TY - JOUR
T1 - Transmyocardial laser revascularization preserves regional myocardial perfusion
T2 - An MRI first pass perfusion study
AU - Mühling, Olaf M.
AU - Wang, Ying
AU - Panse, Prasad
AU - Jerosch-Herold, Michael
AU - Cayton, Mary M.
AU - Wann, L. Samuel
AU - Mirhoseini, Mahmood M.
AU - Wilke, Norbert M.
PY - 2003/1/1
Y1 - 2003/1/1
N2 - Objective: It is controversial whether transmyocardial laser revascularization (TMLR) improves myocardial perfusion. Therefore, we assessed myocardial perfusion before and after TMLR with quantitative magnetic resonance perfusion imaging (MRPI) in an animal study. Methods: One week after partial occlusion of the left circumflex artery (LCx) in 12 pigs, resting perfusion (ml/g/min), perfusion reserve (PR) with adenosine, regional wall thickening (RWT), cardiac output (CO) were quantified with MRI in the LCx (lateral) and LAD (septal) dependent myocardium. Subsequently, six animals were treated with TMLR of the lateral left ventricle (LV). Six animals were left untreated. A final MR was performed 8 weeks later. MRPI data were compared to microsphere-derived blood flow and % LV necrosis (TTC). 'Normal' myocardial perfusion was assessed with MRPI in 12 non-instrumented animals. Results: Resting perfusion prior to TMLR (0.7-0.9±0.3) in the LV-lateral myocardium was preserved after TMLR (1.0±0.3) and decreased without TMLR (0.3±0.1, P<0.05). There was a significant difference (P<0.01) between the TMLR treated and untreated group. Compared to 'normals' (1.2±0.2) perfusion of the LV-lateral wall was not different after TMLR but reduced (P<0.02) without TMLR. PR was not different between TMLR-treated (1.4±0.9) and untreated (1.9±0.6) group but was reduced (P<0.04) compared to PR of 'normals' (2.7±0.8). MRPI data and microsphere-derived perfusion were significantly correlated (P<0.01). RWT in the LCx-dependent myocardium improved (P<0.02) after TMLR. CO decreased (P<0.02) and TTC-staining indicated more LV-necrosis without TMLR (6.6±1.6 vs. 3.7±1.5, P<0.01). Conclusion: TMLR preserves regional myocardial perfusion and improves function as shown with MRPI.
AB - Objective: It is controversial whether transmyocardial laser revascularization (TMLR) improves myocardial perfusion. Therefore, we assessed myocardial perfusion before and after TMLR with quantitative magnetic resonance perfusion imaging (MRPI) in an animal study. Methods: One week after partial occlusion of the left circumflex artery (LCx) in 12 pigs, resting perfusion (ml/g/min), perfusion reserve (PR) with adenosine, regional wall thickening (RWT), cardiac output (CO) were quantified with MRI in the LCx (lateral) and LAD (septal) dependent myocardium. Subsequently, six animals were treated with TMLR of the lateral left ventricle (LV). Six animals were left untreated. A final MR was performed 8 weeks later. MRPI data were compared to microsphere-derived blood flow and % LV necrosis (TTC). 'Normal' myocardial perfusion was assessed with MRPI in 12 non-instrumented animals. Results: Resting perfusion prior to TMLR (0.7-0.9±0.3) in the LV-lateral myocardium was preserved after TMLR (1.0±0.3) and decreased without TMLR (0.3±0.1, P<0.05). There was a significant difference (P<0.01) between the TMLR treated and untreated group. Compared to 'normals' (1.2±0.2) perfusion of the LV-lateral wall was not different after TMLR but reduced (P<0.02) without TMLR. PR was not different between TMLR-treated (1.4±0.9) and untreated (1.9±0.6) group but was reduced (P<0.04) compared to PR of 'normals' (2.7±0.8). MRPI data and microsphere-derived perfusion were significantly correlated (P<0.01). RWT in the LCx-dependent myocardium improved (P<0.02) after TMLR. CO decreased (P<0.02) and TTC-staining indicated more LV-necrosis without TMLR (6.6±1.6 vs. 3.7±1.5, P<0.01). Conclusion: TMLR preserves regional myocardial perfusion and improves function as shown with MRPI.
KW - Cardiovascular surgery
KW - Coronary circulation
KW - Infarction
KW - Microcirculation
KW - NMR
KW - Regional blood flow
KW - Stunning
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UR - http://www.scopus.com/inward/citedby.url?scp=0037214496&partnerID=8YFLogxK
U2 - 10.1016/S0008-6363(02)00647-8
DO - 10.1016/S0008-6363(02)00647-8
M3 - Article
C2 - 12504815
AN - SCOPUS:0037214496
SN - 0008-6363
VL - 57
SP - 63
EP - 70
JO - Cardiovascular research
JF - Cardiovascular research
IS - 1
ER -