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Ann Thorac Surg 2007;84:573
© 2007 The Society of Thoracic Surgeons
Cardiac Surgery Group, Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Groby Rd, Leicester, LE3 9QP United Kingdom
(Email: mg50{at}le.ac.uk).
Patients with severe diffuse coronary artery disease and refractory angina who can not be treated with conventional coronary artery bypass graft surgery or angioplasty represent a clinical challenge due to the absence of proven effective alternative treatments. Therapies such as transmyocardial laser and cardiac denervation have not had the expected results, and our own group demonstrated that although these two treatment modalities can induce angina relief in the short-term, their efficacy was limited (eg, most patients remained with some degree of angina) and their efficacy was also transient (eg, the benefit was partly lost by 42-month follow-up), and this is not associated with detectable improvement in myocardial perfusion as assessed by magnetic resonance imaging [1]. Our group has also found that myocardial revascularization by arterialization of the coronary venous system (eg, grafts connected to the venous system) do not endure [2].
A great variety of angiogenic factors administered in the form of proteins or genes can induce angiogenesis and the growth of collateral arteries leading to an improvement in regional blood flow and the preservation of tissue. However, despite promising laboratory outcomes, the preliminary clinical studies carried out to date have not shown a clear benefit and the real clinical potential of angiogenic factors remains unresolved. More recently the potential of stem cells to differentiate into practically any cell type have been realized and a number of cells have been used in myocardial repair to improve blood flow. There is no doubt that the use of stem cells and genetic modifications have opened up new horizons in angiogenic therapy, but the field is still in its infancy and much more investigation will be required before a wider clinical use is considered.
Lindstedt and co-authors [3] report that the application of negative pressure to the surface of the pig heart increases myocardial blood flow in the normal, ischemic, and reperfused myocardium, and conclude that it may represent a new approach to treat ischemic myocardium. The usefulness of negative pressure for wound healing, including post-sternotomy mediastinitis, is well recognized. A potential mechanism for the beneficial effect of negative pressure may be the stimulation of blood flow that is supported by the findings of Lindstedt and colleagues’ [3] study. However it should be noted that in this study there is a methodological problem that the anterior descending coronary artery was occluded, and the flow changes were assessed in the anterior wall of the right ventricle rather than in the left ventricle. This means that although the reported increase in myocardial blood flow in the normal muscle can be real, the flow changes in the ischemic myocardium need to be confirmed by appropriately designed experiments.
The concept that topical application of negative pressure to the myocardium can be used for increasing the blood flow to ischemic areas of the heart is worth exploring, and if proven to be effective, this may become a valuable therapy to control refractory angina in patients that can not receive conventional revascularization procedures. It can even be argued that the treatment could be useful as an adjuvant to conventional revascularization when complete revascularization can not be achieved. However, before topical negative pressure is considered for clinical use, it would require the demonstration that any increase in blood flow to ischemic myocardium is sufficient to support normal metabolism and function of the affected heart muscle. Furthermore, the application of such a technology would need the design and development of devices that could be selectively applied to the chosen myocardial areas without impairment of the cardiac function.
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