Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to demonstrate the usefulness of fetal magnetic resonance imaging (MRI) in ischemic brain injury. We report seven cases of fetal brain ischemia prenatally suspected on ultrasound (US) and confirmed by fetal MRI. Sonographic abnormalities included ventricular dilatation (n=3), microcephaly (n=1), twin pregnancy with in utero death of a twin and suspected cerebral lesion in the surviving co-twin (n=3). MRI was performed with a 1.0 T unit using half-Fourier acquisition single-shot turbo spin-echo (HASTE) sequences between 28 and 35 weeks of gestation. US and MRI images were compared with pathologic findings or postnatal imaging. MRI diagnosed hydranencephaly (n=1), porencephaly (n=2), multicystic encephalomalacia (n=2), unilateral capsular ischemia (n=1), corpus callosum and cerebral atrophy (n=1). In comparison with US, visualization of fetal brain anomalies was superior with MRI. The present cases demonstrate that MRI is a valuable complementary means of investigation when a brain pathology is discovered or suspected during prenatal US.
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PMID:Fetal magnetic resonance imaging (MRI) of ischemic brain injury. 1155 8

Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 +/- 11 years, 19 coronary artery disease, NYHA 2.2 +/- 0.4, left ventricular ejection fraction 0.42 +/- 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 +/- 3.6 J after 10.3 +/- 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with < or = 8 J. In these patients, the mean defibrillation threshold was 4.0 +/- 2.1 J after 1.4 +/- 0.3 seconds compared to 9.5 +/- 3.1 J after 10.2 +/- 1.1 seconds (P < 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs.
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PMID:Effect of ventricular fibrillation duration on the defibrillation threshold in humans. 1187 30

Cardiac hypertrophy is an adaptive response that compensates for increased workload by normalizing wall stress and preserving cardiac contractile function. In advanced stages, however, clinical and experimental studies have shown that when the high workload is maintained, hypertrophy progresses to ventricular dilatation, contractile dysfunction, and decreased tolerance to ischemia/reperfusion. Development of hypertrophy is accompanied by distinct qualitative and quantitative changes in contractile protein expression and isoform switching, cytosolic calcium regulation, and substrate delivery and use. We have focused our investigations on changes in substrate delivery and capillary density in pressure overload hypertrophy and on the effects that these changes have on tolerance to ischemia/reperfusion. This report summarizes our work in this area using a model of aortic banding in 10-day-old rabbits, which exhibits the same pattern of concentric hypertrophy early, followed by ventricular dilatation and contractile dysfunction that is clinically apparent.
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PMID:Increased susceptibility of hypertrophied hearts to ischemic injury. 1260 12

Improvements in MRI techniques widen the indications for fetal brain imaging and fetal brain injury represents the third indication of fetal brain magnetic resonance imaging (MRI) after the evaluation of suspected central nervous system (CNS) malformations and ventricular dilatation. Optimal MR imaging technique is necessary in order to collect as much data as possible about the fetal brain. Diffusion images can be used routinely in addition to the standard protocol of fetal brain MRI that consists of T1 and T2 weighted images of the fetal brain. Monovoxel proton magnetic resonance spectroscopy can also be performed in utero, but this technique is still more part of research protocol than of routine clinical protocol. Fetal brain injury includes hypoxia-ischemia, congenital infections (especially toxoplasmosis and cytomegalovirus infections), brain damage due to malformation such as vascular brain malformation and heart malformation, pregnancies at risk of fetal brain damage, and even inherited metabolic diseases, especially mitochondrial diseases. MRI findings in fetal brain injury consist of acute or chronic lesions that can be seen alone or in combination. Acute response of the fetal brain is less commonly seen than the chronic response compared to the brain response encountered in the postnatal period.
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PMID:Fetal brain injury. 1509 50

Ventricular remodelling following acute coronary syndromes is both complex and multiform. It is due to the response of the myocardium to the different agressions associated with these syndromes, in particular the ischemia and necrosis downstream of the occluded artery. We must not however neglect the role of the remodelling of the lesions resulting from spontaneous reperfusion or provoked by the cells and tissues associated with coronary microcirculation embolisms and the no-reflow phenomenon. Acute post-infarct remodelling is dominated by early ventricular dilatation which largely affects late prognosis, necrosis elimination and its replacement by a fibrotic scar in parallel with a compensatory hypertrophy of the non-infarcted myocardium. The diverse cellular and molecular components of this remodelling are increasingly well-known, allowing us to better explain the beneficial effects of the currently available medications and providing us with new potential therapeutic targets. A grading of this knowledge associated with the identification of new risk factors and early therapeutic interventions should help us to further limit the deleterious aspects of this remodelling in the goal of preventing, or at least delaying, the devolution towards heart failure.
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PMID:[Early left ventricular remodelling following acute coronary accident]. 1532 14

Several experimental studies have shown that levocarnitine reduces myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism. In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl-CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high-energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti-ischemic properties. In small short-term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end-diastolic pressure. These short-term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g/day by intravenous infusion for 5 initial days and 6 g/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF after discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long-chain acyl-CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative-induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long-chain acyl-CoA; and (4) reducing the ischemia-induced apoptosis and the consequent remodeling of the left ventricle. Propionyl-L-carnitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl-L-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with propionyl-L-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-L-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-L-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.
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PMID:Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: a review. 1559 Oct 5

Because the small leucine-rich proteoglycan decorin has been implicated in regulation of collagen fibrillogenesis leading to proper extracellular matrix assembly, we hypothesized it could play a key role in cardiac fibrosis following myocardial infarction. In this study we ligated the left anterior descending coronary artery in wildtype and decorin-null mice to produce large infarcts in the anterior wall of the left ventricle. At early stages post-coronary occlusion the myocardial infarction size did not appreciably differ between the two genotypes. However, we found a wider distribution of collagen fibril sizes with less organization and loose packing in mature scar from decorin-null mice. Thus, we tested the hypothesis that these abnormal collagen fibrils would adversely affect post-infarction mechanics and ventricular remodeling. Indeed, scar size, right ventricular remote hypertrophy, and left ventricular dilatation were greater in decorin-null animals compared with wildtype littermates 14 days after acute myocardial infarction. Echocardiography revealed depressed left ventricular systolic function between 4 and 8 weeks post-ischemia in the decorin-null animals. These changes indicate that decorin is required for the proper fibrotic evolution of myocardial infarctions, and that its absence leads to abnormal scar tissue formation. This might contribute to aneurysmal ventricular dilatation, remote hypertrophy, and depressed ventricular function.
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PMID:A role for decorin in the remodeling of myocardial infarction. 1594 32

Large numbers of people have anterior myocardial infarctions, many in mid-life, with progressive left ventricular dilatation and heart failure with diminished life expectancy. Myocardial revascularization alone helps ischemia, but does little in cases of large ventricular volume, which is the major determinant of post infarction mortality. Ventricular restoration results in immediate improvement in size and function and when added to revascularization, has markedly improved survival and freedom from congestive heart failure. When coronary bypass is being considered after anterior infarction or in patients with reduced ventricular function, MRI to determine function and viability is recommended. Then a valid, informed judgment can be made about patch reconstruction of the left ventricle.
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PMID:Left ventricular remodeling or restoration for congestive heart failure. 1651 4

This review discusses the application of He-Ne laser irradiation to injured muscles at optimal power densities and optimal timing, which was found to significantly enhance (twofold) muscle regeneration in rats and, even more, in the cold-blooded toads. Multiple and frequent (daily) application of the laser in the toad model was found to be less effective than irradiation on alternate days. It was found that in the ischemia/reperfusion type of injury in the skeletal leg muscles (3 h of ischemia), infrared Ga-Al-As laser irradiation reduced muscle degeneration, increased the cytoprotective heat shock proteins (HSP-70i) content, and produced a twofold increase in total antioxidants. In vitro studies on myogenic satellite cells (SC) revealed that phototherapy restored their proliferation. Phototherapy induced mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) phosphorylation in these cells, probably by specific receptor phosphorylation. Cell cycle entry and the accumulation of satellite cells around isolated single myofibers cultured in vitro was also stimulated by phototherapy. Phototherapy also had beneficial effects on mouse, rat, dog and pig ischemic heart models. In these models, it was found that phototherapy markedly and significantly reduced (50-70%) the scar tissue formed after induction of myocardial infarction (MI). The phototherapeutic effect was associated with reduction of ventricular dilatation, preservation of mitochondria and elevation of HSP- 70i and ATP in the infarcted zone. It is concluded that phototherapy using the correct parameters and timing has a markedly beneficial effect on repair processes after injury or ischemia in skeletal and heart muscles. This phenomenon may have clinical applications.
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PMID:Photoengineering of tissue repair in skeletal and cardiac muscles. 1670 89

Transient ischemic dilatation (TID) of the left ventricle observed during single photon myocardial perfusion emission computed tomography (SPECT) is an important non-perfusion finding that may not only suggest underlying significant (usually multi-vessel) coronary artery disease (CAD) but also an independent prognostic factor of adverse outcomes regardless of abnormal or normal perfusion finding. We present a patient with no significant epicardial coronary disease who had significant TID and considerable decrease in the left ventricular ejection fraction with left ventricular dilatation after a rest-stress Tc-99 tetrofosmin SPECT study in the setting of severe aortic stenosis. With the advent of gated SPECT imaging the additive value of determining rest and post stress EF, as demonstrated in this case, aided in the recognition of TID and transient decrease in the left ventricular ejection fraction. These are not necessarily related to obstructive epicardial coronary disease, but are a result of severe aortic valve disease causing subendocardial ischemia in the setting of multilple other non-ischemic etiologies of TID such as left ventricular hypertrophy and diabetes mellitus.
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PMID:Transient ischemic dilatation of the left ventricle with severe post stress left ventricular dysfunction in the setting of severe aortic stenosis and normal coronary arteries. 1692 2


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