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If Jackson Pollack is the artist, then the recent study in JACCby Saririan and Eisenberg on myocardial laser revascularization is indeed state of the art. The investigators (1)are to be commended for attempting to clarify the work that has been done with this technique, but unfortunately the result is less than satisfactory. To equate Ho:YAG and CO2lasers as well as transmyocardial laser revascularization (TMR) and percutaneous myocardial laser revascularization (PMR) without understanding that vast differences exist in the laser-tissue interactions and in their ability to treat the full thickness of the myocardium is analogous to saying that calcium channel blockers and beta-blockers are of equal importance postmyocardial infarction because they are both “blockers.” This lack of discernment is most obvious in the researchers’ discussion of suggested mechanisms of action.
Throughout the discussion, the investigators list a number of different experiments without identifying what type of laser was used, what type of model was employed, and whether the model employed re-creates the clinical scenario. In addition, they ignore several studies that do clarify the mechanism. These omissions continue when describing the clinical work. Where significant differences exist in the clinical trials, the results are lumped together. In an attempt to tabulate the published series of TMR patients with 12-month follow-up, the researchers ignored over 220 patients who demonstrated a significant perfusion benefit after CO2TMR. The investigators are familiar with these studies, as they do reference them elsewhere in their report. This perfusion benefit has also been demonstrated using the same CO2laser in a randomized clinical trial. Although this is acknowledged by the investigators, it is immediately discounted and considered to be a placebo effect. They claim that a placebo effect can demonstrate an 80% improvement in exertional angina, but this has not been demonstrated at one year, and certainly it has not been demonstrated out beyond five years, as has been reported with CO2TMR.
Moreover, they do not explain how perfusion benefit can be achieved by placebo. They claim that the patients who crossed over from medical therapy to TMR in the aforementioned CO2TMR trial did so owing to a subjective end point of angina and as a result of investigator bias. In fact, crossovers occurred after patients developed unstable angina and were unweanable from intravenous heparin and nitroglycerin after three attempts to decrease this maximal medical therapy. This treatment was not controlled by the investigators and is far from subjective.
Also, comments on the perfusion data from the European CO2TMR trial are misleading. Although it is true that a decrease occurred in the number of myocardial segments with reversible ischemia for patients treated with medical therapy and for TMR, the decrease in the medical management group was due in part to a doubling of the fixed defects. No significant increase occurred in the fixed defects in the TMR group.
To include PMR in this discussion without noting its severe limitations is inappropriate; for example, regardless of the mechanism, a 3- to 4-mm divot created on the subendocardium cannot be considered to be as complete a treatment as a full thickness transmural channel. I do agree with the investigators that a review of the TMR literature suggests that the clinical benefits of PMR are largely due to the placebo effect. Apparently the U.S. Food and Drug Administration (FDA) agrees because the FDA recently deemed Ho:YAG PMR not to be worthy of approval.
- American College of Cardiology Foundation