Circulation. 2006;114:e501-e502
doi: 10.1161/CIRCULATIONAHA.106.620229
(Circulation. 2006;114:e501-e502.)
© 2006 American Heart Association, Inc.
Images in Cardiovascular Medicine |
Coronary Collaterals in Full Effect
Paul Knaapen, MD;
Lucas J. Klein, MD;
Robin Nijveldt, MD;
Tjeerd Germans, MD;
Albert C. van Rossum, MD, PhD;
Carel C. de Cock, MD, PhD
From the Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands.
Correspondence to P. Knaapen, MD, Department of Cardiology, 6D 120, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands. E-mail p.knaapen{at}vumc.nl
A 59-year-old man with no relevant medical history was referred to our clinic for analysis of exertional chest pain. He had noticed slowly progressive symptoms approximately 6 months before referral, although they did not prohibit his daily 12-mile cycling exercise routine. During diagnostic 99m-technetium-sestamibi single photon emission computed tomography treadmill stress testing, the ECG showed pathological ST-segment depression, and the patient had anginal chest pain. Three-dimensional reconstructed scintigraphic perfusion images (Figure 1) displayed a substantial reversible defect in the anterolateral myocardium with only a mild resting perfusion defect in the distal segment of the anterior wall, which coincided with a small area of subendocardial fibrosis visualized by late contrast-enhanced magnetic resonance imaging (Figure 2). Apart from hypokinesia in this segment, contractile function of the left ventricle was normal (online-only Data Supplement Movies I and II). After the nuclear stress test, the patient was admitted and treated with aspirin, ß-blockers, and statins, and coronary angiography was performed. Injection of the contrast agent in the right coronary artery (Figure 3A through Figure 3C, Movies III and IV) revealed an extensive collateral network with complete retrograde filling of the epicardial vessels of the left anterior descending and circumflex artery (grade 3/3 according to the Rentrop collateral flow classification).1 Conversely, there was complete occlusion of the left main coronary artery (Figure 3D, Movie V). No attempts for percutaneous intervention were made, and successful coronary artery bypass grafting was performed within a few days, with subsequent full recovery.

View larger version (19K):
[in this window]
[in a new window]
|
Figure 1. Three-dimensional reconstructed 99m-technetium-sestamibi single photon emission computed tomography images. Tracer uptake during rest is homogeneous, with the exception of a mild defect in the distal segment of the anterior wall. Stress images display a large perfusion defect in the anterolateral myocardium extending to the apex.
|
|

View larger version (97K):
[in this window]
[in a new window]
|
Figure 2. Images from late contrast-enhanced magnetic resonance imaging, 15 minutes after injection of gadolinium-diethylenetriamine pentaacetic acid. Modified vertical long-axis view (A) through the center of contrast enhancement as seen on short-axis images (B), demonstrating the area of subendocardial fibrosis (arrows and dotted line). LA indicates left atrium; LV, left ventricle.
|
|

View larger version (61K):
[in this window]
[in a new window]
|
Figure 3. Right anterior oblique 30° projection of the right coronary artery with complete retrograde filling of the left anterior descending and circumflex artery (A through C). Left anterior oblique 60° of the (occluded) left main stem (D).
|
|
Total occlusion of the left main coronary artery in patients without previous coronary bypass surgery is a rare finding at cardiac catheterization. When encountered, it is usually in the setting of an acute myocardial infarction accompanied by severe left ventricular dysfunction often leading to cardiogenic shock. In this particular case, however, due to the development of extensive right to left collateral blood flow, chronic left main occlusion led to only minor subendocardial scarring with virtually no effect on left ventricular function. Although the pathophysiological determinants for collateral recruitment are largely unknown, the occurrence is related to prolonged periods of ischemia, duration of occlusion, proximal lesion location, and long-term physical exercise.25 These factors have probably contributed to the collateral recruitment in the currently described patient and have resulted in the fortunate final outcome.
 |
Disclosures
|
|---|
None.
 |
Footnotes
|
|---|
The online-only Data Supplement, which contains 5 movies, can be found at http://circ.ahajournals.org/cgi/content/full/114/12/e501/DC1.
 |
References
|
|---|
1. Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects.
J Am Coll Cardiol. 1985; 5: 587592.
[Abstract]2. Werner GS, Ferrari M, Betge S, Gastmann O, Richartz BM, Figulla HR. Collateral function in chronic total coronary occlusions is related to regional myocardial function and duration of occlusion. Circulation. 2001; 104: 27842790.[Abstract/Free Full Text]
3. Piek JJ, van Liebergen RA, Koch KT, Peters RJ, David GK. Clinical, angiographic and hemodynamic predictors of recruitable collateral flow assessed during balloon angioplasty coronary occlusion. J Am Coll Cardiol. 1997; 29: 275282.[Abstract]
4. Senti S, Fleisch M, Billinger M, Meijer B, Seiler C. Long-term physical exercise and quantitatively assessed human collateral circulation. J Am Coll Cardiol. 1998; 32: 4956.[Abstract/Free Full Text]
5. Pohl T, Seiler C, Billinger M, Herren E, Wustmann K, Mehta H, Windecker S, Eberli FR, Meier B. Frequency distribution of collateral flow and factors influencing collateral channel development: functional collateral channel measurement in 450 patients with coronary artery disease. J Am Coll Cardiol. 2001; 38: 18721878.[Abstract/Free Full Text]