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TMR Mechanism of Action
Current theories suggest that the mechanism is a multifactorial process with both short-term and long-term benefits.1 Proposed mechanisms of action for TMR, include:
- Increased perfusion of myocardium via the channels created;
- Increased collateralization via angiogenesis;
- Symptom reduction resulting from disruption of pain fiber function;
- Possible microinfarcts to the myocardium.
Data suggests that much of the immediate benefit of TMR is from denervation,2 while the long-term benefit derives from angiogenesis.3
During a TMR procedure, the laser fiber encounters local pain and sympathetic nerve fibers. As a channel is created, these nerves are severed which interrupts pain signal transmission and decreases the heart’s regional sympathetic tone. In response, two events occur.
- First, there’s a decreased resistance in the local vascular bed which increases the flow reserve and regional blood flow to the myocardium.
- Second, the tissues oxygen demand decreases. The result is an immediate decrease in angina pain.
During channel creation, the laser energy causes a limited focal injury to the myocardium. This injured tissue, known as the border zone, stimulates the angiogenic cascade to begin. Inflammation of the injured tissue produces angiogenic growth factors which stimulate new blood vessel growth within the region. Numerous clinical studies reflect increased perfusion to myocardium treated with TMR.4,5,6
Acting in tandem, denervation and angiogenesis can provide early and long-term benefit after TMR and can provide relief for patients suffering from severe refractory angina.
- Huikeshoven M, et al. Ann Thorac Surg 2002;74:956-970.
- Beek JF, et al. J Thorac Cardiovasc Surg 2004;127:517-524.
- Atluri P, et al. J Thorac Cardiovasc Surg 2008;135:283-291.
- Akay MH, et al. Heart Surg Forum 2009;12:E199-E201.
- Kostkiewicz M, et al. Cardiology 2000;94:173-178.
- Meuller XM, et al. Heart 2001;85:697-701.