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Ann Thorac Surg 2000;70:1134-1138
© 2000 The Society of Thoracic Surgeons
a Division of Cardiac Surgery, Department of Emergency and Transplantation, University of Bari School of Medicine, Bari, Italy
b Institute of Nuclear Medicine, University of Bari School of Medicine, Bari, Italy
Address reprint requests to Dr Bortone, Haemodynamic Laboratory, Division of Cardiac Surgery, University of Bari, Ospedale Consorziale - Policlinico P.zza G. Cesare, 11, 70124 Bari, Italy
e-mail: emobort{at}libero.it
Presented at the Sixth Annual Meeting of Cardiothoracic Techniques and Technologies 2000, Fort Lauderdale, FL, Jan 27–29, 2000.
Background. The aim of our study was to investigate the inflammatory response immediately after percutaneous transmyocardial laser revascularization (PTMR) along with the underlying mechanism of angiogenesis.
Methods. Patients with angina pectoris underwent coronary angiography and were divided into two groups. Group A (n = 10) included patients with obstructed vessels who received PTMR, whereas group B (n = 5) comprised patients who had normal coronary arteries. Blood levels of neutrophils, procalcitonin, troponin-I, myoglobin, and creatine kinase (CK) mass were evaluated in each patient before angiography and monitored up to 48 hours after the procedure. Six patients were injected with 99mTc-leukoscan approximately 60 to 90 minutes after PTMR. During the 240 to 300 minutes after the radionuclide administration, single photon emission tomography (SPET) was performed and compared with conventional 99mTc-sestamibi-SPET.
Results. A significant increase in blood levels of neutrophils and procalcitonin was observed in group A only (p < 0.005). A slight but significant increase of troponin-I was evident in the same group (p < 0.05), and a distinct myocardial uptake of 99mTc-Leukoscan-SPET was observed in each patient along homologous regions treated by PTMR.
Conclusions. The increased amount of neutrophils (both circulating and inside the treated myocardial areas) along with the raised levels of procalcitonin were the immediate reactions to PTMR. This systemic and intramyocardial inflammatory response is the underlying mechanism that gives rise to angiogenesis.
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