The Influence of Myocardial Systolic Shortening on Action Potential Duration Following Changes in Left Ventricular End‐Diastolic Pressure

APD and Systolic Shortening. Introduction: Contraction‐excitation feedback may he an important factor in arrhythmogenesis in patients with heart failure. We have previously demonstrated the contrasting effects of raising left ventricular end‐diastolic pressure on action potential duration in dog and guinea pig hearts. The current study was undertaken to assess whether these differing effects might reflect differences in the effect of varying left ventricular end‐diastolic pressure on systolic shortening in the two models.

[1]  R. Hainsworth,et al.  The use of a microcomputer to automate measurement of action potential duration for both transmembrane and monophasic action potentials , 1993, Physiological measurement.

[2]  D E Hansen,et al.  Mechanoelectrical feedback effects of altering preload, afterload, and ventricular shortening. , 1993, The American journal of physiology.

[3]  R. Hainsworth,et al.  The effects of ventricular end‐diastolic and systolic pressures on action potential and duration in anaesthetized dogs. , 1992, Journal of Physiology.

[4]  J. Cowan,et al.  Contraction-excitation feedback in an ejecting whole heart model--dependence of action potential duration on left ventricular diastolic and systolic pressures. , 1991, Cardiovascular research.

[5]  L. Hondeghem,et al.  Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. , 1990, Circulation.

[6]  D. Hansen,et al.  Stretch-induced arrhythmias in isolated, canine ventricle , 1990 .

[7]  A. Weyman,et al.  Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside. , 1989, Journal of the American College of Cardiology.

[8]  C. Gornick,et al.  Electrophysiological effects of left ventricular free wall traction in intact hearts. , 1989, The American journal of physiology.

[9]  M. Lab,et al.  Effect of changes in load on monophasic action potential and segment length of pig heart in situ. , 1989, Cardiovascular research.

[10]  M. Lab,et al.  ARRHYTHMIA IN HEART FAILURE: ROLE OF MECHANICALLY INDUCED CHANGES IN ELECTROPHYSIOLOGY , 1989, The Lancet.

[11]  D. Kass,et al.  Electrophysiological effect of volume load in isolated canine hearts. , 1989, The American journal of physiology.

[12]  M R Franz,et al.  Mechanically induced action potential changes and arrhythmia in isolated and in situ canine hearts. , 1989, Cardiovascular research.

[13]  H. Calkins,et al.  Effect of acute volume load on refractoriness and arrhythmia development in isolated, chronically infarcted canine hearts. , 1989, Circulation.

[14]  J A Vassallo,et al.  Nonuniform recovery of excitability in the left ventricle. , 1988, Circulation.

[15]  M. Reiter,et al.  Electrophysiological Effects of Acute Ventricular Dilatation in the Isolated Rabbit Heart , 1988, Circulation research.

[16]  S. Gottlieb,et al.  Immediate and long-term pathophysiologic mechanisms underlying the genesis of sudden cardiac death in patients with congestive heart failure. , 1987, The American journal of medicine.

[17]  J. Spear,et al.  The monophasic action potential upstroke: a means of characterizing local conduction. , 1986, Circulation.

[18]  F. Tristani,et al.  Effect of Vasodilator Therapy on Mortality in Chronic Congestive Heart Failure , 1986 .

[19]  C. Gornick,et al.  Electrophysiologic effects of papillary muscle traction in the intact heart. , 1986, Circulation.

[20]  D. Burkhoff,et al.  Mechanoelectrical feedback: independent role of preload and contractility in modulation of canine ventricular excitability. , 1985, The Journal of clinical investigation.

[21]  R. Anderson,et al.  Electrophysiological effects of transient aortic occlusion in intact canine heart. , 1985, The American journal of physiology.

[22]  M. Packer,et al.  Sudden unexpected death in patients with congestive heart failure: a second frontier. , 1985, Circulation.

[23]  J. Cohn,et al.  Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. , 1984, The New England journal of medicine.

[24]  J. Cohn,et al.  Survival in men with severe chronic left ventricular failure due to either coronary heart disease or idiopathic dilated cardiomyopathy. , 1983, The American journal of cardiology.

[25]  M J Lab,et al.  Contraction-excitation feedback in myocardium. Physiological basis and clinical relevance. , 1982, Circulation research.

[26]  J. Covell,et al.  Mechanical induction of paired action potentials in intact heart in situ , 1981 .

[27]  M. Lab.  Mechanically Dependent Changes in Action Potentials Recorded from the Intact Frog Ventricle , 1978, Circulation research.

[28]  F. Kiil,et al.  Preload, contractility, and afterload as determinants of stroke volume during elevation of aortic blood pressure in dogs. , 1973, Cardiovascular research.

[29]  A. J. Brady,et al.  Intracellular recording from moving tissues with a flexibly mounted ultramicroelectrode. , 1956, Science.

[30]  K. Swedberg,et al.  Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). , 1988, The American journal of cardiology.

[31]  J. Cohn.  Effect of vasodilator therapy on mortality in chronic congestive heart failure. , 1988, European heart journal.

[32]  K. Peterson,et al.  Densitometric regional ejection fraction: a new three-dimensional index of regional left ventricular function--comparison with geometric methods. , 1988, Journal of the American College of Cardiology.

[33]  R. Anderson,et al.  Electrophysiologic properties of the myocardial infarction border zone: effects of transient aortic occlusion. , 1986, Surgery.