TL;DR: Shear stress can stimulate the migration and proliferation of endothelial cells and occurred more prominently in the downstream portion of the flow than in the upstream part.
Abstract: We have examined the effect of shear stress on the regenerative response of cultured vascular endothelial cells by using a fluid shear apparatus designed in our laboratory. The shear stress was created on the endothelial cell layer of a fetal calf and grown confluently in a culture dish by whirling the medium, with a rotating disk placed on the fluid surface. The effect of the shear load (0.3-1.7 dyn/cm2) over 24 hr was evaluated by counting the number of regenerated cells in a denuded area that had been created by mechanically removing some cells before rotating the medium. The cell number observed in the denuded area after the exposure to shear stress was about twice as great as that of the static control. The difference was statistically significant (P less than 0.01 to P less than 0.05). Cell migration and proliferation occurred more prominently in the downstream portion of the flow than in the upstream part. The cell number in the downstream portions correlated significantly with the intensity of the applied shear stress (P less than 0.05). These results indicate that shear stress can stimulate the migration and proliferation of endothelial cells.
TL;DR: It is shown that the formula proposed by Friedewald provides a better fit for Japanese people, when k = 4, rather than original k = 5, and a better estimation is gained, if k is rotated according to the triglyceride levels of individual subjects.
Abstract: When direct measurement of serum low density lipoprotein cholesterol (LDL-c) is not available, it can be estimated from total cholesterol (TC), triglycerides (TG) and high density lipoprotein cholesterol (HDL-c) by using the formula proposed by Friedewald: LDL-c = TC-[HDL-c + TG/k], k = 5 This formula assumes the triglyceride/cholesterol ratio in VLDL to be 5:1. However, it is changeable with serum triglyceride levels, and averaged as 4 among Japanese with triglycerides less than 400 mg/dl. The formula provides a better fit for Japanese people, when k = 4, rather than original k = 5. In addition, a better estimation is gained, if k is rotated according to the triglyceride levels of individual subjects; i.e. 3 for those with triglycerides less than 150 mg/dl, 4 for those with triglycerides from 150 to 299 mg/dl, 5 for those with triglycerides from 300 to 400 mg/dl. The percent error of estimation is less than 5% when k = 4, and about 1% when variable k is employed for populations of about 1,000 subjects in number.
TL;DR: In the annuals of autopsy records in Japan, from 1958 to 1977, 377841 autopsy cases are registered with a short summary of the pathology findings, 434 cases with idiopathic, interstitial, viral, non-specific (NSM) and giant cell (GCM) myocarditis were found.
Abstract: In the annuals of autopsy records in Japan, edited by the Japanese Society of Pathology and covering 20 years, from 1958 to 1977, 377841 autopsy cases are registered with a short summary of the pathology findings. Of these, 434 cases with idiopathic, interstitial, viral, non-specific (NSM) and giant cell (GCM) myocarditis were found. The incidences of NSM and GCM were 0.11 and 0.007%, respectively. The annual incidence of NSM showed periodic fluctuations with in 5-year intervals and increased remarkably after 1974. Incidence of GCM showed a similar fluctuation but with a one to two year delay of peaks. The male to female ratio was 1.2 : 1 and the age distribution had two peaked patterns for both sexes, though these peaks were scattered widely from neonate to elderly patients. The regional distribution of NSM showed a concentration in the middle portion of Honshu and its regional annual incidence had propagation waves from the central area to peripheral areas. The same tendency was observed in GCM cases. Hokkaido was characterized by a low incidence of NSM and no GCM. Complications of myocarditis included pancreatitis, pneumonitis, , interstitial nephritis, meningoencephalitis, hepatitis, hepatic cirrhosis and a considerable incidence of malignancies. Antibiotics, antineoplastic agents, steroids and irradiation therapy were the main forms of treatment applied before or after the start of myocarditis.
TL;DR: Clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger, and lines of evidence suggest extension of infarction due to secondary coronary occlusion.
Abstract: In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
TL;DR: An important feature of this mass screening by ECG for heart diseases in pupils and students was the ability to carry out an accurate follow-up in all the phases from primary to precise examination.
Abstract: Mass screening by ECG for heart diseases in pupils and students was performed in Shimane Prefecture; all the children had primary screening and were under the supervision of a pediatric cardiologist in all phases, from primary to precise (tertiary) examination. The precise examination was performed with 2D echo, exercise ECG and/or cardiac catheterization when indicated, and an important feature of this mass screening was the ability to carry out an accurate follow-up in all the phases from primary to precise examination. The number of subjects in the primary screening from 1980 to 1984 was 50758 primary school pupils, 44216 junior high school students and 33480 senior high school students; organic heart diseases not under the supervision of the pediatric cardiologist at the time of mass screening were found in 22 primary school pupils (0.04% of participants in the primary screening), 14 junior high school students (0.03%) and 5 senior high school students (0.01%). Clinically significant arrhythmias without underlying organic heart diseases were discovered by mass screening in 8 primary school pupils (0.02%), 13 junior high school students (0.02%) and 16 senior high school students (0.05%).
TL;DR: Though the induction of VT may not be indicated in every case of VT, it is believed that EPS is required to determine the focus for the operation and to evaluate the precise drug efficacy in rapid VT.
Abstract: Five among 19 cases of sustained ventricular tachycardia (VT) treated in the last two years had left ventricular aneurysms, but the patients denied any previous attack of chest pains that would indicate acute myocardial infarction Laboratory findings including serum electrolytes were normal and no signs of inflammation were found Coronary angiograms were normal but the left ventriculograms showed aneurysms in four patients and akinetic to aneurysmal wall motion in one patient Electrophysiologic studies (EPS) were done in four patients VT was induced reproducibly by programmed electrical stimulation in three patients and it was terminated by programmed stimulation within 30 seconds The foci of VT were determined by EPS One case who showed acceleration of the VT rate following the second induction of VT developed a fulminant course; Adams-Stokes attacks from VT, more than ten times a night in spite of intravenous administration of a large dose of procainamide, were terminated by DC shock VT was determined to originate from the aneurysm that was resected operatively In the other two cases, the foci were resected and the intraoperative EPS confirmed the preoperative foci The postoperative EPS showed no inducibility of VT in three surgical cases Though the induction of VT may not be indicated in every case of VT, we believe that EPS is required to determine the focus for the operation and to evaluate the precise drug efficacy in rapid VT It is further stressed that the sustained VT of our patients including the present five, lasted for several hours until it was terminated in the hospital
TL;DR: During the period from August, 1977 to December, 1984, a total of 3003 patients who received open heart surgery were treated postoperatively at the ICU of National Cardiovascular Center, low cardiac output syndrome (LOS) developed in 669 patients and organ failures due to LOS were studied.
Abstract: During the period from August, 1977 to December, 1984, a total of 3003 patients who received open heart surgery were treated postoperatively at the ICU of National Cardiovascular Center. Low cardiac output syndrome (LOS) developed in 669 (22.3%) patients. Organ failures due to LOS were studied in these patients. Although the overall mortality of postoperative patients was 5.6% and improved to around 4% in the later years, death rate of patients with LOS was persistently high (22.8%) and showed no tendency to improve even in the latest years. Moreover, the clinical results of those LOS patients who developed organ failure were extremely poor; the mortality of patients with respiratory failure (RF) accounted for 36.8% and that of patients with other organ failure exceeded 50%. The incidence of impaired organs in LOS patients was 49.9% in RF, 29.9% in acute renal failure (ARF), 18.4% in hepatic failure (HF), 16.4% in disseminated intravascular coagulation (DIC), 15.5% in central nervous system failure (CNSF), and 11.1% in gastrointestinal bleeding (GIB). Pathophysiological mechanisms as well as the management of these major complications caused by LOS are also discussed. Some patients developed multiple organ failure (MOF). Plasma exchange (PE) was performed on 16 patients who developed MOF. Improvement of various organ functions was obtained and consequently three patients were successfully treated by means of PE. Removal of various substances toxic to organs, supplement of deficient substances and cessation of the vicious cycle produced by the interaction of impaired organs in patients with MOF are major roles of PE in the treatment of MOF.
TL;DR: Since socio-economic conditions have improved, and penicillin has been introduced to control group A streptococcus, mortality and morbidity from RF and RHD have remarkably decreased in well developed countries, and these factors may have contributed predominantly to the sharp decrease in first and recurrent attack of RF in Japan.
Abstract: Rheumatic fever (RF) is the common cause of rheumatic heart disease (RHD) in the 5-30 age group and is usually preceded by group A streptococcal pharyngitis. The annual mortality caused by RF and RHD has changed remarkably in Japan between 1960 and 1981 according to the report of the Ministry of Health and Welfare. The annual incidence of RF among schoolchildren as surveyed from pediatric clinics of 20 major hospitals between 1952 and 1980 varied year by year, and is now steadily declining. Follow-up studies of 287 patients with carditis over ten years showed that cardiac murmur disappeared in 44.9% of total patients within 4 years through use of antibiotic prophylaxis. Other patients continued to have cardiac murmur 10 years after the first attack of RF. Valvular involvement due to RF was mostly confined to mitral valve and the appearance of mitral regurgitation was particularly common in schoolchildren. Survey of RHD in schoolchildren showed that mitral regurgitation was the most common anomaly, but the prevalence rate of RHD decreased from 4.6/1000 population in 1958 to 0.14/1000 population in 1981. By contrast, mitral stenosis was predominant in adults, according to the records of patients admitted in three university hospitals. Since socio-economic conditions have improved, and penicillin has been introduced to control group A streptococcus, mortality and morbidity from RF and RHD have remarkably decreased in well developed countries. These factors may have contributed predominantly to the sharp decrease in first and recurrent attack of RF in Japan.
TL;DR: Large cerebral infarctions were caused by atherosclerosis with or without thrombosis in the proximal circumflex (cortical) cerebral arteries, and hypertensive cerebral hemorrhage was the rupture of arterionecrosis-derived microaneurysms in the distal penetrating cerebral arteries.
Abstract: Large cerebral infarctions were caused by atherosclerosis with or without thrombosis in the proximal circumflex (cortical) cerebral arteries. Hypertension, hypercholesterolemia, hypoxidosis, and vasospasm were considered to induce endothelial cell injuries, which might be the primary events not only in atherosclerosis, but also in arteriosclerosis and arteriosis formation. Morphogenesis of atherosclerosis and causes of associated thrombosis were also discussed. Small cerebral infarcts were produced not only by arteriosclerosis, arteriosis, and atherosclerosis, but also by arterionecrosis-derived microaneurysms occluded by thrombi in the distal penetrating (perforating) cerebral arteries. Pathogenesis and morphogenesis of the arterial lesions were discussed. Recent increase of the arterionecrosis occluded by thrombosis in the pathogenesis of small infarcts (lacunes) was noted. The direct cause of hypertensive cerebral hemorrhage was the rupture of arterionecrosis-derived microaneurysms in the distal penetrating cerebral arteries. The primary change of the arterionecrosis was the medial muscle cell necrosis, the causes of which were considered to be hypertension, aging, poor diet low in cholesterol, vasospasm, and the congenitally poor wall structure of the arteries. The development and healing of experimental arterionecrosis in hypertensive rats were also reported.
TL;DR: Abnormal status of pulmonary circulation may be one of the important determining factors of deterioration by pregnancy in cardiac patients, and the criteria for permitting pregnancy in cardiomegaly and atrial fibrillation are proposed.
Abstract: To evaluate the influence of volume overload by pregnancy on heart diseases, the relations between cardiac status before pregnancy and clinical courses during pregnancy were studied, especially from the viewpoint of pulmonary circulation. In 206 pregnant cardiac patients whose prepregnancy laboratory data were known, the deterioration (appearance or advance of heart failure) during pregnancy was prospectively related to: pulmonary congestion (p less than 0.05), enlarged left atrium (p less than 0.05), atrial fibrillation (p less than 0.01) and right ventricular hypertrophy (p less than 0.005) in mitral stenosis; cardiomegaly (p less than 0.05) and atrial fibrillation (p less than 0.005) in mitral regurgitation; cardiomegaly (p less than 0.005) in congenital heart diseases; and to previous congestive heart failure (p less than 0.005) in total cases. All of the cases with systolic pulmonary artery pressure higher than 50 mmHg deteriorated during pregnancy. Some cases with no deteriorating laboratory findings showed dyspnea suddenly at the end of pregnancy. In 1033 cardiac patients who had experienced pregnancy, deterioration during pregnancy was seen more frequently in cases with mitral valvular diseases that in those with aortic valvular diseases. No deterioration was seen in pulmonary stenosis patients. Abnormal status of pulmonary circulation may be one of the important determining factors of deterioration by pregnancy in cardiac patients. The criteria for permitting pregnancy in cardiac patients are proposed.
TL;DR: It is proposed that AI or BK induced PGI2 generation may be regulated by the increased breakdown of AI orBK, as an autoregulation mechanism, that is derived from increased ACE activity by AI and BK.
Abstract: Prostacyclin (PGI2) generation has been known to be regulated by several endogenous vasoactive substances, and in this study the relationship between angiotensin I-converting enzyme (ACE) related substances and PGI2 generation was investigated using cultured human vascular endothelial cells. Addition of angiotensin I (AI) or bradykinin (BK) enhanced PGI2 generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI2 generation and ACE activity. The enhancement of PGI2 generation induced by AI or BK was not affected by pretreatment with captopril, and angiotensin II (AII) did not show any effect on either PGI2 generation or ACE activity. Through these experimental results, the conversion of AI to AII by ACE was considered not to cause the enhancement of PGI2 generation. Captopril solely inhibited PGI2 generation and the reported hypothesis that captopril enhances PGI2 generation by the accumulation of AI or BK via inhibition of ACE was not confirmed in this experimental system. Rather, it is proposed that AI or BK induced PGI2 generation may be regulated by the increased breakdown of AI or BK, as an autoregulation mechanism, that is derived from increased ACE activity by AI or BK.
TL;DR: The degree of hypertension that produces high vulnerability to stroke and severe damage to the brain after ischemic insult is indicated as beginning at about 180 mmHg.
Abstract: The Wistar rat, with a blood pressure range of 120-160 mmHg, and two strains of spontaneously hypertensive rats (SHR), stroke-prone (SHRSP, range 210-270 mmHg) and stroke-resistant (SHRSR, range 160-240 mmHg), were used to determine the degree of damage after ischemic insult induced by bilateral carotid artery ligation (BLCL) The survival rate and McGraw Stroke Index correlated well with the degree of hypertension After BLCL, impairment of cerebral blood flow is abrupt and residual flow is near zero in rats with initial blood pressures greater than 200 mmHg A markedly deteriorated aerobic metabolism, as measured by the concentrations of ATP, c-AMP and lactate, is seen to precipitate in rats with initial blood pressures greater than 180 mmHg and severe edema occurs if the pressure is more than 160 mmHg The degree of hypertension that produces high vulnerability to stroke and severe damage to the brain after ischemic insult is indicated as beginning at about 180 mmHg
TL;DR: Using monoclonal antibodies specific for human cardiac HC alpha and HC beta, the expression of these isozymes in fetal through adult cardiac tissues is examined and whether isozymic redistribution occurs in pressure overloaded human ventricles is investigated.
Abstract: Cardiac muscles contain at least two isozymes--referred to as alpha(HC alpha) and beta(HC beta)--of the myosin heavy chain. The proportional ratio of these isozymes varies depending upon the developmental stage and the physiological and/or the hormonal milieu of the cell. Using monoclonal antibodies (MoAb) specific for human cardiac HC alpha and HC beta, we have examined the expression of these isozymes in fetal through adult cardiac tissues and investigated whether isozymic redistribution occurs in pressure overloaded human ventricles. We found that although HC alpha was expressed in the atrium from the early embryonic stage, in embryonic ventricular myofibers, only HC beta was expressed without expression of HC alpha, but some myofibers replace HC beta by HC alpha after birth, and these HC alpha containing ventricular myofibers were found to be decreased by pressure overload, which suggested that isozymic redistribution from HC alpha to HC beta also occurred in the ventricles, as well as the atrium. In addition, we also found two subtypes of HC beta (beta 1, beta 2) in the human heart. In the ventricle, both beta 1 and beta 2 was present in all myofibers; in contrast, some myofibers contained beta 1 or beta 2 or both with or without expression of HC alpha in the atrium. beta 1 and beta 2 were distinctive in their expression during the developmental stage, since beta 1 was present in the embryonic heart from the early developmental stage, whereas beta 2 was not present in the early embryonic heart, but began to be expressed in the late embryonic stage.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The electrophysiological effects of antiarrhythmic drugs were tested in 36 patients with recurrent paroxysmal supraventricular tachycardia and disopyramide was less effective than previously reported.
Abstract: The electrophysiological effects of antiarrhythmic drugs were tested in 36 patients with recurrent paroxysmal supraventricular tachycardia (PSVT), 25 of whom had accessory pathway reentrant tachycardia (APRT) and 11 A-V nodal reentrant tachycardia (AVNRT ; 10 of the slow-fast type one of the fast-slow type). The test drugs were procainamide (used in 19 patients), verapamil (in 27), disopyramide (in 31), and propranolol (in 15). The drugs were tested for their ability to terminate episodes of PSVT as well as to inhibit their induction. Procainamide had an inhibitory effect on APRT in nine of 12* patients (75%9 and terminated episodes of APRT in seven of 11* patients (63.6%); in all of them V-A block was responsible for the termination. In four of six* patients (66.7%) with slow-fast AVNRT and in one patient with fast-slow AVNRT, inhibition of the induction of tachycardia attacks was noted after procainamide. Termination of AVNRT was seen in the same number of patients. Verapamil inhibited the induction of APRT in 12 of 18* patients (66.7%) and terminated episodes of APRT in 10 of 16* patients (62.5%), all by A-V block. In six of eight* patients (75%) with slow-fast AVNRT, inhibition of the induction as well as termination of tachycardia were noted after verapamil. Disopyramide had an inhibitory effect on APRT in seven of 23* patients (30.4%) and terminated APRT in five of 21* patients (23.8%) by V-A block, while AVNRT (all slow-fast type) was terminated in only one of eight* patients (12.5%) by disopyramide. Disopyramide was less effective than previously reported. This could be attributed to a relatively low dosage and slow infusion speed. This could be attributed to a relatively low dosage and slow infusion speed. Propranolol inhibited the induction of APRT and terminated episodes of APRT in only one of 10* patients (10%). In two of four* patients (50%) with slow-fast AVNRT, an inhibitory effect by propranolol was noted, but termination was seen in only one patients.
TL;DR: OPC-8212 may be promising for the treatment of congestive heart failure with reduced coronary flow reserve, probably because the increase in MV^^·O2 by positive inotropic effect is offset by a decrease in MV ^O2 due to a decreases in chamber size.
Abstract: The effect of a new inotropic agent, OPC-8212 (2(1H)-quinolinone derivative), on myocardial oxygen consumption (MV^^·O2) following intravenous administration (1 and 3 mg/kg/min) was studied in normal and ischemic failing hearts in open chest dogs. Ischemic failing heart was obtained by intracoronary injection of 15-μm microspheres and volume loading. OPC-8212 significantly increased LV mad dP/dt and decreased mean aortic pressure, whereas heart rate was not altered in both normal and failing hearts. Despite the remarkable positive inotropic effect, this agent did not increase MV^^·O2 in the normal hearts and even decreased MV^^·O2 in the ischemic failing hearts associated with a decrease in LV end-diastolic pressure and hence, LV chamber size. These results indicate that OPC-8212 does not increase myocardial oxygen demand, probably because the increase in MV^^·O2 by positive inotropic effect is offset by a decrease in MV^^·O2 due to a decrease in chamber size. Thus, OPC-8212 may be promising for the treatment of congestive heart failure with reduced coronary flow reserve.
TL;DR: The data suggest that myocardial edema may precede cellular infiltration during the rejection process and it may be suppressed with CYA treatment, which is useful in early detection of acute cardiac allograft rejection and for examining the therapeutic effects of CYA.
Abstract: To determine the changes in myocardial water during acute cardiac rejection and the effects of Ciclosporin (CYA) on the myocardial water, 90 heterotopic cardiac transplants were performed in rats which were divided into 3 groups, namely those receiving 1) Lewis × Lewis isografts, 2) Lewis × Brown Norway allografts and 3) CYA treated allografts (15 mg/kg/day). The water content was measured in both recipient and donor hearts at 2, 4, 6, and 8 days after transplant. Pathological specimens were examined by light and electron microscopy, and scored on a 0 to 4+ scale of increasing evidence of rejection. The water content of the isografts showed no significant change throughout the post operative period. In contrast, the allografts had significant increase of water content as early as 2 days after transplant, compared to the isografts and recipients hearts. A significant difference in cellular infiltration was noted between isograft and allograft 4 days after transplant. CYA suppressed significantly the increase of myocardial water and cellular infiltration in the allografts. These data suggest that myocardial edema may precede cellular infiltration during the rejection process and it may be suppressed with CYA treatment. The measurement of myocardial water may be useful in early detection of acute cardiac allograft rejection and for examining the therapeutic effects of CYA.
TL;DR: By depressing hypothalamic function, centrally injected GABA decreases sympathetic nerve activity to thereby lower blood pressure and heart rate, and in SHR, ICV-injected GABA reversed hypothalamo-sympathetic hyperactivity and thus attenuated hypertension.
Abstract: To determine the central effects of 4-Amino-n-butyric acid (GABA), pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were recorded following the intracerebroventricular (ICV) injection of GABA. In normotensive Wistar rats, anesthetized with urethane, ICV injections of GABA (50-200 μg) reduced sympathetic nerve activity, arterial blood pressure, and heart rate in a dose-dependent manner. Graded electrical stimulation of the ventromedial hypothalamus (50, 100, 150 μA) increased not only mean blood pressure but also the rate of sympathetic nerve firing, and both responses were attenuated by GABA pretreatment (100, 200 μg, ICV). In spontaneously hypertensive rats (SHR), ICV-injected GABA also reduced sympathetic and cardiovascular activity, but the magnitude of depressor responses was significantly larger in SHR than in normotensive Wister Kyoto controls (WKY). Pressor and sympathetic nerve responses elicited by ventromedial hypothalamic stimulation were initially larger in SHR than in WKY, but upon subsequent ICV injection of GABA, hypothalamic responsiveness in SHR was inhibited more prominently and became comparable to that in WKY. These results suggest that by depressing hypothalamic function, centrally injected GABA decreases sympathetic nerve activity to thereby lower blood pressure and heart rate, and in SHR, ICV-injected GABA reversed hypothalamo-sympathetic hyperactivity and thus attenuated hypertension.
TL;DR: The high score for postmyocarditis in DCM could suggest that prior myocarditis is an important causative factor of this disease.
Abstract: From our study employing serial endomyocardial biopsy in patients with acute viral or idiopathic myocarditis, we were able to construct histopathologic criteria for acute, subacute and convalescent myocarditis. We realize that it is difficult for the inexperienced observed to make an appropriate diagnosis of myocarditis or postmyocarditic changes in patients with dilated cardiomyopathy (DCM). In order to overcome this problem, each finding was graded and the scores obtained were analyzed statistically and compared with those from hypertrophic cardiomyopathy (HCM) and chronic right ventricular overloading (CRVO). The scores were obtained by summing the gradings for each of the following findings : increase of fibrocytes, increase of fibroblasts in the interstitium, hypertrophy of myocytes, fragmentation of muscle bundles, interstitial fibrosis, disarrangement of muscle bundles, abnormal branching, variation in size, increased glycogen deposition in the sarcoplasm, scarcity of myofibrils, and nuclear degeneration of myocytes and endocardial thickening. Since the increase in number of fibrocytes was considered important, its value was doubled. Scores in each group were as follows : convalescent myocarditis : 17.1 ± 4.7 (n=10), DCM : 13.2 ± 3.3 (n=47), HCM : 9.7 ± 2.4 (n=20), CRVO : 7.0± 3.6 (n=21). It was found that the scores for cases with myocarditis in the convalescent stage and in DCM were higher than those found for cases with either HCM and CRVO (p < 0.05). In summary, the high score for postmyocarditis in DCM could suggest that prior myocarditis is an important causative factor of this disease.
TL;DR: An autopsied patient who showed typical dilated cardiomyopathy (DCM)-like features and was pathologically diagnosed with hypertrophic cardiopathy (HCM) is presented and a diagnosis of HCM with features of DCM was made.
Abstract: An autopsied patient who showed typical dilated cardiomyopathy (DCM)-like features and was pathologically diagnosed with hypertrophic cardiomyopathy (HCM) is presented. The patient, a 60-year-old male at the time of death, died of intractable congestive heart failure. At autopsy the heart weighted 570g and showed marked left ventricular (LV) dilatation with a thin wall (ventricular septum/free wall of the LV=7mm/8mm). There was no evidence of significant stenosis in the extramural coronary arteries. Massive fibrosis was found in the middle and outer thirds of the ventricular septum and anterior wall of the LV (48% in the ventricular septum and 9% in the free wall of the LV). As myocytes were not present in the area with massive fibrosis, percent area of disarray was calculated excluding the area of massive fibrosis and found to be 30% in the ventricular septum. Based on the marked increase in the percent area of disarray, this case was diagnosed as HCM. The patient's 37-year-old son showed asymmetric septal hypertrophy on echocardiography (ventricular septum/posterior wall of the LV = 15mm / 11mm), marked LV hypertrophy on electrocardiography, and diffuse and marked disarray by endomyocardial biopsy. There were also LV dilatation (LV diastolic dimension =51 mm) and hypokinesis of the LV ; as a result, a diagnosis of HCM with features of DCM was made.
TL;DR: AV pacing provides a great improvement inleft ventricular filling, which cannot be obtained with V pacing even with the compensatory enhancement of left ventricular rapid filling, and these beneficial effects of AV pacing seemed to be greater in patients with impaired left vent cardiac rapid filling.
Abstract: There has been increased interest in the beneficial effects of atrio-ventricular (AV) pacing over ventricular (V) pacing. This study attempted to evaluate the changes in cardiac output and left ventricular filling dynamics when the pacing mode was switched from V pacing to AV pacing. Study population consisted of 26 patients with multiprogrammable AV pacemakers. Cardiac output was determined as a product of echocardiographically determined cross sectional area of the aortic annulus and Doppler-determined velocity integral of left ventricular outflow over systole. Left ventricular peak rapid filling rate (PFR) and peak atrial filling velocity to peak rapid filling velocity ratio (A/R) were determined from measurements at the mitral annulus. Cardiac output showed a significant improvement when the pacing mode was switched from V to AV pacing, and the percent change ranged from 3 to 73% (average 26%). The improvement in cardiac output brought about by AV synchrony was greater in patients with smaller PFR (r = -0.71, p less than 0.01) and larger A/R ratio (r = 0.77, p less than 0.01). On the other hand, PFR was greater with V pacing than with AV pacing. Greater increment of the PFR was produced by the loss of atrial contraction in patients with smaller PFR (r = -0.82, p less than 0.01) and larger A/R ratio (r = 0.76, p less than 0.01). Thus, AV pacing provides a great improvement in left ventricular filling, i.e., cardiac output, which cannot be obtained with V pacing even with the compensatory enhancement of left ventricular rapid filling. These beneficial effects of AV pacing seemed to be greater in patients with impaired left ventricular rapid filling.
TL;DR: In this article, 24-hour recordings of arterial pressure (AP) and heart rate (HR) were performed in 15 normotensives (NT) and 39 patients with essential hypertension (EH) by means of a new portable device with a digital memory for analyzing frequency histograms.
Abstract: For statistical analysis of 24-hour recordings of arterial pressure (AP) and heart rate (HR), it is necessary to establish a theoretical probability density function of the distributions. In the present study, 24-hour recordings of direct AP and HR were performed in 15 normotensives (NT) and 39 patients with essential hypertension (EH) by means of a new portable device with a digital memory for analyzing frequency histograms. In both NT and EH, frequency histograms of AP (systolic and diastolic AP) and HR during a 24-hour period showed bi-modal curves, whereas those made during sleep and waking produced asymmetrical patterns resembling Gamma distribution. From the AP and HR histograms made for each subject during sleep and waking, such parameters as mean (M), standard deviation, mode (Mo), skewness (Sk), kurtosis (K) and minimum values (Mi) were calculated. The Sk and M minus Mo were positive, and K was greater than 3 in both HR and AP histograms; the AP and HR histograms during sleep can be more correctly analyzed with Gamma distribution (mean parameter errors were less than 7.3%) than with Gaussian distribution (in this: S = O, M minus Mo = O, K = 3). The Mi would accord with the location parameter of the Gamma distribution.
TL;DR: This experiment is the first demonstration of the in vivo cardiotoxicity of ECP, which was mild and limited to the right ventricular wall, which differed from those in the mice with EMC virus inoculation, where both the right and left ventricles were involved.
Abstract: We studied the in vivo effects of eosinophilic cationic protein (ECP) on DBA/2 mice, and compared the cardiac lesions caused by ECP with those caused by encephalomyocarditis (EMC) virus. ECP caused myocarditis in two of five mice (40%), and EMC virus did so in five of five mice (100%). Cardiac lesions of ECP were mild and limited to the right ventricular wall, which differed from those in the mice with EMC virus inoculation, where both the right and left ventricles were involved. This experiment is the first demonstration of the in vivo cardiotoxicity of ECP.
TL;DR: Results indicate that an overnight urine specimens are available for assessing dietary intakes of Na and K, as well as protein and sulfur amino acids in field studies.
Abstract: The feasibility of using overnight urine as an alternative to 24-hr urine was examined on measures of dietary intake of sodium (Na), potassium (K) and protein as well as the sulfur amino acids, which are contained mainly in animal protein. It was also of interest whether urinary excretions of taurine (Tau : final metabolite of sulfur amino acids, contained mainly in animal protein) and excretions of 3-methylhistidine (3-MHis : the product of breakdown of skeletal muscle protein, quantitatively excreted into urine) were appropriate in assessing the dietary intake of animal protein and total protein, respectively. Overnight urine specimens were collected from 16 subjects (19 to 60 years old) with normotension or borderline hypertension without complications. Creatinine (Cr) ratios to Na, K, urea nitrogen (UN) and inorganic sulfate (SO4) derived from overnight urine and from 24-hr urine specimens showed significant correlations . Similar correlations were also found for the Na/K and SO4/UN rations between overnight and 24-hr urine specimens. Concentrations of Tau and 3-MHis ( mmol per g Cr) of overnight urine specimens were strong correlated with 24-hr urinary excretions of Tau and 3-MHis (μmol per day), respectively. Furthermore, significant correlations were found between 24-hr urinary excretions of UN and 3-MHis and between those of SO4 and Tau. These results indicate that an overnight urine specimens are available for assessing dietary intakes of Na and K, as well as protein and sulfur amino acids in field studies.
TL;DR: The exercise tolerance in post-operative tetralogy patients was found to be within the normal range as long as their hemodynamic operative result was satisfactory, but the limited capability of increasing heart rate with exercise could present a potential problem in the long-term prognosis.
Abstract: Twenty-one patients with tetralogy of Fallot following intracardiac repair underwent a treadmill test for evaluation of their exercise capacity. They were divided into two groups according to their post-operative hemodynamic status, the good results group and the poor result group. The maximum oxygen consumption during exercise was significantly decreased in the poor result group, but that of the good result group showed no significant difference from the control group. However, the maximum heart rate in both the good and the poor result groups was significantly lower than that of the control group. Thus, the exercise tolerance in post-operative tetralogy patients was found to be within the normal range as long as their hemodynamic operative result was satisfactory, but the limited capability of increasing heart rate with exercise could present a potential problem in the long-term prognosis.
TL;DR: The results suggest that AMN possesses a dominant vasodilating effect in addition to its inotropic effect, which would greatly benefit the treatment of refractory heart failure, and are the characteristic cardiovascular hemodynamic effects of as if catecholamine and a Vasodilator were combined.
Abstract: The hemodynamic effects of a newly developed inotropic agent, amrinone (AMN) were studied and compared with those of dopamine (DA) and dobutamine (DB) in forty patients with pump failure due to acute myocardial infarction. Hemodynamic measurements were taken using a Swan-Ganz thermodilution catheter before and 5, 10, 15, 30, 60, 90 and 120 minutes after intravenous injection of AMN (1-2 mg/kg) for 3 minutes in eight patients, and also before and during drip infusion (3-7 μg/kg/min) of DA in fifteen patients and DB in seventeen patients. AMN showed maximal increases in CI, SVI and SWI, and maximal lowering in CVP and SVR 5 minutes after intravenous injection, while maximal lowering in PCWP occurred 10 minutes after injection. These significant hemodynamic changes lasted for 60 minutes after injection. Comparing the maximal hemodynamic effects occurring 5 minutes after injection of AMN with those of DA and DB, it was found that AMN increased CI to almost the same degree as DA, and lowered CVP and PCWP much more compared to DB. These results suggest than AMN possesses a dominant vasodilating effect in addition to its inotropic effect, which would greatly benefit the treatment of refractory heart failure ; AMN are the characteristic cardiovascular hemodynamic effects of as if catecholamine and a vasodilator were combined.
TL;DR: It is postulated that hypertension has a deleterious effect on myocardial energy metabolism in ischemic heart, even when cardiac mechanical function is maintained.
Abstract: The difference between normotensive rats (WKY) and spontaneously hypertensive rats (SHR) in functional and metabolic responses to ischemia was studied. Systolic arterial blood pressure of SHR (171.2 ± 2.9 mmHg) was significantly higher than that of WKY (135.3 ± 1.2 mmHg), and the left ventricular mass of SHR was larger than that of WKY. Hearts isolated from either WKY or SHR were perfused by the working heart technique. Ischemia was induced by lowering the afterload pressure of the working heart. Ischemia produced cardiac arrest, and decreased the tissue levels of adenosine triphosphate and creatine phosphate in both WKY and SHR. Recovery of mechanical function of the heart during reperfusion following ischemia in SHR was better than that in WKY, while recovery of the high-energy phosphates level in SHR was less prominent than in WKY. It is postulated that hypertension has a deleterious effect on myocardial energy metabolism in ischemic heart, even when cardiac mechanical function is maintained.
TL;DR: A case of right adrenal pheochromocytoma masquerading as a dilated cardiomyopathy masqueraders as well as the findings of increased plasma and urinary epinephrine and norepinephrine values is described.
Abstract: A case of right adrenal pheochromocytoma masquerading as a dilated cardiomyopathy is described. This patient was normotensive throughout 8 years of observation. Hyperglycemia and an abnormal glucose tolerance test were a clue to the diagnosis which was confirmed by the findings of increased plasma and urinary epinephrine and norepinephrine values. In patients with dilated cardiomyopathy the possibility of a pheochromocytoma should be considered.
TL;DR: PEEP and ECUM are beneficial for patients with refractory heart failure due to reduction in preload due to an increased intrathoracic pressure and a decreased systemic venous return with PEEP, or due to removal of excess fluid with ECUM, and improvement of the oxygenation of the blood.
Abstract: We studied the effects of positive end-expiratory pressure (PEEP) ventilation in ten patients with acute myocardial infarction (nine in Killip class III, one in Killip class IV; pulmonary capillary wedge pressure greater than 24 mmHg) and of extracorporeal ultrafiltration method (ECUM) in seven patients with refractory heart failure due to acute myocardial infarction and others. Application of PEEP resulted in significant increases in PaO2 and SaO2 and decrease in PaCO2. Significant reduction in mean pulmonary arterial and pulmonary capillary wedge pressures and heart rate was observed, while stroke work index increased significantly. There was a significant correlation between changes in stroke work index and PaO2 after the application of PEEP. The use of ECUM removed fluid of 1416 +/- 662 ml (680-2800 ml) with the ultrafiltration flux rate being 478 +/- 223 ml/hour. Significant decreases in mean pulmonary arterial, pulmonary capillary wedge and central venous pressures were observed, while PaO2 increased significantly. BUN and serum creatinine levels increased significantly, and total protein and serum albumin tended to increase. There was a significant correlation between fluid removed and change in PaO2 after the use of ECUM. Thus, PEEP and ECUM are beneficial for patients with refractory heart failure. The mechanism(s) are: reduction in preload due to an increased intrathoracic pressure and a decreased systemic venous return with PEEP, or due to removal of excess fluid with ECUM, and improvement of the oxygenation of the blood.
TL;DR: It is suggested that insulin attenuates the pressor responsiveness to alpha agonist and angiotensin II, which may be one of the significant mechanisms in insulin-induced vasodilation.
Abstract: The effects of insulin on pressor responsiveness to α agonist (phenylephrine) and angiotensin II, and baroreflex function were studied in fifteen diabetic patients without autonomic neuropathy. The dose of phenylephrine required to increase systolic pressure by 25 mmHg (PD25) was significantly increased from 38 ± 7 to 62 ± 9 μg (p < 0.05) after IV injection of 4 U of Actrapid monocomponent insulin. The dose of angiotensin II required to increase systolic pressure by 30 mmHg (AD30) was also increased from 0.29 ± 0.07 to 0.48 ± 0.10 μg (p < 0.01). Following insulin administration, the dose-response curves for phenylephrine and angiotensin II were shifted to the right. The baroreflex sensitivity was not affected by insulin. In contrast, there was no significant change in PD25, AD30 or baroreflex sensitivity after the injection of saline. These results suggest that insulin attenuates the pressor responsiveness to α agonist and angiotensin II, which may be one of the significant mechanisms in insulin-induced vasodilation.