A compare between myocardial topical negative pressure levels of -25 mmHg and -50 mmHg in a porcine model

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Abstract

Background
Topical negative pressure (TNP), widely used in wound therapy, is known to stimulate wound edge blood flow, granulation tissue formation, angiogenesis, and revascularization. We have previously shown that application of a TNP of -50 mmHg to the myocardium significantly increases microvascular blood flow in the underlying tissue. We have also shown that a myocardial TNP levels between -75 mmHg and -150 mmHg do not induce microvascular blood flow changes in the underlying myocardium. The present study was designed to elucidate the difference between- 25 mmHg and -50 mmHg TNP on microvascular flow in normal and ischemic myocardium.

Methods
Six pigs underwent median sternotomy. The microvascular blood flow in the myocardium was recorded before and after the application of TNP using laser Doppler flowmetry. Analyses were performed before left anterior descending artery (LAD) occlusion (normal myocardium), and after 20 minutes of AD occlusion (ischemic myocardium).

Results
A TNP of -25 mmHg significantly increased microvascular blood flow in both normal (from 263.3 ± 62.8 U before, to 380.0 ± 80.6 PU after TNP application, * p = 0.03) and ischemic myocardium (from 58.8 ± 17.7 PU before, to 85.8 ± 20.9 PU after TNP application, * p = 0.04). TNP of -50 mmHg also significantly increased microvascular blood flow in both normal (from 174.2± 20.8 PU before, to 240.0 ± 34.4 PU after TNP application, * p = 0.02) and ischemic myocardium (from 44.5 ± 14.0 PU before, to 106.2 ± 26.6 PU after TNP application, ** p = 0.01).

Conclusion
Topical negative pressure of -25 mmHg and -50 mmHg both induced a significant increase in microvascular blood flow in normal and in ischemic myocardium. The increase in microvascular blood flow was larger when using -25 mmHg on normal myocardium, and was larger when using -50 mmHg on ischemic myocardium; however these differences were not statistically significant.

Pages

Background
TNP produces a mechanical stress and a pressure gradient across the tissue which may cause a surge of blood to the area. Mechanical forces and increased blood flow are known to stimulate granulation tissue formation, i.e. endothelial proliferation, capillary budding and angiogenesis3,4. Poststernotomy mediastinitis is a strong predictor for poor long-term survival after coronary artery by-pass surgery (CABG), when using conventional wound healing techniques (closed irrigation, delayed wound closure, or reconstructing with momentum or pectoral flaps)5,6. Braxton and coworkers demonstrated that actuarial survival after 10 years was 39% in patients with oststernotomymediastinitis and 70% in patients without mediastinitis6. Milano and collages have suggested that mediastinitis may cause negative long-terms effects on several organs such as the heart and kidneys5. Lately, the usefulness of TNP in the treatment of poststernotomy mediastinitis has been well recognized among cardiothoracic surgeons around the world, due to excellent clinical outcome7,8.

Pages

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