Posterior fascicular block versus posteroinferior myocardial infarction in left posterior excitation disturbances.

To delineate electrocardiographic similarities and differences in ventricular depolarization between left posterior fascicular block and posteroinferior myocardial infarction, these lesions were produced in two and three stage experiments in dogs and baboons. The observed QRS changes of left posterior fascicular block were found to be immediate, little influenced by healing of the acute lesion, and partially correctable by pacing viable myocardium distal to the block. In contrast, the QRS changes of posteroinferior myocardial infarction occurred later with cicatrization and were essentially unaffected by pacing. The intrinsic deflection in direct posterior epicardial leads was more delayed by left posterior fascicular block than by posteroinferior myocardial infarction. Both lesions accounted for Q waves in leads II, III and aVF. However, R amplitude in these same leads was increased after left posterior fascicular block but decreased after posteroinferior myocardial infarction. The mean QRS axis in the frontal plane was shifted toward the vertical in left posterior fascicular block but little changed or shifted slightly away from the vertical in posteroinferior myocardial infarction. When left posterior fascicular block and posteroinferior myocardial infarction coexist, there may be masking, imitation or enhancement of the effects of one lesion by the presence of the other. To assist in recognition, distinguishing features are described.

Arterial pressure contour analysis for estimating human vascular properties.

The form of an arterial blood pressure curve during the diastolic portion of the cardiac cycle was here employed to identify parameters in a third-order model of the vascular system. Calculated elastic and intertial characteristics of this fitted model then became clinically accessible indices of corresponding real vascular properties. This technique incurred no risk and little discomfort for the patient. Tested in theory, in animal experimentation, and in human observations, our procedure utilized a Gauss-Newton algorithm via digital computer to provide rapid model solutions from different starting values, from multiple measurements sites, and from normal or diseased patients. Model parameters thus determined defined ranges of normal variation and suggested a less compliant arterial bed in hypertensive than in normotensive patients.