopsies were performed in patients with repetitive ventricular tachycardia (VT; 8 patients) or ventricular premature beats (1 patient) which showed left bundle branch block morphology in electrocardiograms. These 9 males patients ranging in age from 21-55 years (mean 37.7 years) revealed enlargement and/or asynergy of the right ventricle in the ventriculogram. Randomly selected biopsied patients with dilated cardiomyopathy (DCM; 18 patients) and chronic right ventricular overloading (14 patients) who did not show the above-described arrhythmias served as controls. A histopathological analysis revealed advanced myocardal interstitial fibrosis associated with an increase in fatty tissue in 8 of the 9 patients (89%). Moreover, advanced hypertrophy of myocytes (grades 2 or more of our criteria), disarrangement of muscle bundles and endocardial thickening were prominent with incidences of 75%, 75% and 78%, respectively. Incidence of all findings was more pronounced in the ARVD group. suggestiveness of post-myocarditic change in the biopsied specimen was high in 1 patient, showing a lower incidence (12%) than the DCM group (17%). From these results, we can conclude that different etiological factors may be the based of these pathological changes. We believe that the presence of a large amount of fatty tissue within the myocardial tissue is an important element in the etiology of ventricular arrhythmias as it has also been recognized in patients with non-ARVD idopathic ventricular tachycardia in our biopsy series.

Abstract: Alterations in the phospholipid component of membranes were studied in acute myocardial ischemia with respect to sarcoplasmic reticulum (SR) and mitochondria (Mt) in the carine heart and compared with changes in the phospholipid composition of intact membrane treated with exogenous phospholipases (PLases)A2 and C, in order to examine the mechanism of ischemic degradation. As early as 30 min after coronary ligation, the total phospholipid content of SR and Mt decreased significantly, 16.0% and 5.6% respectively. The patterns of SR and Mt phospholipids from the ischemic myocardia did not differ on the chromatograms from those of the non-ischemic myocardia, and no significant increases in lysophospholipids were found for up to 3 hrs. Among the components of phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE) decreased mainly during ischemia, and depletion of PC exceeded that of PE in SR. PLase C hydrolysed phospholipids yielded no lysophospholipids, compared to the production of a large amount of lysophospholipids by PLase A2. It was concluded that degradation of membrane phospholipids occurs in the early stage of myocardial ischemia mainly in PC and PE, which are the major components of membrane phospholipids. This may be an expression of irreversible changes, and the activation of PLase C was considered to play an important role in their degradation.

Abstract: The intra-arterial blood pressure (BP) was measured during 24 hours on 52 patients with essential hypertension using a portable device. The minimum BP inherent to each subject (base BP) was determined from the systolic and diastolic BP histograms during sleep. In this study the systolic and diastolic BPs were presented as a mean BP (BP) and a base BP, and the average of BPs during waking hours was considered as the sum of the base BP and the additional BP increment. The clinical significance of the base BP and BP increment was examined by comparing them with the results of clinical examinations. The comparison showed that the base BP was closely related with the left ventricular hypertrophy and severity of hypertension, while the BP increment correlated with the baroreflex sensitivity and plasma norepinephrine concentration. In this paper, a new tonometry was developed to indirectly record the BP of the superficial temporal artery. The tonometry correlated well with the intra-arterial BP measurement, and was available for the indirect base BP evaluation at an outpatient-clinic.

Abstract: To investigate a relation between circadian blood pressure and heart rate variation, intra-arterial blood pressure (BP) and heart rate (HR) were recorded during 24 hours in 53 untreated essential hypertensives (EH), 8 secondary hypertensives, 10 normotensives (NT), and 3 patients with Shy-Drager syndrome. Values of systolic BP (SBP) and HR were sampled at about 10 second intervals throughout the 24-hour to calculate the coefficient of correlation between SBP and HR (rSBP-HR). A significant positive correlation was found between SBP and HR levels in each subject of EH with WHO stage I and II, along with NT (average rSBP-HR = 0.59, 0.40, and 0.54 respectively, p less than 0.001). Low coefficients of correlation were found in the EH with WHO Stage III (r = 0.16) and the patients with pheochromocytoma (r = 0.05). In contrast, a significant negative correlation was found in the patients with Shy-Drager syndrome (r = -0.44, p less than 0.001). Since HR is controlled mainly by the autonomic nervous system (ANS), the results suggest that the circadian variation of SBP is also mainly controlled by the ANS in the subjects with high rSBP-HR and that of SBP controlled by the other factors in subjects with low rSBP-HR.

Abstract: In order to clarify whether hemodialysis treatment accelerates atherosclerosis, forty-two patients undergoing chronic hemodialysis were investigated. Because it is non-invasive and repeatable, aortic calcification on chest-XP was used as an index of atherosclerosis. No patients had evidence of calcified atherosclerosis at the start of hemodialysis therapy. The patients were divided into three groups according to vascular changes. Group 1 (20 patients) showed no calcification during the observation period. Group 2 (11 patients) had mild or moderate aortic calcification (thin linear aortic calcification). In group 3 (11 patients), massive and severe calcification was accelerated by hemodialysis. 18 parameters which might be considered to promote atherosclerosis were evaluated in each group. The age in group 3 was 53.8 +/- 10.4 (mean +/- standard deviation) years, which was older than the 42.1 +/- 12.6 year age in group 1 (p less than 0.025). Duration of dialysis in group 3 was 121.9 +/- 30.5 months, which was significantly longer than the 82.0 +/- 31.0 months in group 2 (p less than 0.01) and the 77.3 +/- 55.3 months in group 1 (p less than 0.025). Serum HDL-cholesterol levels in groups 2 (23.0 +/- 4.5 mg/dl) and 3 (20.9 +/- 6.6 mg/dl) were significantly lower than the 28.6 +/- 8.3 mg/dl in group 1, (p less than 0.025 and p less than 0.05, respectively). Serum parathormone-C level in group 3 was 14.7 +/- 8.6 ng/ml, which was significantly higher than the 6.1 +/- 6.0 ng/ml level in group 1 (p less than 0.01) and the 5.0 +/- 7.8 ng/ml level in group 2 (p less than 0.025). In discriminant analysis, age, duration of dialysis, hematocrit, serum HDL-cholesterol, parathormone-C, and alkaline phosphatase level were the independent factors used to distinguish the three groups. These findings suggest that 1) aging is a basal factor in the promotion of atherosclerosis, 2) hypo-HDL cholesterolemia is a major factor in the early phase of atherosclerosis, 3) hyperparathyroidism could have an important role in the late phase of atherosclerosis, 4) dialysis itself might promote atherosclerosis directly, and 5) blood pressure level is not major factor for atherosclerosis over a long observation period, at least in our study.

Abstract: In 23 patients with recurrent sustained ventricular tachycardia (VT) which originated from the left ventricle, endocardial catheter mapping has performed. In an additional 14 patients we also stimulated their left ventricle for non-sustained VT. Multiple sites could be mapped for the recording of local electrical activity, for pacing and for the induction of VT. These procedures could be done without complication. A careful, reasonable, and safe method of endocardial mapping will facilitate clinical electrophysiologic study.

Abstract: In order to clarify the relation between salt sensitivity and changes in intracellular sodium ([Na]i) and free calcium concentration ([Ca2+]i) after salt loading, [Na]i and [Ca2+]i were determined in lymphocytes of twenty patients with essential hypertension under a low salt diet (3 g/day) and a high salt diet (20 g/day) for seven days, respectively. They were classified as "salt-sensitive" (n=10) or "nonsalt-sensitive" (n=10) on the basis of the changes in blood pressure after salt loading. Both lymphocytic [Na]i and [Ca2+]i were significantly increased with salt loading in salt-sensitive patients (p<0.05 for both), while they were not affected by salt loading in nonsalt-sensitive patients. Lymphocytic [Ca2+]i showed a positive correlation with lymphocytic [Na]i under both low salt diet (r=0.62, p<0.01) and high salt diet (r=0.70, p<0.01) in all patients in both groups. In addition, a close and positive correlation was observed between the changes in lymphocytic [Na]i and those in lymphocytic [Ca2+]i after salt loading in all patients in both groups (r=0.80, p<0.001). These results suggest that the increase in [Ca2+]i, possibly linked with the increase in [Na]i, may be involved in elevation of blood pressure in the salt-sensitive patients after salt loading.

Abstract: Using fluorescent calcium indicator quin2, we studied intracellular free calcium concentration in platelets that have a number of features similar to vascular smooth muscle cells. Intracellular free calcium concentration in platelets of male SHR was significantly higher at 4, 11 and 28 weeks old compared with age-matched male WKY. However, no significant difference was observed in platelets cytosolic free calcium level of DOCA-salt hypertensive and two-kidney, one clip hypertensive rats in the chronic stage. Cardiac Ca++ channels were estimated by means of radioligand binding method with [3H]-nimodipine. No significant changes were observed in the concentration and affinity of cardiac Ca++ channel in SHR, DOCA-salt hypertensive and two-kidney, one clip hypertensive rats. Calmodulin levels in mesenteric arteries of SHR were significantly decreased in comparison with those of WKY. However no significant differences were observed in DOCA-salt hypertensive rats in the chronic stage. These results indicate that the increase in intracellular free calcium concentration of SHR is not the secondary change caused by high blood pressure. It is impossible to detect the ratio of the three states (open, resting and inactivated) of Ca++ channel. Therefore, there remains a possibility of the changes in the ratio of the states of Ca++ channel. The observed abnormalities of Ca++ regulation may contribute to the pathogenesis of hypertension.

Abstract: To evaluate the role of the renal dopaminergic system on renal water-sodium metabolism patients with essential hypertension (EHT), urinary excretion of dopamine, urinary excretion of sodium (UNaV) and fractional excretion of sodium (FENa) were all investigated before and after the administration of dopamine (3 micrograms/kg/min, intravenous infusion for 60 minutes), dopamine antagonist, metoclopramide (8 mg/m2 BSA, intravenous injection) or mild sodium loading in both normotensive subjects and benign EHT. In the basal values, no significant difference in urinary excretion of free (u-fDA), conjugated (u-cDA) or total dopamine (u-tDA) was found between normotensives and hypertensives. However, low renin EHT showed a pronounced reduction in u-fDA compared with normotensis subject and (NT) normal renin EHT. In this study, a significant reduction of u-cDA and of u-tDA was also found in those patients with low renin essential hypertension. In the normotensive and essential hypertensive groups UNaV or FENa showed a positive correlation with u-fDA (measured simultaneously), but not with u-tDA or u-cDA. The regression line between u-fDA and UNaV or FENa in EHT was shifted towards a lower u-fDA level than in NT. UNaV and FENa were increased by dopamine infusion and were decreased by metoclopramide injection in both NT and EHT. Changes of UNaV and FENa following dopamine or metoclopramide, showed a negative correlation with u-fDA measured immediately before the administration of these drugs. The enhanced natriuretic response to infused dopamine and the attenuated antinatriuretic response to injected metoclopramide were significant in low renin EHT, when compared with NT or normal renin EHT patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract: 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 blockers. 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: 1) an increase of VPCs at higher heart rates (positive correlation) in 16 patients, 2) an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in 13 patients, 3) an increase at low heart rates and flat curve at high heart rates ( positive-flat correlation) in 5 patients, 4) a linear decrease (negative correlation) in 1 patient, and 5) 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<0.01); atenolol was effective in 5 of 6 patients of P group only 1 of 10 patients of NP group (p<0.05). Both drugs reduced the slope of a positive correlation. These results suggest that: 1) VPCs which increase at higher heart rates may be related to triggered activity, and 2) 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.

Abstract: The present study was designed to evaluate the role of the presynaptic α2-adrenoceptor in the pathogenesis of hypertension. Norepinephrine overflow during sympathetic nerve stimulation and its changes by presynaptic α2-adrenoceptor inhibition were examined in the perfused mesenteric vasculatures of young and adult spontaneously hypertensive rats (SHR) compared with age-matched Wistar Kyoto rats (WKY). Electrical sympathetic nerve stimulation caused significantly greater overflow of endogenous norepinephrine from the adrenergic nerve terminals in young SHR than in age- matched WKY. Yohimbine, an α2-adrenoceptor blocking agent, facilitated norepinephrine overflow from the adrenergic nerve terminals. The effects of yohimbine on norepinephrine overflow and pressor responses to electrical nerve stimulation were less in young SHR than in age-matched WKY. Norepinephrine overflow in adult SHR was similar to that in adult WKY, and differences in the effect of yohimbine on norepinephrine overflow between SHR and WKY were not marked at this chronic stage. These results suggest that enhanced norepinephrine overflow in the mesenteric vasculatures can be observed only in young SHR; this may be due in part to an impaired negative feed-back mechanism on the nerve terminals by presynaptic 2-adrenoceptors.

Abstract: An animal model of dilated cardiomyopathy following encephalomyocarditis (EMC) virus has been developed. Virus was isolated from mouse hearts and viral antigens were detected in the myocardium until the second week of infection, but neither was found thereafter. Differences were found among different strains of mice in the frequency of occurrence and severity of myocarditis, and even in the character of the pathologic lesions. Thus, genetic factors may play an important role in the pathogenesis. Autoantibodies against heart developed and the distribution of cardiac myosin isoenzymes was altered during the course of myocarditis. Virus, vaccine, maternal vaccination, recombinant interferon alpha A/D and ribavirin were effective in protecting the mice from developing myocarditis. This animal model is suitable for studying the pathogenesis of viral myocarditis and evaluating preventive and therapeutic interventions of the condition.

Abstract: The gross anatomic and microscopic appearance of the hearts of young and adult WKY/NCrj rats was examined in comparison with that of normotensive Wistar and SHR/NCrj rats In a substantial number of the WKY rats, the heart weight and thickness of ventricular septum were much greater than those of the Wistar and SHR rats The ventricular septum to left ventricular free wall thickness ratio was greater than 13 in about one sixth of the WKY rats In most of the hypertrophied WKY hearts, the transverse area of the left ventricular cavity was smaller in relation to the wall area than in the Wistar and SHR rat hearts, although in a few it was greater Abnormal fiber arrangement, myocyte hypertrophy, and myocardial fibrosis were far more prominent in the hypertrophied myocardium of the WKY rats compared with the Wistar of SHR rats Intramural arteries with marked wall thickening existed frequently in the hypertrophied and dilated hearts Electron microscopic examination revealed marked disarrangement of bundles of myofilaments and widened Z-bands in the hypertrophied myocardium blood pressure was not elevated in the rats with cardiac hypertrophy These findings show that a disease of the myocardium with the pathologic features similar to those of hypertrophic cardiomyopathy in man occurs spontaneously in rats

Abstract: Westudiedthemetabolicandcardiacresponsestoexercisebyexpiratorygasanalysisin40patientswitholdmyocardialinfarctionand33normalsedentarymales.Onthebasisofexerciseenergymetabolism, theelevationoftherespiratoryquotient(RQ;RQ=VCO2/VO2)duringexerciseiscausedbytheincreaseofbloodlactateduetotheaugmentedanaerobicmetabolism.Functionalaerobicimpairment(FAI)inourstudywassignificantlyadvancedinthecontrolgroupandtheNYHAfunctionalclassI, classIIandclassIIIgroups, thatis, 2.3±11.2%, +14.8±10.4%, +27.8±13.8%and+49.4±2.8%respectively.TheRQvaluesweresimilaramongallgroups;0.29±0.09respectively.Functionalchronotropicimpairment(FCI)forthesamegroupswas0.9±7.0%, +1.4±6.1%, +3.8±4.8%and+8.7±6.0%, andthatoftheclassIIIgroupwassignificantlylargerthanthatofthecontrolgroup.Thus, intheclassIIIcongestiveheartfailuregroup, thechronotropicresponsetothemetabolicrequirementwasimpairedincomparisontothecontrolgroup.ItwasconcludedthatthereducedchronotropicreservewaspresentinNYHAclassIIIpatientswitholdmyocardialinfarction, andthatthismechanismmightcontributetoadecreaseinthepumpreserveoftheheart, resultinginfurtherimpairmentofphysicalcapacityinthesepatients.

Abstract: The characteristics of 24-hour blood pressure variation in hypertensive patients were assessed using new indices of variability. Blood pressure of 43 inpatients with essential hypertension was measured using a portable device without disturbing daily behaviors. Variances in systolic and diastolic pressure values obtained for a day (SDd2), and short-term (SDh2) and long-term (SD242) variances were calculated; their relationship was expressed as SDd2 =SDh2 + SD242. SDh and SD24 were expedient in assessing the relatively fast and slow blood-pressure variations, respectively. The results showed that the ratio SDh2/SDd2 (percentile of the short-term variance in a whole-day variance) increased and therefore SD242/SDd2 decreased as age increased for both systolic and diastolic pressures. It was found, moreover, that systolic SDh was significantly related to age and baroreflex sensitivity, and systolic SD24 to the heart rate during waking hours. The physiological and clinical significance of SDh and SD24 is discussed, briefly, including arterial wall stiffness.

Abstract: To clarify the patho-etiologic factors of Japanese myocardial infarction, a comparative pathological study of myocardial infarction in the Osaka, Akita, Wakayama, and Hokkaido districts, and an extensive histopathological study of 94 autopsy cases with acute myocardial infarct (AMI) in less than 4 weeks at Osaka were carried out. Although AMI in Akita was highly complicated by hypertension, AMI in Osaka was associated with a history of diabetes mellitus and hypercholesterolemia, especially in the young generation (under 59 years of age); hypercholesterolemia was related to the occurrence of AMI. Moreover, in spite of increases in transmural myocardial infarct (TMI) in Osaka, Hokkaido and Wakayama, Akita showed an equal ratio of TMI and subendcardial myocardial infarct. In AMI in Osaka, significant stenosis (more than 75% stenosis) of the coronary artery was of the same grade between the proximal and distal portions in the epicardial coronary artery. AMI in Akita, however, showed more severe stenosis in the proximal than the distal portion. A high incidence (88.3%) of thrombosis formation corresponding to the site of infarction was observed in AMI in Osaka. Moreover, ruptured atheromatous plaques were identified as being responsible for 62.6% of the coronary thrombosis cases, and a high incidence (70.0%) of foamy cell infiltration was disclosed. Thus, it can be concluded that ruptured atheromatous plaque is a major factor in the progression of coronary atherosclerosis and/or thrombosis, which might be due to the process of plaque softening.

Abstract: To determine the prognostic factors of dilated cardiomyopathy (DCM), a retrospective long-term investigation of 111 patients seen between 1967 and 1983 was carried out. Fifty-four deaths were divided into 3 subgroups: (1): sudden death (n=6); (2): sudden death on the basis of heart failure (n=17); (3): refractory heart failure death (n=31). Multivariate analysis was employed to ascertain the prognostic score, which was constructed from the grading of the New York Heart Association functional classification, the cardiothoracic ratio, electrocardiographic findings and cardiac function. Individual variables were indicated on the first (I)0 and second (II) principal component axes. The mean center points for the death modes were as follows: (1): I=-0.4, II=+0.8, (2): I=+0.7, II=+1.1 (3): I=+1.4, II=-0.8. Surviving cases (n-57) showed I=-0.6, II=+0.1. Forty-one cases examined during 1984-1985 were analyzed to evaluate the prognostic efficacy of this score. Fourteen of 17 cases (82%) located in the refractory heart failure death group died within one year ater determination of the prognosis, showing thereby that the prognositc determination by multivariate analysis is effective.

Abstract: The case reported here showed a radiological appearance of hypoplasia of the right lung, dextroposition of the heart, and a curved vascular shadow in the right lower lung field known as a scimitar sign. However, a computed tomography of the chest showed this abnormal vascular shadow draining into the left atrium (pseudo-scimitar sign). Therefore, in patients with a radiological appearance of the scimitar syndrome, computed tomography of the chest should be indicated to rule out the pseudoscimitar sign.

Abstract: In order to define indications for newly developing aggressive managements for patients with acute myocardial infarction, an analysis of therapeutic results was made on 1,060 patients admitted to our coronary care unit (CCU). The total mortality was 14.9%, and 143 patients (13.5%) died from cardiac complications. These 143 patients were divided according to causes of death listed in Killip's classification. In the Killip class 4 group, mortality was as high as 86.6%, and all patients with previous infarction and/or hemodynamic abnormality of Forrester's subset 4 died. Pump failure caused death in 100 patients, of whom 69 were in a state of cardiogenic shock at the time of their admission. On the other hand, 58 patients, accounting for 40.6% of the cardiac deaths, were in Killip's class 1 or 2 at admission. In these 58 patients, 23 died from free wall rupture and/or perforation of the interventricular septum. Another 27 patients expired from reinfarction or infarct size extension and/or post-infarction angina. Thus, we can say that the major causes of death of patients in CCU are cardiogenic shock, reinfarction and cardiac rupture. We could not save these patients by using conventional CCU managements. Newly developing aggressive techniques, such as intracoronary thrombolysis and artificial hearts, seem to be indicated for these potentially fatal patients, while the effectiveness of these techniques should be verified as to such patients.