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Coronary vascular function is improved in ischemic patients after continuous‐flow left ventricular assist device implantation (1071.8)
Author(s) -
Deeter Lance,
Diakos Nikos,
Stehlik Josef,
Selzman Craig,
Kfoury Abdallah,
Reid Bruce,
Saidi Abdulfatah,
WeverPinzon Omar,
Verma Divya,
Yen ChiGang,
Uzoigwe Emmanuella,
Guo Shawn,
Li Dean,
Drakos Stavros,
Symons J David
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1071.8
Subject(s) - coronary arteries , medicine , cardiology , ventricle , sodium nitroprusside , implant , heart failure , myocardial infarction , endothelial dysfunction , transplantation , vasodilation , artery , surgery , nitric oxide
Continuous‐flow left ventricular assist devices (LVADs) are used in heart failure (HF) patients either as a bridge to transplantation or as a permanent (destination) therapy. HF is precipitated by myocardial infarction (MI) in most (ischemic; I) but not all (non‐ischemic; NI) patients. We hypothesized that coronary vascular dysfunction is greater in I (63±2 y; n=12) vs. NI (53±5 y; n=17) male HF patients, and that dysfunction is reversed by LVAD support. Arteries from a transmural biopsy of the left‐ventricle were obtained, and concentration‐response curves to bradykinin (BK, 10 ‐6 to 10 ‐10 M) and sodium nitroprusside (SNP, 10 ‐4 to 10 ‐9 M) were completed after vessels were precontracted to ~65% of maximal tension development. Maximal BK‐induced vasorelaxation was less (p<0.05) in arteries from I (68±8%; n=21 arteries, 195±20 µm i.d.) vs. NI (87±3%; n=33 arteries, 213±17 µm i.d.) patients, while responses to SNP (~90%) were similar between groups. These findings indicate endothelial dysfunction is greater in I vs. NI patients at the time of LVAD implant. Next we assessed vascular reactivity in 6 I (58±6 y) and 4 NI (49±11 y) patients wherein samples were obtained at implant and explant (239±51 days later). Maximal BK‐induced vasorelaxation was greater (p<0.05) in coronary arteries from I patients at explant (87±6%, n=14 arteries, 305±30 μm i.d.) vs. implant (53±11%, n=12 arteries, 204±33 μm i.d.). Maximal BK‐induced vasorelaxation was similar in coronary arteries from NI patients obtained at explant (79±8%, n=7 arteries, 232±21 μm i.d.) and implant (72±17%, n=5 arteries, 135±13 μm i.d.). Responses to SNP were similar (~93%) at implant and explant for I and NI patients. Our data demonstrate that endothelial dysfunction in patients with advanced ischemic cardiomyopathy is improved through LVAD support.