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Divergent effects of losartan and metoprolol on cardiac remodeling, c-kit+ cells, proliferation and apoptosis in the left ventricle after myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature97093
Source
Clin Transl Sci. 2009 Dec;2(6):422-30
Publication Type
Article
Date
Dec-2009
Author
Raisa Serpi
Anna-Maria Tolonen
Olli Tenhunen
Oskari Pieviläinen
Anna-Maria Kubin
Tommi Vaskivuo
Ylermi Soini
Risto Kerkelä
Hanna Leskinen
Heikki Ruskoaho
Author Affiliation
Institute of Biomedicine, Department of Pharmacology and Toxicology, Biocenter, Oulu, Finland.
Source
Clin Transl Sci. 2009 Dec;2(6):422-30
Date
Dec-2009
Language
English
Publication Type
Article
Keywords
Animals
Antihypertensive Agents - pharmacology - therapeutic use
Apoptosis - drug effects
Cell Count
Cell Proliferation - drug effects
Heart Ventricles - drug effects - physiopathology
Interleukin-1beta - metabolism
Losartan - pharmacology - therapeutic use
Metoprolol - pharmacology - therapeutic use
Myocardial Infarction - complications - drug therapy - pathology - physiopathology
Neovascularization, Pathologic - complications - physiopathology
Proto-Oncogene Proteins c-kit - metabolism
Rats
Ventricular Function, Left - drug effects
Ventricular Remodeling - drug effects
Abstract
There is strong evidence for the use of angiotensin converting enzyme inhibitors and beta-blockers to reduce morbidity and mortality in patients with myocardial infarction (MI), whereas the effect of angiotensin receptor blockers is less clear. We evaluated the effects of an angiotensin receptor blocker losartan and a beta-blocker metoprolol on left ventricular (LV) remodeling, c-kit+ cells, proliferation, fibrosis, apoptosis, and angiogenesis using a model of coronary ligation in rats. Metoprolol treatment for 2 weeks improved LV systolic function. In contrast, losartan triggered deleterious structural remodeling and functional deterioration of LV systolic function, ejection fraction being 41% and fractional shortening 47% lower in losartan group than in controls 2 weeks after MI. The number of c-kit+ cells as well as expression of Ki-67 was increased by metoprolol. Losartan-induced thinning of the anterior wall and ventricular dilation were associated with increased apoptosis and fibrosis, while losartan had no effect on the expression of c-kit or Ki-67. Metoprolol or losartan had no effect on microvessel density. These results demonstrate that beta-blocker treatment attenuated adverse remodeling via c-kit+ cells and proliferation, whereas angiotensin receptor blocker-induced worsening of LV systolic function was associated with increased apoptosis and fibrosis in the peri-infarct region.
PubMed ID
20443934 View in PubMed
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Effect on exercise performance of enalapril therapy initiated early after myocardial infarction. Nordic Enalapril exercise Trial.

https://arctichealth.org/en/permalink/ahliterature50206
Source
J Am Coll Cardiol. 1993 Oct;22(4):975-83
Publication Type
Article
Date
Oct-1993
Author
K. Dickstein
T. Aarsland
Author Affiliation
Medical Department, Central Hospital in Rogaland, Stavanger, Norway.
Source
J Am Coll Cardiol. 1993 Oct;22(4):975-83
Date
Oct-1993
Language
English
Publication Type
Article
Keywords
Administration, Oral
Age Factors
Aged
Double-Blind Method
Enalapril - pharmacology - therapeutic use
Exercise Test
Exertion
Heart Failure, Congestive - complications - physiopathology
Hemodynamic Processes - drug effects
Humans
Infusions, Intravenous
Male
Middle Aged
Myocardial Infarction - complications - drug therapy - pathology - physiopathology
Research Support, Non-U.S. Gov't
Time Factors
Abstract
OBJECTIVES. The Nordic Enalapril Exercise Trial was a multicenter subtrial of the Cooperative New Scandinavian Enalapril Survival Study (CONSENSUS II) designed to evaluate the effect on maximal exercise performance of a 6-month period of enalapril treatment initiated early after myocardial infarction. BACKGROUND. When begun early after myocardial infarction, converting enzyme inhibition therapy has been shown to attenuate infarct expansion and reduce left ventricular volume. Therapy has been associated with improved exercise performance. METHODS. Three hundred twenty-seven men (mean age 63.3 +/- 10.9 years) with documented acute myocardial infarction were randomized to treatment with enalapril or placebo on a double-blind basis. Intravenous enalaprilat or placebo therapy was initiated within 24 h after the onset of symptoms. Oral therapy was continued at a target dose of 20 mg/day. Patients exercised maximally at 1 month and 6 months after infarction to symptom-limited end points on a cycle ergometer with a 20 W/min incremental protocol. RESULTS. The treatment and control groups were comparable in patient age, concurrent therapy and type and site of infarction. At 1 month, for all patients, mean total work performed was 34.9 +/- 20.9 kJ in the enalapril group (n = 169) versus 28.5 +/- 20.6 kJ in the placebo group (n = 158) (difference = 18.4%, p 70 years old (difference = 41.4%, p
PubMed ID
8409072 View in PubMed
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Left ventricular thrombosis after anterior myocardial infarction with and without thrombolytic treatment.

https://arctichealth.org/en/permalink/ahliterature54764
Source
J Intern Med. 1995 Jun;237(6):563-9
Publication Type
Article
Date
Jun-1995
Author
T. Mooe
D. Teien
K. Karp
P. Eriksson
Author Affiliation
Department of Internal Medicine, Umeå University Hospital, Sweden.
Source
J Intern Med. 1995 Jun;237(6):563-9
Date
Jun-1995
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Female
Heart Diseases - etiology - physiopathology - prevention & control
Humans
Male
Middle Aged
Myocardial Infarction - complications - drug therapy - pathology - physiopathology
Prospective Studies
Research Support, Non-U.S. Gov't
Streptokinase - therapeutic use
Thrombolytic Therapy
Thrombosis - etiology - physiopathology - prevention & control
Treatment Outcome
Ventricular Function, Left - drug effects
Abstract
OBJECTIVES. To examine the incidence of left ventricular thrombus in patients with anterior myocardial infarction, with and without streptokinase treatment. To identify predictors of thrombus development. DESIGN. Consecutive patients prospectively studied during the hospitalized period. Echocardiography was performed within 3 days of admission and before discharge. SETTING. Umeå University Hospital, a teaching hospital in Northern Sweden. SUBJECTS. Ninety-nine patients with anterior myocardial infarction of whom 74 were treated with streptokinase. MAIN OUTCOME MEASURES. Left ventricular thrombus and left ventricular segmental myocardial function. RESULTS. During the hospital stay, a thrombus developed in 46% (95% confidence interval [CI], 35-57%) of the patients in the thrombolysis group and in 40% (95% CI, 21-59%) of the patients in the non-thrombolysis group. No difference in left ventricular segmental myocardial function was found between the thrombolysis and non-thrombolysis groups at hospital discharge. No embolic events were observed. The occurrence of a left ventricular thrombus at hospital discharge was significantly associated with previous myocardial infarction, peak enzyme levels, left ventricular global and segmental dysfunction and an increased dose of peroral diuretics or use of parenteral diuretics. In a multiple logistic regression model, left ventricular segmental dysfunction was the most important predictor of left ventricular thrombus. CONCLUSION. Thrombolytic treatment with streptokinase does not prevent the development of a left ventricular thrombus but the risk of embolic complications is low. The left ventricular segmental myocardial score can be used to assess the risk of thrombus development, also, after thrombolysis.
PubMed ID
7782728 View in PubMed
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