Key result
In a pig model of chronic myocardial ischemia, endocardial unipolar voltage was significantly reduced in ischemic compared to non-ischemic zones (9.9±3.3 vs 13.3±3.3 mV, P=0.03).
Why the study?
Does endocardial unipolar voltage mapping correlate with myocardial perfusion in a pig model of chronic myocardial ischemia?
Does endocardial unipolar voltage mapping correlate with myocardial perfusion in a pig model of chronic myocardial ischemia?
Endocardial unipolar voltage mapping correlates with endomyocardial blood flow, suggesting its potential utility in assessing chronic myocardial ischemia.
Supports voltage mapping for ischemia assessment in animal models; leaves open human validation before clinical use.
In Brief Background Recent clinical studies using a non-fluoroscopic three-dimensional (3D) left ventricular (LV) mapping system suggested reduced endocardial voltage amplitudes measured in zones sustaining myocardial ischemia or infarction. However, the direct relationship between myocardial perfusion and endomyocardial voltage amplitudes has not been fully elucidated. Methods In a pig model of chronic myocardial ischemia (n=20), LV endocardial unipolar voltage (UpV) mapping was performed using the Biosense 3D navigation system (Johnson and Johnson, Warren, New Jersey, USA) 4 weeks after ameroid constrictor placement around the left circumflex coronary artery. Echocardiography was used to assess regional changes in myocardial wall thickening (MT) and fluorescent microspheres (4×106/injection) were used to quantify rest regional myocardial blood flow (MBF) in ischemic (left circumflex) and remote non-ischemic (left anterior descending) regions. Results UpV measurements were reduced in ischemic compared to non-ischemic zones (9.9±3.3 compared with 13.3±3.3 mV, P=0.03). This corresponded to changes in endocardial MBF and MT, which were both noted to be significantly reduced in the ischemic compared to the non-ischemic area (MBF, 0.50±0.16 compared with 0.74±0.15 ml/g per min, P=0.001; MT, 26.1±12.0 compared with 37.4±10.1%, P=0.003). A positive linear correlation was found between UpV at rest and endomyocardial (but not epicardial) perfusion: UpV (mV)=7.8+5.9×MBFendocardial (r=0.32, P=0.05). Conclusions Chronic myocardial ischemia, resulting in reduced perfusion and function at rest (that is, hibernating myocardium), is characterized by a significant reduction (≈25%) in endocardial UpV potentials, which correlates with reduced endomyocardial blood flow and tissue perfusion at rest. In the current study, we assessed the direct relationship between myocardial tissue perfusion and endomyocardial voltage amplitude using a chronic ischemia pig ameroid model. Unipolar voltage (UpV) was measured using a left ventricular electromechanical mapping system. Ischemic zones, characterized by reduced myocardial perfusion and wall thickening had significantly reduced UpV values compared to non-ischemic zones (9.9±3.3 vs.13.3±3.3 mV p=0.03). A positive linear correlation was found between UpV at rest and endomyocardial (but not epicardial) perfusion: UpV (mV)=7.8+5.9 x MBFendocardial (r=0.32, p=0.048) suggesting an association between reduced endocardial UpV potentials and chronic endomyocardial ischemia.
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Fuchs et al. (2005) studied Chronic myocardial ischemia (n=20). Left ventricular endocardial unipolar voltage (UpV) mapping vs. Non-ischemic zones was evaluated on Endocardial unipolar voltage (UpV) (p=0.03). In a pig model of chronic myocardial ischemia, endocardial unipolar voltage was significantly reduced in ischemic compared to non-ischemic zones (9.9±3.3 vs 13.3±3.3 mV, P=0.03).
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