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 clinical features and long-term outcome of seven patients with delayed cerebral radiation necrosis (DCRN) are described. Radiotherapy had been given for pituitary tumour (1), astrocytoma (2), pinealoma (2), craniopharyngioma (1) and parotid carcinoma (1). The mean latency to onset of the first neurological symptoms was 22 months (range 6-40 months), and mean duration of follow-up was 86 months (range 60-126). Three patients died at a mean of 84 months after radiotherapy (range 62-98). A fourth patient probably died from metastatic disease. Three patients remain alive, albeit severely disabled, after 5-10 years. The illness typically ran a stepwise course, with fits and stroke-like episodes occurring against a background of progressive dementia and somnolence. CT and MRI scans showed progressive ventricular dilatation associated with cerebral atrophy and diffuse or focal changes in the white matter. Four patients had had two or more neurosurgical procedures after the radiotherapy. In only one of the seven patients was the diagnosis made at presentation. DCRN produces a distinctive clinical picture, yet remains a poorly recognized complication of cranial irradiation.
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PMID:Delayed cerebral radiation necrosis. 815 88

The goal of this study was to elucidate the ability of the left ventricle to accommodate an increase in preload (Frank-Starling mechanism) in the presence of congestive heart failure (CHF) but in the absence of the complicating effects of hypertrophy and fibrosis. To accomplish this, the effects of volume loading were examined in eight conscious dogs during the control state and after 3 wk of right ventricular pacing (240 beats/min). CHF increased heart rate (by 16 +/- 5 from 92 +/- 5 beats/min), left ventricular (LV) end-diastolic pressure (by 17 +/- 2 from 10 +/- 1 mmHg), and LV end-diastolic volume (EDV; by 23 +/- 4 from 57 +/- 3 ml). Despite reduced LV ejection fraction (from 54 +/- 3 to 31 +/- 3%), there was no significant change in cardiac output (2.5 +/- 0.3 l/min) compared with control (2.7 +/- 0.2 l/min). Stroke volume was preserved (control 19 +/- 2 ml; CHF 18 +/- 2 ml) at a constant heart rate by a shift to the right in the relationship between LV stroke volume and EDV, indicating the importance of chronic ventricular dilatation in maintaining pump performance. In the control state, acute volume load increased LV EDV (by 17 +/- 2 ml) and stroke volume (by 11 +/- 2 ml), whereas in CHF it did not increase LV EDV or stroke volume. Scanning electron microscopy revealed areas of reduced collagen weave pattern surrounding myofibers. Myocyte cross-sectional area by transmission electron microscopy was significantly reduced, and there were multiple electron-dense expansions of the Z lines with disruption of the normal lateral sarcomere alignment. These morphological findings suggest that chronic ventricular dilatation utilized in CHF results from myocyte stretch and morphological intracellular rearrangement. Furthermore, the failing heart cannot further augment stroke volume by acutely increasing EDV in CHF, suggesting that the Frank-Starling reserve is essentially exhausted.
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PMID:Exhaustion of Frank-Starling mechanism in conscious dogs with heart failure. 823 98

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28

A major consequence of chronic cardiac dysfunction is chronic overload of contractile myocardium. Various aetiologies, in reaction to this, may induce compensatory mechanisms consisting of excentric (dilatation) and concentric hypertrophy. Chronic left ventricular dysfunction is caused most frequently by myocardial infarction. Left ventricular dilatation and hypertrophy occurs in patients with extensive infarction. Dilatation may at first be compensatory, restoring stroke volume within 4 weeks of the infarct. However, as dilatation progresses, left ventricular ejection fraction and stroke volume deteriorate during exercise and at rest, and finally pulmonary capillary wedge pressure increases and patients become symptomatic 1.5-3 years after the infarct. Major determinants of progressive left ventricular dilatation and deterioration of haemodynamics are a depressed left ventricular ejection fraction, angiographically determined infarct size, stroke volume early (4 days) after myocardial infarction, infarct location (anterior/inferior) and the grade (TIMI) of perfusion of the infarct-associated coronary artery. Chronic loading and unloading may accelerate or decelerate this process. Efficiency and energy reserve (phosphocreatine) of the dilated ventricles is reduced. Further intrinsic changes in surviving myocardium include morphological and functional disturbance of coronary microcirculation.
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PMID:Cardiac dysfunction and development of heart failure. 837 Mar 60

Following a myocardial infarction the patient with a dilated heart is at greater risk for arrhythmias, congestive failure and sudden death. Studies of myocardial infarction in experimental animals have shown that, with infarcts involving up to 20% of the left ventricle, hypertrophy of surviving myocytes occurs and there are minimal hemodynamic changes. Infarctions greater than 20% induce little additional hypertrophy, and develop increased left ventricular filling pressures and cardiac dilatation. It has been suggested that inadequate hypertrophy of residual myocardium may be a reason for the progressive left ventricular dilatation which occurs after large myocardial infarcts. There are data in humans and animals suggesting that the mass of the left ventricle following a myocardial infarction correlates with improvement in systolic function. Studies from our laboratories have previously shown that 2-tetradecylglycidic acid, an inhibitor of carnitine palmitoyl transferase I, inhibits mitochondrial long-chain fatty acid oxidation and causes myocardial hypertrophy when given to rats by mouth for 7-28 days. We carried out studies to see whether induction of additional myocardial hypertrophy by means of feeding tetradecylglycidic acid might prevent pathologic dilation following a large (50%) infarct in rats. Treatment of control and infarcted rats with tetradecylglycidic acid for 10 days resulted in myocardial hypertrophy in both groups. The rats with myocardial infarction treated with tetradecylglycidic acid had an increase in peak developed left ventricular pressure during abrupt aortic occlusion and lower left ventricular end-diastolic volumes, when compared to untreated rats with myocardial infarction, while the stroke volume was maintained. Thus induction of myocardial hypertrophy with an inhibitor of long-chain fatty acid oxidation retarded the process of left ventricular dilatation and had beneficial effects on systolic function following a large myocardial infarction.
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PMID:A role of fatty acid oxidation in cardiac hypertrophy. 840 20

We report an autopsy case of a 19 year-old man with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) a subgroup of mitochondrial encephalomyopathy presenting cardiomyopathy. He had repeatedly suffered from transient unconsciousness, hemiplegia, hemianopsia and convulsion attacks since the age of 9, and he died of severe congestive heart failure. In laboratory findings, blood lactate and pyruvate were markedly increased. Skeletal muscle biopsy demonstrated numerously scattered ragged-red fibers with modified Gomori's trichrome staining. Enzymatic activities of the mitochondrial respiratory chain showed a marked decrease of NADH cytochrome c reductase (complex I). In postmortem examination, the heart was 310g in weight and had right ventricular dilatation. Microscopically, degenerated and scattered myocardial cells (ragged-red fibers), interstitial edema and microvascular hyperplasia were demonstrated in the myocardium. Under the electron microscope, abnormal mitochondria proliferated and myofibrils were unusually sparse. Immunohistochemical studies with specific antibodies against the mitochondrial electron transfer enzyme subunits revealed a reduction of immunoreactive materials for complex I in the myocardium. These results suggested the relationship of myocardial disorders and decreased activity of complex I in electron transfer enzymes in this patient.
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PMID:[A study of myocardial disorders in an autopsy case of mitochondrial encephalomyopathy]. 846 36

Survival after myocardial infarction decreases with left ventricular dilatation, although dilatation at 4 weeks was found to be compensatory. To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 days (range, 2-6 days) and 4 weeks (range, 3-5 weeks) to 6 months (range, 5-8 months) after infarction and were repeated during supine bicycle exercise at 50 W. In patients with small infarction, end-diastolic volume (mL/m2) decreased from 4 days to 6 months; ejection fraction (%), stroke volume (mL/m2), and end-systolic volume (mL/m2) remained unchanged. Stroke index rose during exercise at 4 weeks and 6 months. In patients after large infarction (n = 37), left ventricular end-systolic volume index (4 days, 38 +/- 3; 4 weeks, 47 +/- 3*; 6 months, 52 +/- 3*; *p < 0.05 versus 4 days) and end-diastolic volume indexes (4 days, 72 +/- 3; 4 weeks, 86 +/- 5*; 6 months, 92 +/- 5*; *p < 0.05 versus 4 days, +p < 0.05 versus 4 weeks) increased at constant wedge pressure. Stroke index remained restored beyond 4 weeks after infarction (4 days, 35 +/- 2; 4 weeks, 42 +/- 2*; 6 months, 42 +/- 2*; p < 0.05 versus 4 days) and rose during exercise at 4 weeks (rest, 45 +/- 2; exercise, 55 +/- 3; p < 0.05) but not at 6 months (rest, 42 +/- 3; exercise, 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation to cardiac dysfunction after myocardial infarction. 848 38

In the present investigation, we estimated both the evolution and the severity of ischemic damage following unilateral carotid occlusion (UCO) in Mongolian gerbils by using conventional magnetic resonance imaging (MRI, i.e. T2 weighted imaging) and histological techniques. Immediately after UCO, the animals showed different clinical effects. The mortality (46%) detected within the first 48h was considered an "stroke-sensitivity", the "stroke-resistant" animals showed wide variability in terms of both temporal evolution and the extent of ischemic damage. The signal hyperintensity and negative MRI observed during the first 30h after UCO did not always correlate with the cerebral damage presented after 14 days, although a close correlation was established between the T2 weighted images taken more than 30h after UCO and neuropathology: the gerbils negative to imaging showed no morphological changes, whereas an enhanced signal was always prognostic of ischemic injury. Moreover, late MRI documented ventricular dilatation. Histopathology showed that the ischemic damage differed among the stroke-resistant gerbils and was often bilateral. The present study confirms the differences in gerbil susceptibility to hemispheric infarction after permanent UCO and suggests that conventional MRI may be a useful non-invasive method for i) identifying the stroke-resistant animals prone to mature ischemic injury and ii) monitoring the evolution of therapeutic efficacy without sacrificing animals.
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PMID:Variable response of the Mongolian gerbil to unilateral carotid occlusion: magnetic resonance imaging and neuropathological characterization. 861 12

The renin-angiotensin and adrenergic nervous systems are cross-regulated compensatory mechanisms that are induced or activated in the failing heart. In ventricular myocardium, the activation of one of these systems leads to activation or induction of the other, resulting in co-amplification of cellular mechanisms that result in cardiac myocyte hypertrophy, hyperplasia of nonmyocytic tissue components, increased contractility and heart rate, and increased ventricular volume. Although these changes serve to stabilize stroke volume and cardiac output following an insult to the myocardium, the chronic and continual activation of these systems produces ventricular dilatation and deleterious remodelling at a chamber level and progressive myocyte dysfunction at a cellular level. Because these systems are cross-regulated, inhibition of one of them attenuates the activity of the other. This appears to be especially true in the failing heart, where angiotensin converting enzyme inhibitors can produce substantial anti-adrenergic effects in individuals with high levels of adrenergic activation. The anti-adrenergic properties of angiotensin converting enzyme inhibitors may be at least partially responsible for the salutary effects of these agents in the clinical setting of heart failure or ischaemic heart disease.
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PMID:Anti-adrenergic effects of angiotensin converting enzyme inhibitors. 886 34

Severe stroke is an emergency and requires rapid neurological assessment and diagnosis. CT scan is the first diagnostic step with the aim of finding out the extent, localization and possible pathophysiology of ischaemia in order to direct specific diagnostic and therapeutic options. An intracranial haemorrhage must be excluded. Early CT signs, including the size of the hypodensity and brain swelling, are important prognostic markers. Extracranial and transcranial Doppler sonography are valid for primary assessment of vascular pathophysiology and haemodynamics in most cases. Cerebral angiography should be performed if acute occlusion of the basilar artery or middle cerebral artery trunk is suspected and intra-arterial thrombolysis is a potential therapy. Intravenous thrombolyis has been proven to be effective in improving outcome in severe stroke; it is safe if the exclusion criteria are strictly applied. Prevention of secondary complications of stroke include general medical treatment with control of blood pressure, infections and cardiac and respiratory function, anti-coagulation. anti-oedematous treatment and surgical decompressive therapy for cerebellar and MCA space-occupying infarcts. Monitoring in the ICU is recommended. The medical therapy of intracerebral haemorrhage consists of control of ventilation and blood pressure, seizure prevention and anti-oedema treatment. Treatment of secondary ICH due to anti-coagulation or thrombolysis consists of administration of specific antidotes and the correction of the coagulopathy. Ventricular drainage should be performed when there is marked ventricular dilatation due to obstruction or blood in the ventricles. Most patients with cerebellar haemorrhage of more than 3 cm in diameter should undergo surgery to avoid brain-stem compression and hydrocephalus. In younger patients, non-dominant hemisphere putaminal and lobar haemorrhages with lateral displacement of midline structures and extensive oedema should be evacuated if the patient's level of consciousness deteriorates rapidly, or if the elevation of ICP cannot be controlled pharmacologically, and herniation is incipient. New techniques such as stereotactic and endoscopic evacuation still need to be tested prospectively. Patient selection for surgery should be cautious considering age, clinical status and possible contraindications such as cerebral amyloid angiopathy and coagulation disorders. Stroke therapy is rapidly becoming a focus of research and major changes in diagnostic and therapeutic options can therefore be expected.
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PMID:Severe stroke. 911 74


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