When compared side-by-side, these results indicate a difference between the CO2 and the Ho:YAG laser systems when TMR is performed. This is likely due to differences in the laser–tissue interactions for these different wavelengths of light.
Although the channel created when using the Ho:YAG can be less than the diameter of the channel created by the CO2 laser; it causes up to six times as much damage to the tissue. This creates more necrotic tissue in an already ischemic heart. Following this necrosis, collagen is laid down in the lasered area and Ho:YAG TMR does not accentuate the growth of angiogenesis in viable myocardium and can potentially further impair already ischemic tissue.
Previous publications have investigated the differences in myocardial damage between the CO2
and the Ho:YA Glaser. Kitade et al. found that when the Ho:YAG laser was fired, a layer of 760 ± 288 μm of thermal damage was created. When the CO2
laser was fired, a layer of 249 ± 83 μm of thermal damage was created. This study also found that the CO2
laser was more appropriate for end-stage myocardial ischemia then a Ho:YAG laser; in terms of the damage created [11
]. Another study investigated the vascular response of TMR as a relation to the scar size left by the laser [12
]. They reported that the angiogenic response to TMR is limited to the channel scar and related to the scar size. With a smaller scar channel (CO2
laser) there is greater angiogenesis in the scar. Additional experiments of histologically tracking laser tissue interactions over time revealed that the acute thermal injury and initial scarring at 2–3 weeks was greater with a Ho:YAG laser than with a CO2
]. There was scar contracture over time and at 6 weeks there was little difference between the groups. Moving beyond these histologic reports, Eckstein et al. [14
] concluded from their trial that a Ho:YAG laser did not provide acute improvement of myocardial perfusion.
The channel created by the single pulse of the CO2
laser creates less trauma and fibrosis in the surrounding tissue and may engender an angiogenic response that allows for recovery of myocardial function in the ischemic area. Krabatsch et al. [15
] found that the CO2
laser did not cause significant collateral damage to the myocardium and therefore resulted in minimal tissue fibrosis and more healthy tissue remained. In contrast, the Ho:YAG laser requires multiple blast-like pulses to traverse the myocardium, such firing damages the surrounding tissue creating more scar. This scarring of the myocardium leads to fibrosis that negatively impacts the contractile function of the heart. This is not to say that the Ho:YAG laser does not relieve angina but the mechanism of action is unlikely to be due to improved perfusion and function. Previous clinical studies have shown little to no perfusion benefits with Ho:YAG TMR [3
]. In contrast, the CO2
laser offers a superior environment for stimulating angiogenesis and subsequent blood flow as has been reported clinically [4
Confirmatory of our findings is a recent report of a cohort of patients 12 years after being treated with Ho:YAG TMR. The study found that cases of angina returned in treated patients after 3 years [21
]. This was not seen in a report of CO2
treated TMR patients out to 7 years post-treatment [22
It has been suggested that the scar tissue generated from the revascularization techniques can have a beneficial outcome. The new scar tissue can help to redistribute cardiac wall stress, penetrating all three layers of cardiac muscle acting as redistributing points to reduce interfascicular tension [23
]. We have previously seen that focal injury caused by laser kinetic energy that leads to scarring and angiogenesis can have an impact on myocardial function and that the balance of fibrosis and perfusion is important [24
]. One limitation of the present study is that unlike these reports we did not focus on the histologic findings but on the functional results. As noted many previous reports have discussed the different laser–tissue interactions with these two wavelengths of light and resultant tissue level findings. Our inclusion of histologic findings was not to be the foundation of the study therefore semi-quantitative methods were employed. Accurately tracking the laser injury histologically over time is difficult and it may be more clinically relevant to determine if the laser–tissue interaction with either scarring or angiogenesis led to changes in myocardial contractility. We endeavored to describe the ensuing functional impact.