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)

Two grams of methylprednisolone was administratered to ten patients with acute myocardial infarction at an average of 13 hours from the onset of symptoms; pain in the chest was not relieved in six of the ten patients. In one hour, no significant improvement was noted in the function of the ischemic segments (examined using a multiaxis echocardiographic method) or in the S-T segments of the 12-lead electrocardiogram. Left ventricular filling pressure soon increased by an average of 4 mm Hg (P less than 0.005), without ventricular dilatation or a Frank-Starling response, suggesting a decrease (ischemic?) in myocardial compliance. Cardiac output by Swan-Ganz thermodilution later increased by 21 percent (P less than 0.01) when a decrease in peripheral vasoconstriction was evident. In contrast, small-dose beta-adrenergic blockade using 0.2 mg of pindolol intravenously after administration of methylprednisolone immediately relieved pain in the chest in all six patients. Elevation of the S-T segments was reduced by 34 percent (P less than 0.05) within 15 minutes, and the contractile function of the ischemic segments improved markedly, by 3 mm or to 34 percent of normal, from the 4 percent of normal before administration of pindolol (P less than 0.005). Hemodynamic function did not deteriorate in the eight patients with uncomplicated infarction or moderate left ventricular failure. Therapy with pindolol thus reduced clinical, electrocardiographic, and myocardial mechanical signs of acute ischemia safely, while administration of methylprednisolone had no short-term protective effect.
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PMID:Failure of methylprednisolone to protect acutely ischemic myocardium: a contrast with subsequent beta-adrenergic blockade in man. 34 14

One hundred thirty-four patients with redistribution on a thallium-201 exercise test who did not experience angina (group 1) were compared with 134 patients also having redistribution who had angina during the test (group 2). The groups were matched by age, sex, and peak exercise heart rate. Although patients in both groups achieved an equivalent exercise level, patients in group 1 had less frequent (53 vs 71%, p less than 0.005) and less severe (0.15 +/- 0.13 vs 0.20 +/- 0.13 mV, p less than 0.005) ischemic ST-segment depression. Group 1 also had less ischemic thallium-201 images in terms of the number of redistributing defects, the severity of the worst redistributing defect, and an ischemic index composite of both extent and severity. Patients in group 1 were less likely to undergo early revascularization (12 vs 29%, p less than 0.005), but in the remaining patients the occurrence of adverse cardiac events was similar (21% vs 29%, p = not significant). By multivariate analysis, only the ischemic index correlated with early revascularization in group 1 (p = 0.0017), whereas the percent maximal predicted heart rate correlated best in group 2 (p = 0.0003). In group 1 the ratio of lung/heart thallium-201 uptake correlated best with an outcome of nonfatal myocardial infarction or cardiac death (p = 0.0024); in group 2 the presence of fixed left ventricular dilatation did (p = 0.0022). Thus, patients with exercise-induced thallium-201 redistribution without angina have less ischemia than patients experiencing angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Silent versus symptomatic ischemia during a thallium-201 exercise test. 174 60

Over a 5-year period, 1,292 patients had operation on their native mitral valves. Ischemia was the cause of mitral insufficiency in 84 patients (6.5%). Sixty-five patients (77.4%) had mitral valve repair. Mean age was 66 +/- 10 years; 35 patients (53.8%) were women. Mean degree of preoperative insufficiency was 3.2 +/- 0.7; mean preoperative New York Heart Association functional class was 3.3 +/- 0.7. Eleven patients (16.9%) had acute and 54 (83.1%) had chronic mitral insufficiency. Valve prolapse was present in 26 patients (40%). Restrictive leaflet motion secondary to regional or global left ventricular dilatation occurred in 39 patients (60%). All patients had associated myocardial revascularization followed by transatrial valvuloplasty. Multiple techniques were employed to achieve valve competence: leaflet resection (3), chordal shortening (15), papillary muscle reimplantation (10), papillary muscle shortening (3), and annuloplasty (63). There were six (9.2%) hospital deaths (acute, 9.1%; chronic, 9.3% [not significant]; prolapse, 11.5%; restrictive, 7.7% [not significant]). The mean degree of postoperative mitral insufficiency was 0.6 +/- 0.8 in 51 patients. At a mean follow-up of 3.1 +/- 1.6 years, patient survival was 96% for patients with valve prolapse and 48% for those with restrictive leaflet motion (p = 0.02). New York Heart Association functional class was improved in all groups. Ischemic mitral insufficiency is an uncommon cause of mitral valve disease that is amenable to repair in the majority of cases of both acute and chronic onset. The operative mortality is low, and operation is associated with superior survival in patients with valve prolapse.
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PMID:Mitral valve repair for ischemic mitral insufficiency. 161 Feb 45

We describe two cases of prolonged postischemic ventricular dilatation during myocardial scintigraphy with 99mTc MIBI, the new perfusion tracer that has only negligible redistribution. Ventricular dilatation, caused by true chamber dilatation and/or subendocardial ischemia, was still present over two hours after the induced ischemic episode, suggesting a prolonged duration of such a commonly believed fleeting scintigraphic finding.
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PMID:Transient prolonged postischemic ventricular dilatation documented by 99mTc MIBI scan. 182 21

There is a complex network of collagen throughout the heart. It is composed of a hierarchy of fibrils and fibers ranging from 10 nm to 2-3 microns in diameter. This network can be broken down by ischemia, adriamycin administration, or disulfide administration in laboratory animals. Following loss due to coronary artery ligation, the ischemic area begins bulging within 3 h. General loss of portions of the collagen matrix is induced by intravenous oxidizing glutathione, and results in marked diffuse ventricular dilatation. Generalized collagen loss in the ventricles, as induced by disulfide administration or adriamycin infusion, persists for 6 months at which time evidence of some replacement is visible, and evidence of diffuse fibrosis is present. In humans, cardiac dilatation occurs in a variety of disease states without overstretch of sarcomeres. This presumes rearrangement of the muscle bundles, which can only occur with marked alterations of the collagen matrix. Ventricular dilatation, associated with viral myocarditis or puerperal cardiomyopathy, may persist for months, suggesting the collagen loss, as with the experimental animals, takes many months to repair. The cardiac dilatation may ameliorate, or, in some patients, deteriorate into heart failure. The animal experiments with loss of the collagen matrix, ventricular dilatation, and failure to replace the matrix for many months provide an explanation for persistent cardiac dilatation in various human diseases.
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PMID:Myocardial connective tissue alterations. 209 Dec 28

In order to study myocardial and clinical events during transient coronary occlusion in humans, two-dimensional echocardiography was continuously performed in 15 patients undergoing 49 balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). Transient segmental asynergy developed in all patients 8 +/- 3 seconds after balloon inflation and returned to baseline 19 +/- 8 seconds after balloon deflation. Segmental dyskinesis was seen in only 8 of 11 patients undergoing PTCA of the left anterior descending artery (LAD). A wall motion score, based on degree of asynergy of 13 segments of the left ventricle, was significantly higher during LAD than during right coronary artery inflation (7.9 +/- 1.3 vs 4.0 +/- 1.4, p less than 0.01). Left ventricular size index increased significantly during balloon inflation, from 179 +/- 9 to 196 +/- 10 mm (p less than 0.01). Four patients developed transient ST segment changes in the extremity leads of the ECG and five patients had angina pectoris. The very first sign of ischemia in three patients, who developed all of these symptoms together, was consistently asynergy, followed by ECG changes, and last, angina pectoris. Thus during PTCA, transient asynergy and left ventricular dilatation develop, which are often clinically silent.
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PMID:Two-dimensional echocardiography during percutaneous transluminal coronary angioplasty. 294 Aug 52

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)
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PMID:[Cerebral ischemia (1)--Reversibility of ischemic lesion and CT findings]. 320 63

We examined the effects of left ventricular dilatation on epicardial pacing threshold, conduction velocity, and effective refractory period (ERP) in the isolated, retrograde perfused rabbit heart. Left ventricular size was modified by acutely changing the volume of a fluid-filled balloon anchored within the vented left ventricle. Increases in left ventricular volume, associated with increases in left ventricular end-diastolic pressure from 0 +/- 1 to 35 +/- 2 mm Hg, were not associated with significant changes in pacing threshold or conduction velocity. The left ventricular ERP decreased significantly with an added volume of 1.5 ml (91.4 +/- 5.5 msec) compared with starting volume (117.7 +/- 3.8 msec, p less than 0.01). Right ventricular ERP did not change significantly with increases in left ventricular volume. The left and right ventricular ERPs were comparable at starting volume (117.7 +/- 3.8 and 117.6 +/- 3.5 msec, respectively; p = NS) but were significantly different with an added volume of 1.5 ml (91.4 +/- 5.5 and 112 +/- 5.6 msec, p less than 0.05). These changes were independent of coronary perfusion pressure and paced cycle length, suggesting that ischemia is an unlikely explanation for the observed effects. Changes in left ventricular volume decreased left ventricular ERP in a regionally heterogeneous manner, increasing the temporal dispersion of recovery over the left ventricle nearly twofold. Induced ventricular arrhythmias (ventricular tachycardia or fibrillation) were significantly more frequent at high (35%) than at low (3%) volumes during left ventricular pacing. We conclude that ventricular dilatation is associated with increased dispersion of refractoriness in this model, a finding that correlates with propensity for reentrant arrhythmias.
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PMID:Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart. 334 78

The clinical characteristics and prognosis of 16 cases of mitral regurgitation (MR) secondary to Kawasaki disease (KD) were studied, and its pathogenesis was discussed. The observation period ranged from 3 years and 17 months to 15 years. Six of the 16 patients died, and 10 are alive. MR has disappeared spontaneously in 2 of these survivors. Thirteen of the 16 patients were male and 3 were female, there being a predominance in male, which is a striking contrast to rheumatic mitral regurgitation which is predominant in females. The age at the time of diagnosis ranged from 3 months to 7 years. The appearance time of MR showed two different patterns, one with early onset within a few weeks to one month after affliction with KD and the other with MR developing months or years later during the course of the follow-up. The cardiothoracic ratio was greater in those who had a progressively downhill course, and whose sigma RV1-6 decreased with time course. This was considered to be due to the decrease of the remaining functioning myocardial mass. The outcome of the patients with a severe degree of coronary arterial stenosis and occlusion observed on the coronary angiogram was poor. The prognosis of the patients with severe left coronary arterial stenosis was especially poor. MR due to KD is regarded as a new clinical entity, and its pathogenesis is thought to be due to ischemia, papillary muscle dysfunction, coronary angitis, myocardial failure and valvulitis. Incidence of MR will increase when examined by Doppler echocardiography especially in the acute stage. Our experience as well as that of others indicates the presence of valvulitis, myocarditis or left ventricular dilatation leading to MR in the acute stage.
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PMID:Mitral regurgitation in Kawasaki disease. 342 45

Reversible myocardial depression, manifested by ventricular dilatation and decreased ejection fraction, is common in human septic shock. A proposed mechanism, based on animal studies, is myocardial ischemia resulting from inadequate coronary blood flow. Coronary flow observations have not been reported for human septic shock. To determine whether myocardial depression in human septic shock is associated with reduced coronary flow, thermodilution coronary sinus catheters were placed in seven patients with septic shock for measurements of coronary flow and myocardial metabolism. Four of the seven patients developed myocardial depression. These patients had coronary flow similar to or higher than that of control subjects and similar to that of the other three patients, who did not develop myocardial depression. None of the patients had net myocardial lactate production. In general, compared with values in control subjects, the oxygen content difference (arterial minus coronary sinus) was narrowed, and the fractional extraction of arterial oxygen was diminished. This pattern of disordered coronary autoregulation is analogous to the pattern of arteriovenous shunting in other organs in patients with septic shock. The preservation of coronary flow, the net myocardial lactate extraction, and the increased availability of oxygen to the myocardium argue against global ischemia as the cause of myocardial depression in human septic shock.
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PMID:The coronary circulation in human septic shock. 394 66


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