Angiotensin-converting enzyme inhibitor therapy affects left ventricular mass in patients with ejection fraction > 40% after acute myocardial infarction.

[1]  K. Chatterjee,et al.  Coronary vasodilation induced by angiotensin-converting enzyme inhibition in vivo: differential contribution of nitric oxide and bradykinin in conductance and resistance arteries. , 1996, Circulation.

[2]  C. Pepine.  Ongoing clinical trials of angiotensin-converting enzyme inhibitors for treatment of coronary artery disease in patients with preserved left ventricular function. , 1996, Journal of the American College of Cardiology.

[3]  S. Oparil,et al.  Increased ACE and chymase-like activity in cardiac tissue of dogs with chronic mitral regurgitation. , 1995, The American journal of physiology.

[4]  G. Aurigemma,et al.  Serial echocardiographic-Doppler assessment of left ventricular geometry and function in rats with pressure-overload hypertrophy. Chronic angiotensin-converting enzyme inhibition attenuates the transition to heart failure. , 1995, Circulation.

[5]  M. Quiñones,et al.  Effects of long-term enalapril therapy on cardiac structure and function in patients with left ventricular dysfunction. Results of the SOLVD echocardiography substudy. , 1995, Circulation.

[6]  Raymond C. Schneider,et al.  ISIS-4: A randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58 050 patients with suspected acute myocardial infarction , 1995, The Lancet.

[7]  G. Lamas,et al.  Effects of captopril on ischemic events after myocardial infarction. Results of the Survival and Ventricular Enlargement trial. SAVE Investigators. , 1994, Circulation.

[8]  S. Yusuf,et al.  Emerging role of angiotensin-converting enzyme inhibitors in cardiac and vascular protection. , 1994, Circulation.

[9]  H. Schunkert,et al.  Angiotensin‐Converting Enzyme Inhibition Prolongs Survival and Modifies the Transition to Heart Failure in Rats With Pressure Overload Hypertrophy Due to Ascending Aortic Stenosis , 1994, Circulation.

[10]  D. King,et al.  Three-dimensional echocardiography: in vitro and in vivo validation of left ventricular mass and comparison with conventional echocardiographic methods. , 1994, Journal of the American College of Cardiology.

[11]  Gruppo Italiano per lo Studio della Soprawivenza nell'Inf Miocardico..  GISSI-3: effects of lisiriopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction , 1994, The Lancet.

[12]  G. Lamas,et al.  Quantitative Two-Dimensional Echocardiographic Measurements are Major Predictors of Adverse Cardiovascular Events After Acute Myocardial Infarction: The Protective Effect of Captopril , 1994, Circulation.

[13]  J. Ambrose.  The open artery: beyond myocardial salvage. , 1993, The American journal of cardiology.

[14]  J. Sadoshima,et al.  Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro , 1993, Cell.

[15]  M. Kronenberg,et al.  Effects of the angiotensin converting enzyme inhibitor enalapril on the long-term progression of left ventricular dilatation in patients with asymptomatic systolic dysfunction. SOLVD (Studies of Left Ventricular Dysfunction) Investigators. , 1993, Circulation.

[16]  S. Yusuf,et al.  Effects of the Angiotensin Converting Enzyme Inhibitor Enalapril on the Long‐term Progression of Left Ventricular Dilatation in Patients With Asymptomatic Systolic Dysfunction , 1993, Circulation.

[17]  D. King,et al.  Three‐dimensional Echocardiography , 1993, American journal of cardiac imaging.

[18]  J. Sadoshima,et al.  Critical Role of the AT1 Receptor Subtype , 2005 .

[19]  L Axel,et al.  Regional differences in function within noninfarcted myocardium during left ventricular remodeling. , 1993, Circulation.

[20]  M. Rousseau,et al.  Effects of long-term enalapril therapy on left ventricular diastolic properties in patients with depressed ejection fraction. SOLVD Investigators. , 1993, Circulation.

[21]  S. Yusuf,et al.  Effects of Long‐term Enalapril Therapy on Left Ventricular Diastolic Properties in Patients With Depressed Ejection Fraction , 1993 .

[22]  K. Thygesen,et al.  Effects of Captopril on Ischemia and Dysfunction of the Left Ventricle After Myocardial Infarction , 1993, Circulation.

[23]  W. Linz,et al.  Ramiprilat increases bradykinin outflow from isolated hearts of rat , 1993, British journal of pharmacology.

[24]  B. Pitt,et al.  Effect of enalapril on myocardial infarction and unstable angina in patients with low ejection fractions , 1992, The Lancet.

[25]  E. J. Brown,et al.  Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. , 1992, The New England journal of medicine.

[26]  S. Yusuf,et al.  Effects of the angiotensin converting enzyme inhibitor enalapril on the long-term progression of left ventricular dysfunction in patients with heart failure. SOLVD Investigators. , 1992, Circulation.

[27]  A. Moss,et al.  Interrelation of left ventricular ejection fraction, pulmonary congestion and outcome in acute myocardial infarction. , 1992, The American journal of cardiology.

[28]  M. Laks,et al.  Functional significance of post-myocardial infarction left ventricular hypertrophy: a beneficial response. , 1992, American heart journal.

[29]  J. Cohn,et al.  Hemodynamic, left ventricular structural and hormonal changes after discrete myocardial damage in the dog. , 1992, Journal of the American College of Cardiology.

[30]  G. Blackwell,et al.  Time-varying wall stress: an index of ventricular vascular coupling. , 1991, The American journal of physiology.

[31]  G. Lamas,et al.  Activation of neurohumoral systems following acute myocardial infarction. , 1991, The American journal of cardiology.

[32]  G. Lamas,et al.  Patency of the infarct-related coronary artery and ventricular geometry. , 1991, The American journal of cardiology.

[33]  M. Rabinov,et al.  Inhibition of angiotensin converting enzyme by ramipril in serum and tissue of man. , 1991, Journal of hypertension.

[34]  H. Schunkert,et al.  Tissue-specific activation of cardiac angiotensin converting enzyme in experimental heart failure. , 1991, Circulation research.

[35]  H. Crijns,et al.  Prediction of uneventful cardioversion and maintenance of sinus rhythm from direct-current electrical cardioversion of chronic atrial fibrillation and flutter. , 1991, The American journal of cardiology.

[36]  C. Johnston,et al.  REDUCTION IN LEFT VENTRICULAR MASS IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS GIVEN ENALAPRIL , 1991, Clinical and experimental pharmacology & physiology.

[37]  G. Gamble,et al.  Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition , 1991, The Lancet.

[38]  S. Litwin,et al.  Contractility and Stiffness of Noninfarcted Myocardium After Coronary Ligation in Rats: Effects of Chronic Angiotensin Converting Enzyme Inhibition , 1991, Circulation.

[39]  K. Baker,et al.  Renin-angiotensin system involvement in pressure-overload cardiac hypertrophy in rats. , 1990, The American journal of physiology.

[40]  B. Healy,et al.  Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy. , 1990, Circulation.

[41]  R. Tomanek,et al.  Role of lowering arterial pressure on maximal coronary flow with and without regression of cardiac hypertrophy. , 1989, The American journal of physiology.

[42]  M. Laks,et al.  Functional significance of hypertrophy of the noninfarcted myocardium after myocardial infarction in humans. , 1989, Circulation.

[43]  S. Goldman,et al.  Importance of Venodilatation in Prevention of Left Ventricular Dilatation After Chronic Large Myocardial Infarction in Rats: A Comparison of Captopril and Hydralazine , 1989, Circulation research.

[44]  D. Ganten,et al.  Converting enzyme inhibition specifically prevents the development and induces regression of cardiac hypertrophy in rats. , 1989, Clinical and experimental hypertension. Part A, Theory and practice.

[45]  A. Rumley,et al.  Neuroendocrine activation after acute myocardial infarction. , 1988, British heart journal.

[46]  G. Lamas,et al.  Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. , 1988, The New England journal of medicine.

[47]  J. Travis.  Structure, function, and control of neutrophil proteinases , 1988 .

[48]  J. Michel,et al.  Myocardial effect of converting enzyme inhibition in hypertensive and normotensive rats. , 1988, The American journal of medicine.

[49]  M. Pfeffer,et al.  Angiotensin converting enzyme inhibition and ventricular remodeling in heart failure. , 1988, The American journal of medicine.

[50]  N. Sharpe,et al.  TREATMENT OF PATIENTS WITH SYMPTOMLESS LEFT VENTRICULAR DYSFUNCTION AFTER MYOCARDIAL INFARCTION , 1988, The Lancet.

[51]  G. Freeman,et al.  Reduction of left ventricular mass in normal rats by captopril. , 1987, Cardiovascular research.

[52]  W. Nichols,et al.  Ventricular/vascular interaction in patients with mild systemic hypertension and normal peripheral resistance. , 1986, Circulation.

[53]  P. Anversa,et al.  Myocardial Infarction in Rats: Infarct Size, Myocyte Hypertrophy, and Capillary Growth , 1986, Circulation research.

[54]  M. Pfeffer,et al.  Survival after an experimental myocardial infarction: beneficial effects of long-term therapy with captopril. , 1985, Circulation.

[55]  M. Pfeffer,et al.  Influence of Chronic Captopril Therapy on the Infarcted Left Ventricle of the Rat , 1985, Circulation research.

[56]  Miles Be,et al.  Letter: Serum-phenytoin. , 1976 .