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)

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
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PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.
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PMID:Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations. 114 6

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

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

The prognostic implications of the presence of mitral regurgitation (MR) in patients with recent myocardial infarction has not been clarified yet. In March 1983, we undertook a prospective study in patients surviving a first episode of acute myocardial infarction. Over a 4-year period, 266 patients entered the study. Left ventriculography documented the presence of MR in 51 patients, while 215 did not have angiographic evidence of MR. The presence of MR was associated with larger infarcts, as shown by greater values of peak CK (P less than 0.05) and by the prevalence of Q-wave vs non-Q-wave infarctions (P less than 0.05). Transient left ventricular failure during hospitalization was more frequent in patients with MR (P less than 0.05), while the occurrence of early post-infarction angina was similar in the two groups of patients. No difference was found in the extent of coronary disease, yet patients with MR had higher values of left ventricular end diastolic pressure (LVEDP) (P less than 0.005) and a lower ejection fraction (EF) (P less than 0.001). Patients with MR had a reduced exercise capacity (P less than 0.005), but signs of myocardial ischaemia were similarly distributed in the two groups. Patients with anterior infarcts and MR had higher left ventricular volumes than patients without MR, while no difference was found between patients with and patients without MR and inferior infarction, suggesting that left ventricular dilatation may play an important role in the pathogenesis of MR in patients with anterior but not in those with inferior infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical significance of mitral regurgitation in patients with recent myocardial infarction. 339 Nov 84

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.
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PMID:Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia. 339 67

Dilated cardiomyopathy is a moderately common syndrome resulting from many causes, many of which are yet to be defined. The syndrome is relatively easy to diagnose in its late congestive stage if valvular abnormality, hypertensive disease, and gross myocardial infarction are absent. However, it should be suspected in patients with undiagnosed chest pain, in patients whose severe arrhythmia has no obvious cause, and in any patient with demonstrable ventricular dilatation or systolic malfunction. It may follow infections, especially viral ones and is found in many deficiency diseases, especially diabetes. Repeated episodes of angina due to epicardial disease may result in myocardial "stunning" with ultimate dilation and failure. Microvascular spasm or occlusion may be etiologically important. Dilated cardiomyopathy may be a manifestation of toxins, with ethanol being the most important. Immune mechanisms may play a major role, either independently or in connection with other factors. Early diagnosis may be made with the help of echocardiography, radionuclide angiography, and even coronary arteriography. Gallium scan may be helpful, and if positive myocardial biopsy is indicated. Therapy includes classic measures for congestive failure if it is present: cardiac glycosides, diuretics, antiarrhythmics, and anticoagulants. There is evidence that vasodilators, calcium channel blockers, and beta-adrenergic blockers may be helpful for both general and specific reasons, but these should be used with care. Prednisone and azathioprine may help if there is an inflammatory component. Cardiac replacement remains an ultimate measure.
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PMID:Dilated cardiomyopathy: current concepts. 372 Feb 70

Left ventricular function and exercise capacity were assessed in 79 patients randomised to receive intravenous and oral propranolol (n = 44) or conventional therapy (n = 35) within four hours of onset of their first myocardial infarction. Cineangiocardiography and exercise testing were performed four weeks after infarction to allow for maximum recovery of myocardial function. Left ventriculography showed no improvement in ejection fraction or preservation of regional contractile function in patients treated with propranolol compared with controls. A trend towards smaller end diastolic volumes was seen in the propranolol group (mean (SD) 151(42) ml) compared with controls (167(42) ml). Exercise duration and frequency of angina were not significantly different in the two groups. It is concluded that limitation of infarct size by propranolol does not lead to a significant improvement in ventricular systolic function, although left ventricular dilatation may be reduced. These findings are consistent with the known effect of early intravenous beta blockade which limits infarct size by preservation of subepicardial myocardium.
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PMID:Effect of early treatment with propranolol on left ventricular function four weeks after myocardial infarction. 405 76

This study set out to determine the pathophysiologic changes in the left ventricle during atrial pacing in 22 patients with coronary artery disease. Graduated right atrial pacing to a rate of 160 beats/min, or the induction of angina pectoris or significant ST depression was undertaken. Ventricular volumes were measured at rest and at rates of 100, 120, 140 and 160 beats/min using radionuclide angiography. The volumes at a pacing rate of 100 beats/min were used as a reference standard (100%). In the 22 patients with coronary artery disease, left ventricular end-diastolic volume decreased from 118 +/- 3% at rest to 80 +/- 5% at a rate of 160 beats/min; stroke volume from 121 +/- 3% to 54 +/- 5%; and ejection fraction (EF) from 49 +/- 3% to 37 +/- 5%. End-systolic volume decreased from 118 +/- 4% at rest, reached its minimal value of 94 +/- 5% at a rate of 120 beats/min and then increased slightly to 106 +/- 9% at 160 beats/min. Cardiac output and blood pressure did not change significantly. Compared to the control group of 10 normal subjects, the patients had a significantly smaller decrease in end-diastolic volume and end-systolic volume than in normal control subjects. EF in the normal subjects did not change. Blood pressure, cardiac output and stroke volume were similar in both groups. Atrial pacing tachycardia induced reversible ventricular dysfunction with a decrease in EF. Stroke volume was maintained because of relative ventricular dilatation.
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PMID:Left ventricular volumes and function during atrial pacing in coronary artery disease: a radionuclide angiographic study. 669 79

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.
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PMID:A prospective study of heart disease in diabetes mellitus. 670 23


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