Evolution and resolution of long-term cardiac memory

Cardiac memory (CM) refers to T-wave changes induced by ventricular pacing or arrhythmia that accumulate in magnitude and duration with repeated episodes of abnormal activation. We report herein the kinetics of long-term CM and its association with the ventricular action potential. Dogs were paced f...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1998-05, Vol.97 (18), p.1810-1817
Main Authors: SHVILKIN, A, DANILO, P. JR, JIE WANG, BURKHOFF, D, ANYUKHOVSKY, E. P, SOSUNOV, E. A, HARA, M, ROSEN, M. R
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Biological and medical sciences
Cardiac Pacing, Artificial
Cycloheximide - pharmacology
Dogs
Electrocardiography
Endocardium - physiology
Female
Fundamental and applied biological sciences. Psychology
Heart
Heart - physiology
Long-Term Potentiation
Male
Muscle Proteins - biosynthesis
Protein Synthesis Inhibitors - pharmacology
Time Factors
Ventricular Function
Vertebrates: cardiovascular system
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Summary:Cardiac memory (CM) refers to T-wave changes induced by ventricular pacing or arrhythmia that accumulate in magnitude and duration with repeated episodes of abnormal activation. We report herein the kinetics of long-term CM and its association with the ventricular action potential. Dogs were paced from the ventricles at rates of 110 to 120 bpm for approximately 3 weeks. CM characterized by gradual sinus rhythm T vector rotation toward the paced QRS vector evolved in all dogs regardless of pacing site (left ventricular [LV] anterior apex or base, posterior LV, or right ventricular free wall). Cardiac hemodynamics and myocardial flow (microsphere studies) were unaltered by the pacing. Recovery time for the memory T wave to return to control increased with duration of the previous pacing. The protein synthesis inhibitor cycloheximide markedly (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.97.18.1810