This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Solomon, S. D. Articles by Pfeffer, M. A. Search for Related Content PubMed PubMed Citation Articles by Solomon, S. D. Articles by Pfeffer, M. A. Related Collections Remodeling ACE/Angiotension receptors Acute myocardial infarction Related Article

(Circulation. 2002;106:2167.)
© 2002 American Heart Association, Inc.

Editorial

Renin-Angiotensin System and Cardiac Rupture After Myocardial Infarction

Scott D. Solomon, MD; Marc A. Pfeffer, MD, PhD

From the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Scott D. Solomon, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail ssolomon@rics.bwh.harvard.edu

Key Words: Editorials • renin • angiotensin • myocardial infarction

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Of all the mechanical complications after acute myocardial infarction (MI), cardiac rupture remains the most devastating, dramatic, and deadly. Continued improvements in the care of patients with acute MI have decreased the incidence of cardiac rupture over the past decade to under 3% in patients receiving reperfusion therapy,¹ although autopsy evaluation of patients who died suddenly with acute MI has suggested a higher incidence.^2,3 Without extremely prompt surgical intervention, patients with cardiac rupture rarely survive.

See p 2244

Cardiac rupture in humans generally occurs after transmural MI. Patients who rupture the free wall of the left ventricle typically develop hemopericardium and cardiac tamponade, whereas septal rupture leads to ventricular septal defect. Rupture can occur as early as the first day after infarction, although it most often occurs later in the first week in the setting of myocardial necrosis and neutrophilic infiltration.⁴ A combination of factors, both pathological and physiological, make the infarct region most vulnerable within the first 7 to 10 days. This is when cardiac tissue in the involving infarct region is weakest and most friable. As ventricular enlargement and infarct thinning commence, regional wall stress can increase precipitously. While prompt reperfusion therapy is thought to lower the incidence of rupture, delayed reperfusion may be associated with an increased risk of rupture.⁵ Treatment with steroids or nonsteroidal antiinflammatory agents may also be associated with an increased risk of rupture.^6,7

While the initial phases of acute infarction are characterized pathologically by neutrophil infiltration and myocyte necrosis, the healing phase of . . . [Full Text of this Article]

Related Article:

Targeted Deletion of Angiotensin II Type 2 Receptor Caused Cardiac Rupture After Acute Myocardial Infarction

Sahoko Ichihara, Takaaki Senbonmatsu, Edward Price, Jr, Toshihiro Ichiki, F. Andrew Gaffney, and Tadashi Inagami
Circulation 2002 106: 2244-2249. [Abstract] [Full Text]

This article has been cited by other articles:

				W. Huang, J. Rubinstein, A. R. Prieto, L. V. Thang, and D. H. Wang Transient Receptor Potential Vanilloid Gene Deletion Exacerbates Inflammation and Atypical Cardiac Remodeling After Myocardial Infarction Hypertension, February 1, 2009; 53(2): 243 - 250. [Abstract] [Full Text] [PDF]

				G. Weissman, C. C. Kwon, R. K. Shaw, and J. F. Setaro Free-Wall Rupture of the Myocardium Following Infarction: A Changing Clinical Portrait in the Reperfusion Era: A Case Report Angiology, October 1, 2006; 57(5): 636 - 642. [Abstract] [PDF]

				V. L. Sales, G. K. Sukhova, M. A. Lopez-Ilasaca, P. Libby, V. J. Dzau, and R. E. Pratt Angiotensin Type 2 Receptor Is Expressed in Murine Atherosclerotic Lesions and Modulates Lesion Evolution Circulation, November 22, 2005; 112(21): 3328 - 3336. [Abstract] [Full Text] [PDF]