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Ann Thorac Surg 1996;61:772-773
© 1996 The Society of Thoracic Surgeons
Division of Thoracic Surgery, Medical College of Pennsylvania, Hahnemann University, Allegheny Campus, 320 E North Ave, Pittsburgh, PA 15212
To the Editor:
I read with interest the contribution by Chiu and associates [1]. Although the terms ``molecular'' cardiomyoplasty [2] and ``cellular'' cardiomyoplasty may be misnomers, I agree with Dr Chiu's conclusions that ``confirmation of their findings and its functional capabilities could have important clinical implications.'' On the other hand, I disagree with their description of a method of myocardial cryoinjury implied to be original to them.
In 1987 my colleagues and I [3] described cryoinjury to produce left ventricular dysfunction. This was part of a study on the effects of electrical stimulation on fibers of skeletal muscle used for dynamic cardiomyoplasty. Twenty dogs underwent transferral of the latissimus dorsi muscle onto the heart and wrapped around the ventricles, either after ischemic injury (coronary ligation, n = 10), cryoinjury of the free (anterior) left ventricular wall (n = 5), partial wall resection (n = 1), or no injury at all (n = 4).
Cryoinjury was induced by applying a flat 3-cm-diameter copper disc connected to a CE-4 Cryosurgery Unit (Frigitronics. Shelton, CT), and circulating liquid nitrogen at -196°C through it for 4 ± 1 minutes. The depth of freezing was monitored using a 7.5-MHz linear ultrasound transducer connected to an intraoperative ultrasound machine.
Of the 5 cryoinjured dogs, 3 were long-term survivors, 1 had a fatal arrhythmia after receiving a rather extensive cryoinjury, and the other was sacrificed 4 weeks postoperatively to study the injured left ventricle. The histopathologic findings in this last case led to ``Part of [the] studies in the first series of experiments [which] were carried out by Dr Race L Kao at the Allegheny-Singer Research Institute (Chairman: Dr George Magovern, Sr), Pittsburgh, PA'' [1].
We concluded from that early series that cryoinjury was safer than coronary artery ligation as an experimental model of permanent myocardial damage, if not necessarily of congestive heart failure. It is highly controllable in extension and depth of injury and does not cause life-threatening arrhythmias if one stays away from the upper anteroseptal wall.
The only discrepancy we find between the methods we originally described and the one now described by Chiu and associates is the time of cryoprobe application: 4 ± 1 minutes in our series versus 20 to 25 minutes in theirs. Perhaps the fact that their cryoprobe is kept at -160°C, as opposed to -196°C when we created the model, may allow them to stay on the ventricular wall that long without generating fatal transoperative complications.
I suggest that detailed description of the predictability of their application of the technique for extent of injury and short-term and long-term consequences would be helpful to those requiring myocardial injury models for evaluation of cellular, pharmacologic, and mechanical support.
References
Division of Cardiovascular and Thoracic Surgery, The Montreal General Hospital, 1650 Cedar Ave, Rm C9-169 Montreal, PQ, H3G 1A4, Canada
Department of Surgery, Box 70575, James H.Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0575
To the Editor:
By ``cellular cardiomyoplasty,'' we tried to describe our approach to ``repair the heart using cells,'' because our report was on implanting satellite cells into damaged myocardium to repair it by growing new cardiac muscle. This is a new field, and Dr Christlieb is welcome to offer better terms if he believes ours is a misnomer.
We are surprised by his statement that he disagrees with ``...their description of a method of myocardial cryoinjury implied to be original to them.'' We did not claim or imply originality of the cryoinjury model. We simply described how we did it. Cryoinjury for cardiac research and surgery goes back to at least 1951 [1], and had been described by numerous authors. Furthermore, the technique of cryoinjury should be adapted to the specific purpose of its use. Creation of left ventricular aneurysm or failure [2], interruption of conduction pathways and destruction of arrhythmogenic tissue, or, as in our study [3], as a means to create homogeneous scar simply to demonstrate new muscle tissue within the scar, all can be achieved by optimizing the individual cryoinjury protocol. Thus, there is no single ``correct'' way to create a cryoinjury.
Incidentally, we appreciate the opportunity to collaborate with Dr George Magovern's group at Pittsburgh as Dr Kao did his early work there, and this was acknowledged in our article. Since the submission of our manuscript, an article by the Pittsburgh group had appeared [4], which should be of interest for readers who are following the progress with this approach.
References
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