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A comparison of mechanical and laser transmyocardial revascularization for induction of angiogenesis and arteriogenesis in chronically ischemic myocardium

G. Chad Hughes, MD^*,*, Shankha S. Biswas, MD^*, Bangliang Yin, MD^*, Dmitri V. Baklanov, MD^*, Brian H. Annex, MD, R. Edward Coleman, MD, Timothy R. DeGrado, PhD, Carolyn K. Landolfo, MD, FACC, Kevin P. Landolfo, MD^* and James E. Lowe, MD, FACC^*

^* Departments of Surgery and Medicine, Division of Cardiovascular and Thoracic Surgery, Duke University Medical Center, Durham, North Carolina, USA
Division of Cardiology, Duke University Medical Center, Durham, North Carolina, USA
Department of Radiology, Duke University Medical Center, Durham, North Carolina, USA

View larger version (141K): [in a new window]   Figure 1 Coronary angiogram performed immediately prior to euthanasia (six months post-transmyocardial implant) in a representative animal demonstrating experimental model with location of hydraulic occluder (radiolucent and not seen) and ultrasonic flow probe around proximal left circumflex (LCx) coronary artery indicated. Note normal left anterior descending (LAD) coronary artery, high-grade stenosis of proximal LCx, and multiple transmyocardial implants in lateral and posteroinferior walls of the left ventricle.

View larger version (111K): [in a new window]   Figure 2 Transmyocardial implant (TMI) device. The helical TMI is constructed of stainless steel and has a large anchor coil (on right in figure) on one end to prevent migration once the device has been implanted in the myocardium. For implantation, the TMI is mounted on a stainless steel delivery device (not shown), which has a sharp needle-like tip allowing it to pierce the epicardium. This places the distal end of the TMI into the epicardium; the TMI coil is then twisted through the myocardium using the delivery device such that the TMI spans the entire wall of the heart. An indicator on the delivery device confirms transmural penetration, after which the delivery device is removed, leaving the TMI intact.

View larger version (128K): [in a new window]   Figure 3 Transthoracic echocardiogram in a representative animal after transmyocardial implant (TMI) placement. Note the multiple TMI devices in the chronically ischemic left circumflex (LCx) distribution (lateral and posteroinferior walls of the left ventricle). Arrows in the upper right indicate the location of the papillary muscles. The LCx distribution lies between the papillary muscles and has been entirely treated with TMI devices.

View larger version (124K): [in a new window]   Figure 4 Representative postmortem radiograph of an explanted heart demonstrating all 16 transmyocardial implants to be intact and in good position.

View larger version (74K): [in a new window]   Figure 5 Masson trichrome staining (x100) showing (A) hypocellular transmyocardial implant channel remnant filled with blue-staining connective tissue. Large region devoid of connective tissue within channel remnant is prior location of coil of implant device, which has been removed post mortem. Similar-appearing region six months post-transmyocardial laser revascularization is shown in (B).

View larger version (46K): [in a new window]   Figure 6 Endogenous endothelial alkaline phosphatase staining (original magnification x100) of representative sections from hibernating myocardium treated with sham redo-thoracotomy (A), transmyocardial implant (TMI) (B), and holmium yttrium:aluminum:garnet transmyocardial laser revascularization (TMR) (C). Note the significantly greater blue-staining intensity, characteristic of endothelial cells, in (C) compared with (B) and (A). The number of blue-staining blood vessels is greater both within and adjacent to the TMR channel remnant (C) compared with that seen with TMI (B).

View larger version (14K): [in a new window]   Figure 7 Quantitative (A) vascular and (B) arteriolar density analysis. See text for details. TMI = transmyocardial implant; TMR = transmyocardial laser revascularization.

View larger version (44K): [in a new window]   Figure 8 Anti-smooth muscle actin (HHF-35) staining (original magnification x40) of representative sections from hibernating myocardium treated with sham redo-thoracotomy (A), transmyocardial implant (B), and holmium:yttrium-aluminum-garnet transmyocardial laser revascularization (C). Note numerous red-staining arterioles in (C) compared with (B) and (A).