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Ann Thorac Surg 1998;65:1200
© 1998 The Society of Thoracic Surgeons

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Correspondence

Why Do Channels Remain Patent After Transmyocardial Laser Revascularization?

^a 4101 S Wappel Dr, Columbia, MO 65203 USA

Previously in this journal [1], I described how transmyocardial laser revascularization (TLR) had led to the formation of myocardial pseudovascular tubes. Now, I would like to present another case of the same phenomenon and to formulate some ideas concerning its pathogenesis.

Mack and associates [2] have studied channels after TLR and compared them with myocardial channels formed by mechanical means. At 72 hours after TLR, both types of channels were obstructed by alleged thrombus (see Mack and associates’ Figure 1). Thirty days after TLR, 56% ± 7.3% of the lased channels were patent (see their Figure 2), whereas all channels formed mechanically underwent healing (see their Figure 3). Mack and associates [2] believe that growth factors promoted by laser injury might have led to angiogenesis and the recanalization of lased channels. This hypothesis is contradicted, however, by the absence of organized thrombus in the patent channels (see their Figure 2), and another explanation must be found.

I propose that the lased channel in their Figure 1 [2] is obstructed by damaged hyalinized cardiomyocytes, which will fragment eventually into eosinophilic droplets similar to red cells [1]. This interpretation is based (1) on the interstitial tissue septa still visible in the peripheral parts of the channel and (2) on the cell nuclei situated in the same location and aligned into parallel rows, indicating derivation from highly organized tissue and not from haphazardly located inflammatory cells infiltrating thrombus.

It has been proposed that the fragmentation of hyalinized cardiomyocytes into eosinophilic droplets is a morphologic manifestation of their apoptotic death and that eosinophilic droplets are apoptotic bodies [3]. In contradistinction to accidental cell death, apoptosis does not provoke inflammation and blood coagulation, ie, the phenomena that are followed by healing reaction. Both appear absent from the channel in Figure 1 [2] and from the channels presented in Figure 4 by Horvath and associates [4]. This explains why these channels do not heal and become patent when eosinophilic droplets are eliminated [1]. This fact may be exploited purposely in TLR. If the optimal level of laser energy is used, which induces apoptosis and not accidental cell death, one may obtain myocardial channels that become and remain patent. This hypothesis is in full agreement with the observation that the fragmentation of cardiomyocytes into eosinophilic droplets in some pathologic states leads to tissue defects that do not heal either [5]. Would it be possible to exploit the same principle in laser angioplasty? Would one obtain the reduction of atherosclerotic plaques without inflammation, healing, and restenosis?

References

1. Beranek J.T. Pseudovascular tubes obscure transmyocardial revascularization. Ann Thorac Surg 1997;63:597-598.[Free Full Text]
2. Mack C.A., Magovern C.J., Hahn R.T., et al. Channel patency and neovascularization after transmyocardial revascularization using an excimer laser. Results and comparisons to nonlased channels. Circulation 1997;96(Suppl 2):65-69.
3. Beranek J.T. Apoptosis is the main mechanism of cardiomyocyte death in the hyperacute rejection of heart xeno- and allografts. Transplantation 1997;64:1632-1633.[Medline]
4. Horvath K.A., Smith W.J., Laurence R.G., Schoen F.J., Appleyard R.F., Cohn L.H. Recovery and viability of an acute myocardial infarct after transmyocardial laser revascularization. J Am Coll Cardiol 1995;25:258-263.[Abstract]
5. Beranek J.T. Hyalin degeneration in the cardiomyopathy of overload. J Mol Cell Cardiol 1995;27:847.[Medline]

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This Article 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 Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Beranek, J. T. Search for Related Content PubMed PubMed Citation Articles by Beranek, J. T.