Hypertensive left ventricular hypertrophy risk: beyond adaptive cardiomyocytic hypertrophy

被引:54
作者
Frohlich, Edward D. [1 ]
Gonzalez, Arantxa [2 ]
Diez, Javier [2 ,3 ]
机构
[1] Ochsner Clin Fdn, New Orleans, LA USA
[2] Univ Navarra, Ctr Invest Med Aplicada, Div Cardiovasc Sci, Pamplona 31008, Spain
[3] Univ Navarra, Univ Clin, Dept Cardiol & Cardiovasc Surg, Pamplona 31008, Spain
关键词
arterial hypertension; hypertensive heart disease; left ventricular hypertrophy; myocardial hypertrophy; myocardial remodelling; COMPENSATED CARDIAC-HYPERTROPHY; CONVERTING ENZYME-INHIBITOR; ANGIOTENSIN-II; BLOOD-PRESSURE; HEART-FAILURE; DIASTOLIC DYSFUNCTION; TRANSCRIPTION FACTOR; MYOCARDIAL FIBROSIS; CARDIOVASCULAR RISK; RECEPTOR ANTAGONISM;
D O I
10.1097/HJH.0b013e328340d787
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
The heart is a remarkably adaptive organ, capable of increasing its minute output and overcoming short-term or prolonged pressure overload. The structural response, in addition to the foregoing functional demands, is that of myocardial hypertrophy. Then, why should an adaptive response increase cardiovascular risk in hypertensive patients with left ventricular hypertrophy (LVH)? Evidence shows that the functional performance of hypertrophied cardiomyocytes is impaired, and that additional alterations develop in cardiomyocytes themselves, the extracellular matrix and the intramyocardial vasculature, leading to myocardial remodelling and providing the basis for the adverse prognosis associated with pathological LVH in hypertensive patients (i.e., hypertensive heart disease, HHD). As molecular information accumulates, the pathophysiological understanding and the clinical approach to HHD are changing. The time has come to develop novel diagnostic and therapeutic strategies aimed at improving the prognosis of HHD on the basis of reversing or even preventing the aforementioned changes in the ventricular myocardium. J Hypertens 29:17-26 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
引用
收藏
页码:17 / 26
页数:10
相关论文
共 113 条
[1]   Central blood pressure measurements and antihypertensive therapy a consensus document [J].
Agabiti-Rosei, Enrico ;
Mancia, Giuseppe ;
O'Rourke, Michael F. ;
Roman, Mary J. ;
Safar, Michel E. ;
Smulyan, Harold ;
Wang, Ji-Guang ;
Wilkinson, Ian B. ;
Williams, Bryan ;
Vlachopoulos, Charalambos .
HYPERTENSION, 2007, 50 (01) :154-160
[2]  
Agodoa L, 2007, J HYPERTENS, V25, P951
[3]   Roles of cardiac transcription factors in cardiac hypertrophy [J].
Akazawa, H ;
Komuro, I .
CIRCULATION RESEARCH, 2003, 92 (10) :1079-1088
[4]   Compensated cardiac hypertrophy is characterised by a decline in palmitate oxidation [J].
Akki, Ashwin ;
Smith, Katie ;
Seymour, Anne-Marie L. .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2008, 311 (1-2) :215-224
[5]   Western diet impairs metabolic remodelling and contractile efficiency in cardiac hypertrophy [J].
Akki, Ashwin ;
Seymour, Anne-Marie L. .
CARDIOVASCULAR RESEARCH, 2009, 81 (03) :610-617
[6]   INCREASED MYOTHERMAL ECONOMY OF ISOMETRIC FORCE GENERATION IN COMPENSATED CARDIAC-HYPERTROPHY INDUCED BY PULMONARY-ARTERY CONSTRICTION IN THE RABBIT - A CHARACTERIZATION OF HEAT LIBERATION IN NORMAL AND HYPERTROPHIED RIGHT VENTRICULAR PAPILLARY-MUSCLES [J].
ALPERT, NR ;
MULIERI, LA .
CIRCULATION RESEARCH, 1982, 50 (04) :491-500
[7]  
AOKI H., 2001, Hear. Physiol. Pathophysiol, P1065, DOI DOI 10.1016/B978012656975-9/50060-2
[8]   Intracellular angiotensin II induces cell proliferation independent of AT1 receptor [J].
Baker, Kenneth M. ;
Kumar, Rajesh .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2006, 291 (05) :C995-C1001
[9]   Evidence of a novel intracrine mechanism in angiotensin II-induced cardiac hypertrophy [J].
Baker, KM ;
Chernin, MI ;
Schreiber, T ;
Sanghi, S ;
Haiderzaidi, S ;
Booz, GW ;
Dostal, DE ;
Kumar, R .
REGULATORY PEPTIDES, 2004, 120 (1-3) :5-13
[10]   Molecular regulation of cardiac hypertrophy [J].
Barry, Sean P. ;
Davidson, Sean M. ;
Townsend, Paul A. .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2008, 40 (10) :2023-2039