ArticleJournal of cardiac failure2007
Left atrial reverse remodeling in dogs with moderate and advanced heart failure treated with a passive mechanical containment device: an echocardiographic study.
Article in Journal of cardiac failure, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- The echocardiography in the cardiovascular laboratory: a guide to research with animals.Arquivos brasileiros de cardiologia · 2014Review
- Control of autocrine and paracrine myocardial signals: an emerging therapeutic strategy in heart failure.Heart failure reviews · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAssessment of global left ventricular (LV) remodeling is important in evaluating the efficacy of pharmacologic and device therapies for the treatment of chronic heart failure (HF). The effects of pharmacologic or device therapies on global left atrial (LA) remodeling in HF, although also important, are not often examined. We showed that long-term therapy with the Acorn Cardiac Support Device (CSD), a passive mechanical ventricular containment device, prevents or reverses LV remodeling in dogs with HF. This study examined the effects of the CSD on global LA remodeling in dogs with moderate and advanced HF. METHODS AND
resultsStudies were performed in 24 dogs with coronary microembolization-induced HF. Of these, 12 had moderate HF (ejection fraction, EF 30% to 40%) and 12 advanced HF (EF < or = 25%). In each group, the CSD was implanted in 6 dogs and the other 6 served as controls. Dogs were followed for 3 months in the moderate group and 6 months in the advanced HF group. LA maximal volume (LAVmax), LA volume at the onset of the p-wave (LAVp), LA minimal volume (LAVmin), LA active emptying volume (LAAEV), and LA active emptying fraction (LAAEF) were measured from 2-dimensional echocardiograms obtained before CSD implantation and at the end of the treatment period. Treatment effect (delta) comparisons between CSD-treated dogs and controls showed that CSD therapy significantly decreased LA volumes (deltaLAVmax: 3.33 +/- 0.70 vs. -2.87 +/- 1.31 mL, P = .002; 7.77 +/- 1.76 versus -0.37 +/- 0.87 mL, P = .002) and improved LA function (deltaLAAEF: -6.00 +/- 1.53 versus 1.85 +/- 1.32%, P = .003; -2.39 +/- 1.10 versus 3.13 +/- 1.66%, P = .02) in the moderate HF and advanced HF groups, respectively.
conclusionsProgressive LA enlargement and LA functional deterioration occurs in untreated dogs with HF. Monotherapy with the CSD prevents LA enlargement and improves LA mechanical function in dogs with moderate and advanced HF indicating prevention or reversal of adverse LA remodeling.
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Registered trials
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