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Results for “Body Surface Potential Mapping”

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PubMed1979

Body surface potential maps in patients with pulmonic valvular and aortic valvular stenosis of mild to moderate severity.

Multiple-lead surface potential maps were compared throughout ventricular activation in nine patients with mild-to-moderate pulmonic stenosis and in 12 patients with mild-to-moderate aortic stenosis. Abnormal patterns of potential distribution were found in aortic stenosis, including three patients without electrocardiographic evidence of left ventricular enlargement. When related to the onset of depolarization, abnormal departures started later, peaked later, lasted longer, and were more intense, more uniform and discrete in aortic stenosis. In pulmonic stenosis, abnormal departures started earlier, but were more dispersed in timing and location than in aortic stenosis. The left ventricle appears to be the more remote, though more powerful and compact, generator. The right ventricular shell, however, is nearer to the surface, and is more anatomically extended in surface area, permitting much wider shifts in wavefront location and orientation as a result of small differences in pressure, or volume, or location of the heart in the thorax.

Aortic Valve Stenosis↗
PubMed1988

P wave changes in body surface potential maps due to increasing heart rate during exercise in normals.

Exercise-induced changes in P maps were investigated in normal subjects (n = 20) in order to clarify the basic changes in P maps caused by exercise in patients with ischemic heart disease or by exercise-induced dysfunction of the left ventricle in patients with various heart diseases. Maps were obtained using an 87 lead-point system (HPM-6500, Chunichi-Denshi Corporation) and were recorded at rest and at heart rates up to 140/min in 20/min steps under graded bicycle ergometric exercise. P waves were divided into 3 phases (initial, middle and terminal) by locating the maximum. Maps were characterized by the distribution pattern of the positive and negative potentials in each frame. Peak voltages increased proportionally to the increase in heart rate. We observed a decrease in P wave duration concomitant with the increase in heart rate. Time from P onset to peak voltage increased slightly. We believe these findings to be due to the acceleration of sympathetic nerve tone accompanying exercise. We observed 2 patterns: type A showed the relatively short middle and terminal phases, and type B a prolongation of the middle phase and a shortening of the terminal phase. We consider the differences between types A and B to be partly due to individual differences in the degree of increase in pulmonary air volume and sympathetic nerve tone influence on the atria. In evaluating the exercise-induced P map changes, special consideration should be paid to the changes due to increase in heart rate.

Adult↗