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

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.
 ...
PMID:Cerebral hemodynamic and metabolic effects of chronic alcoholism. 270 68

Two hundred and twenty-one patients with cerebral cerebral ischemic attack in the middle cerebral artery territory were investigated. Those patients manifested several clinical types, TIA: 31, stroke with full recovery: 50, minor completed stroke: 54 and major completed stroke: 86 cases. CT classification was made 3 weeks after the ischemic attack based on the characteristic arterial topography. We discussed in this paper what kind of ischemic lesion had greater possibility of recovery from ischemic lesion had greater possibility of recovery from ischemia focusing on the retrospective study of clinical symptoms, CT classification and angiographic findings. We also referred to the other factors influencing the reversibility of an ischemia such as lacunae and PVH (periventricular hypodensity). The extent of and LDA on CT scan closely correlated with clinical symptoms, CT classification and angiographic findings. We also referred to the other factors influencing the reversibility of an ischemia such as lacunae and PVH (periventricular hypodensity). The extent of an LDA on CT scan closely correlated with clinical types (Table 2). The reversibility of type I was excellent, however aged patients over 70 with PVH and ventricular dilatation developed permanent neurological impairment associated with dementia. The reversibility of a small infarction in the basal ganglia (type II) depended mainly on the involvement of the internal capsule. Infarction involving a cortex (type IV and type V) invariably resulted in permanent neurological deficits except for the rare cases with involvement of silent areas. CT classification of type III, so called demarcation zone infarction, developed various clinical types, and showed transient functional disturbance of the cortex without an infarction i the cortico-subcortical region.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Cerebral ischemia (1)--Reversibility of ischemic lesion and CT findings]. 320 63

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.
 ...
PMID:Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia. 339 67

A rare case of extracranial internal carotid occlusion with a coexisting ipsilateral internal carotid aneurysm is reported. A 50-year-old male had a sudden onset of severe headache, vomiting and right motor weakness on May 14, 1984. Two days later the patient was transferred to our hospital. On admission he was alert but presented with nuchal rigidity and right moderate hemiparesis. He had an episode of a blunt head injury 12 years previously, but no history of hypertension, diabetes mellitus or cerebral stroke. A computed tomography revealed mild subarachnoid hemorrhage and mild ventricular dilatation. A cerebral angiography did not demonstrate any aneurysms but it revealed occlusion of the right internal carotid artery at the cervical bifurcation. The repeated angiography on May 31 disclosed a saccular aneurysm arising anteromedially at the level of the junction of the right posterior communicating artery and the internal carotid artery. The cervical internal carotid artery remained occluded at the same site. The middle cerebral artery was supplied through the well-developed posterior communicating artery, and the right anterior cerebral artery was supplied through the anterior communicating artery. Clipping of the aneurysm was attempted but it was forcibly trapped because of premature bleeding on June 5. The right V-P shunt was performed for the progressive ventricular dilatation on June 12. The patient was discharged with no paresis on June 20. It has been well known that the uni- or bilateral carotid occlusion, whatever the origins are, are often associated with cerebral aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Extracranial internal carotid occlusion and coexisting ipsilateral intracranial internal carotid aneurysm]. 361 34

A canine sepsis model that simulates the human cardiovascular response to septic shock was produced in 10 conscious unsedated dogs by implanting an Escherichia coli-infected clot into the peritoneum, resulting in bacteremia. By employing serial, simultaneous measurements of radionuclide scan-determined left ventricular (LV) ejection fraction (EF) and thermodilution cardiac index (CI), the end-diastolic volume index (EDVI) was calculated (EDVI = stroke volume index divided by EF). By using three different methods of quantifying serial ventricular performance (EF, shifts in the Starling ventricular function curve using EDVI vs. stroke work index, and the ventricular function curve response to volume infusion), this study provides evidence (P less than 0.01) that septic shock produces a profound, but reversible, decrease in systolic ventricular performance. This decreased performance was not seen in controls and was associated with ventricular dilatation (P less than 0.01); the latter response was dependent on an adequate volume infusion. Further studies of EDVI and pulmonary capillary wedge pressure during diastole revealed a significant, though reversible, shift (P less than 0.001) in the diastolic volume/pressure (or compliance) relationship during septic shock.
 ...
PMID:Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock. 372 79

To assess the comparative cardiac effects of hemodialysis and continuous ambulatory peritoneal dialysis (CAPD), we performed M-mode echocardiography prior to and immediately following hemodialysis on 56 patients and during the dwell phase of CAPD on 39 patients. Hemodialysis produced a significant increase in the mean velocity of circumferential fiber shortening (VCF, an index of left ventricular systolic function) in patients with low VCF prior to dialysis, but resulted in no significant change in VCF in patients with normal predialysis VCF. Hemodialysis produced a significant increase in VCF in patients with a normal predialysis left ventricular end-diastolic volume index (LVEDVI), but resulted in no significant change in VCF in patients with left ventricular dilatation prior to dialysis. Hemodialysis produced a significant decrease in mean LVEDVI and mean stroke index, but resulted in no significant change in mean cardiac index due to a reflex increase in heart rate. Mean LVEDVI, mean stroke index, and VCF values in patients on CAPD were not significantly different from those observed immediately following hemodialysis. Mean cardiac index and mean heart rate were significantly lower in CAPD patients than in posthemodialysis patients. Pericardial effusion was observed in 25% of hemodialysis patients and 5% of CAPD patients (p less than 0.05). We conclude (1) the effects of hemodialysis on left ventricular performance are variable and depend in part on predialysis left ventricular volume and left ventricular systolic function, (2) except for a lower cardiac index, left ventricular hemodynamics for CAPD patients resemble those of posthemodialysis patients, and (3) pericardial effusion occurs with significantly higher frequency in patients on hemodialysis than in those on CAPD.
 ...
PMID:Comparative cardiac effects of hemodialysis and continuous ambulatory peritoneal dialysis. 394 41

Semantic difficulties arise when hypertrophic obstructive cardiomyopathy is seen without obstruction and with congestive failure, and also when congestive cardiomyopathy is seen with gross hypertrophy but without heart failure. Retention of a small left ventricular cavity and a normal ejection fraction characterizes hypertrophic cardiomyopathy at all stages of the disorder. Congestive cardiomyopathy is recognized by the presence of a dilated left ventricular cavity and reduced ejection fraction regardless of the amount of hypertrophy and the presence or not of heart failure. Longevity in congestive cardiomyopathy seems to be promoted when hypertrophy is great relative to the amount of pump failure as measured by increase in cavity size. Conversely, death in hypertrophic cardiomyopathy is most likely when hypertrophy is greatest at a time when outflow tract obstruction has been replaced by inflow restriction caused by diminishing ventricular distensibility. Hypertrophy is thus beneficial and compensatory in congestive cardiomyopathy, whereas it may be the primary disorder and eventual cause of death in hypertrophic cardiomyopathy. Reasons are given for believing that hypertension may have been the original cause of left ventricular dilatation in some case of congestive cardiomyopathy in which loss of stroke output thenceforward is followed by normotension. Development of severe hypertension in these patients after recovery from a prolonged period of left ventricular failure with normotension lends weight to this hypothesis. No fault has been found in the large or small coronary arteries in either hypertrophic cardiomyopathy or congestive cardiomyopathy when they have been examined in life by selective coronary angiography, or by histological methods in biopsy or post-mortem material. Coronary blood supply may be a limiting factor in the compensatory hypertrophy of congestive cardiomyopathy, and the ability to hypertrophy may explain the better prognosis of some patients. In hypertrophic cardiomyopathy excessive metabolic demand may not be met, and inadequacy of blood flow may contribute both to sudden death and to progressive replacement fibrosis in this disease. Histochemical and ultrastructural methods have failed to show any fundamental differences between hypertrophic cardiomyopathy and congestive cardiomyopathy, whereas conventional histology permits recognition of hypertrophic cardiomyopathy and distinction both from congestive cardiomyopathy and from ;normal' secondary hypertrophy in organic aortic stenosis.
 ...
PMID:Ventricular hypertrophy in cardiomyopathy. 425 44

Since elevation of plasma concentrations of free fatty acids (FFA) increases myocardial oxygen consumption without influencing mechanical performance in normal hearts, it was the purpose of this study to determine whether FFA would modify mechanical performance at limited oxygen supply. Left coronary blood flow was reduced by gradual clamping of a shunt from the left carotid artery until moderate ventricular dilatation supervened. Left ventricular systolic pressure (LVSP), its maximal rate of rise (dP/dt) and stroke volume (SV) were unchanged or slightly reduced. The ischemia resulted in a decrease in myocardial oxygen consumption (MVO(2)) from 9.7+/-1.1 ml/min to 7.9+/-0.8 ml/min, and myocardial lactate uptake was reduced or reversed to excretion. Increasing the plasma concentrations of FFA from 359+/-47 muEq/1 to 3688+/-520 muEq/1 by intravenous infusion of a triglyceride emulsion and heparin resulted in further ventricular dilatation, accompanied by increased excretion of lactate. The ventricular decompensation and enhancement of anaerobic myocardial metabolism associated with increased uptake of FFA was not related to changes in coronary flow, MVO(2), or LVSP. dP/dt and SV were virtually unchanged. Intravenous infusion of glucose/insulin, which lowered plasma concentrations of FFA, reversed ventricular dilatation and lactate excretion. The data support the hypothesis that high concentrations of FFA play a significant role in increasing myocardial oxygen requirement and thereby promote depression of contractility of the hypoxic heart in experimental animals.
 ...
PMID:Effect of free fatty acids on myocardial function and metabolism in the ischemic dog heart. 503 25

The spontaneously hypertensive rat (SHR) exhibits both a compensated phase of cardiac hypertrophy in which forward output is maintained despite persistently elevated systemic arterial pressures and a decompensated phase in which cardiac performance has deteriorated in spite of further hypertrophic growth. To determine whether chronic antihypertensive therapy prevents the development of heart failure and the progression of cardiac hypertrophy in SHR with advanced hypertension, captopril (2 g/l of drinking water), a converting enzyme inhibitor, was administered to 14 month old female SHR and normotensive American Wistar rats (NWR) for 10 months. The severe left ventricular hypertrophy of the 24 month old untreated SHR (4.37 +/- 0.2 mg/g v. 2.50 +/- 0.06 mg/g, untreated NWR) was markedly reduced (P less than 0.02) by captopril (3.01 +/- 0.1 mg/g). Chronic therapy prevented the reduction of both baseline and maximal cardiac indices in SHR, but did not alter blood flow in NWR. Left ventricular dilatation was present in 24 month old SHR and, as peak stroke volume index was diminished, the ejection fraction index of the SHR was reduced. Captopril restored this index in SHR to normal. The relation of ejection fraction index and afterload (peak systolic wall stress) was depressed in untreated SHR, but was normal in treated SHR. Thus, chronic therapy with captopril prevented the development of severe cardiac dysfunction and produced a marked regression of cardiac hypertrophy in SHR with advanced hypertensive heart disease.
 ...
PMID:Prevention of the development of heart failure and the regression of cardiac hypertrophy by captopril in the spontaneously hypertensive rat. 622 Aug 93

This study analyzes and compares systemic and coronary hemodynamics in patients with essential hypertension in relation to hypertrophic heart disease of nonhypertensive origin. Left ventricular function (as assessed from the cardiac index, stroke volume index, ejection fraction, mean velocity of circumferential fiber shortening, mean normalized systolic ejection rate, and isovolumic indexes) may be normal in patients with hypertensive hypertrophy, even with a large increase in muscle mass and in the presence of concomitant coronary artery disease. Left ventricular function is impaired when regional contraction abnormalities or ventricular dilatation, or both, occur and is inversely related to both cardiac size and systolic wall stress. Coronary blood flow (+ 18%), coronary resistance (+ 38%), and myocardial oxygen consumption (MVO2) (+ 21%) are increased in essential hypertension. Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. Coronary reserve may remain normal in both moderate and excessive hypertrophy, provided systolic wall stress and hence the myocardial oxygen consumption are not increased. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption.
 ...
PMID:The coronary circulation in hypertensive heart disease. 624 Apr 56


<< Previous 1 2 3 4 5 6 7 8 Next >>