Circulation, Vol 74, 693-702, Copyright © 1986 by American Heart Association
RG McKay, MA Pfeffer, RC Pasternak, JE Markis, PC Come, S Nakao, JD Alderman, JJ Ferguson, RD Safian and W Grossman
Dilatation of infarcted segments (infarct expansion) may occur during
recovery from myocardial infarction, but the fate of noninfarcted segments
is uncertain. Accordingly, left ventricular geometric changes were assessed
by left ventricular angiography and M mode echocardiography on admission
and 2 weeks later in 30 patients with their first acute transmural
myocardial infarction. All patients demonstrated chest pain, ST segment
elevation with subsequent development of Q waves (15 anterior, 15
inferior), and elevation of cardiac enzymes. Sequential left ventricular
angiographic and hemodynamic findings were available in these patients by
virtue of their participation in a study of thrombolysis in acute
myocardial infarction. By that study design, all patients treated
successfully with thrombolytic therapy and demonstrating improvement of
flow in an occluded coronary artery underwent repeat cardiac
catheterization. At 2 weeks there was a significant decrease in left
ventricular and pulmonary capillary wedge pressures (p less than .01),
whereas both left ventricular end-diastolic (LVEDV) and end-systolic
(LVESV) volume indexes increased (p less than .01). The increase in LVEDV
correlated directly with the percentage of the ventriculographic silhouette
that was akinetic or dyskinetic at the initial catheterization (r = .71, p
less than .001). To assess regional changes in both infarcted and
noninfarcted segments, serial endocardial perimeter lengths of both the
akinetic-dyskinetic segments (infarction zone) and of the remainder of the
cardiac silhouette (noninfarction zone) were measured in all patients who
demonstrated at least a 20% increase in their LVEDV at 2 weeks after
myocardial infarction. Notably, there was a mean increase of 13% in the
endocardial perimeter length of infarcted segments and a 19% increase in
the endocardial perimeter length of noninfarcted segments. Serial M mode
echocardiographic studies showed no significant change in the wall
thickness of noninfarcted myocardial segments. Hemodynamic changes that
occurred in this subgroup of patients included significant decreases in
left ventricular end-diastolic and pulmonary capillary wedge pressures (p
less than .05) and significant increases in angiographic cardiac index (p
less than .01) and LVESV index (p less than .01). We conclude that in
patients who manifest cardiac dilatation in the early convalescent period
after myocardial infarction, there is remodeling of the entire left
ventricle including infarct expansion of akinetic-dyskinetic segments and
volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT
400 WORDS)
ARTICLES
Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion
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P. Uusimaa, J. Risteli, M. Niemela, J. Lumme, M. Ikaheimo, A. Jounela, and K. Peuhkurinen Collagen Scar Formation After Acute Myocardial Infarction : Relationships to Infarct Size, Left Ventricular Function, and Coronary Artery Patency Circulation, October 21, 1997; 96(8): 2565 - 2572. [Abstract] [Full Text] |
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G. D. Pennock, D. D. Yun, P. G. Agarwal, P. H. Spooner, and S. Goldman Echocardiographic changes after myocardial infarction in a model of left ventricular diastolic dysfunction Am J Physiol Heart Circ Physiol, October 1, 1997; 273(4): H2018 - H2029. [Abstract] [Full Text] [PDF] |
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S. Basu, R. Senior, U. Raval, R. van der Does, T. Bruckner, and A. Lahiri Beneficial Effects of Intravenous and Oral Carvedilol Treatment in Acute Myocardial Infarction : A Placebo-Controlled, Randomized Trial Circulation, July 1, 1997; 96(1): 183 - 191. [Abstract] [Full Text] |
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P. Dubach, J. Myers, G. Dziekan, U. Goebbels, W. Reinhart, P. Vogt, R. Ratti, P. Muller, R. Miettunen, and P. Buser Effect of Exercise Training on Myocardial Remodeling in Patients With Reduced Left Ventricular Function After Myocardial Infarction : Application of Magnetic Resonance Imaging Circulation, April 15, 1997; 95(8): 2060 - 2067. [Abstract] [Full Text] |
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R. S. Vasan and D. Levy The Role of Hypertension in the Pathogenesis of Heart Failure: A Clinical Mechanistic Overview Arch Intern Med, September 9, 1996; 156(16): 1789 - 1796. [Abstract] [PDF] |
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R. L. Duerr, M. D. McKirnan, R. D. Gim, R. G. Clark, K. R. Chien, and J. Ross Jr Cardiovascular Effects of Insulin-Like Growth Factor-1 and Growth Hormone in Chronic Left Ventricular Failure in the Rat Circulation, June 15, 1996; 93(12): 2188 - 2196. [Abstract] [Full Text] |
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G. Melillo, J. A.C. Lima, R. M. Judd, P. J. Goldschmidt-Clermont, and H. S. Silverman Intrinsic Myocyte Dysfunction and Tyrosine Kinase Pathway Activation Underlie the Impaired Wall Thickening of Adjacent Regions During Postinfarct Left Ventricular Remodeling Circulation, April 1, 1996; 93(7): 1447 - 1458. [Abstract] [Full Text] |
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R. S. Vasan, E. J. Benjamin, and D. Levy Congestive Heart Failure With Normal Left Ventricular Systolic Function: Clinical Approaches to the Diagnosis and Treatment of Diastolic Heart Failure Arch Intern Med, January 22, 1996; 156(2): 146 - 157. [Abstract] [PDF] |
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H. Ito, A. Maruyama, K. Iwakura, S. Takiuchi, T. Masuyama, M. Hori, Y. Higashino, K. Fujii, and T. Minamino Clinical Implications of the `No Reflow' Phenomenon : A Predictor of Complications and Left Ventricular Remodeling inReperfused Anterior Wall Myocardial Infarction Circulation, January 15, 1996; 93(2): 223 - 228. [Abstract] [Full Text] |
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J. Kajstura, X. Zhang, Y. Liu, E. Szoke, W. Cheng, G. Olivetti, T. H. Hintze, and P. Anversa The Cellular Basis of Pacing-Induced Dilated Cardiomyopathy : Myocyte Cell Loss and Myocyte Cellular Reactive Hypertrophy Circulation, October 15, 1995; 92(8): 2306 - 2317. [Abstract] [Full Text] |
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K. M. McDonald, J. Mock, A. D'Aloia, T. Parrish, K. Hauer, G. Francis, A. Stillman, and J. N. Cohn Bradykinin Antagonism Inhibits the Antigrowth Effect of Converting Enzyme Inhibition in the Dog Myocardium After Discrete Transmural Myocardial Necrosis Circulation, April 1, 1995; 91(7): 2043 - 2048. [Abstract] [Full Text] |
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R. J. Cody Comparing Angiotensin-Converting Enzyme Inhibitor Trial Results in Patients With Acute Myocardial Infarction Arch Intern Med, September 26, 1994; 154(18): 2029 - 2036. [Abstract] [PDF] |
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N. G. Uren, T. Crake, D. C. Lefroy, R. de Silva, G. J. Davies, and A. Maseri Reduced Coronary Vasodilator Function in Infarcted and Normal Myocardium after Myocardial Infarction N. Engl. J. Med., July 28, 1994; 331(4): 222 - 227. [Abstract] [Full Text] |
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D. L. Groden Vasodilator Therapy for Congestive Heart Failure: Lessons From Mortality Trials Arch Intern Med, February 22, 1993; 153(4): 445 - 454. [Abstract] [PDF] |
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J. J. Popma and E. J. Topol Adjuncts to Thrombolysis for Myocardial Reperfusion Ann Intern Med, July 1, 1991; 115(1): 34 - 44. [Abstract] [PDF] |
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S.G. Ray, H.M. McAlpine, J.J. Morton, B. Leckie, and H.J. Dargie Importance of RAA System and the Treatment of Patients with ACE Inhibition After Myocardial Infarction Angiology, April 1, 1991; 42(4): 268 - 272. [Abstract] [PDF] |
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G. K. Lund, C. B. Higgins, M. F. Wendland, N. Watzinger, H.-J. Weinmann, and M. Saeed Assessment of Nicorandil Therapy in Ischemic Myocardial Injury by Using Contrast-enhanced and Functional MR Imaging Radiology, December 1, 2001; 221(3): 676 - 682. [Abstract] [Full Text] [PDF] |
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