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Potential Reduction of Interstitial Myocardial Fibrosis With Renal Denervation
Author(s) -
Doltra Adelina,
Messroghli Daniel,
Stawowy Philipp,
Hassel JanHendrik,
Gebker Rolf,
Leppänen Olli,
Gräfe Michael,
Schneeweis Christopher,
Schnackenburg Bernhard,
Fleck Eckart,
Kelle Sebastian
Publication year - 2014
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.114.001353
Subject(s) - medicine , myocardial fibrosis , extracellular fluid , extracellular , cardiology , magnetic resonance imaging , ejection fraction , fibrosis , muscle hypertrophy , left ventricular hypertrophy , hypertensive heart disease , diastole , urology , heart failure , blood pressure , radiology , biology , microbiology and biotechnology
Background Hypertensive cardiomyopathy is characterized by myocyte hypertrophy and interstitial fibrosis. The effects of renal denervation ( RD ) on the heart are poorly understood. New magnetic resonance imaging techniques (extracellular volume fraction) permit the quantitative assessment of myocardial fibrosis. Our aim was to study the effects of RD on myocardial fibrosis. Methods and Results Twenty‐three patients with resistant hypertension undergoing RD and 5 resistant hypertensive controls were prospectively included. Cardiac magnetic resonance imaging at 1.5 T was performed before RD and at 6‐month follow‐up. Indexed left ventricular mass, septal extracellular volume fraction, and indexed absolute extracellular volume (a quantitative measure of extracellular matrix) were quantified. All data are reported as mean±SD deviation (median). Decreases in systolic (161.96±19.09 [160] versus 144.78±16.48 [143] mm Hg, P <0.0001) and diastolic (85.61±12.88 [83] versus 80.39±11.93 [81] mm Hg, P =0.018) blood pressures and in indexed left ventricular mass (41.83±10.20 [41.59] versus 37.72±7.44 [38.49] g/m 1.7 , P =0.001) were observed at follow‐up only in RD patients. No significant differences in extracellular volume were found (26.24±3.92% [26.06%] versus 25.74±4.53% [25.63%], P =0.605). A significant decrease in absolute extracellular volume was observed after 6 months in RD patients exclusively (10.36±2.25 [10.79] versus 9.25±2.38 [9.79] mL/m 1.7 , P =0.031). This effect was observed independently of blood pressure reduction. Conclusions RD significantly decreases left ventricular mass, while extracellular volume remains stable. Our results suggest that the observed left ventricular mass decrease was due not exclusively to a reversion of myocyte hypertrophy but also to an additional reduction in collagen content, indicating interstitial myocardial fibrosis.

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