Myocardial structure and function differ in systolic and diastolic heart failure

被引:529
作者
van Heerebeek, L
Borbély, A
Niessen, HWM
Bronzwaer, JGF
van der Velden, J
Stienen, GJM
Linke, WA
Laarman, GJ
Paulus, WJ
机构
[1] VU Med Ctr, Lab Physiol, NL-1081 BT Amsterdam, Netherlands
[2] VU Med Ctr, Dept Physiol, NL-1081 BT Amsterdam, Netherlands
[3] VU Med Ctr, Dept Pathol, NL-1081 BT Amsterdam, Netherlands
[4] VU Med Ctr, Dept Cardiol, NL-1081 BT Amsterdam, Netherlands
[5] VU Med Ctr, Inst Cardiovasc Res, NL-1081 BT Amsterdam, Netherlands
[6] Univ Munster, Physiol & Biophys Unit, Munich, Germany
[7] Dept Cardiol, Amsterdam, Netherlands
关键词
myocardium; heart failure; diastole; hypertrophy; collagen;
D O I
10.1161/CIRCULATIONAHA.105.587519
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: To support the clinical distinction between systolic heart failure (SHF) and diastolic heart failure (DHF), left ventricular (LV) myocardial structure and function were compared in LV endomyocardial biopsy samples of patients with systolic and diastolic heart failure. Methods and Results: Patients hospitalized for worsening heart failure were classified as having SHF (n = 22; LV ejection fraction (EF) 34 +/- 2%) or DHF (n = 22; LVEF 62 +/- 2%). No patient had coronary artery disease or biopsy evidence of infiltrative or inflammatory myocardial disease. More DHF patients had a history of arterial hypertension and were obese. Biopsy samples were analyzed with histomorphometry and electron microscopy. Single cardiomyocytes were isolated from the samples, stretched to a sarcomere length of 2.2 mu m to measure passive force (F-passive), and activated with calcium-containing solutions to measure total force. Cardiomyocyte diameter was higher in DHF (20.3 +/- 0.6 versus 15.1 +/- 0.4 mu m, P < 0.001), but collagen volume fraction was equally elevated. Myofibrillar density was lower in SHF (36 +/- 2% versus 46 +/- 2%, P < 0.001). Cardiomyocytes of DHF patients had higher F-passive (7.1 +/- 0.6 versus 5.3 +/- 0.3 kN/m(2); P < 0.01), but their total force was comparable. After administration of protein kinase A to the cardiomyocytes, the drop in Fpassive was larger (P < 0.01) in DHF than in SHF. Conclusions: LV myocardial structure and function differ in SHF and DHF because of distinct cardiomyocyte abnormalities. These findings support the clinical separation of heart failure patients into SHF and DHF phenotypes.
引用
收藏
页码:1966 / 1973
页数:8
相关论文
共 42 条
[1]   Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart [J].
Abel, ED ;
Kaulbach, HC ;
Tian, R ;
Hopkins, JCA ;
Duffy, J ;
Doetschman, T ;
Minnemann, T ;
Boers, ME ;
Hadro, E ;
Oberste-Berghaus, C ;
Quist, W ;
Lowell, BB ;
Ingwall, JS ;
Kahn, BB .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (12) :1703-1714
[2]   Enteroviral protease 2A cleaves dystrophin: Evidence of cytoskeletal disruption in an acquired cardiomyopathy [J].
Badorff, C ;
Lee, GH ;
Lamphear, BJ ;
Martone, ME ;
Campbell, KP ;
Rhoads, RE ;
Knowlton, KU .
NATURE MEDICINE, 1999, 5 (03) :320-326
[3]   Left ventricular systolic performance, function, and contractility in patients with diastolic heart failure [J].
Baicu, CF ;
Zile, MR ;
Aurigemma, GP ;
Gaasch, WH .
CIRCULATION, 2005, 111 (18) :2306-2312
[4]   Cardiomyocyte stiffness in Diastolic heart failure [J].
Borbély, A ;
van der Velden, J ;
Papp, Z ;
Bronzwaer, JGF ;
Edes, I ;
Stienen, GJM ;
Paulus, WJ .
CIRCULATION, 2005, 111 (06) :774-781
[5]   Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy [J].
Bronzwaer, JGF ;
Heymes, C ;
Visser, CA ;
Paulus, WJ .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (01) :H10-H16
[6]   Endomyocardial nitric oxide synthase and the hemodynamic phenotypes of human dilated cardiomyopathy and of athlete's heart [J].
Bronzwaer, JGF ;
Zeitz, C ;
Visser, CA ;
Paulus, WJ .
CARDIOVASCULAR RESEARCH, 2002, 55 (02) :270-278
[7]   Contribution of left ventricular diastolic dysfunction to heart failure regardless of election fraction [J].
Brucks, S ;
Little, WC ;
Chao, T ;
Kitzman, DW ;
Wesley-Farrington, D ;
Gandhi, S ;
Shihabi, ZK .
AMERICAN JOURNAL OF CARDIOLOGY, 2005, 95 (05) :603-606
[8]   Heart failure with a normal ejection fraction - Is it really a disorder of diastolic function? [J].
Burkhoff, D ;
Maurer, MS ;
Packer, M .
CIRCULATION, 2003, 107 (05) :656-658
[9]   PRESSURE-INDUCED AND VOLUME-INDUCED LEFT-VENTRICULAR HYPERTROPHIES ARE ASSOCIATED WITH DISTINCT MYOCYTE PHENOTYPES AND DIFFERENTIAL INDUCTION OF PEPTIDE GROWTH-FACTOR MESSENGER-RNAS [J].
CALDERONE, A ;
TAKAHASHI, N ;
IZZO, NJ ;
THAIK, CM ;
COLUCCI, WS .
CIRCULATION, 1995, 92 (09) :2385-2390
[10]   The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus [J].
Finck, BN ;
Lehman, JJ ;
Leone, TC ;
Welch, MJ ;
Bennett, MJ ;
Kovacs, A ;
Han, XL ;
Gross, RW ;
Kozak, R ;
Lopaschuk, GD ;
Kelly, DP .
JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (01) :121-130