Circulation, Vol 90, 1410-1422, Copyright © 1994 by American Heart Association
EO Weinberg, FJ Schoen, D George, Y Kagaya, PS Douglas, SE Litwin, H Schunkert, CR Benedict and BH Lorell
BACKGROUND: We tested the hypotheses that long-term administration of the
angiotensin-converting enzyme (ACE) inhibitor fosinopril will regress
hypertrophy, modify the transition to heart failure, and prolong survival
in rats with chronic left ventricular (LV) pressure overload due to
ascending aortic stenosis. METHODS AND RESULTS: Aortic stenosis was created
in weanling male Wistar rats by a stainless steel clip placed on the
ascending aorta. Age-matched control animals underwent a sham operation
(Sham group, n = 57). Six weeks after surgery, rats with aortic stenosis
were randomized to receive either oral fosinopril 50 mg.kg-1.d-1 (Fos/LVH
group, n = 38) or no drug (LVH group, n = 36) for 15 weeks. Pilot studies
confirmed that this dosage produced significant inhibition of LV tissue ACE
in vivo. Animals were monitored daily, and survival during the 15-week
treatment period was assessed by actuarial analysis. At 15 weeks, in vivo
LV systolic and diastolic pressures and heart rate were measured. To assess
contractile function, the force-calcium relation was evaluated by use of
the isovolumic buffer-perfused, balloon-in-LV heart preparation at
comparable coronary flow rates per gram LV weight. Quantitative morphometry
was performed. Mortality during the 15-week trial was significantly less in
the Fos/LVH group than in the LVH group (3% versus 31%, P < .005). No
deaths occurred in the Sham group. In vivo LV systolic pressure was similar
between Fos/LVH and LVH hearts (223 +/- 10 versus 232 +/- 9 mm Hg) and
significantly higher than the Sham group (99 +/- 3 mm Hg, P < .05). In
vivo LV diastolic pressure was significantly lower in Fos/LVH hearts than
in LVH hearts (10 +/- 2 versus 15 +/- 2 mm Hg), and both were significantly
higher than in the Sham group (5 +/- 1 mm Hg, P < .05). Heart rate was
similar among all groups. Despite equivalent elevation of LV systolic
pressure, fosinopril resulted in regression of myocyte hypertrophy in
Fos/LVH versus LVH (myocyte cell width, 14.8 +/- 0.5 versus 20.8 +/- 2.2
microns, P < .05) to normal levels (Sham, 16.3 +/- 0.9 microns).
Quantitative morphometry demonstrated that the regression of LV myocyte
hypertrophy in the Fos/LVH group was associated with a relative increase in
the fractional volume of fibrillar collagen and noncollagen interstitium.
In the isolated heart experiments, LV systolic developed pressure relative
to perfusate [Ca2+] was significantly higher in Fos/LVH hearts than in LVH
hearts. The improvement in systolic function was not related to any
difference in myocardial high-energy phosphate levels, since LV ATP and
creatine phosphate levels were similar in Fos/LVH and LVH hearts.
CONCLUSIONS: In rats with ascending aortic stenosis, chronic ACE inhibition
with fosinopril improved survival, decreased the extent of LV hypertrophy,
and improved cardiac function despite persistent elevation of LV systolic
pressure. The favorable effects of fosinopril may be related in part to
inhibition of the effects of cardiac ACE on myocyte hypertrophy rather than
to systemic hemodynamic mechanisms.
ARTICLES
Angiotensin-converting enzyme inhibition prolongs survival and modifies the transition to heart failure in rats with pressure overload hypertrophy due to ascending aortic stenosis
Charles A. Dana Research Institute, Boston, MA.
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D. Grimm, D. Elsner, H. Schunkert, M. Pfeifer, D. Griese, G. Bruckschlegel, F. Muders, G. A.J Riegger, and E. P Kromer Development of heart failure following isoproterenol administration in the rat: role of the renin-angiotensin system Cardiovasc Res, January 1, 1998; 37(1): 91 - 100. [Abstract] [Full Text] [PDF]
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W. W. Brooks, O. H. L. Bing, K. G. Robinson, M. T. Slawsky, D. M. Chaletsky, and C. H. Conrad Effect of Angiotensin-Converting Enzyme Inhibition on Myocardial Fibrosis and Function in Hypertrophied and Failing Myocardium From the Spontaneously Hypertensive Rat Circulation, December 2, 1997; 96(11): 4002 - 4010. [Abstract] [Full Text]
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Y. Ishigai, T. Mori, T. Ikeda, A. Fukuzawa, and T. Shibano Role of bradykinin-NO pathway in prevention of cardiac hypertrophy by ACE inhibitor in rat cardiomyocytes Am J Physiol Heart Circ Physiol, December 1, 1997; 273(6): H2659 - H2663. [Abstract] [Full Text] [PDF]
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W. W. Brooks, O. H. L. Bing, C. H. Conrad, L. O'Neill, M. T. Crow, E. G. Lakatta, D. E. Dostal, K. M. Baker, and M. O. Boluyt Captopril Modifies Gene Expression in Hypertrophied and Failing Hearts of Aged Spontaneously Hypertensive Rats Hypertension, December 1, 1997; 30(6): 1362 - 1368. [Abstract] [Full Text]
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M. Takemoto, K. Egashira, H. Tomita, M. Usui, H. Okamoto, A. Kitabatake, H. Shimokawa, K. Sueishi, and A. Takeshita Chronic Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade : Effects on Cardiovascular Remodeling in Rats Induced by the Long-term Blockade of Nitric Oxide Synthesis Hypertension, December 1, 1997; 30(6): 1621 - 1627. [Abstract] [Full Text]
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J. Fareh, R. M. Touyz, E. L. Schiffrin, and G. Thibault Cardiac Type-1 Angiotensin II Receptor Status in Deoxycorticosterone Acetate–Salt Hypertension in Rats Hypertension, November 1, 1997; 30(5): 1253 - 1259. [Abstract] [Full Text]
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F. G. Spinale, M. de Gasparo, S. Whitebread, L. Hebbar, M. J. Clair, D. M. Melton, R. S. Krombach, R. Mukherjee, J. P. Iannini, and S.-J. O Modulation of the Renin-Angiotensin Pathway Through Enzyme Inhibition and Specific Receptor Blockade in Pacing-Induced Heart Failure : I. Effects on Left Ventricular Performance and Neurohormonal Systems Circulation, October 7, 1997; 96(7): 2385 - 2396. [Abstract] [Full Text]
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C. D. Thienelt, E. O. Weinberg, J. Bartunek, and B. H. Lorell Load-Induced Growth Responses in Isolated Adult Rat Hearts : Role of the AT1 Receptor Circulation, June 17, 1997; 95(12): 2677 - 2683. [Abstract] [Full Text]
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N. Ito, J. Bartunek, K. W. Spitzer, and B. H. Lorell Effects of the Nitric Oxide Donor Sodium Nitroprusside on Intracellular pH and Contraction in Hypertrophied Myocytes Circulation, May 6, 1997; 95(9): 2303 - 2311. [Abstract] [Full Text]
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E. O. Weinberg, M. A. Lee, M. Weigner, K. Lindpaintner, S. P. Bishop, C. R. Benedict, K. K. L. Ho, P. S. Douglas, E. Chafizadeh, and B. H. Lorell Angiotensin AT1 Receptor Inhibition : Effects on Hypertrophic Remodeling and ACE Expression in Rats With Pressure-Overload Hypertrophy due to Ascending Aortic Stenosis Circulation, March 18, 1997; 95(6): 1592 - 1600. [Abstract] [Full Text]
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R. J. Wiesner, H. Ehmke, J. Faulhaber, R. Zak, and J. C. Ruegg Dissociation of Left Ventricular Hypertrophy, ß-Myosin Heavy Chain Gene Expression, and Myosin Isoform Switch in Rats After Ascending Aortic Stenosis Circulation, March 4, 1997; 95(5): 1253 - 1259. [Abstract] [Full Text]
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Y. Kagaya, R. J. Hajjar, J. K. Gwathmey, W. H. Barry, and B. H. Lorell Long-term Angiotensin-Converting Enzyme Inhibition With Fosinopril Improves Depressed Responsiveness to Ca2+ in Myocytes From Aortic-Banded Rats Circulation, December 1, 1996; 94(11): 2915 - 2922. [Abstract] [Full Text]
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R. M. Touyz, J. Fareh, G. Thibault, and E. L. Schiffrin Intracellular Ca2+ Modulation by Angiotensin II and Endothelin-1 in Cardiomyocytes and Fibroblasts From Hypertrophied Hearts of Spontaneously Hypertensive Rats Hypertension, November 1, 1996; 28(5): 797 - 805. [Abstract] [Full Text]
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C.-P. Cheng, M. Suzuki, N. Ohte, M. Ohno, Z.-M. Wang, and W. C. Little Altered Ventricular and Myocyte Response to Angiotensin II in Pacing-Induced Heart Failure Circ. Res., May 1, 1996; 78(5): 880 - 892. [Abstract] [Full Text]
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N. Iwai, H. Shimoike, and M. Kinoshita Cardiac Renin-Angiotensin System in the Hypertrophied Heart Circulation, November 1, 1995; 92(9): 2690 - 2696. [Abstract] [Full Text]
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S. E. Litwin, S. E. Katz, E. O. Weinberg, B. H. Lorell, G. P. Aurigemma, and P. S. Douglas 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 Circulation, May 15, 1995; 91(10): 2642 - 2654. [Abstract] [Full Text]
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H. Schunkert, J.-i. Sadoshima, T. Cornelius, Y. Kagaya, E. O. Weinberg, S. Izumo, G. Riegger, and B. H. Lorell Angiotensin II–Induced Growth Responses in Isolated Adult Rat Hearts : Evidence for Load-Independent Induction of Cardiac Protein Synthesis by Angiotensin II Circ. Res., March 1, 1995; 76(3): 489 - 497. [Abstract] [Full Text]
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