Medical therapy can improve the biological properties of the chronically failing heart - A new era in the treatment of heart failure

被引:383
作者
Eichhorn, EJ
Bristow, MR
机构
[1] UNIV TEXAS, SW MED CTR, DEPT INTERNAL MED, DIV CARDIOL, DALLAS, TX USA
[2] UNIV COLORADO, HLTH SCI CTR, DIV CARDIOL, DENVER, CO 80262 USA
[3] UNIV TEXAS, VET ADM MED CTR, CARDIAC CATHETERIZAT LAB IIIA2, DALLAS, TX 75216 USA
关键词
heart failure; remodeling; myocardial contraction;
D O I
10.1161/01.CIR.94.9.2285
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Myocardial failure has been considered to be an irreversible and progressive process characterized by Ventricular enlargement, chamber geometric alterations, and diminished pump performance. However, more recent evidence has suggested that certain types of medical therapy may lead to retardation and even reversal of the cardiomyopathic process. In the failing heart, long-term neurohormonal/autocrine-paracrine activation results in abnormalities in myocyte growth, energy production and utilization, calcium flux, and receptor regulation that produce a progressively dysfunctional, mechanically inefficient heart. Interventions such as ACE inhibition and beta-blockade result in a reduction in the harmful long-term consequences of neurohormonal/autocrine-paracrine effects and retard the progression of left ventricular dysfunction or ventricular remodeling. Furthermore, in subjects with idiopathic dilated or ischemic cardiomyopathy, antiadrenergic therapy with beta-blocking agents appears to be able to partially reverse systolic dysfunction and ventricular remodeling. Although the precise mechanisms underlying this latter effect have not yet been elucidated, the general mechanism appears to be via improvement in the biological function of the cardiac myocyte. Such an improvement in the intrinsic defect(s) responsible for myocardial failure will likely translate into important clinical benefits.
引用
收藏
页码:2285 / 2296
页数:12
相关论文
共 156 条
  • [1] ABRAHAM WT, 1995, J INVEST MED S2, V43, pA316
  • [2] [SAR1]ANGIOTENSIN-2 RECEPTOR-MEDIATED STIMULATION OF PROTEIN-SYNTHESIS IN CHICK HEART-CELLS
    ACETO, JF
    BAKER, KM
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 258 (03): : H806 - H813
  • [3] ANDERSON JL, 1995, AM J CARDIOL, V75, P1220
  • [4] ANVERSA P, 1991, LAB INVEST, V64, P441
  • [5] ALTERATIONS IN SARCOPLASMIC-RETICULUM GENE-EXPRESSION IN HUMAN HEART-FAILURE - A POSSIBLE MECHANISM FOR ALTERATIONS IN SYSTOLIC AND DIASTOLIC PROPERTIES OF THE FAILING MYOCARDIUM
    ARAI, M
    ALPERT, NR
    MACLENNAN, DH
    BARTON, P
    PERIASAMY, M
    [J]. CIRCULATION RESEARCH, 1993, 72 (02) : 463 - 469
  • [6] RENIN-ANGIOTENSIN SYSTEM INVOLVEMENT IN PRESSURE-OVERLOAD CARDIAC-HYPERTROPHY IN RATS
    BAKER, KM
    CHERNIN, MI
    WIXSON, SK
    ACETO, JF
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (02): : H324 - H332
  • [7] HISTOLOGIC AND BIOCHEMICAL CORRELATES OF LEFT-VENTRICULAR CHAMBER DYNAMICS IN MAN
    BASHORE, TM
    MAGORIEN, DJ
    LETTERIO, J
    SHAFFER, P
    UNVERFERTH, DV
    [J]. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1987, 9 (04) : 734 - 742
  • [8] ANGIOTENSIN-II AND LEFT-VENTRICULAR GROWTH IN NEWBORN PIG-HEART
    BEINLICH, CJ
    WHITE, GJ
    BAKER, KM
    MORGAN, HE
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1991, 23 (09) : 1031 - 1038
  • [9] THE CELLULAR BASIS OF DILATED CARDIOMYOPATHY IN HUMANS
    BELTRAMI, CA
    FINATO, N
    ROCCO, M
    FERUGLIO, GA
    PURICELLI, C
    CIGOLA, E
    SONNENBLICK, EH
    OLIVETTI, G
    ANVERSA, P
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (01) : 291 - 305
  • [10] BISHOPRIC NH, 1992, J BIOL CHEM, V267, P20932