Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the early topographic changes after acute transmural myocardial infarction, we studied 28 patients during the first two weeks after infarction by serial two-dimensional echocardiography. Regional end-diastolic segment lengths and wall thicknesses for anterior and posterior left ventricular walls were calculated. Eight patients showed infarct expansion, with disproportionate dilatation and transmural thinning in the infarcted zone, that was significantly different (P less than 0.005) from changes in non-infarcted regions. This regional expansion led to an overall left ventricular dilatation in these eight patients of 25 per cent compared to 5 per cent in the 20 patients without infarct expansion. Although the eight patients with regional expansion did not have significantly higher peak creatine kinase or Killip classification, they had a significantly greater eight-week mortality (four of eight versus none of 20, P less than 0.004). Thus, regional cardiac dilatation may be an early, lethal consequence of transmural infarcts, and appears to be an important mechanism of acute cardiac dilatation after myocardial infarction.
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PMID:Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography. 75 78

Low-dose intravenous nitroglycerin infusion can be safely administered during acute myocardial infarction to unload the left ventricle and salvage ischemic myocardium and left ventricular geometry and function. In an experimental conscious dog model, low-dose infusion titrated to decrease mean blood pressure by 10% over the first 6 hours after coronary artery ligation resulted in 51% decrease in infarct size, 54% decrease in preload, and more than 50% increase in collateral blood flow. The same benefits were seen when methoxamine was given to counteract that 10% decrease in blood pressure. Similar short-term nitroglycerin infusion also limited remodeling in the dog model. More important, no myocardial salvage was seen with excessive nitroglycerin-induced hypotension to levels less than 80 mm Hg. Clinically, prolonged low-dose nitroglycerin infusion was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients with acute infarction: 154 received nitroglycerin and 156 received placebo. Nitroglycerin was titrated to reduce mean blood pressure by 10% in normotensive patients and up to 30% in hypertensive (blood pressure greater than 140/90 mm Hg) patients, but not to less than 80 mm Hg. Nitroglycerin produced several benefits compared with placebo: (1) smaller creatine kinase infarct size; (2) less regional left ventricular dysfunction, better global ejection fraction, and less infarct expansion and thinning; (3) better clinical functional status and hemodynamics; (4) fewer inhospital complications such as acute left ventricular failure and dilation due to marked infarct expansion, left ventricular thrombus, cardiogenic shock, and infarct extension; and (5) fewer deaths up to 1 year in patients with anterior Q-wave infarction.
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PMID:Intravenous nitroglycerin unloading in acute myocardial infarction. 183 97

The ultrastructure of skeletal muscle and activity of some enzymes of energy metabolism were studied to assess the effect of a deficiency of dietary energy and subsequent nutritional rehabilitation in 24 young, growing, healthy rhesus monkeys. Electron microscopy of muscles on energy-deficient animals showed thinning of myofibrils with widening of interfibrillar space and enlargement and accumulation of mitochondria at subsarcolemmal level. There was an apparent significant reduction in the fiber size. Muscle samples from each animal were analyzed for enzymes representative of glycolysis (phosphofructokinase [PFK] and lactate dehydrogenase [LDH], citric-acid cycle (isocitric dehydrogenase [ICDH] and citrate synthase [CS] and regeneration of ATP (creatine kinase [CK]. PFK and LDH activities were significantly augmented in energy-deficient animals. The increase in LDH activity resulted from a large increase in MU (skeletal muscle) LDH subunit. The activities of CS and ICDH were reduced. No alteration of CK in muscle and serum was observed. The morphological structure and enzyme activities returned to normal after nutritional rehabilitation.
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PMID:Ultrastructure and activity of some enzymes of energy metabolism of skeletal muscle in experimental energy deficiency. 310 25

To determine 1) whether the effect of intravenous nitroglycerin (NG) therapy during acute myocardial infarction on creatine kinase infarct size is influenced by infarct location (anterior vs. inferior), timing (therapy less than 4 hours vs. greater than or equal to 4 hours after onset of pain), and dose response (mean blood pressure greater than or equal to 80 mm Hg vs. less than 80 mm Hg during the first 12 hours) and 2) whether NG therapy modifies infarct expansion, 310 patients were randomly allocated to NG (n = 154) and control (n = 156) groups. NG infusion was titrated to lower mean blood pressure by 10% in normotensive and 30% in hypertensive patients, but not below 80 mm Hg, and was maintained for 39 hours. Measurements included clinical variables, creatine kinase infarct size (geq) as well as left ventricular (LV) asynergy, LV ejection fraction, expansion index, and thinning ratio on serial two-dimensional echocardiography. Compared with controls, creatine kinase infarct size was less in the NG group (41 vs. 55 geq, p less than 0.001), in anterior (44 vs. 58 geq, p less than 0.05), and inferior (39 vs. 53 geq, p less than 0.025) NG subgroups, and in early than late NG subgroups (43% vs. 22% decrease). Other indexes of infarct size also improved (p less than or equal to 0.05) with NG compared with controls. Thus, by 10 days, LV asynergy was 40% less, LV ejection fraction was 22% more, and Killip class score was 41% less. A negative effect of mean blood pressure less than 80 mm Hg with NG was reflected in these indexes. In addition, expansion index increased (p less than 0.001) by 31% and thinning ratio decreased (p less than 0.001) by 17% in controls by 10 days but remained unchanged with NG. Infarct-related major complications were less frequent in the NG than the control groups: infarct expansion syndrome (2% vs. 15%, p less than 0.0005), LV thrombus (5% vs. 22%, p less than 0.0005), cardiogenic shock (5% vs. 15%, p less than 0.005), and infarct extension (11% vs. 22%, p less than 0.025). Mortality was less in NG than in control groups in-hospital (14% vs. 26%, p less than 0.01), at 3 months (16% vs. 28%, p less than 0.025) and 12 months (21% vs. 31%, p less than 0.05), but this advantage was only found in the anterior subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location. 313 26

Two groups of chronically instrumented, conscious baboons were studied. The effects of coronary artery occlusion for 3 hours and reperfusion for 1 week were examined on measurements of left ventricular function, ischemic-zone wall thickness, regional myocardial blood flow, arrhythmias, and extent of necrosis. The experimental group of animals (n = 7) was treated with the calcium channel blocker nisoldipine (0.1 microgram/kg/min) from 1 hour after coronary occlusion to 3 hours after coronary reperfusion. The control group (n = 6) received the vehicle (n = 4) or saline (n = 2). The effects of coronary artery occlusion and reperfusion on arterial pressure, left ventricular systolic pressure, heart rate, and left ventricular dP/dt were similar in both groups. Systolic wall thickening was reversed to paradoxical wall thinning during occlusion in both groups, and there was no recovery to systolic wall thickening over the 1-week period in either group. There were differences in regional blood flow; during coronary artery occlusion, nisoldipine increased blood flow significantly in the endocardium and epicardium of nonischemic and ischemic zones. There was a major difference in the number of arrhythmic beats per minute on reperfusion; during reperfusion, the number of arrhythmias rose markedly in the vehicle-treated group but actually fell in the nisoldipine-treated group. The size of areas at risk, infarcts, infarcts related to the area at risk, and amount of total creatine kinase (CK) and MB-CK appearing in blood were not significantly different in the two groups. Thus, in the conscious baboon, nisoldipine administered 1 hour after coronary artery occlusion exerted a marked effect in diminishing reperfusion-induced arrhythmias and improved blood flow to the ischemic zone during occlusion but did not salvage ischemic tissue.
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PMID:Effects of calcium channel blocker on responses of blood flow, function, arrhythmias, and extent of infarction following reperfusion in conscious baboons. 333 53

To investigate the clinical application of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI) in the management of acute myocardial infarction (AMI), we examined 44 patients with AMI within 1 month after onset. Enhanced images were classified into 4 types: nontransmural (type 1), transmural and homogeneous (type 2), transmural and marginal (type 3), and no enhancement (type 4). Each enhancement pattern was correlated with angiographic and thallium-201 imaging results. The redistribution images of thallium were graded on a 4-point scale from 0 (normal) to 3 (markedly reduced or absent activity). The percentage of the perimeter affected by asynergy was obtained from the left ventriculogram. Peak creatine kinase and the percentage of asynergic perimeter were significantly higher in type 3 than in other type patients. End-diastolic volume index was significantly higher in type 3 than in type 2 patients. Left ventricular ejection fraction was lowest, and end-systolic volume index, thallium-201 score, and incidence of wall thinning on MRI were highest in type 3 patients. Therefore, the transmural and marginal enhancement pattern (type 3) was compatible with extensive myocardial infarction with infarct expansion and less viable myocardium. In the other types, the infarction was small to moderate in size and left ventricular function was well preserved. Thus, Gd-DTPA-enhanced MRI may be useful in the evaluation of left ventricular function and myocardial viability of the infarct region after AMI.
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PMID:Gadolinium-enhanced magnetic resonance imaging in acute myocardial infarction. 788 81

In order to forecast the clinical course of acute myocardial infarction (MI), the time course of the functional changes of the left ventricular myocardium that result in remodeling was evaluated with two-dimensional echocardiography (2DE). The study group comprised 45 patients with anterior MI treated with successful percutaneous transluminal coronary angioplasty. 2DE studies were performed on days 1, 3, 7 and 14; months 1 and 3 and 1 year after MI, and the following parameters were recorded: (1) infarcted wall thickness, (2) traced length of the endocardium and of the epicardium on end-diastolic apical long axis images, and (3) wall motion score (total of asynergy scores of 16 segments of left ventricle (LV); normal: 0, hypokinesis: 1, akinesis: 2, dyskinesis: 3). According to the peak creatine kinase (CK) level, patients were classified into L group (CK > or =8000 U/L, n=16), M group (8000> CK > or =4000, n=13) and S group (CK <4000, n=16). The following results were obtained. (1) There was progressive thinning of the infarcted myocardium up to 1 month after (1 day: 9.3+/-1.7, 14 days: 6.3+/-1.7 vs 1 month: 5.9+/-1.8 mm, p<0.05; vs 1 year: 5.9+/-1.9 mm, NS). (2) Dilatation of the LV cavity occurred shortly after MI and continued up to 14 days (endocardium at 14 days: 176.8+/-13.6 vs 1 day: 164.1+/-11.4 mm, p<0.01; vs 1 year: 176.3+/-12.7 mm, NS). (3) The wall motion score improved rapidly by 14 days, and continued to improve gradually to 1 year (1 day: 12.2+/-3.4, 14 days: 6.8+/-4.0, 1 year: 4.6+/-3.1). (4) The expansion ratio (endocardial length at 14 days/1 day) was significantly greater in the L group than in the S group (p<0.05). Comparing the groups, the LV cavity of the L group remained dilated up to 14 days, whereas that of the S and M groups was dilated up to 7 days (L group 14 days: 179.3+/-11.9 vs 1 day: 156.9+/-9.2mm, p<0.01; vs 1 year: 180.0+/-14.1 mm, NS) (S group 7 days: 171.7+/-13.6 vs 1 day: 161.5+/-7.2 mm, p<0.01; vs 1 year: 172.7+/-14.4 mm, NS) (M group 7 days: 170.5+/-10.5 vs 1 day: 157.7+/-14.5 mm, p<0.05; vs 1 year: 177.08+/-9.6 mm, NS). Serial 2DE on days 1 and 14 after MI were useful for evaluating the course of LV remodeling and to forecast cardiac function in the chronic phase of MI. Determining the length of hospital stay on the basis of infarction size is justified.
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PMID:Time course of left ventricular remodeling after myocardial infarction: a two-dimensional echocardiographic study. 1087 32

The aim of the present retrospective study was to clarify the histopathologic substrates of left ventricular myocardium with transient asynergy due to acute ischemic insult in man. Three patients who had had prolonged chest pain, new abnormal Q waves and new ST segment elevation were studied. There was no significant elevation of serum creatine phosphokinase activity in two of the three patients. Echocardiograms on admission or the next day showed severe hypokinetic or akinetic motion and thinning of the anteroseptal and apical portions of the left ventricle and regional dilatation of the same portions. Disappearance of the abnormal Q waves, ST segment elevation resolution, and early T wave inversion were observed later. Complete improvement of the echocardiographic abnormalities was confirmed after a few weeks in all patients. Manifest ischemic lesions of subendocardial scars of the anteroseptal region of the left ventricle were detected in only one of the three cases by gross examination. However, on microscopic examination, islands of necrotic myocytes were interspersed with islands of viable cells throughout the jeopardized region in one case, although the scattered necrotic foci were restricted to the subendocardium and the trabeculae. Normal myocardium and subendocardial scars were observed in the other two cases. In conclusion, left ventricular myocardium with transient asynergy. detected clinically during acute ischemic attack, consists of normal myocardium or small ischemic lesions primarily in the subendocardium.
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PMID:Clinicopathological characteristics of left ventricular myocardium with transient asynergy: report of three cases. 1138 83

Muscle ring finger (MuRF)1 is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates and heterodimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal, whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy, indicating cooperative control of muscle mass by MuRF1 and MuRF2. To identify the unique role that MuRF1 plays in regulating cardiac hypertrophy in vivo, we created transgenic mice expressing increased amounts of cardiac MuRF1. Adult MuRF1 transgenic (Tg(+)) hearts exhibited a nonprogressive thinning of the left ventricular wall and a concomitant decrease in cardiac function. Experimental induction of cardiac hypertrophy by transaortic constriction (TAC) induced rapid failure of MuRF1 Tg(+) hearts. Microarray analysis identified that the levels of genes associated with metabolism (and in particular mitochondrial processes) were significantly altered in MuRF1 Tg(+) hearts, both at baseline and during the development of cardiac hypertrophy. Surprisingly, ATP levels in MuRF1 Tg(+) mice did not differ from wild-type mice despite the depressed contractility following TAC. In comparing the level and activity of creatine kinase (CK) between wild-type and MuRF1 Tg(+) hearts, we found that mCK and CK-M/B protein levels were unaffected in MuRF1 Tg(+) hearts; however, total CK activity was significantly inhibited. We conclude that increased expression of cardiac MuRF1 results in a broad disruption of primary metabolic functions, including alterations in CK activity that leads to increased susceptibility to heart failure following TAC. This study demonstrates for the first time a role for MuRF1 in the regulation of cardiac energetics in vivo.
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PMID:Cardiac muscle ring finger-1 increases susceptibility to heart failure in vivo. 1949 99

Angiotensin II receptor blockers (ARBs) are used for the treatment of patients with heart failure and hypertension. Yet their safety has been questioned by some who observed delayed cardiac healing and scar thinning after myocardial infarction (MI). To clarify potential efficacy and safety of ARBs, we administered Azilsartan medoxomil, a prodrug of an ARB (Takeda Pharmaceutical Company Limited), assessed cardiac fibrosis (hydroxyproline content), left ventricular (LV) wall thickness (premortem echocardiography and caliper measurement at necropsy), and LV mass and cardiac function with high-resolution ultrasound in mice with either surgically induced LV pressure overload (aortic banding) or acute MI. Drug-treated aortic-banded mice exhibited less LV wall thickness, hypertrophy, and dilation compared with that exhibited by controls. Survival in drug-treated MI mice was greater though not significantly. Drug-treated mice with acute MI exhibited less cardiomyocyte injury reflected by LV creatine kinase content and less LV hypertrophy and dilation. Thus, Azilsartan exerted favorable biological effects on the hearts of mice subjected to LV pressure overload or MI without compromising survival consistent with its potential utility and tolerability in patients with analogous conditions.
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PMID:The efficacy and tolerability of azilsartan in mice with left ventricular pressure overload or acute myocardial infarction. 2342 90


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