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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to characterise patients without overt heart failure and with a left ventricular ejection fraction > or = 40% 2-7 days following an acute myocardial infarction. Patients with an ejection fraction > or = 40% (n = 868) had a lower prevalence of anterior myocardial infarction (p < 0.001) and lower levels of N-terminal pro-ANP (atrial natriuretic peptide) (p < 0.001) than those with ejection fraction < 40% (n = 305). Patients with ejection fraction > or = 40% had smaller left ventricular volume and mass (p < 0.001). Pro-ANP levels did not correlate significantly with left ventricular volume or ejection fraction in this group. Among patients with ejection fraction < 40%; statistically significant correlations between pro-ANP levels and both ejection fraction and left ventricular endsystolic volume were found. 64% and 61% of patients in the two groups were given thrombolytic treatment. In this study, most patients with acute myocardial infarction had an ejection fraction > or = 40%. Pro-ANP levels were not correlated with the ejection fraction or left ventricular volume. Approximately two thirds of the patients received thrombolytic treatment.
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PMID:[Echocardiographic findings, pro-ANP and treatment in acute myocardial infarction without overt heart failure]. 1049 98

Anterior infarction changes ventricular shape and volume. Akinesia is most commonly observed after early reperfusion. Dyskinesia develops in the absence of reperfusion. Both produce heart failure by dysfunction of the remote muscle. Traditional surgery deals with dyskinesia. This study evaluates surgical anterior ventricular endocardial restoration (SAVER), an operation that excludes the apical and septal scar in both akinesia and dyskinesia. A new international group of cardiologists and surgeons from 13 centers, the RESTORE Group) investigated SAVER in ischemic cardiomyopathy following anterior infarction. From January 1998 to July 2000, 662 patients underwent surgery. Early and 3-year outcomes were investigated. Concomitant procedures included coronary artery bypass grafting (CABG) in 92%, mitral repair in 22%, and mitral replacement in 3%. Hospital mortality was 7.7%. Mortality among 606 patients with SAVER and CABG alone was 4.9%. It was 8.1% among 147 patients who underwent concomitant mitral valve repair. Few patients required IABPs (8.4%), LVADs (0.4%), or ECMO (0.6%). Postoperatively, ejection fraction increased from 29.7% +/- 11.3% to 40.0% +/- 12.3% and left ventricular end systolic volume decreased from 96 +/- 63 to 62 +/- 39 mL/m(2) (P <. 05). At 3 years, the survival rate was 89.4% +/- 1.3%. Survival was lower among those with preoperative volume >80 mL/m(2) compared with volume < or = 80 mL/m(2) (83.5% +/- 3.3% v 94.5% +/- 2.0%). Freedom from readmission to hospital for heart failure was at 88.7% at 3 years and was not related to preoperative volume. SAVER is a safe and effective procedure for treating the remodeled dilated anterior ventricle following anterior myocardial infarction.
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PMID:Surgical anterior ventricular endocardial restoration (SAVER) for dilated ischemic cardiomyopathy. 1180 40

A 54-year-old man who was admitted due to cardiogenic shock as a result of a large anterior myocardial infarction 3 days previously was about to die, despite reperfusion therapy, application of an intra-aortic balloon pump, mechanical ventilation and maximal medical therapy. After insertion of a percutaneous left ventricular assist device, the patient was haemodynamically stable. After 11 days, the assist device was weaned and was removed. One day later, the patient died due to progressive heart failure. This case shows that a percutaneously inserted left ventricular assist device is effective in patients with severe, refractory cardiogenic shock, and is relatively simple to insert in the heart catheterisation room. However, it is still not clear what the recovery possibilities of the heart are following a large myocardial infraction, which factors may influence this recovery, and what the applicability of such a ventricular assist device might be in bridging the recovery period.
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PMID:[Percutaneous insertion of a left ventricular assist device for cardiogenic shock in a patient with a myocardial infarction]. 1263 49

The object of this study of acute anterior myocardial infarction uncomplicated by cardiogenic shock, a context in which the role of intra-aortic balloon pumping (IABP) remains controversial, was to analyse the effects of IABP on coronary flow in the culprit artery. Twenty-one patients admitted for angioplasty in the acute phase of anterior myocardial infarction were included. The IABP was performed in 6 patients (Group 1) because of clinical signs of cardiac failure. Fifteen patients (Group 2) had no signs of cardiac failure. Coronary flow velocity was recorded by a Doppler catheter after successful angioplasty. The following parameters were analysed: average peak velocity (APV), average diastolic peak velocity (ADPV), average systolic peak velocity (ASPV), diastolic to systolic velocity ratio (DSVR) and maximum peak velocity (MPV). Intra-aortic balloon pumping was associated with an increase in the diastolic indices (APV 17.9 +/- 3.5 vs 14.9 +/- 3.6 cm/s; p < 0.05; ADPV 27.6 +/- 5.2 vs 19.7 +/- 4.7 cm/s; p < 0.05), and a decrease in the systolic index ASVP (3.8 +/- 1.3 vs 7.6 +/- 2.6 cm/s; p < 0.05). The diastolic indices recorded with IABP did not change in Group 2. The velocity spectra changed with the appearance of abnormalities usually described in the presence of microcirculatory abnormalities ("no reflex" phenomenon): decrease in anterograde systolic flow, rapid deceleration of diastolic velocities with appearance of a retrograde systolic flow. The authors conclude that IABP increases diastolic velocities of coronary flow in the acute phase of revascularised anterior myocardial infarction complicated by left ventricular failure but does not seem to be accompanied by improved myocardial perfusion.
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PMID:[Intra-aortic balloon pumping and variations in flow in the dilated coronary artery in acute myocardial infarction]. 1274 8

Matrix metalloproteinase-2 (MMP-2) is prominently overexpressed both after myocardial infarction (MI) and in heart failure. However, its pathophysiological significance in these conditions is still unclear. We thus examined the effects of targeted deletion of MMP-2 on post-MI left ventricular (LV) remodeling and failure. Anterior MI was produced in 10- to 12-wk-old male MMP-2 knockout (KO) and sibling wild-type (WT) mice by ligating the left coronary artery. By day 28, MI resulted in a significant increase in mortality in association with LV cavity dilatation and dysfunction. The MMP-2 KO mice had a significantly better survival rate than WT mice (56% vs. 85%, P < 0.05), despite a comparable infarct size (50 +/- 3% vs. 51 +/- 3%, P = not significant), heart rate, and arterial blood pressure. The KO mice had a significantly lower incidence of LV rupture (10% vs. 39%, P < 0.05), which occurred within 7 days of MI. The KO mice exerted less LV cavity dilatation and improved fractional shortening after MI by echocardiography. The LV zymographic MMP-2 level significantly increased in WT mice after coronary artery ligation; however, this was completely prevented in KO mice. In contrast, the increase in the LV zymographic MMP-9 level after MI was similar between KO and WT mice. MMP-2 activation is therefore considered to contribute to an early cardiac rupture as well as late LV remodeling after MI. The inhibition of MMP-2 activation may therefore be a potentially useful therapeutic strategy to manage post-MI hearts.
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PMID:Targeted deletion of MMP-2 attenuates early LV rupture and late remodeling after experimental myocardial infarction. 1277 62

From the available data, one cannot conclude whether thrombolytic therapy is beneficial or detrimental in patients older than age 75 years with acute myocardial infarction. Data favor the use of primary percutaneous transluminal coronary angioplasty rather than thrombolysis in eligible patients older than age 75 years with acute myocardial infarction to reduce mortality, recurrent myocardial infarction, stroke, and intracranial hemorrhage. High-risk elderly patients with acute myocardial infarction, such as those with a large anterior myocardial infarction complicated by heart failure and hypotension, those with persistent ischemic pain or marked ST-segment changes, those with hemodynamic instability, and those at high risk for stroke or bleeding complications, should, especially, be treated with percutaneous transluminal coronary angioplasty.
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PMID:Thrombolytic therapy is indicated for patients over 75 years of age with st-elevation acute myocardial infarction: antagonist viewpoint. 1461 Mar 82

Heparin-induced thrombocytopenia (HIT) type II is an acquired thrombophylic state and life-threatening immune complication of a heparin treatment mainly clinically manifested by marked thrombocytopenia, frequently by arterial and venous thrombosis, and sometimes by skin changes. Functional assay as heparin aggregation test and 14C-serotonin release assays are used in diagnostics as well as antigen assays of which detection tests for heparin-platelet factor 4 antibodies are most frequently used. Considering the fact that there is no single reliable assays for HIT II detection available, sometimes it is necessary to combine both of the above-mentioned types of assays. We present the case of a 57-year-old patient with an acute anterior myocardial infarction with cardiac insufficiency of III and IV degree according to Killip, recurrent ventricular fibrillation and diabetes mellitus type II developing thrombocytopenia to 37 x 10(9)/l accompanied with typical skin changes. The diagnosis was confirmed by the heparin aggregation test. The second patient aged 70 undergoing the treatment for anteroseptal myocardial infarction and reinfarction of the inferior wall complicated by a cardiogenic shock and acute right bundle branch block developed thrombocytopenia 59 x 10(9)/l on the third day of the heparin therapy, with the remark that he had received a heparin therapy during the first infarction as well. Antibodies against heparin-platelet factor 4 were detected by particle gel ID-HPF4 immuno-assay. In both patients, the disease had a lethal outcome despite all then available therapeutic measures applied. Further on we discuss advantages of certain types of tests, a therapy doctrine, need for urgent therapeutic measures, inclusive of the administration of antithrombins, avoidance of harmful procedures like low-molecular-weight heparins administration and prophylactic platelet transfusion as well as preventive measures.
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PMID:[Thrombocytopenia induced by type II heparin and myocardial infarct: 2 case reports]. 1522 63

A 54-year-old man with ischemic mitral regurgitation and severe heart failure due to broad myocardial infarction successfully underwent mitral valve plasty and coronary artery bypass grafting under beating heart. He had an old anterior myocardial infarction and was admitted to our hospital with acute inferior myocardial infarction. Two weeks later, the cathetelization revealed moderate mitral regurgitation and triple vessel coronary artery disease. We selected antegrade continuous blood perfusion for myocardial protection on operation. He recovered uneventfully and discharged on postoperative day 31. We could perform this procedure safety and satisfactorily, we could this procedure for heart valve operation with other complications.
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PMID:[Mitral valve plasty and coronary artery bypass grafting under beating heart cardiopulmonary bypass for severe left ventricular dysfunction; report of a case]. 1555 34

Anterior myocardial infarction produces abrupt left ventricular (LV) dysynergy and global systolic dysfunction. Rapid intense neurohumoral activation, infarct expansion, and early ventricular chamber dilatation all contribute to restoring a normal stroke volume despite a persistently depressed ejection fraction. Continued neurohumoral activation provokes late remodeling of the remote non-infarcted myocardium, characterized by an abnormal progressively increasing LV volume/mass ratio that leads to further LV remodeling. Heart failure is a progressive disorder of LV remodeling. Heart failure from post-infarction remodeling is unique because of the persistent non-functioning scar that self- perpetuates abnormal loading conditions and neurohumoral activation. Medical therapy attenuates remodeling and improves survival but does not change the size of the scar. Surgical ventricular restoration to exclude the non-functioning infarct from the ventricular cavity decreases ventricular volumes, increases global ejection fraction, attenuates neurohumoral activation and yields an excellent 5-year survival. Combined medical and surgical therapy is recommended in this patient population.
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PMID:Heart failure following anterior myocardial infarction: an indication for ventricular restoration, a surgical method to reverse post-infarction remodeling. 1588 71

A 65-year old patient was admitted after having sustained a ventricular septum rupture 18 days after an anterior myocardial infarction. He developed acute heart failure. Given the extremely high perioperative risk in surgical approaches in this setting, we decided for a transcatheter closure of the defect with an exclusively venous approach. After a complete recovery, the patient underwent open heart surgery with aorto coronary bypass, aneurysmectomy, and removal of the closure device. This case demonstrates that transcatheter closure of a post infarction ventricular septum rupture is a technically feasible and suitable method.
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PMID:Transcatheter closure of a ruptured ventricular septum after myocardial infarction using a venous approach. 1620 Apr 84


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