Myocardial effects of aldosterone antagonism in heart failure with preserved ejection fraction
| Autor: | Graham Fent, James R. J. Foley, Mark T. Kearney, Klaus K. Witte, Katrina Bounford, Peter P Swoboda, Laura E Dobson, Petra Bijsterveld, Sven Plein, Bara Erhayiem, Adam K McDiarmid, John P Greenwood, Tarique A Musa, Keith Tyndall, Pankaj Garg |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
heart failure with preserved ejection fraction medicine.medical_specialty Time Factors Magnetic Resonance Imaging (MRI) Magnetic Resonance Imaging Cine Spironolactone 030204 cardiovascular system & hematology Ventricular Function Left cardiovascular magnetic resonance 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine Extracellular fluid medicine Humans 030212 general & internal medicine extracellular volume Aged Mineralocorticoid Receptor Antagonists Original Research Aged 80 and over Heart Failure Aldosterone Ventricular Remodeling Myocardial tissue business.industry Myocardium Stroke Volume medicine.disease Fibrosis Remodeling Treatment Outcome England chemistry Heart failure Cardiology Female Cardiology and Cardiovascular Medicine Antagonism Heart failure with preserved ejection fraction business |
| Zdroj: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
| Popis: | Background Spironolactone may have prognostic benefit in selected patients with heart failure with preserved ejection fraction. This study assessed the myocardial tissue effects of spironolactone in heart failure with preserved ejection fraction. Methods and Results A 1:1 randomized controlled study of 6 months of spironolactone versus control in heart failure with preserved ejection fraction. The primary outcome was change in myocardial extracellular volume fraction by cardiovascular magnetic resonance as a surrogate of diffuse fibrosis. Of 55 randomized patients, 40 (20 women; age, 75.2±5.9 years) completed follow‐up (19 treatment, 21 control). A significant change in extracellular volume over the study period was not seen (treatment, 28.7±3.7% versus 27.7±3.4% [ P =0.14]; controls, 27.6±3.4% versus 28.3±4.4% [ P =0.14]); however, the rate of extracellular volume expansion was decreased by spironolactone (−1.0±2.4% versus 0.8±2.2%). Indexed left ventricular mass decreased with treatment (104.4±26.6 versus 94.0±20.6 g/m 2 ; P =0.001) but not in controls (101.4±29.4 versus 104.0±32.8 g/m 2 ; P =0.111). Extracellular mass decreased by 13.8% (15.1±4.8 versus 13.0±3.4 g/m 2 ; P =0.003), and cellular mass decreased by 8.3% (37.6±10.0 versus 34.3±7.9 g/m 2 ; P =0.001) with spironolactone, but was static in controls. Conclusions Spironolactone did not lead to significant change in extracellular volume. However, spironolactone did decrease rate of extracellular expansion, with a decrease in the mass of both cellular and extracellular myocardial compartments. These data point to the mechanism of action of spironolactone in heart failure with preserved ejection fraction, including a direct tissue effect with a reduction in rate of myocardial fibrosis. |
| Databáze: | OpenAIRE |
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