[Image and biochemical diagnosis of acute myocardial infarction].
Explore the source record for details and available documents.
Antibodies, Monoclonal↗
Biomedical subjects
K Yamaoki
Publications and source records attributed to K Yamaoki.
Effect of long-term treatment with beta-blocker on cardiac hypertrophy in SHR.
Recent studies suggest that beta-blocker treatment may attenuate cardiac hypertrophy induced by pressure overload in the spontaneously hypertensive rat (SHR), but the effect of this therapy on the reconstitution of the intracellular constituents in the heart that occurs during the development of cardiac hypertrophy has not been examined. In this study, we investigated the effect of chronic administration of carteolol (4 mg/kg/day p.o.) or propranolol (20 mg/kg/day p.o.), beta-blockers with distinct modes of action, on the composition of cardiac myosin isozymes and histological findings as well as heart weight. Therapeutic periods were 4, 12 or 30 weeks. Though blood pressure was not significantly reduced, the development of cardiac hypertrophy was suppressed as evidenced by left ventricular weight in both groups of carteolol- and propranolol-treated SHR for all therapeutic periods. Again, beta-blocker treatment for 12 weeks alleviated myocardial degeneration and reactive fibrosis which were observed in all cases of age-matched untreated SHR. However the extent of the transition of cardiac myosin isozymes from V1 to V2 or V3 were essentially the same among all groups including untreated SHR. These results indicate that chronic administration of beta-blockers attenuates the development of cardiac hypertrophy and degeneration without affecting the transition of myosin isozymes which is thought to be a kind of biochemical adaptation of the myocardium to overload.
Adrenergic beta-Antagonists↗
Endothelin: a potent vasoconstrictor associated with coronary vasospasm.
Endothelin, administered into the coronary arteries of anesthetized dogs, produced a profound and long-lasting reduction in coronary blood flow with electrocardiographical evidence of myocardial ischemia. Coronary angiography revealed delayed filling of the distal branches and, in some cases, cessation of the blood flow distal to the epicardial portions of coronary arteries. The coronary vasoconstriction induced by endothelin subsided after intracoronary administration of nitroglycerin. Pretreatment with the Ca2+-channel antagonist, nitrendipine, suppressed endothelin-induced vasoconstriction. These findings suggest that endothelin, produced by vascular endothelial cells, may contribute to the pathogenesis of coronary vasospasm.
Animals↗
The possible role of endothelin-1 in the pathogenesis of coronary vasospasm.
We investigated the in vivo vasoconstrictor effects of endothelin-1 (ET-1) on canine coronary arteries and the regulation of ET-1 gene expression with special reference to the pathogenesis of coronary vasospasm. ET-1, administered into the coronary arteries of anesthetized dogs, produced a profound and long-lasting reduction in coronary blood flow with myocardial ischemia. Coronary angiography revealed delayed filling of the distal branches and, in some cases, total occlusion in the epicardial portions of coronary arteries. The coronary vasoconstriction induced by ET-1 subsided after intracoronary administration of nitroglycerin. Pretreatment with the Ca2+-channel antagonist, nitrendipine, suppressed ET-1-induced vasoconstriction. In cultured porcine aortic endothelial cells, ET-1 gene expression was induced by agents related to thrombus formation, such as thrombin and transforming growth factor beta (TGF beta). These findings suggest that ET-1, produced by vascular endothelial cells, may contribute to the regulation of coronary circulation and the pathogenesis of coronary vasospasm with respect to intimal injury and subsequent thrombus formation.
Angiocardiography↗
Quantification of myocardial infarct size after coronary reperfusion by serum cardiac myosin light chain II in conscious dogs.
The effects of early coronary artery reperfusion on the relation between the extent of myocardial infarction and serum levels of cardiac myosin light chain II or plasma creatine kinase levels were evaluated in the conscious dog. Hydraulic occluders were placed on the left anterior descending arteries of 38 dogs. Seven to 10 days later, myocardial infarction was produced. Coronary reperfusion was performed 3 hours (group A1, n = 13) and 6 hours (group A2, n = 12) after the occlusion. In the other 13 dogs, coronary occlusion was sustained throughout the course of the experiment (group B). Seven days after the occlusion, the heart was cut from the apex to the base into 4-mm slices, and infarct size was determined macroscopically. Rapid appearance and early peaking of creatine kinase were observed in group A. Cumulative release of creatine kinase significantly correlated with infarct size in group A (infarct size ranged from 0.1 to 20.1 g, r = 0.90) and group B (from 0.6 to 26.8 g, r = 0.91). However, since creatine kinase release in group A was greater in comparison with that from infarcts of the same size in group B, the slope of the regression line for group A was significantly steeper (p less than 0.05). Cardiac myosin light chain II appeared as early as creatine kinase did and continued to be elevated for 7 days. A very close relation was observed between infarct size and total cardiac myosin light chain II release (r = 0.87 for group A, and r = 0.88 for group B) or peak level of light chain II (r = 0.85 for group A, and r = 0.81 for group B). In addition, the slopes of the regression lines for infarct size and both peak and total release of light chain II did not differ between group A and group B. On histological examination, viable myocardium was frequently observed in the epicardium of the ischemic area in group A1; therefore, infarct size was greater in group B than in group A1 (p less than 0.05). Also, myocardial creatine kinase content in the epicardium of the center of the ischemic area in group A1 was greater than that in group B. Cardiac myosin light chain II release in group A1 was less than that in group B, whereas no difference was found in plasma creatine kinase release among groups A1, A2, and B.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
High renin hypertension in the elderly.
This paper describes clinical features of high renin hypertension in the elderly. Peripheral plasma renin activity ranged from 0 to 20.1 ng/ml/hr in 59 hypertensive in-patients aged 70 to 86. The patients were divided into 2 groups: 9 cases with plasma renin activity greater than or equal to 3.0 ng/ml/hr (high renin group) and the remaining 50 with plasma renin activity less than 3.0 ng/ml/hr (control group). The development of hypertension differed between the 2 groups. Six of the high renin group (66.7%) had a history of acceleration of previously mild hypertension, while only 3 of the control group (6.0%) had this history (p less than 0.01). The frequencies of high diastolic blood pressure (greater than or equal to 120 mmHg), massive proteinuria (at least 3.0 g/day), hypokalemia (serum potassium less than or equal to 3.0 mEq/L) and high serum cholesterol (greater than or equal to 250 mg/100 ml) were significantly greater in the high renin group than in the control group (p less than 0.01, respectively). Renovascular hypertension was suspected in 6 patients from the high renin group (66.7%), as compared with 1 of the control group (2.0%) (p less than 0.001). There was massive proteinuria in 3 of 6 patients with renovascular hypertension in the high renin group and 2 showed nephrotic syndrome. Thus, two-thirds of the elderly patients with high renin hypertension had probable renovascular hypertension with a history of rapid progression of hypertension.
Aged↗
Evaluation of regurgitant fraction of the left ventricle by gated cardiac blood-pool scanning using SPECT.
Regurgitant fraction (RF) of patients with and without mitral regurgitation (MR) and/or aortic regurgitation (AR) was evaluated by gated cardiac blood-pool scanning using single photon emission computed tomography (SPECT). Using the stroke count image of a short-axis tomogram to separate the right atrium and ventricle, the left ventricular stroke count (LVSC) and right ventricular stroke count (RVSC) were determined. The RF equaled (LVSC - RVSC)/LVSC. Calculated RF in 14 subjects without significant regurgitation by contrast angiography was 5.8 +/- 5.9% (mean +/- s.d.), RF of 17 cases with angiographic regurgitation was 42.5 +/- 16.8% (p less than 0.001). The sensitivity of the radionuclide method compared to angiography was 94% (16/17 cases), and specificity was 100% (14/14 cases). RF of mild Re (1+ or 2+) was 26.0 +/- 8.9% (n = 6) and RF of severe Re (3+ or 4+) was 51.5 +/- 12.7% (n = 11) (p less than 0.001). Correlation between the RF determined with the radionuclide method and with cardiac catheterization was good (y = 5.85 + 0.700 x, r = 0.821, n = 17). We conclude that RF of MR and/or AR can be accurately evaluated by gated cardiac blood-pool scanning using SPECT.
Cardiac Catheterization↗
Transmitral reversed blood flow during mid- and end diastole in constrictive pericarditis.
Explore the source record for details and available documents.
Adult↗
Peculiar mitral valve and papillary muscle lesions induced by vagus manipulations in rabbits. An experimental model for nonrheumatic mitral regurgitation.
Peculiar lesions of mitral valves and papillary muscles developed in 50 to 80% of rabbits after clipping (N = 38), crushing (N = 15) or electrical stimulation (N = 44) of their cervical vagi. Both right and left vagus manipulations induced similar cardiac lesions. The earliest manifestation was bleeding of the mitral leaflets, which was followed by swelling and fibrosis of the papillary muscles. Ventricular arrhythmias and systolic murmurs were frequently associated with the vagus manipulations. During or just after electrical stimulation of the vagus, ventricular premature contractions (VPCs) were observed in 30 of 44 animals. Twenty-nine of these 30 animals with VPCs (96.7%) were found to have mitral valve and/or papillary muscle lesions at autopsy, whereas only 5 of 14 animals without VPCs (35.7%) had the cardiac lesions. These results indicate that the occurrence of these ventricular arrhythmias during vagus manipulations was closely related with the mitral valve and papillary muscle lesions.
Animals↗
[Single Master's two step test and arrhythmias].
Explore the source record for details and available documents.
Adult↗
[High renin hypertension in the elderly].
Explore the source record for details and available documents.
Aged↗
Effects of steroid treatment on release of cardiac myosin light chain II in acute myocardial infarction in dogs.
The effect of methylprednisolone sodium succinate (MP) on release of myosin light chain II (LCII) from the myocardium was studied in experimental myocardial infarction (MI). Acute MI was produced in conscious, closed-chest dogs by ligating the left anterior descending coronary artery beyond the first diagonal branch. MP, 30 mg/kg, was administered intravenously just before and 24 hours after MI. After MI, LCII levels in the serum were determined serially up to 240 hours. MI size was determined histologically 10 days after MI. In the MP group, LCII levels in the serum within 72 hours were lower than in the control, and cumulative LCII release for 3 days decreased from 530 +/- 159 to 310 +/- 101 ng/ml (mean +/- standard deviation) (p less than 0.001). However, the peak LCII level appeared later (control vs MP, 63 +/- 27 vs 122 +/- 25 hours, p less than 0.001), and the peak LCII level and cumulative LCII release for 10 days were not decreased by MP treatment. MI size also was not reduced by MP (11.0 +/- 4.4% vs 11.8% +/- 4.5% of the left ventricle, difference not significant). Since the rate of disappearance of LCII is rapid and was not affected by MP, these results suggest that MP treatment early after acute MI delays breakdown of myosin filaments, but cannot prevent it.
Acetylglucosaminidase↗
Reduced number of erythrocyte sodium pump units in essential hypertension.
The number of sodium pump units of erythrocytes measured with ouabain binding assay was significantly lower in 17 patients with essential hypertension (0.538 +/- 0.020 pmol/10(9) cells) than in 13 normotensive controls (0.673 +/- 0.031 pmol/10(9) cells) (p less than 0.01) and it was inversely correlated with erythrocyte sodium concentration (r = -0.86, p less than 0.01).
Adult↗
Reconstitution of heavy chain and light chain 1 in cardiac subfragment-1 from hyperthyroid and euthyroid rabbit hearts.
It is now established that cardiac myosin from hyperthyroid rabbit hearts (TXM) exhibits high Ca2+ ATPase activity. The high Ca2+ ATPase activity of TXM was completely retained in cardiac myosin subfragment-1 (S-1) (1.33 +/- 0.04 mumol Pi/mg per min; euthyroid, 0.51 +/- 0.04). Cardiac S-1 from hyperthyroid and euthyroid rabbits (TXS-1 and NS-1) had the same pattern in SDS-polyacrylamide gel electrophoresis. The possible influence of heavy and light chains of TXM on increasing the ATPase activity was examined by reconstitution in the S-1 preparation. Crosswise reconstitution was performed using cardiac S-1 heavy chain (90,000 daltons) and light chain 1 (LC1) (27,000 daltons) from hyperthyroid and euthyroid hearts. Reconstitution was verified by using radiolabeled LC1. More than 95% of S-1 was recovered with full ATPase activity. When TXS-1 was reconstituted with LC1 from euthyroid hearts, the reconstituted molecule retained high ATPase activity. On the other hand, NS-1 reconstituted with LC1 from hyperthyroid hearts failed to increase the ATPase activity. The ATPase activity of S-1 was determined by the source of the heavy chain. These results suggest that the high Ca2+ ATPase activity of cardiac myosin and S-1 from hyperthyroid animals arises from the molecular alteration of the heavy chain induced by thyroxine administration.
Animals↗
Serial changes in cytosolic, mitochondrial, and lysosomal enzymes and cardiac myosin light chain II in plasma following coronary ligation in conscious closed-chest dogs.
We studied serial changes in various myocardial enzymes and cardiac myosin light chain II (LCII) in plasma following coronary ligation in 14 conscious closed-chest dogs. Cytoplasmic enzymes [creatine phosphokinase (CPK) and supernatant glutamic oxaloacetic transaminase (sGOT)] reached maximum at 12-24 hr and returned to normal at 72-96 hr. The mitochondrial isozyme of GOT (mGOT) began to rise at 6-9 hr, peaked at 12-30 hr (4.8-42.2 IU/liter), and stayed higher at 96 hr than before infarction. Glutamate dehydrogenase (GLDH), another mitochondrial enzyme, began to elevate at 6-16 hr and reached maximum at 24-60 hr (6.2-20.5 U/liter); GLDH also showed higher levels at 96 hr than before infarction. N-Acetyl-beta-glucosaminidase (NAG), a lysosomal enzyme, showed a biphasic pattern in every case. The first peak appeared at 3-12 hr, and the second one at 36-72 hr. Myosin LCII began to rise at 3-9 hr, peaked at 30-120 hr (34-136 ng/ml), and remained elevated for 7 to 10 days. Determination of these myocardial enzymes or LCII in plasma is useful for the diagnosis of acute myocardial infarction.
Acetylglucosaminidase↗
Myocardial infarct size from serum cardiac myosin light chain. Clinical and experimental studies.
The relationship between myocardial infarct size and serum cardiac light chain (LC) levels was studied in experimental and clinical myocardial infarction. In dogs with left anterior descending coronary artery occlusion, regression analysis showed good correlation between infarct size and LC II release, but CPK-MB release failed to correlate with infarct size because of a decreasing value of cumulative CPK with larger sized infarctions. In patients with acute myocardial infarction, Peak LC I levels correlated well with CPK release, since the phenomenon of the decreased CPK release in larger sized infarction was not so distinctive in human cases. Thus, LC determination may better quantitate the extent of myocardial damage as well as provide a specific and sensitive method for diagnosis of acute myocardial infarction.
Animals↗
Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes.
The relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.
Animals↗
An extensive primary myocardial fibrosis in progressive systemic sclerosis--a case report with autopsy findings.
An extensive myocardial fibrosis due to progressive systemic sclerosis (PSS) was described in a 36-year-old normotensive woman without pulmonary hypertension. An electrocardiogram showed low voltage and a pseudo-infarctional pattern in leads V1 through V3. Right ventricular dilatation and generalized left ventricular hypokinesis were present, but her pulmonary artery pressure was normal. Serum creatine kinase (CK) was elevated to 2305 U/L and CK-MB isoenzyme was as high as 7.1%. Simultaneously performed isoenzyme analysis of CK from the homogenate of the skeletal muscle of the patient showed a similar pattern, thus confirming that serum CK originated mainly from the skeletal muscle lesions. Autopsy findings demonstrated diffuse myocardial fibrosis and relatively unremarkable changes in the lungs and the kidneys. Our case serves as a warning that primary myocardial fibrosis could be, in some cases, so extensive that it might lead to a rapidly aggravated myocardial dysfunction and eventual death.
Adult↗