This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gerber, B. L. Articles by Melin, J. A. Search for Related Content PubMed PubMed Citation Articles by Gerber, B. L. Articles by Melin, J. A.

CLINICAL STUDIES

Myocardial perfusion and oxygen consumption in reperfused noninfarcted dysfunctional myocardium after unstable angina

Direct evidence for myocardial stunning in humans

Bernhard L. Gerber, MD^*,1, William Wijns, MD, Jean-Louis J. Vanoverschelde, MD, FACC^*, Guy R. Heyndrickx, MD, Bernard De Bruyne, MD, Jozef Bartunek, MD and Jacques A. Melin, MD^*

^* Division of Cardiology and Positron Emission Tomography Laboratory, University of Louvain Medical School, Brussels, Belgium
Cardiovascular Center, Onze Lieve Vrouw-Ziekenhuis, Aalst, Belgium

Manuscript received December 2, 1998; revised manuscript received June 29, 1999, accepted August 27, 1999.

Reprint requests and correspondence: Dr. William Wijns, Cardiovascular Center, Onze-Lieve Vrouwziekenhuis, Moorselbaan 164, B-9300 Aalst, Belgium
william.wijns{at}olvz-aalst-.be

OBJECTIVES

To positively establish the diagnosis of myocardial stunning in patients with unstable angina and persistent wall motion abnormalities after reperfusion by coronary angioplasty.

BACKGROUND

Although myocardial stunning is thought to occur in several clinical conditions, definite proof of its existence in humans is still lacking, owing to the difficulty of measuring myocardial blood flow (MBF) in absolute terms.

METHODS

We studied 14 patients with unstable angina due to proximal left anterior descending coronary artery disease who presented persistent anterior wall motion abnormalities despite revascularization of the culprit lesion by percutaneous coronary angioplasty (PTCA) and who did not have clinical evidence of necrosis. Dynamic positron emission tomography (PET) with [¹³N]-ammonia and [¹¹C]-acetate was performed 48 h after PTCA to determine absolute MBF and oxygen consumption (MVO₂). Regional wall thickening and regional cardiac work were determined using two-dimensional echocardiography. Improvement of segmental wall motion abnormalities was followed for a median of 4 months (1.5 to 14 months).

RESULTS

As judged from the changes in segmental wall motion score, regional dysfunction was spontaneously reversible in 12/14 patients and improved from 2.2 ± 0.3 to 1.2 ± 0.3 at late follow-up (p < 0.001). With PET, [¹³N]-ammonia MBF was similar among dysfunctional and remote normally contracting segments (85 ± 29 vs. 99 ± 20 ml·min^–1·100g^–1, p = not significant [n.s.]), thus demonstrating a perfusion-contraction mismatch. Despite the reduced contractile function, dysfunctional myocardium presented near normal levels of MVO₂ (6.5 ± 4.2 vs. 8.0 ± 1.9 ml·min^–1·100g^–1, p = n.s.). Consequently, the regional myocardial efficiency (regional work divided by MVO₂) of the dysfunctional myocardium was found to be markedly decreased as compared with normally contracting myocardium (6 ± 6% vs. 26 ± 6%, p < 0.001).

CONCLUSIONS

This study demonstrates that human dysfunctional myocardium capable of spontaneously recovering contractile function after unstable angina endures a state of perfusion-contraction mismatch. These data for the first time provide unequivocal direct evidence for the existence of acute myocardial stunning in humans.

Abbreviations and Acronyms   ECG = electrocardiogram   LAD = left anterior descending coronary artery   MBF = myocardial blood flow   MVO2 = myocardial oxygen consumption   PET = positron-emission tomography   PTCA = percutaneous coronary angioplasty

This article has been cited by other articles:

				P. Knaapen, T. Germans, J. Knuuti, W. J. Paulus, P. A. Dijkmans, C. P. Allaart, A. A. Lammertsma, and F. C. Visser Myocardial Energetics and Efficiency: Current Status of the Noninvasive Approach Circulation, February 20, 2007; 115(7): 918 - 927. [Full Text] [PDF]

				A. N. Mazzadi, X. Andre-Fouet, N. Costes, P. Croisille, D. Revel, and M. F. Janier Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2570 - H2582. [Abstract] [Full Text] [PDF]

				G. R. Heyndrickx Early reperfusion phenomena. Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2006; 10(3): 236 - 241. [Abstract] [PDF]

				R. G. Weiss, G. Gerstenblith, and P. A. Bottomley ATP flux through creatine kinase in the normal, stressed, and failing human heart PNAS, January 18, 2005; 102(3): 808 - 813. [Abstract] [Full Text] [PDF]

				B. L. Gerber, J. Garot, D. A. Bluemke, K. C. Wu, and J. A.C. Lima Accuracy of Contrast-Enhanced Magnetic Resonance Imaging in Predicting Improvement of Regional Myocardial Function in Patients After Acute Myocardial Infarction Circulation, August 27, 2002; 106(9): 1083 - 1089. [Abstract] [Full Text] [PDF]

				S. Verma, P. W.M. Fedak, R. D. Weisel, J. Butany, V. Rao, A. Maitland, R.-K. Li, B. Dhillon, and T. M. Yau Fundamentals of Reperfusion Injury for the Clinical Cardiologist Circulation, May 21, 2002; 105(20): 2332 - 2336. [Full Text] [PDF]

				E. Barnes, R. J. C. Hall, D. P. Dutka, and P. G. Camici Absolute blood flow and oxygenconsumption in stunned myocardiumin patients with coronary artery disease J. Am. Coll. Cardiol., February 6, 2002; 39(3): 420 - 427. [Abstract] [Full Text] [PDF]