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THE JOURNAL OF CARDIOVASCULAR SURGERY
Rivista di Chirurgia Cardiaca, Vascolare e Toracica
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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ORIGINAL ARTICLES CARDIAC SECTION
The Journal of Cardiovascular Surgery 2003 December;44(6):681-84
Noninvasive characterization of myocardium after transmyocardial laser revascularization
Jones J. W. 1, Richman B. W. 1, Baldwin J. C. 2, Losanoff J. E. 1
1 Department of Surgery, University of Missouri-Columbia, MO, USA,
2 Dartmouth Medical School, Hanover, NH, USA
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Aim. The therapeutic mechanism of transmyocardial revascularization (TMR) is not yet fully understood, and continues to be a subject of controversy and active research. Immediate direct laser channel flow, gradual angiogenesis, denervation, and perioperative infarction of the ischemic area have been all discussed, without clear evidence indicating superiority of individual factors.
Methods. We utilized a prospective noninvasive physiologic dynamic method to assess laser-related myocardial injury. The study protocol included EKGs and echocardiograms, including intraoperative transesophageal echocardiograms (TEE) on consecutive TMR patients. CPK-MB was measured postoperatively, with 5 samples at 6-hour intervals.
Results. Fifty male patients averaging 62 years old were enrolled in the study. Two patients experienced postoperative myocardial infarctions, from which 1 died. The average CPK-MB values were 12.8±1.28 immediately after surgery, 19.2±2.4 at 6 h, 15.2±2.3 at 12 h, 12.2±6.3 at 18 h, and 11.7±1.3 at 24 h. In only 5 patients were the CPK-MB values over 30 units at their peak. The intraoperative wall motion remained unchanged in the patients studied, both using TEE and transthoracic echography.
Conclusion. Significant myocardial injury after TMR appears unlikely, as indicated by CPK-MB and myocardial wall dynamics. Furthermore, TMR does not seem to aggravate baseline myocardial ischemia. We found no evidence to support a hypothesis that surgical myocardial injury constitutes the mechanism of therapeutic action in TMR.