Left ventricular electromechanical mapping to assess efficacy of phVEGP(165) gene transfer for therapeutic angiogenesis in chronic myocardial ischemia

Citation
Pr. Vale et al., Left ventricular electromechanical mapping to assess efficacy of phVEGP(165) gene transfer for therapeutic angiogenesis in chronic myocardial ischemia, CIRCULATION, 102(9), 2000, pp. 965-974
Citations number
27
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
0009-7322 → ACNP
Volume
102
Issue
9
Year of publication
2000
Pages
965 - 974
Database
ISI
SICI code
0009-7322(20000829)102:9<965:LVEMTA>2.0.ZU;2-4
Abstract
Background-NOGA left ventricular (LV) electromechanical mapping (EMM) can b e used to distinguish among infarcted, ischemic, and normal myocardium. We investigated the use of percutaneous LV EMM to assess the efficacy of myoca rdial gene transfer (GTx) of naked plasmid DNA encoding for vascular endoth elial growth factor (phVEGF(165)), administered during surgery by direct my ocardial injection in patients with chronic myocardial ischemia. Methods and Results-A total of 13 consecutive patients (8 men, mean age 60. 1+/-2.3 years) with chronic stable angina due to angiographically documente d coronary artery disease, all of whom had failed conventional therapy (dru gs, PTCA, and/or CABG), were treated with direct myocardial injection of ph VEGF(165) via a minithoracotomy. Foci of ischemic myocardium were identifie d on LV EMM by preserved viability associated with an impairment in linear local shortening, Myocardial viability, defined by mean unipolar and bipola r voltage recordings greater than or equal to 5 and greater than or equal t o 2 mV, respectively, did not change significantly after GTx. Analysis of l inear local shortening in areas of myocardial ischemia, however, disclosed significant improvement after (15.26+/-0.98%) versus before (9.94+/-1.53%, P = 0.004) phVEGF(165) GTx. The area of ischemic myocardium was consequentl y reduced from 6.45+/-1.37 cm(2) before GTx to 0.95+/-0.41 cm(2) after GTx (P = 0.001). These findings corresponded to improved perfusion scores calcu lated from single-photon emission CT-sestamibi myocardial perfusion scans r ecorded at rest (7.4+/-2.1 before GTx versus 4.5+/-1.4 after GTx, P = 0.009 ) and after pharmacological stress (12.8+/-2.7 before GTx versus 8.5+/-1.7 after GTx, P = 0.047). Conclusions-The results of EMM constitute objective evidence that phVEGF(16 5) GTx augments perfusion of ischemic myocardium. These findings, together with reduction in the size of the defects documented at rest by serial sing le-photon emission CT-sestamibi imaging, suggest that phVEGF(165) GTx may s uccessfully rescue foci of hibernating myocardium.