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At least 829 records · Page 46Linked to original sources
PubMed1998

The role of endothelin-1 in the aorta of post-infarct left ventricular dysfunction rats treated with captopril.

OBJECTIVES: There is little information available regarding local vasomotor regulating processes in chronic heart failure. In this study, we tested the hypothesis that chronic heart failure impaired the endothelial function, and long term captopril treatment might reverse endothelial activity through tissue endothelin (ET) pathway. METHODS: Forty Sprague-Dawley rats were divided into 4 groups including 15 rats in each of the sham-operated with or without captopril-treated groups and 5 rats in each of large infarcted with or without captopril-treated groups. RESULTS: Concentration-response curves obtained in aortic rings without endothelium revealed no difference in nitroprusside-induced relaxation. With endothelium, rightward shifting was noted only in the untreated large infarct group during acetylcholine-induced relaxation. As compared to the non-treated group, plasma ET-1 concentrations were lower in the captopril-treated with or without large infarct groups. However, endothelin-like immunoreactivity in endothelial cells and cytoplasma of smooth muscle cells of the media of the aorta were lower only in the non-treated large infarct group. CONCLUSIONS: Endothelial function was impaired in the chronic heart failure model. Coverting enzyme inhibitor might improve endothelial function through the Local endothelin pathway.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

[Heart tomography with 99mTc sestamibi and echocardiography with dobutamine in the identification of reversible left ventricular dysfunction in patients with acute myocardial infarction].

INTRODUCTION: We investigated the role of technetium-99m (99mTc) sestamibi cardiac imaging and dobutamine echocardiography in detecting myocardial viability early after acute myocardial infarction. MATERIAL AND METHODS: Nineteen patients (mean age 52 +/- 10 years) underwent coronary angiography, low-dose dobutamine echocardiography and rest 99mTc sestamibi imaging within 10 days of myocardial infarction. All patients were revascularized. Resting echocardiogram was repeated 8 months later to evaluate segmental functional recovery. RESULTS: Sixty-one of 108 akinetic or dyskinetic segments at baseline showed functional recovery after revascularization. Sensitivity in predicting segmental functional recovery was 87% for sestamibi imaging and 66% for dobutamine echocardiography (p < 0.001), while specificity and accuracy were comparable. Sestamibi activity was the strongest predictor of segmental functional recovery (p < 0.001). CONCLUSIONS: Dobutamine echocardiography predicts functional recovery after myocardial infarction. However, sestamibi imaging is useful to identify patients with dysfunctional segments without contractile reserve which may benefit by revascularization.

Cardiotonic Agents↗
PubMedDate not supplied

[Reversible left ventricular dysfunction in coronary disease (part one): myocardial stunning].

INTRODUCTION: The concept of myocardial stunning has been proposed by Braunwald and Kloner in early 1980's and is defined as transient postischemic myocardial dysfunction that persists after reperfusion, despite the absence of irreversible damage and restoration of normal or near normal coronary flow. Thus, the hallmark of stunned myocardium is the mismatch between coronary flow and myocardial function. MYOCARDIAL STUNNING: The two most plausible hypotheses used to explain the pathogenetic mechanisms of myocardial stunning are calcium and oxyradical hypotheses. According to the first one, myocardial stunning is the result of impaired calcium homeostasis caused either by calcium overload or decreased responsiveness of myofilaments to calcium. The oxyradical hypothesis postulates that generation of free oxygen radicals depresses myocardial function after the ischemic episode. The exact mechanism is unknown, but it is probably due to extreme reactivity of oxyradicals that bind to some cellular components, impairing membrane permeability and function of various cell organelle. Stunned myocardium can be seen in numerous clinical situations in which myocardial ischemia has been followed by reperfusion. These include: coronary artery bypass surgery, acute myocardial infarction, stable, unstable and variant angina, percutaneous transluminal coronary angioplasty and cardiac transplantation. DISCUSSION AND CONCLUSION: In majority of these situations, stunned myocardium is usually well tolerated. However, there is a group of high-risk patients in whom prolonged myocardial dysfunction due to stunning can cause serious hemodynamic instability, which requires pharmacological and/or mechanical support. Therefore, in order to avoid these situations, some authors have suggested that stunned myocardium should be prevented, rather than treated. Since stunned myocardium is by definition reperfused, with normal or near normal coronary flow, treatment is reserved only for those patients in whom stunned region is large enough to cause low cardiac output and hypotension. Revascularisation is usually unnecessary; however, there are situations in which episodes of repetitive stunning cause chronic myocardial dysfunction along with hibernated myocardium, when myocardial revascularization would be beneficial.

Animals↗
PubMed2000

[Comparison of the effectiveness of crystalloid and warm blood cardioplegia in patients with significant left ventricular dysfunction].

UNLABELLED: In a group of 84 patients undergoing elective coronary artery bypass surgery and with the ejection fraction lower than 40% two types of myocardial protection were studied. Group I (41 cases) was given intermittent cold crystalloid cardioplegia and group II (43 patients) was given intermittent warm blood cardioplegia followed by normothermic reperfusion. Preoperative, intraoperative and postoperative data were retrospectively collected. There were no differences between the two groups except more rhythm disturbances in group I and higher incidence of neurological complications in group II. CONCLUSIONS: Warm blood cardioplegia is an effective, cheap and practical myocardial protection technique.

Adult↗
PubMed2001

Sandwich ELISA for proANP 1-98 facilitates investigation of left ventricular dysfunction.

Proatrial natriuretic peptides are proposed to be sensitive and specific markers for various stages of heart deficiency. Here we present a rapid and specific sandwich immunoassay for the measurement of proANP 1-98 in biological fluids like plasma, serum urine. No sample preparation prior to the assay is necessary. Polyclonal antibodies specific for distinct epitopes of proANP 1-98, predicted to be highly immunogenic, were raised in sheep and purified by immunoaffinity chromatography prior to use in the assay. Antigen binding sites of the antibodies were determined by epitope mapping with a set of peptide fragments. The capture antibody, specific for proANP 16-23, is coated directly onto microtiter plates. Recombinant proANP 1-98 is used as a standard. The biotinylated detection antibody, specific for proANP 80-88, is incubated simultaneously with 20microl of sample for 150 min. Signal is generated with a streptavidin-HRPO-conjugate and TMB as substrate. The detection limit of the assay is 50 pmol/l; intraassay CVs are below 5%, interassay CVs are lower than 10%. Dilution curves show good linearity, recovery of synthetic peptide ranged between 85% and 91%. Reference values from healthy volunteers range from 0 to 2000 pmol/l in human plasma. We conclude this assay is a easy to handle, quick and reliable method for routine measurement of proANP 1-98 and the presented manuscript describes the procedure and performance of this ELISA in detail.

Animals↗