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 aim of this study was to determine whether the percentage of akinesia on echocardiography during the acute phase of transmural anterior myocardial infarction could predict secondary left ventricular dilatation. The study group comprised 24 patients (18 men and 6 women) with an average age of 59 years. The patients underwent two echocardiographic examinations, the first during the acute (< 72 hours) phase and the second, 6 months later. Ventricular volumes were calculated by the ellipse monoplane method in the apical 4 chamber view. The percentage of akinesia was defined as the ratio between the length of the akinetic segment and the left ventricular end diastolic perimeter in the apical 4 chamber view. An increase in end diastolic volume (83 +/- 25 vs 62 +/- 18 ml/m2; p < 0.01) and in end systolic volume (51 +/- 27 vs 34 +/- 11 ml/m2; p < 0.01) was observed 6 months after infarction without a significant change in ejection fractions (42 +/- 17% vs 44 +/- 10%). The percentage of akinesia in the acute phase was > 30% in 15 patients (Group I) and < 30% in 9 patients (Group II). The increase in ventricular volumes at 6 months after infarction was significant in Group I (p < 0.02) but not in Group II. At 6 months after infarction, the end systolic volumes were greater (60 +/- 27 vs 37 +/- 22 ml/m2, p < 0.5) and the ejection fractions were lower (35 +/- 13% vs 53 +/- 18%, p < 0.01) in Group I than in Group II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Left ventricular dilatation after primary transmural anterior myocardial infarction. Influence of the percentage of akinesia on echocardiography]. 129 91

We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months. No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [+/- SEM] of 21 +/- 8 ml (P less than 0.02) in the placebo group, but by only 10 +/- 6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P less than 0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P less than 0.05). Patients given captopril also had increased exercise capacity (P less than 0.05). This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.
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PMID:Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. 296 17

To evaluate pathologic features of myocardial infarction of the right ventricle (MI-RV), we analyzed 106 autopsy cases with transmural myocardial infarction (MI) (fresh in 46 cases and healed in 60). Anterior MI was observed in 47, posterior MI in 54 and lateral in 5. There were 13 cases (12%) with MI-RV (anterior in 1 case and posterior in 12), which included 10 cases with fresh MI and 3 with healed MI. All cases with MI-RV had associated transmural interventricular septal infarction. Of the 13 cases with MI-RV, 9 (69%) had right ventricular dilatation (RVD) and 2 had right ventricular hypertrophy. Extensive MI-RV (more than 1/3 of the right ventricle) was observed in 8 (89%) of those with RVD. Of 93 cases of MI without MI-RV, 14 (16%) had RVD. The incidence of RVD was greater in cases with MI-RV than in those without (p less than 0.005). All 12 cases with posterior MI-RV had significant (greater than or equal to 75%) narrowing of the right coronary artery (RCA), and 19 cases (87%) of those with posterior MI without MI-RV, had similar lesions. In conclusion, the incidence of RVD and significant narrowing of RCA was greater in cases with posterior MI-RV than in those with posterior MI.
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PMID:Pathologic study of myocardial infarction of the right ventricle. 296 27

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

The purpose of this study was to evaluate the detectability of stress-induced ischemic lesion in patients with previous myocardial infarction using single photon emission computed tomography (SPECT) producing thallium-201 (T1-201) myocardial perfusion imagings (MPI). Seventy patients underwent stress SPECT by symptom-limited graded bicycle ergometer exercise using a dual-headed rotating gamma camera (Toshiba GCA70A) equipped with a computer system (GMS90). After intravenous administration of 2.5 mCi of T1-201, stress SPECT data at 10 minutes and delayed SPECT data at 3 hours after the injection were collected in the 64 X 64 matrix form covering 360 degrees directions by camera sweep of 180 degrees in 6 minutes, which were immediately followed by conventional planar imagings (PL). Transaxial tomographic image reconstruction was performed by convolution method using a Shepp-Logan's filter. Thereafter, sagittal and coronal tomographic images were reconstructed for about 2 minutes. Image interpretation was assessed visually. The results were as follows: Sensitivity and specificity in detecting the affected vessel with more than 75% stenosis by segmental analysis of myocardial images were higher by SPECT than by PL (LAD 89% and 65%, LCX 68% and 56%, RCA 89% and 76% in sensitivity and LAD 94% and LCX 75%, 92% and 94%, RCA 81% and 59% in specificity, respectively). Sensitivity in detecting both single (82%) and multivessel disease (76%) was fairly high. Detectability of stress-induced ischemia (i.e. occurrence of a new defect in patients with previous myocardial infarction and ST-segment depression in ECG) was significantly higher in SPECT (67%) than in PL (39%, p less than 0.005) and in ECG (39%, p less than 0.005). A perfusion defect in the extensive anterior wall, marked left ventricular dilatation and the widening of the angle toward the apex composed of septal and anterolateral walls in transaxial images were the findings characteristic of anterior myocardial infarction with severe dyskinesis. We conclude that stress SPECT is a useful noninvasive technique for the documentation of the number of vessels affected and severe wall motion abnormality of the LV and for the detection of stress-induced ischemia in previous myocardial infarction.
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PMID:[Detectability of stress-induced ischemic lesion in previous myocardial infarction using 201T1 myocardial single photon emission computed tomography]. 633 58

In a series of 75 consecutive patients with transmural acute myocardial infarction (AMI) a right-to-left ventricular filling pressure ratio equal to or greater than 0.65 (RVFP/LVFP greater than or equal to 0.65) was assumed to be indicative of associated right ventricular infarction (RVI). Out of 45 patients with inferoposterior myocardial infarction, 11 (24%) had such hemodynamic evidence of right ventricular infarction (group A). The remaining 34 patients with inferoposterior myocardial infarction (group B) and the 30 patients with anterior myocardial infarction did not. Time-motion and two-dimensional echocardiographic examinations were performed 7-10 days after admission in the 62 patients who survived. Right ventricular wall asynergy was found in six of eight group A patients. In three of these, right ventricular dilatation was also present. No patient in group B with inferior infarction or with anterior infarction showed abnormal right ventricular wall motion. While hemodynamic monitoring seems presently the most specific diagnostic method and it is of invaluable help in the choice of the best pharmacological therapy of right ventricular failure due to RVI, two-dimensional echocardiography is probably highly sensitive and specific for the diagnosis of RVI, by detecting RV wall motion and thickening abnormalities. Due to advantages, such as noninvasivity and repeatibility, two-dimensional echocardiography can be used in the selection of patients who deserve hemodynamic monitoring and in follow-up studies.
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PMID:Echocardiographic features of right ventricular infarction. 674 96

Prevention of post-infarction ventricular remodeling is an important therapeutic aim since left ventricular dilatation is one of the most important prognostic post-infarction determinants. Early reperfusion and chronic treatment with ACE-inhibitors are able to limit remodeling by means of two distinct mechanisms. Early reperfusion limits the extent of the infarcted area by salvaging a part of the myocardial area at risk of necrosis. ACE-inhibition, on the other hand, by reducing afterload, facilitates cardiac ejection and therefore tends to reduce left ventricular volume. Remodeling could be limited also by drugs which, like L-carnitine, act, as has been demonstrated by experimental studies, on the use of energy substrates both in the area at risk of necrosis and in the area subjected to a greater wall stress because of remodeling and which will progressively dilate over time. The CEDIM study is a double-blind, randomized, placebo-controlled, multicentre trial which has involved 36 Heart Divisions. The CEDIM study aims at evaluating the effects of L-carnitine on left ventricular function, as assessed by echocardiography, in patients with acute anterior myocardial infarction.
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PMID:[Prevention of post-infarction remodelling with L-carnitine: multicenter study CEDIM (L-Carnitine digital echocardiography myocardial infarction)]. 763 89

The purpose of this investigation was to study whether favorable renal effects might contribute to the influence of captopril in offsetting ventricular dilatation after infarction. Effective renal plasma flow and glomerular filtration rate were estimated by isotope injection methods in 20 patients on days 2, 7, 8, 42 and 180 after a first transmural anterior myocardial infarction. After measurements on day 7, patients were randomized to receive either captopril 25 mg 3 times daily (n = 10) or placebo (n = 10) for the remainder of the study. At baseline (day 7) there were no differences between the 2 treatment groups in radionuclide left ventricular ejection fraction, effective renal plasma flow, glomerular filtration rate or neurohormones. Left ventricular ejection fractions (40 +/- 4% [mean +/- 2 SD] at baseline) were higher in the captopril- than the placebo-treated patients on days 42 (p < 0.05) and 180 (p < 0.01) after infarction. Effective renal plasma flow became significantly higher at all time points after randomization in the captopril-treated group than in the placebo group (p < 0.001). A similar but lesser trend was observed for glomerular filtration rate. Plasma atrial natriuretic factor and aldosterone were significantly higher in the placebo group (p < 0.05). Renal hemodynamic indexes were directly correlated with and neurohumoral indexes inversely correlated with ejection fractions. In a second group of 12 patients with higher baseline ejection fractions (48 +/- 4%) after an inferior infarction, none of these beneficial effects of captopril were demonstrable. It is proposed that in the setting of left ventricular dysfunction after infarction, a prompt and sustained improvement in renal hemodynamics, by reducing inappropriate fluid retention and thus ventricular preload, may be one contributory mechanism by which captopril prevents progression of left ventricular dilatation.
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PMID:Effectiveness of captopril in reversing renal vasoconstriction after Q-wave acute myocardial infarction. 836 82

We measured left ventricular volume in 70 asymptomatic patients after first Q-wave anterior myocardial infarction in order to determine whether ventricular dilatation occurs and whether there is evidence for its attenuation or prevention by treatment with captopril or xamoterol--PRevention Of VEntricular Dilatation?: the PROVED? study. 77% of patients received thrombolytic treatment. Patients were randomised a mean of 11 days after infarction to receive either captopril 25 mg three times daily, xamoterol 200 mg twice daily or matching placebo. After 6 months of treatment, 6 patients from the placebo group (n = 24), 1 from the captopril group (n = 23) and 3 from the xamoterol group (n = 23) had been withdrawn from the study because of clinical complications. Left ventricular volume was measured using magnetic resonance imaging, before randomisation and after 6 months of treatment. Changes in left ventricular end-diastolic and end-systolic volume after 6 months of treatment were defined prospectively as the primary endpoints. Mean initial end-diastolic volume index was 85 (S.D. 19) ml/m2, mean end-systolic volume index was 45 (S.D. 18) ml/m2, and mean ejection fraction was 48 (S.D. 11)% for the whole group. There was no significant change in left ventricular volume index in the placebo or either treatment group after 6 months of treatment. Only minimal left ventricular dilatation was evident at 11 days. No further increase in left ventricular volume occurred after six months and there was no additional benefit from treatment with either captopril or xamoterol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular volume in thrombolysed patients with acute anterior myocardial infarction: the effect of captopril and xamoterol. 852 9

Progressive left ventricular dilatation is an important determinant of prognosis after myocardial infarction. The association of this process with the occurrence of ventricular arrhythmias is less well established. Of 153 patients with a first anterior myocardial infarction treated with thrombolytic therapy, 34 (22%) had high-grade ventricular arrhythmias (Lown 4A and B) during Holter monitoring after 1 year. Patients with high-grade ventricular arrhythmias had a larger end-systolic volume (38 +/- 12 vs 25 +/- 11 mL/m2; P < .001) at hospital discharge and more left ventricular dilatation (10 +/- 18 vs 1 +/- 9 mL/m2; P = .011) during the follow-up period. Increased end-systolic volume at discharge and subsequent dilatation proved to be independent predictors of high-grade ventricular arrhythmias. Six patients died suddenly during the first 12 months after myocardial infarction. Four of these patients had an enlarged end-systolic volume (> 22 mL/m2) at discharge, and the three patients who died suddenly after 3 months showed a significant increase in end-systolic volume from discharge to 3 months compared to survivors (16 +/- 6 vs 2 +/- 9; P = .008). Left ventricular remodeling after myocardial infarction is an independent predictor of the occurrence of ventricular arrhythmias late after myocardial infarction.
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PMID:Left ventricular dilatation and high-grade ventricular arrhythmias in the first year after myocardial infarction. CATS Investigators. Captopril and Thrombolysis Study. 942 Jun 28


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