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 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

The relation of global and regional right and left ventricular function during the acute phase after a first myocardial infarction was assessed by first pass radionuclide angiography in 20 patients (10 after anterior and 10 after inferior myocardial infarction). The right ventricular ejection fraction did not differ significantly between the groups, but left ventricular ejection fraction was significantly depressed after anterior myocardial infarction. There was evidence of right ventricular dilatation and impaired transit in the group with inferior infarction. Five patients with anterior infarction and six with inferior infarction had abnormal right ventricular ejection fractions. Right ventricular wall motion abnormalities affected the septal wall in the group with anterior infarction and the free wall in the group with inferior infarction. The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with anterior infarction there was a significant linear relation between right and left ventricular ejection fraction, whereas in the group with inferior infarction there was not. Thus right ventricular dysfunction commonly occurs after both anterior and inferior myocardial infarction. Right and left ventricular impairment are related after anterior myocardial infarction, but are independent after inferior myocardial infarction. Finally, the different effects of anterior and inferior myocardial infarction on right ventricular function may be explained by differences in septal and free wall involvement.
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PMID:Global and regional right ventricular function after acute myocardial infarction: dependence upon site of left ventricular infarction. 362 Feb 49

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

To assess the prevalence and significance of left ventricular dilatation in patients with severe left ventricular dysfunction secondary to coronary artery disease (or coronary artery cardiomyopathy), we studied 70 patients with an ejection fraction of 35 percent or less and one-vessel coronary artery disease (n = 14) or with multivessel coronary artery disease (n = 56). None had had a recent myocardial infarction or valvular heart disease. Patients who underwent myocardial revascularization during follow-up were excluded. The left ventricular end-diastolic volume (measured by contrast ventriculography) was less than 110 ml/sq m in 14 patients (20 percent) (group 1), and was 110 ml/sq m or more in 56 patients (80 percent) (group 2). There were no differences between the two groups in age, sex, diabetes mellitus, hypertension, extent of coronary artery disease, or left ventricular asynergy. Patients in group 1 had lower pulmonary arterial wedge pressure (13 +/- 6 vs 22 +/- 10 mm Hg; p = 0.0008), lower left ventricular end-diastolic pressure (21 +/- 6 vs 27 +/- 9 mm Hg; p = 0.007), and higher left ventricular ejection fraction (31 +/- 2 vs 25 +/- 7 percent; p = 0.001) than patients in group 2. At a mean follow-up of 27 months, 24 patients had died of cardiac causes, all of whom were in group 2. Survival was significantly better in group 1 than in group 2 (Mantel-Cox, p = 0.009). Survival analysis (Cox models) of 20 clinical, hemodynamic, and angiographic variables showed that ejection fraction (chi2 = 13.6; p less than 0.001) and end-diastolic volume chi2 = 4.7; p = 0.03) were the most significant predictors of death. Thus, minimally dilated coronary artery cardiomyopathy is a distinct entity with favorable hemodynamics. Prognostically, the end-diastolic volume adds significant predictive information to the ejection fraction among conservatively treated patients.
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PMID:Coronary artery cardiomyopathy. Hemodynamic and prognostic implications. 394 48

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

Myocardial infarction following coronary occlusion limits the effectiveness of emergency coronary artery bypass operations. We designed and evaluated a transvenously introduced balloon-tipped catheter and an electrocardiogram-activated pumping system for perfusing ischemic myocardium by retrograde pulsation of oxygenated blood into the coronary veins during diastole. Balloon deflation during systole allowed for normal venous drainage. Four groups of dogs (n = 26) were instrumented with sonomicrometry crystals and catheters to measure regional and global left ventricular function. Two groups of dogs had chronic left ventricular (LVH) produced by prior aortic banding (left ventricular mass 174 gm versus 115 gm for control dogs of equal body weight, p less than or equal to 0.05). The left anterior descending coronary artery (LAD) was occluded for 40 minutes; after 10 minutes left ventricular function was severely depressed in all groups (less than or equal to 0.05 compared to baseline). Groups 1 (normal left ventricle, n = 8) and 2 (LVH, n = 5) had no further therapy for the following 30 minutes. Groups 3 (normal left ventricle, n = 8) and 4 (LVH, n = 5) received 30 minutes of coronary vein retroperfusion (CVRP) 10 minutes following the LAD occlusion. CVRP restored 37% of systolic shortening, whereas there was no restoration of systolic shortening in control dogs (p less than or equal to 0.001). All other physiological and hemodynamic parameters including heart rate, cardiac output, aortic pressure, dP/dt, and left ventricular dilatation were normalized during CVRP while remaining severely depressed in control dogs (p less than or equal to 0.05). Following restoration of arterial flow at 40 minutes, 10 of 13 CVRP-treated dogs recovered normal left ventricular function while only two of 13 untreated dogs survived. CVRP offers a transvenous approach for modifying myocardial ischemia prior to emergency coronary artery bypass grafting.
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PMID:Modification of myocardial ischemia in normal and hypertrophied hearts utilizing diastolic retroperfusion of the coronary veins. 621 Aug 8

Necropsy findings were examined in 20 male patients with end-stage renal disease associated with longstanding spinal cord injury and treated with maintenance hemodialysis. All patients exhibited cardiovascular abnormalities. Fibrinous pericarditis was found in 50% of the patients. Left and right ventricular hypertrophy was present in 45% and 20% of the cases, respectively. The respective incidences of left and right ventricular dilatation were 40% and 30%. Cardiac amyloidosis was noted in 25% of the cases, whereas myocardial fibrosis was found in 45% of the patients. Valvular abnormalities were limited to one case of aortic stenosis and two cases of mitral ring dilatation. No evidence of infective endocarditis was observed despite the high incidence of infections in this population. Whereas 45% of the patients exhibited some degree of coronary arteriosclerosis, none exhibited evidence of acute myocardial infarction and only one showed pathologic changes consistent with old myocardial infarction. Aortic atherosclerosis was noted in the majority of patients.
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PMID:Cardiovascular pathology in dialysis patients with spinal cord injury. 622 12

Ventricular performance was assessed in rats three weeks following coronary artery ligation and the subsequent production of a wide range of infarct sizes. The entire spectrum of ventricular dysfunction was observed, from minimal impairment to overt congestive heart failure. Rats with small infarcts ejected normal baseline and volume-stressed forward outputs from a modestly dilated ventricular chamber. Rats with moderate infarcts exhibited normal baseline hemodynamics but had a reduced reserve flow capacity when challenged with a volume load despite considerable ventricular dilatation. Rats with large infarcts demonstrated frank congestive heart failure with elevations in both left and right ventricular filling pressures and consequent right ventricular hypertrophy; marked reductions in both baseline and volume-stressed forward outputs; and ventricular volumes that were twice those of rats without infarcts. Thus, a progressive impairment in ventricular performance and an increase in chamber volume occurred in relation to infarct size in rats with healed myocardial infarction.
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PMID:Ventricular performance in rats with myocardial infarction and failure. 623 4

Quantitative radionuclide angiography (with the first pass technique and a computerized multicrystal camera) was used to evaluate hemodynamic changes in three subject groups during symptom-limited upright exercise. The 12 normal subjects had significant increases in heart rate, stroke volume, left ventricular ejection fraction and cardiac output during exercise; changes in end-diastolic and end-systolic volumes were not significant. In the 24 patients with coronary artery disease there were significant increases in heart rate and cardiac output during exercise, but insignificant changes in end-diastolic, end-systolic and stroke volumes and ejection fraction. The change in diastolic volume in these patients was determined by the extent of coronary artery disease, propranolol therapy, end point of exercise and presence of collateral vessels. Furthermore, patients with previous myocardial infarction had a lower ejection fraction and higher end-diastolic and end-systolic volumes during exercise than those without myocardial infarction. In the 12 patients with chronic aortic regurgitation of moderate to severe degree, there was a decrease in the end-diastolic volume during exercise. This response was distinctly different from that of the normal subjects or the patients with coronary artery disease. All three groups had a significant decrease in pulmonary transit time during exercise. It is concluded that changes in cardiac output in normal subjects during upright exercise are related to augmentation of stroke volume and tachycardia, whereas in patients with coronary artery disease they are related mainly to tachycardia. Left ventricular dilatation during exercise occurred in some normal subjects and in patients with coronary artery disease but was not a consistent finding. However, a decrease in left ventricular end-diastolic volume is common in patients with aortic regurgitation. Such a decrease may be explained by a reduction in the regurgitant volume per beat caused by shortening of the diastolic filling period or a decrease in systemic vascular resistance, or both.
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PMID:Quantitative radionuclide angiography in assessment of hemodynamic changes during upright exercise: observations in normal subjects, patient with coronary artery disease and patients with aortic regurgitation. 626 23

Out of 178 consecutive patients with acute inferior wall myocardial infarction submitted to technetium-99 m pyrophosphate scintigraphy, 49 (27.5%) were found to have concomitant right ventricular infarction. Gated blood pool scans showed right ventricular abnormalities in 21 out of 26 patients who were submitted to this investigation (right ventricular asynergy: 16 cases; right ventricular dilatation: eight cases; decreased right ventricular ejection fraction: 16 cases). Complications were common in the acute stage. Shock was noted in 19 cases (eight related to bradycardia, three related to relative hypovolaemia and eight instances of true cardiogenic shock). Atrial fibrillation (seven patients), ventricular fibrillation (eight patients) and severe atrioventricular conduction disorders (13 patients) were also frequent. In spite of this, the in-hospital mortality was low: three deaths occurred (6.1%), one from heart failure, two others from posterior septal rupture. All patients were followed up for one year or more. Six additional deaths were noted (three from left cardiac failure, two from recurrent anterior wall infarction and one from massive pulmonary embolism). Clinical assessment, haemodynamic measurements and gated blood pool scans showed significant improvement of right ventricular function with return to normal in those cases with small right ventricular infarcts as judged from technetium-99 m pyrophosphate scintigraphy. In spite of the complications seen in the initial period, patients with a right ventricular infarction have a good overall prognosis and the long-term outcome, primarily determined by the left-sided lesions, is often favourable.
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PMID:Right ventricular myocardial infarction diagnosed by 99 m technetium pyrophosphate scintigraphy: clinical course and follow-up. 629 41


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