Electroanatomic mapping during sinus rhythm allows accurate 3D characterization of infarct architecture and defines the relationship of electrophysiological and anatomic abnormalities. This technique may prove useful in devising anatomically based strategies for ablation of ventricular tachycardia.
The somatosensory evoked potential (SEP) measured in response to median nerve stimulation was correlated with cortical and white matter cerebral blood flow (CBF), adenosine triphosphate (ATP), and lactate levels in 14 cats subjected to graded hemorrhagic hypotension following bilateral carotid artery ligation. Three additional cats served as controls. Regional CBF was determined by the hydrogen clearance method, and the time for conduction of the sensory stimulus from the thalamus to the cortex (the thalamocortical conduction time), was used to assess SEP latency changes. A reproducible sequence of changes occurred in the SEP as ischemia developed. There was an early conduction delay that correlated well with mild white matter ischemia. Amplitude reductions in the SEP began as significant cortical ischemia occurred. The cortical SEP was abolished when white matter CBF and ATP fell to critical levels.
The electrical impedance properties of healthy and infarcted left ventricular myocardium differ markedly. The properties of the infarction border zone are intermediate between healthy and infarcted myocardium. Impedance may be a useful assay of cardiac tissue content and adaptable for cardiac mapping in vivo. Condensed Abstract. To delineate the electrical impedance properties of healthy and chronically infarcted left ventricular myocardium emphasizing the infarction border zone, impedance was measured in chronically infarcted ovine hearts. Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the infarction border zone in transition between healthy myocardium and dense infarction. This correlated with a decreasing myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as measurement frequency decreased. There was a direct association between impedance and electrogram characteristics. Endocardial impedance, measured in vivo using an electrode catheter inserted percutaneously, distinguished between healthy and infarcted myocardium
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