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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infarct expansion, defined as an alteration in the ventricular topography due to thinning and lengthening of the infarcted segment, develops within the first few hours of the acute symptoms, mostly in patients with a large, transmural, anterior myocardial infarction. Shape changes, peculiar to risk region location and due to disparity in regional ventricular architecture, could be posited as the first step in the process of infarct expansion, with various cellular mechanisms contributing to subsequent continued early and late ventricular dilation. Because the increase in left ventricular volume is expected to be linearly dependent on the extent of the infarction, limiting infarct size, by thrombolysis, would proportionally reduce enlargement of the cavity. The effect of thrombolysis on left ventricular volume, however, seems not to be completely accounted for by the lessening effect of reperfusion on infarct size, because data suggest a restraining effect of reperfusion on the process of ventricular dilation in addition to the lessening effect on infarct size. If this turns out to be true, then the achievement of a patent vessel even beyond the time period when that patency may be expected to salvage myocardium would be further justified. Theoretical predictions substantiate the potential effectiveness in restraining ventricular dilation of stiffening of the necrotic region alone, independently of myocardial salvage in infarcted patients. The process of progressive ventricular dilation involves not only a primary alteration in function of the infarcted region, but also a time-dependent secondary change in the noninfarcted tissue itself, finalized to restore stroke volume despite a persistently depressed ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular remodeling and infarct expansion. 827 68

The prevalence of left ventricular (LV) thrombosis and incidence of arterial embolism after acute anterior myocardial infarction (AAMI) treated with streptokinase 1.5 x 10(6) IU intravenously was studied in 136 patients enrolled consecutively in five cardiological centres. Adjunctive antithrombotic therapy was administered according to the routine of each centre. Thrombus formation was studied by two-dimensional echocardiography, and events of arterial embolism recorded. LV thrombosis was found in 37 (27.2%) of the patients. In a subgroup of 53 patients receiving post-thrombolytic therapy with acetylsalicylic acid only, a thrombus developed in 14 (26.4%). The thrombus prevalence among patients given high-dose heparin was significantly lower than among those receiving either low-dose heparin or no heparin (4/30 vs 33/106, P = 0.045). Logistic regression analysis suggested that severe LV wall motion abnormality (P < 0.001) and avoidance of treatment with high-dose heparin (P = 0.023) were independent predictors of LV thrombus formation. Only one patient (0.7%) suffered arterial embolism (ischaemic stroke). In conclusion, LV thrombosis is frequent after thrombolytic therapy for AAMI, and impaired LV wall motion represents an independent predisposing factor. Low-dose heparin and acetylsalicylic acid seem less effective for LV thrombus prophylaxis than high-dose heparin. The incidence of arterial embolism is low.
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PMID:Left ventricular thrombosis and arterial embolism after thrombolysis in acute anterior myocardial infarction: predictors and effects of adjunctive antithrombotic therapy. 829 30

The authors used Thoratec left ventricular assist devices (VADs) for more than 30 days in eight patients. There were five left atrial (LA) (total, 513 days; range, 33-202 days) and three left ventricular (LV) cannulations (total, 484 days; range, 44-247 days). The flow provided by LA cannulation was less than that provided by LV cannulation. However, serial measurements of hematologic, renal, and hepatic function were similar for patients with LA and those with LV cannulation throughout support. Plasma free hemoglobin and lactate dehydrogenase (LDH) levels were similar for LA and LV patients. The five LA patients had one transient ischemic attack, one reversible ischemic neurologic deficit, and one stroke. The LV patients had no neurologic events (p = 0.20; LA versus LV total neurologic events). One LA patient and one LV patient died during support. Three LA patients underwent transplant, and one LA patient recovered native cardiac function. Two LV patients underwent transplant. In certain situations (e.g., recent anterior myocardial infarction; small left ventricular dimensions) LA cannulation may be advantageous. Neurologic events may be more common in LA patients, but in our small group this difference could be attributable to chance alone. LA or LV cannulation for a Thoratec VAD can provide adequate circulatory support for more than 30 days.
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PMID:Left atrial or ventricular cannulation beyond 30 days for a Thoratec ventricular assist device. 857 58

In 53 patients with recent (< 6 hrs) acute myocardial infarction a study was undertaken to evaluate the safety of conjunctive therapy with streptokinase (1.5 mln U), aspirin (150 mg) and low molecular weight heparin (Fraxiparine). Patients were treated with Fraxiparine 250 U anti-Xa IC/kg/24 hrs iv for 2 days (with bolus 12.5 U anti-Xa IC/kg), and 125 U anti-Xa IC/kg twice a day sc for 5 subsequent days. Clinical course in one-year observation was compared regarding the time the therapy was initiated. In the group undergoing therapy 3-6 hrs after the infarct had occurred 4 (7.5%) patients died (2 during hospitalization, 2 after discharge). In 31 patients treated within 3 hrs of the myocardial infarction there were fewer cases of recurrent myocardial infarction, unstable angina or congestive heart failure necessitating rehospitalization their (9.1%) than in 22 patients included in the treatment regimen between 3 rd and 6th h of the infarction (27.3%). Earlier thrombolysis was also connected with higher left ventricular ejection fraction (55 +/- 8% vs 49 +/- 10%) and more frequent peak CK-MB values 12 hrs after thrombolysis (81% and 68% of patients respectively). Neither symptomatic deep vein thrombosis nor pulmonary embolism was detected. The left ventricular thrombosis was diagnosed by echocardiography in 4 of 20 patients (20%) with the first anterior myocardial infarction. There was neither bleeding requiring blood transfusion nor cerebrovascular stroke. The treatment with Fraxiparine did not induce the prolongation of APTT values. Conjunctive thrombolytic therapy with low molecular weight heparin was safe and followed by a favorable outcome of the acute myocardial infarction, especially if instituted within the first 3 hrs after the onset of infarction.
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PMID:[Low molecular weight heparin (Fraxiparine) as adjunctive therapy with thrombolysis for acute myocardial infarction: a pilot study with a one year follow up]. 867 95

To investigate the role of left ventricular (LV) diastolic function in the maintenance of exercise capacity in patients with systolic dysfunction, symptom-limited cardiopulmonary exercise testing combined with radionuclide ventriculography was performed in 24 patients with an LV ejection fraction < 35% after anterior myocardial infarction. The ratio of pulmonary artery wedge pressure (PAWP) to LV end-diastolic volume (EDV), an index of global diastolic function, correlated significantly with peak oxygen consumption at peak exercise (r = -0.55; p = 0.006), whereas ejection fraction at peak exercise did not. The change in PAWP/EDV ratio from rest to peak exercise was related to the increases in stroke volume (r = -0.54; p = 0.006) and cardiac output (r = -0.51; p = 0.01) during exercise, but the change in ejection fraction was not. Resting hemodynamics did not differ between patients with preserved exercise capacity (group 1, n = 8) and those with exercise impairment (group 2, n = 16). At peak exercise, stroke volume, cardiac output, and EDV were significantly higher, and PAWP and PAWP/EDV ratio were significantly lower in group 1 than in group 2, but ejection fraction and end-systolic volume were similar in both groups. Although the incidences of hypertension, LV hypertrophy, and infarct-related coronary artery lesions did not differ between the two groups, group 2 had a significantly higher incidence of non-infarct-related coronary artery lesions than group 1 (p < 0.05). Thus in patients with LV systolic dysfunction after anterior myocardial infarction, the major cause of exercise impairment and failure to increase LV performance during exercise was diastolic dysfunction associated with the presence of non-infarct-related coronary artery lesions with the potential for exercise-induced ischemia of the noninfarcted areas.
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PMID:Importance of left ventricular diastolic function on maintenance of exercise capacity in patients with systolic dysfunction after anterior myocardial infarction. 900 95

Alteplase (recombinant tissue plasminogen activator; rt-PA) is a thrombolytic agent that when given in an accelerated regimen with intravenous heparin has survival advantages compared with streptokinase in the treatment of acute myocardial infarction, as shown by the results of the Global Utilisation of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) trial. Although alteplase is more fibrin-specific than streptokinase, alteplase therapy is associated with a small relative increase in the incidence of haemorrhagic stroke, but appears to cause a small relative decrease in the incidence of major bleeding. Because alteplase has a higher acquisition cost than alternative thrombolytic agents, analyses have been undertaken to assess whether administration of alteplase after myocardial infarction is a cost-effective use of healthcare resources. In retrospective analyses undertaken before completion of the GUSTO trial, it was generally assumed, on the basis of better 90-minute patency rates, that alteplase would provide survival advantages compared with streptokinase or conventional nonthrombolytic therapy. Alteplase had acceptable cost-effectiveness ratios compared with conventional therapy and streptokinase therapy from both third-party payer and hospital perspectives. Subgroup analyses demonstrated that alteplase was more cost effective when given early after symptom onset and when given to patients with large infarcts. Prospective evaluations of the cost effectiveness of alteplase in 3-hour and accelerated regimens have similarly demonstrated that alteplase therapy after myocardial infarction improves survival at an 'acceptable' cost. The largest prospective evaluation undertaken to date was performed in conjunction with the GUSTO trial. Primary analysis, on the basis of the clinical findings of the GUSTO trial and prospective collection of cost data from US patients, revealed that the cost-effectiveness ratio for accelerated alteplase therapy compared with streptokinase was $US32,687 (1993 dollars) per year of life saved (YLS). This value is most relevant for US patients and lies within the definition of 'cost effective' if $US50,000/YLS is the benchmark for acceptable use of resources. The cost-effectiveness ratio for alteplase was most sensitive to assumptions regarding long term survival and cost differences after the first year following treatment. In subgroup analyses, alteplase was a cost-effective treatment option for all elderly patients (> 60 years of age) and all patients > 40 years of age with anterior infarction. Alteplase therapy appears to have in-hospital costs/charges similar to those for primary percutaneous transluminal coronary angioplasty (PTCA), mainly because PTCA appears to have a favourable effect on duration of hospitalisation. Given the technical expertise and facilities required for PTCA, it is likely that thrombolytic therapy will remain the management option of choice in most centres. In conclusion, under the conditions of the GUSTO study, accelerated alteplase in combination with intravenous heparin confers survival advantages compared with streptokinase therapy. While decision-makers must choose how best to use their available healthcare resources, pharmacoeconomic evaluations have confirmed that, on the basis of accepted benchmark values, alteplase therapy is a cost-effective therapeutic option for the treatment of acute myocardial infarction, especially in elderly patients with either anterior or inferior infarcts and nearly all patients with anterior myocardial infarction. Thus, on the basis of clinical and economic data, predominantly provided by the GUSTO trial, alteplase is a cost-effective first-line management option for acute myocardial infarction.
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PMID:Alteplase: a pharmacoeconomic evaluation of its use in the management of myocardial infarction. 1017 69

The effect of beta-blockade on left ventricular (LV) remodeling, when added to angiotensin-converting enzyme inhibition (ACEI) after anterior myocardial infarction (MI), is incompletely understood. On day 2 after coronary ligation-induced anteroapical infarction, 17 sheep were randomized to ramipril (ACEI, n = 8) or ramipril and metoprolol (ACEI-beta, n = 9). Magnetic resonance imaging was performed before and 8 wk after MI to measure changes in LV end-diastolic, end-systolic, and stroke volume indexes, LV mass index, ejection fraction (EF), and regional percent intramyocardial circumferential shortening. (123)I-labeled m-iodobenzylguanidine (MIBG) and fluorescent microspheres before and after adenosine were infused before death at 8 wk post-MI for quantitation of sympathetic innervation, blood flow, and blood flow reserve in adjacent and remote noninfarcted regions. Infarct size, regional blood flow, blood flow reserve, and the increase in LV mass and LV end-diastolic and end-systolic volume indexes were similar between groups. However, EF fell less over the 8-wk study period in the ACEI-beta group (-13 +/- 11 vs. -22 +/- 4% in ACEI, P < 0.05). The ratio of adjacent to remote region (123)I-MIBG uptake was greater in ACEI-beta animals than in the ACEI group (0.93 +/- 0.06 vs. 0.86 +/- 0.07, P < 0.04). When added to ACE inhibition after transmural anteroapical MI, beta-blockade improves EF and adjacent regional sympathetic innervation but does not alter LV size.
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PMID:Beta-blockade improves adjacent regional sympathetic innervation during postinfarction remodeling. 1051 78

The presence of a cerebral pathology or of previous hemorrhagic cerebrovascular accidents is considered a contraindication to fibrinolytic therapy during acute myocardial infarction due to the elevated risk of intracranial hemorrhage. Lytic therapy reduces early mortality by 25-50% in patients with anterior myocardial infarction, and logistic considerations make primary angioplasty unfeasible in most clinical centers. Present guidelines exclude most patients who are at risk of a hemorrhagic stroke from fibrinolytic therapy, depriving some of them of a cure which has been demonstrated to be effective. Here we describe 2 cases of patients who had previously been treated for cerebral aneurysms and who were later treated with fibrinolytics during the course of an acute myocardial infarction. Based on the observation of these 2 cases and on the data available in the literature, we identified some patients with cerebral aneurysms or cerebral artero-venous malformations, whose pathology, once adequately corrected, cannot be considered an absolute contraindication to lytic therapy in the presence of a large myocardial infarction, when an emergency coronary angioplasty cannot be performed.
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PMID:[Is a previous neurosurgical intervention a contraindication to fibrinolytic therapy? Description of two cases and review of the literature]. 1093 40

Left ventricular thrombus (LVT) is a frequent complication in patients with acute anterior myocardial infarction (MI) and in those with dilated cardiomyopathy (DCM). The clinical importance of LVT lies in its potential to embolize. The current treatment of patients with acute MI centers on reperfusion, and although controversial, the incidence of LVT complicating acute anterior MI is probably reduced when compared with historical controls. Nevertheless, stroke continues to be a clinically important complication of acute MI and is most common in patients with anterior MI, in part secondary to embolization of LVT. Therapeutic anticoagulation during acute MI reduces the incidence of LVT, and long-term anticoagulation has been associated with a reduction in recurrent infarction and ischemic stroke, but carries hemorrhagic risk. Primary treatment strategies for patients with acute MI center on reperfusion therapy followed by antiplatelet agents and pharmacologic blockade of abnormal neurohumoral mechanisms. Strategies to prevent stroke following infarction include risk stratification for development of LVT and embolism. For patients with anterior MI, particularly those with apical akinesis or dyskinesis, therapeutic anticoagulation reduces the number of LVT and cardioembolic strokes. However, the absolute number of ischemic strokes prevented with this strategy may only be marginal, given the anticoagulation risk, particularly if antiplatelet agents are used concurrently. An attractive alternative strategy is echocardiographic evaluation following anterior infarction with therapeutic anticoagulation reserved for those with demonstrable thrombus. The efficacy of this strategy, however, never has been proven in a clinical study. Primary prevention of cardioembolic stroke through therapeutic anticoagulation is controversial in patients with DCM; the greatest benefit would be expected for those with severe left ventricular dysfunction. If LVT is detected during the course of MI or DCM, therapeutic anticoagulation is usually indicated with the expectation that the majority of thrombi will resolve without clinical evidence of systemic embolism. Additional therapeutic intervention is rarely needed.
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PMID:Left Ventricular Thrombus. 1169 71

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


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