CLINICAL RESEARCH: CORONARY ARTERY DISEASE
Angina pectoris prior to myocardial infarction protects against subsequent left ventricular remodeling
Scott D. Solomon, MD, FACC*,*,
Nagesh S. Anavekar, MBBS (Hons), FRACP*,
Sally Greaves, MD ,
Jean L. Rouleau, MD, FACC ,
Charles Hennekens, MD ,
Marc A. Pfeffer, MD, PhD, FACC* HEART Investigators
* Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
Green Lane Hospital, Auckland, New Zealand
Cardiovascular Division, University of Toronto Health Network, Toronto, Canada
University of Miami, Boca Raton, Florida, USA
Manuscript received July 18, 2003;
revised manuscript received September 12, 2003,
accepted September 23, 2003.
* Reprint requests and correspondence: Dr. Scott D. Solomon, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA.
ssolomon{at}rics.bwh.harvard.edu
OBJECTIVES: To investigate the hypothesis that prior angina pectoris confers protection from remodeling occurring after myocardial infarction (MI), we analyzed echocardiograms from the Healing and Early Afterload Reducing Therapy (HEART) trial.
BACKGROUND: Ischemia occurring before MI has been shown to reduce infarct size in experimental models and to improve outcomes in patients. The extent to which ischemia occurring before MI influences subsequent changes in ventricular size and function is unclear.
METHODS: We studied 283 patients enrolled in the HEART trial who had echocardiograms at days 1 and 90 after MI. Left ventricular (LV) dilation from days 1 to 90 was used as a measure of LV remodeling. We explored the relationship between symptomatic angina occurring before infarction and subsequent LV remodeling.
RESULTS: In patients who reported angina (n = 111) during the three months preceding MI, LV volume change was –0.73 ± 2.6 ml over the 90-day post-MI period, compared with 6.8 ± 2.6 ml for patients (n = 172) without angina (p = 0.017). In contrast, there were no differences in changes in ejection fraction based on prior angina. Maximal creatine kinase was significantly lower in patients with prior angina (2,119 ± 1,729 vs. 2,701 ± 2,088, p = 0.016). In a multivariate model, prior angina remained protective for ventricular remodeling after adjusting for age, gender, baseline ejection fraction, Killip class, baseline end-diastolic volume, and drug treatment group (p = 0.042). However, the protective effect of pre-infarction angina appeared to be attenuated in diabetic patients.
CONCLUSIONS: Ischemic symptoms occurring before MI may protect against LV remodeling. These protective effects may be secondary to recruitment of collaterals or ischemic preconditioning of the myocardium, and they appear to be attenuated in diabetic patients.
|
Abbreviations and Acronyms
| | CK | = creatine kinase | | HEART | = Healing and Early Afterload Reducing Therapy trial | | LV | = left ventricle/ventricular | | MI | = myocardial infarction |
|
This article has been cited by other articles:
|
|
|
|
 
K. Boengler, R. Schulz, and G. Heusch
Loss of cardioprotection with ageing
Cardiovasc Res,
July 15, 2009;
83(2):
247 - 261.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Ishii, T. Amano, T. Matsubara, and T. Murohara
Pharmacological Intervention for Prevention of Left Ventricular Remodeling and Improving Prognosis in Myocardial Infarction
Circulation,
December 16, 2008;
118(25):
2710 - 2718.
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Ferdinandy, R. Schulz, and G. F. Baxter
Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning
Pharmacol. Rev.,
December 1, 2007;
59(4):
418 - 458.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Pocar, A. Moneta, A. Grossi, and F. Donatelli
Coronary Artery Bypass for Heart Failure in Ischemic Cardiomyopathy: 17-Year Follow-Up
Ann. Thorac. Surg.,
February 1, 2007;
83(2):
468 - 474.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. M. Pitcher, M. Wang, B. M. Tsai, A. Kher, N. T. Nelson, and D. R. Meldrum
Endogenous estrogen mediates a higher threshold for endotoxin-induced myocardial protection in females
Am J Physiol Regulatory Integrative Comp Physiol,
January 1, 2006;
290(1):
R27 - R33.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Monteiro, L. Goncalves, and L. A Providencia
Diabetes and cardiovascular disease: the road to cardioprotection
Heart,
December 1, 2005;
91(12):
1621 - 1625.
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Lucchinetti, R. da Silva, T. Pasch, M. C. Schaub, and M. Zaugg
Anaesthetic preconditioning but not postconditioning prevents early activation of the deleterious cardiac remodelling programme: evidence of opposing genomic responses in cardioprotection by pre- and postconditioning
Br. J. Anaesth.,
August 1, 2005;
95(2):
140 - 152.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. A. Nath, J. P. Grande, A. J. Croatt, E. Frank, N. M. Caplice, R. P. Hebbel, and Z. S. Katusic
Transgenic Sickle Mice Are Markedly Sensitive to Renal Ischemia-Reperfusion Injury
Am. J. Pathol.,
April 1, 2005;
166(4):
963 - 972.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. A. Rongen, W. J.G. Oyen, B. P. Ramakers, N. P. Riksen, O. C. Boerman, N. Steinmetz, and P. Smits
Annexin A5 Scintigraphy of Forearm as a Novel In Vivo Model of Skeletal Muscle Preconditioning in Humans
Circulation,
January 18, 2005;
111(2):
173 - 178.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. da Silva, E. Lucchinetti, T. Pasch, M. C. Schaub, and M. Zaugg
Ischemic but not pharmacological preconditioning elicits a gene expression profile similar to unprotected myocardium
Physiol Genomics,
December 15, 2004;
20(1):
117 - 130.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Does Pre-MI Angina Protect Against Post-MI LV Remodeling?
Journal Watch Cardiology,
July 23, 2004;
2004(723):
6 - 6.
[Full Text]
|
|
|
|
