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J Thorac Cardiovasc Surg 1995;110:280-281
© 1995 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Surgery
Division II
Kobe University School of Medicine
Kobe, Japan
Reply to the Editor:
We agree with Mr. El Oakley that Odim, Adoumie, and Chiu
1 showed increased coronary sinus blood flow during cardiac assistance. We further concur that Odim's group suggested that cardiomyoplasty may increase oxygen extraction but that the coronary arteries adjust by increasing coronary artery flow during burst stimulation. Their findings were nearly consistent with our findings, which showed enhanced coronary arterial blood flow velocity during cardiac assistance with cardiomyoplasty.
2
We also agree that incomplete muscle wrap may lessen the effect of cardiomyoplasty on coronary arterial blood flow. Although the muscle flap wrapped the ventricles completely and coronary arterial flow velocity was measured in the left main coronary artery in our study, muscular compression of the heart cannot be fully evaluated until the muscle flap is completely adherent. Recently, Soltero and colleagues
3 reported significant reduction of flow through the left anterior descending and circumflex coronary arteries immediately after posterior cardiomyoplasty in dogs.
These contradictory findings may be attributable to several factors, including methods, the measuring point, stimulation mode, and coronary arterial pressure. As we explained in the discussion section of our article, the Doppler catheter system can minimize the motion artifact during contraction of the latissimus dorsi muscle flap because the catheter can be fixed at the end of the main trunk of the left coronary artery, where muscle contraction may not directly affect the diameter of the vessels. Left ventricular pressure in systole was augmented approximately 16% from 84.6 ± 3.8 mm Hg in control animals to 97.1 ± 3.4 mm Hg in those with cardiomyoplasty. However, the left ventricle moved toward the base of the heart during contraction of the latissimus dorsi muscle, and we could not obtain a constant signal when the Doppler catheter was placed in the left anterior descending artery. In contrast, augmentation of left ventricular pressure was approximately 100% in the study reported by Soltero and associates
3 (from 100 to 200 mm Hg in their figure). This marked increase may be important to exacerbate the adverse effect of cardiomyoplasty on the coronary arterial flow in their study. In addition, as we described in our discussion, additional increase in perfusion pressure will not increase coronary arterial flow when coronary perfusion pressure is high.
4 In our study, initial perfusion pressure was set at about 60 mm Hg and autoregulation was partially abolished. Increases in coronary perfusion pressure, from 60 to 70 mm Hg, and in stroke volume may enhance the coronary arterial flow, in association with an increase in coronary arterial flow velocity.
Limitations of our study include use of unconditioned skeletal muscle, use of an acute heart failure model, and use of normal canine heart. As Soltero's group pointed out, hemodynamics of coronary blood flow may be significantly different in a dilated failing heart compared with a normal heart, especially in the long term after cardiomyoplasty. We are currently using the Doppler guidewire system to evaluate long-term effects of cardiomyoplasty on coronary arterial blood flow in canine hearts. This information will resolve the contradictory findings and be useful in clarifying the mechanisms of augmentation by cardiomyoplasty.
References
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