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ular muscle. We have three comments on their letter. First, their technique can be effective for some forms of the tetralogy that have tubular tunnel-type stenosis of the right ventricular outflow tracts. The configuration of the right ventricular outflow tract, however, varies from patient to patient, and with patient age. We think that some degree of muscle resection is indispensable to the development of hypoplastic pulmonary arteries in the majority of cases. Second, if no muscle resection is rationalized, the innovative technique described by Puga and associates (21 has some advantages, because it does not require extracorporeal circulation. Finally, Dr Nair and associates unfortunately did not state the size of the pulmonary arteries (ie, McGoon ratio) of their patients; the preoperative angiogram showed that their patient had good size of the pulmonary arteries, which was considered to be amenable to corrective repair.

Yutaka Okita, M D Shigehito Miki, M D Department of Cardiovascular Surgery Tenri Hospital 200 Mishima, Tenri, Nara Japan 632

References 1. Okita Y, Miki S, Kusuhara K, et al. Palliative reconstruction of right ventricular outflow tract in tetralogy with hypoplastic pulmonary arteries. Ann Thorac Surg 1990;49:775-9. 2. Puga FJ, Uretzky G. Establishment of right ventriclehypoplastic pulmonary artery continuity without the use of extracorporeal circulation. J Thorac Cardiovasc Surg 1982;83: 7480.

Cooling Jacket Modifications To the Editor: Daily and associates [ l ] recently reemphasized the many advantages of myocardial protection jackets. I share their appreciation of those advantages, and have enjoyed them ever since introducing the first true myocardial protection jacket more than a decade ago [2]. One of those advantages is freedom from concern about phrenic nerve injury. Such injury results from freezing of the phrenic nerve, and has not been reported with properly used cold saline solution lavage of the pericardium-whether the cold saline solution is outside a jacket or inside a jacket. It is no surprise that some years ago Rousou and co-workers [3] were able to induce phrenic nerve injury after using the BonchekShiley myocardial protection jacket incorrectly by placing alcohol rather than saline solution around the cooling coils [3, 41. That improper maneuver allows the saline solution circulating in the jacket to be supercooled below the freezing point of water, which is equivalent to placing ice in the pericardium-exactly what one wishes to avoid with a jacket! Indeed, Rousou and co-workers noticed that the supercooled fluid in the jacket would freeze to slush if the fluid stopped circulating. After abandoning the use of alcohol, they did not experience phrenic nerve injury (personal communication). It is disappointing that in their recent article Daily and associates once again asserted that the Bonchek-Shiley jacket can cause phrenic nerve injury, and to support this assertion they cited a portion of Rousou’s study without providing the explanation that Rousou and co-workers themselves provided. In more than 1,000 valve operations with the Bonchek-Shiley jacket, my colleagues and I have never observed phrenic nerve injury. Daily has previously argued that this could be merely a

failure of detection due to the lack of phrenic nerve stimulation studies in our patients [5]. This same complaint could be made about every other report on methods of topical cardiac hypothermia. Presumably, Daily believes we might have overlooked subclinical phrenic nerve injury. If a subclinical condition is never observed clinically, however, it is not relevant. It should not be necessary to rehash these stale arguments. They have been published before, and my purpose in writing is only to refer readers who are interested in this controversy to those letters (61, which should constitute a sufficient exchange of views. To summarize as simply as possible: cold saline solution lavage of the pericardium does not cause phrenic nerve injury, and enclosing the saline solution in a plastic jacket will not enable it to do so unless the saline solution is supercooled! When coronary blood flow is interrupted, myocardial hypothermia enhances myocardial protection. More than 10 years ago, the BonchekShiley jacket was introduced as a straightforward means of accomplishing this objective. Although we have not found it necessary to add bulky insulating pads or metal strips, others may prefer such accessories. However, those choices should be made on the basis of complete information, which we have attempted to provide.

Lawrence 1. Bonchek, M D 555 N Duke St Lancaster, PA 17603

References 1. Daily PO, Kinney TB. Optimizing myocardial hypothermia: 11. Cooling jacket modifications and clinical results. Ann Thorac Surg 1991;51:284-9. 2. Bonchek LI, Olinger GN. An improved method of topical cardiac hypothermia. J Thorac Cardiovasc Surg 1981;82:87%82. 3. Rousou JA, Parker T, Engelman RM, Breyer RH. Phrenic nerve paresis associated with the use of iced slush and the cooling jacket for topical hypothermia. J Thorac Cardiovasc Surg 1985;89:921-5. 4. Bonchek LI. Phrenic nerve paresis associated with myocardial protection jacket [Letter]. J Thorac Cardiovasc Surg 1985;90: 7954. 5 . Daily PO. Reply to: Myocardial protection jacket for topical hypothermia [Letter]. J Thorac Cardiovasc Surg 1987;94:792-3. 6 . Bonchek LI. Myocardial protection jacket for topical hypothermia. J Thorac Cardiovasc Surg 1987;94:792-5.

Blood Versus Oxygenated Crystalloid Cardioplegia To the Editor: We read with interest the paper by Coetzee and co-workers [ l ] comparing oxygenated crystalloid and blood cardioplegia in baboons. We were initially impressed with the conclusion that the results demonstrated greater maintenance of myocardial contractility with the use of an oxygenated crystalloid cardioplegic solution than with a blood-based solution. However, after examining this report more closely, we believe this conclusion is unjustified. In this study 12 indices of global cardiac function were measured on two occasions after cardioplegic arrest, making 24 values in all. None of these showed significant differences between the two groups. A disturbing fact was that the prearrest control values of first derivative of left ventricular pressure, stroke volume, left ventricular stroke work, and right ventricular stroke work were substantially lower in the blood cardioplegic group than in the crystalloid cardioplegic group. Four of the 12

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indices were stroke-related and therefore could be affected by the faster heart rate in the blood cardioplegic group, but this would not explain the fact, for example, that the first derivative of left ventricular pressure in the crystalloid cardioplegic group was 43%higher under control conditions than in the blood cardioplegic group. None of these differences reached statistical significance, but this could be due to the small numbers in each group (n = 5). When one normalizes the postbypass values in relation to the prebypass values, one finds that in all cases the stroke work and first derivative of left ventricular pressure values in the supposedly inferior blood cardioplegic group were somewhat greater than those in the crystalloid cardioplegic group, eg, 20 minutes after bypass, recovery of stroke work for the blood cardioplegic group was 79% and that for the crystalloid group was 61%; first derivative of left ventricular pressure was 132% for the blood cardioplegic group and 113% for the crystalloid group. These differences were probably not statistically significant, but there appeared to be a consistent trend in favor of blood cardioplegia. The only significant differences in function that were detected between the oxygenated crystalloid and blood cardioplegic groups were in 2 of the 10 measurements of regional function, and then only after these had been normalized in terms of the prearrest control values. It was disturbing to note that whereas the percentage recovery of end-systolic pressure-length relationship was greater in the crystalloid than in the blood cardioplegic group, the "regional stroke work" in normalized terms appeared, if anything, to be greater in the blood cardioplegic group than in the crystalloid cardioplegic group 10 minutes after bypass. In summary, out of a total of 34 hemodynamic measurements, only two showed significant differences between groups and even these were only significant at the 5% level. Thus we believe that a more correct conclusion from this study would be that no important difference in efficacy had been demonstrated between oxygenated crystalloid and blood cardioplegia.

Ann Thorac Surg 1991;52:3447

tion. Medications included digoxin and warfarin sodium (Coumadin). On examination she was a thin woman with a blood pressure of 12470 mm Hg and a heart rate of 64 beats/min. There was mild to moderate left ventricular dysfunction with severe tricuspid regurgitation and a normal prosthetic mitral valve on cardiac catheterization. The patient underwent tricuspid valve replacement. At operation, numerous dense adhesions were noted to surround the entire heart and great vessels. The prosthetic mitral valve appeared normal and the tricuspid valve was replaced with a porcine valve. On weaning from bypass the patient was noted to be in a nodal rythmn. On the third postoperative day the nodal rhythm deteriorated to atrial flutter with complete heart block requiring ventricular pacing through the temporary epicardial wires placed at operation. The digoxin level was subtherapeutic. After a week of observation the patient's heart rate failed to return to an adequate level and pacemaker insertion was planned with epicardial leads. At operation the anterior surface of the right ventricle was found to be covered not only with chronic fibrosis but with acute inflammatory tissue as well. Four different implant sites were tested and the lowest threshold obtained was 2.5 V. The R-wave was 3.8 mV. Two Medtronic Sutureless Epicardial leads (model 6917-A53T; Medtronic, Irving, TX) were placed and sensed and paced well.

Franklin Rosenfeldt, FRACS Andrew Cochrane, FRACS Baker Medical Research Institute PO Box 348 Prahran, 3181 Victoria, Australia

A

Reference 1. Coetzee A, Roussouw G , Fourie P, Lochner A. Preservation of myocardial function and biochemistry after blood and oxygenated crystalloid cardioplegia during cardiac arrest. Ann Thorac Surg 1990;50:230-7.

Epicardial Lead Failure Due to Dense Scarring: A Solution

To the Editor:

The safety and benefit of epicardial pacing have been demonstrated in numerous reports. Today, surgeons are called on to place epicardial pacing electrodes when transvenous pacing is unsuccessful or contraindicated. We present 2 cases of epicardial lead failure due to excessive surface scarring and our solution to the problem. The first patient, a 36-year-old woman with a history of childhood rheumatic fever, had undergone mitral valve commisurotomy for mitral stenosis at age 20 years and mitral valve replacement 11 years later. She was seen at our institution with increased lethargy, bilateral pedal edema, and abdominal disten-

B Fig 1. (A) Medtronic Sutureless Myocardial Pacing Lead (Model 6917-35T), unmodified form. ( B ) Modified epicardial lead: note elongation of the coil with maintenance of the normal spiral architecture.

Blood versus oxygenated crystalloid cardioplegia.

CORRESPONDENCE Ann Thorac Surg 345 1991;52344-7 ular muscle. We have three comments on their letter. First, their technique can be effective for s...
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