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)

When fed furazolidone, 700 ppm, with their mash, most turkey poults develop dilated cardiomyopathy characterized by gross left ventricular dilatation with thinning of both the left ventricular free wall and ventricular septum. Birds fed propranolol, but not digoxin, did not develop this cardiomyopathy. It is not known what pharmacologic property of propranolol conferred protection or if mammals would receive similar protection.
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PMID:Protection of turkeys against furazolidone-induced cardiomyopathy. 668 89

A 50-year-old South American Indian woman, a native of Brazil and now a resident of Shiga Prefecture, was admitted to our hospital because of dyspnea on exertion. We initially suspected dilated cardiomyopathy due to an enlarged and diffusely hypokinetic left ventricle (LV) on echocardiogram. Coronary arteriograms were normal, and histological examination of right ventricular endomyocardial biopsy specimens showed findings compatible with chronic myocarditis. Magnetic resonance imaging revealed localized thinning and a small apical aneurysm at the LV. Since she had previously lived in a high-risk region for Chagas' disease, two immunological examinations for Trypanosoma cruzi were performed. The results of both tests were compatible with the disease. Recently, an increasing number of patients with Chagas' disease have been found in the United States among immigrants from South American countries, and the risk of transmission of the disease through contaminated blood transfusion is becoming a national problem. We report this case with reference to the present state of the problem in the United States and the potential problems it presents in Japan because of the marked increase in the number of immigrants from the affected area.
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PMID:A highly suspected case of chronic Chagas' heart disease diagnosed in Japan. 765 15

Turkey poults fed furazolidone (Fz) in high concentrations (700 ppm) develop dilated cardiomyopathy (Fz-DCM). We tested whether five cardioactive agents were cardioprotective in this model of heart failure, ie, whether they prevented dilatation and wall thinning and improved contractile performance. We compared the effects of chronic administration of a beta 1-selective and a nonselective beta-receptor antagonist, an alpha-receptor antagonist, and two Ca2+ channel antagonists in the presence of Fz administration. The greatest cardioprotection was found with treatment with either propranolol or nifedipine. At the gross morphological level, the effect of propranolol (a nonselective beta-adrenergic antagonist) was greater than the effect of atenolol (a selective beta 1-adrenergic antagonist), and the effect of nifedipine was greater than that of verapamil (Ca2+ channel antagonists), with all agents more cardioprotective than phenoxybenzamine (an alpha 1-adrenergic > alpha 2-adrenergic antagonist). Differences in cardioprotective efficacy of each agent increased with increased concentration. These data indicate that the dose and choice of a specific type of Ca2+ channel antagonist or beta-receptor antagonist might be important in the treatment of dilated cardiomyopathy. All agents that were cardioprotective caused similar functional improvements at both the whole heart and isolated muscle levels. Compared with control animals, Fz-DCM animals showed a significant reduction in peak left ventricular (LV) developed pressure (92 +/- 17 versus 143 +/- 24 mm Hg, P < .05), +dP/dt (1151 +/- 219 versus 2454 +/- 549 mm Hg/s), and -dP/dt (1128 +/- 291 versus 1875 +/- 396 mm Hg/s), with a significant increase in LV end-diastolic volumes (2.8 +/- 0.7 versus 0.16 +/- 0.1 mL for control animals, P < .05). In contradistinction, LV + dP/dt and -dP/dt values for animals receiving Fz plus a cardioactive agent that demonstrated cardioprotection were not significantly different from control values. Peak LV developed pressures were also similar for Fz animals receiving an agent that demonstrated cardioprotection and control animals not receiving any pharmacologic agent. Isolated muscles from Fz-DCM animals as well as animals receiving Fz plus cardioprotective pharmacologic agents responded normally with regard to increasing extracellular Ca2+ concentrations. Peak twitch forces were greater for animals receiving cardioprotective agents plus Fz than control animals not receiving any pharmacologic agents or Fz alone. At higher stimulation rates, Fz-DCM muscles demonstrated a significantly reduced peak twitch force (4 +/- 0.5 versus 1.5 +/- 0.4 g/mm2 for control muscles versus Fz-DCM muscles, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differences in cardioprotective efficacy of adrenergic receptor antagonists and Ca2+ channel antagonists in an animal model of dilated cardiomyopathy. Effects on gross morphology, global cardiac function, and twitch force. 822 79

The pathomorphologic features of hypertrophic cardiomyopathy simulating dilated cardiomyopathy in the late stage (HCM-DCM) were compared with those of ordinary hypertrophic cardiomyopathy (HCM). Seven autopsied hearts with HCM-DCM and 11 with HCM were assessed quantitatively using an image analyzer. Unlike HCM, significant left ventricular enlargement and wall thinning were observed in HCM-DCM, and the percentage areas of massive fibrosis and disarray were significantly greater. In HCM-DCM, the disarray was distributed diffusely, whereas massive fibrosis was distributed more intensively in the ventricular septum and anterior wall than in the lateral and posterior wall. Narrowing of intramyocardial small arteries was observed more frequently in HCM-DCM, especially in the ventricular septum and anterior wall, than in HCM. These results suggest that the enlargement and wall thinning of the left ventricle in HCM-DCM are attributable to non-uniform progression of massive fibrosis, which is closely related to small-arterial lesions.
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PMID:Pathological analysis of hypertrophic cardiomyopathy simulating dilated cardiomyopathy. 834 7

M-mode echocardiography and Doppler were used to assess the effects of phosphodiesterase inhibition on subendocardial function in dilated cardiomyopathy, and in particular, to study interactions with both systolic and diastolic left ventricular function. Twelve adult patients with dilated cardiomyopathy were studied (6 ischemic in origin and 6 idiopathic), 7 of whom were being considered for cardiac transplantation. Cardiac index increased without significant change in heart rate or blood pressure. Longitudinal mitral ring motion, which had been uniformly reduced, increased markedly after intravenous milrinone. Left ventricular cavity size decreased, and shortening fraction, posterior wall thickness, and rates of posterior wall thickening and thinning increased markedly. Left atrial pressure decreased, and isovolumic relaxation time increased. However, the peak velocity and duration of the transmitral E wave increased, with no change in the A wave. Improved longitudinal (subendocardial) function was reflected by improved posterior wall dynamics, and early filling, possibly by augmentation of restoring forces. Thus, severely reduced subendocardial function in dilated cardiomyopathy is potentially reversible, with marked effects on systolic and diastolic function. These previously unrecognized actions of milrinone provide further evidence to justify its short-term use in supporting the severely depressed myocardium.
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PMID:Effects of intravenous milrinone on left ventricular function in ischemic and idiopathic dilated cardiomyopathy. 842 84

In the normal myocardium matrix metalloproteinases (MMP) are present in the latent form. To examine whether MMP are activated following infarction or idiopathic dilated cardiomyopathy (DCM), we extracted and measured MMP activity in tissue derived from 7 explanted, failing human hearts due to either previous myocardial infarction (MI) or DCM. MMP activity in infarcted left ventricle (LV), noninfarcted LV and right ventricle (RV) from MI patients, as well as tissue from either ventricle of DCM patients, were compared to the activity of donor heart tissue. SDS-PAGE and dye-binding assays were used to determine total protein concentration, while collagenase activity was measured by SDS-PAGE type substrate gels embedded with type I gelatin (zymography). Accuracy of the zymographic technique was shown for tissue samples as small as 0.05 mg and was comparable to results obtained by a spectrophotometric method. After normalization for total protein concentration, we found 3 +/- 1% collagenase activity in normal atrial tissue which could be activated to 80-90% by trypsin or plasmin, indicating that collagenase is normally inactive or in a latent form in human heart. In endo- and epimyocardium of infarcted LV, on the other hand, collagenase activity was 85-95% and 10-20%, respectively, while 5-10% and 3-5%, respectively, in noninfarcted LV. In DCM, collagenolytic activity in the endo and epimyocardium was 75 +/- 5 and 35 +/- 5% in the LV and 35 +/- 7 and 20 +/- 5% in the RV, respectively. Thus, in dilated failing human hearts secondary to previous MI or DCM, MMP activity is increased. This is particularly the case within the endomyocardium of the infarcted and noninfarcted portions of either ventricle with MI and in both ventricles in DCM. This suggests that an activation of collagenase throughout the myocardium may contribute to its remodeling that includes ventricular dilatation and wall thinning.
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PMID:Matrix metalloproteinase activity expression in infarcted, noninfarcted and dilated cardiomyopathic human hearts. 871 34

New indications have recently appeared for cardiac pacing with haemodynamic and antiarrhythmic objectives without any symptomatic bradycardia. The best documented indication, though relatively rare, is stimulation of obstructive hypertrophic cardiomyopathy; initially reserved for cases with favorable results of an acute haemodynamic test, it is now used in other cases without this criterion; hypertrophic cardiomyopathy without permanent obstruction, atrial fibrillation or left bundle branch block. The improvement observed during follow-up is always greater as a real remodeling of the myocardium seems to occur with ventricular dilatation and/or septal thinning. However, the position of the atrial, and above all, of the ventricular pacing catheters is critical as is regulation of the pacemaker which should allow complete ventricular capture with an AV delay allowing good filling. The follow-up of these patients must therefore be regular and the effects on longevity are unknown. DDD pacing has also been proposed in dilated cardiomyopathy. The results are contradictory and only very selected cases with left bundle branch block and long PR interval seem justified with, again, optimisation of the pacing sites with high septal or biventricular stimulation. Recurrent atrial tachycardia, special algorithms preventing extrasystoles have been tried with variable results. In cases with inter-atrial block, atrial resynchronisation by bi-atrial stimulation has been assessed with promising results but many technical problems remain unsolved.
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PMID:[New indications for cardiac pacing]. 872 1

201Tl myocardial SPECT is known for better sensitivity, specificity, and accuracy than planar images in detecting coronary artery disease and diagnosing myocardial viability. SPECT images are also superior to planar images in diagnostic sensitivity and anatomical orientation. However, as limitation of the spatial resolution of the machine, we often encounter poor SPECT plower image quality in patients with decreased wall thickness. To test the accuracy of SPECT images in patients with marked thinning of the left ventricular wall, as occurs in dilated cardiomyopathy, we performed a experimental study using myocardial phantom with 7 mm wall thickness. Tomographic image of the phantom images were rather heterogeneous, though no artificial defect was located. Dilated cardiomyopathy is thought to be characterized by patchy defects in the left ventricle. Careful attention should be given to elucidating myocardial perfusion in patients with a thin left ventricle wall, as there are technical limitations in addition to clinical features.
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PMID:[Effect of wall thickness of left ventricle on 201Tl myocardial SPECT images: myocardial phantom study]. 880 47

M-mode indices of left ventricular dimension and posterior wall thickness were derived from echocardiograms of children presenting with dilated cardiomyopathy/myocarditis and were related to outcome. Echocardiograms from 16 of 18 children were manually digitized to obtain changes of left ventricular dimension and posterior wall thickness throughout the cardiac cycle. Indices of ventricular function and the ratio of end-diastolic posterior wall thickness to cavity dimensions were obtained. Patients were divided into group I (alive, n = 7), and group II (died, n = 6 or heart transplantation, n = 3) at median follow-up of 25 months. No significant difference was seen for the shortening fraction, the percentage of posterior wall thickening or the normalized peak rate of left ventricular filling. The normalized peak rate of posterior wall thinning was greater in group II. The posterior wall thickness to cavity dimension ratio was higher in group I (median = 0.19) than group II (median = 0.13) (P < 0.005). Five of six survivors, whose ventricular function improved, had ratios > 0.17. All but one with a ratio < or = 0.16 remained with a dilated heart, died or required transplantation (P = < 0.01). A relatively thicker posterior wall (ratio > 0.17) was associated with better prognosis and recovery. This index should be taken into account in decision-making regarding timing for cardiac transplantation.
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PMID:Prognostic value of posterior wall thickness in childhood dilated cardiomyopathy and myocarditis. 886 65

Anthracyclines, potent cytotoxic agents used to treat a broad spectrum of malignancies, are limited in their use by an attendant risk of cardiotoxicity. Malignancies affect all age ranges, and anthracyclines are used in all age ranges, thereby exposing a broad population of patients to the development of heart disease. For some treated patients, anthracyclines affect cardiac muscle, resulting in cardiomyopathy. The type and degree of cardiomyopathy, as well as when during or after treatment the condition occurs, are dependent on what risk factors are present. Age is a major risk factor. Children and adults may develop restrictive and dilated cardiomyopathy. The length of subsequent survival and amount of subsequent somatic growth may influence late anthracycline-associated cardiac outcome. Early cardiotoxicity, occurring during or within 1 year of completion of treatment, is the largest risk factor for the development of late cardiotoxicity, which occurs beyond a year of completion of treatment. Risk factors, which appear to be specific for early cardiotoxicity in children, include black race, trisomy 21, and the use of amsacrine therapy after anthracycline therapy. More cardiotoxic effects are seen in survivors of childhood cancer, the longer from completion of treatment a patient is followed. Cumulative as well as peak anthracycline doses affect adults and children alike, and cardiotoxicity occurs early and late. In adults, left ventricular contractility is affected by anthracyclines. Children may manifest impairment of left ventricular contractility and increased afterload due to thinning of left ventricular walls. Patients with an early presentation of depressed left ventricular contractility are likely to show progression of cardiac disease with time. In addition, female gender appears to affect early and late cardiotoxicity in both adults and children, although this risk factor has been described predominantly in the survivors of childhood cancer. Thus, although anthracycline chemotherapy has improved overall survivorship of patients with cancer, there is a significant risk of cardiotoxicity associated with this class of drugs.
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PMID:Epidemiology of anthracycline cardiotoxicity in children and adults. 976 28


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