Tachycardia-induced cardiomyopathy: A reversible form of left ventricular dysfunction

Packer, Douglas L.; Bardy, Gust H.; Worley, Seth J.; Smith, Mark S.; Cobb, Frederick R.; Coleman, R. Edward; Gallagher, John J.; German, Lawrence D.

doi:10.1016/0002-9149(86)90836-2

Cited by 482 publications

(197 citation statements)

References 37 publications

Supporting

Mentioning

169

Contrasting

Unclassified

Order By: Relevance

“…We studied a specific animal model of CHF, which has a clinical counterpart in tachycardia-induced ventricular cardiomyopathies 28 but which may be different in specific aspects of pathophysiology from other forms of clinical CHF. Furthermore, such issues as the rate of development of CHF, the neuroendocrine response, and the distribution of hemodynamic load may be important determinants of ionic changes.…”

Section: Potential Limitationsmentioning

confidence: 99%

Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology

et al. 2000

View full text Add to dashboard Cite

Background-Congestive heart failure (CHF) is frequently associated with atrial fibrillation (AF), but little is known about the effects of CHF on atrial cellular electrophysiology. Methods and Results-We studied action potential (AP) properties and ionic currents in atrial myocytes from dogs with CHF induced by ventricular pacing at 220 to 240 bpm for 5 weeks. Atrial myocytes from CHF dogs were hypertrophied (meanϮSEM capacitance, 89Ϯ2 pF versus 71Ϯ2 pF in control, nϭ160 cells per group, PϽ0.001). CHF significantly reduced the density of L-type Ca 2ϩ current (I Ca ) by Ϸ30%, of transient outward K ϩ current (I to ) by Ϸ50%, and of slow delayed rectifier current (I Ks ) by Ϸ30% without altering their voltage dependencies or kinetics. The inward rectifier, ultrarapid and rapid delayed rectifier, and T-type Ca 2ϩ currents were not altered by CHF. CHF increased transient inward Na ϩ /Ca 2ϩ exchanger (NCX) current by Ϸ45%. The AP duration of atrial myocytes was not altered by CHF at slow rates but was increased at faster rates, paralleling in vivo refractory changes. CHF created a substrate for AF, prolonging mean AF duration from 8Ϯ4 to 535Ϯ82 seconds (PϽ0.01). Conclusions-Experimental CHF selectively decreases atrial I to , I Ca , and I Ks , increases NCX current, and leaves other currents unchanged. The cellular electrophysiological remodeling caused by CHF is quite distinct from that caused by atrial tachycardia, highlighting important differences in the cellular milieu characterizing different clinically relevant AF

show abstract

Section: Potential Limitationsmentioning

confidence: 99%

Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology

et al. 2000

View full text Add to dashboard Cite

show abstract

“…Persistent rapid pacing in larger laboratory species can cause cardiomyopathy and heart failure (Packer et al, 1986;Calderone et al, 1991). Although b-blockers yield a number of changes that may ultimately contribute to the overall efficacy in the setting of heart failure, reduction in HR by bblockers can reduce myocardial oxygen consumption and prolong diastolic period with increased coronary blood flow.…”

Section: X-j Du Et Almentioning

confidence: 99%

I_f channel inhibitor ivabradine lowers heart rate in mice with enhanced sympathoadrenergic activities

Gao

et al. 2004

British J Pharmacology

View full text Add to dashboard Cite

1 Ivabradine selectively reduces heart rate (HR) by inhibiting the cardiac pacemaker I f current, thus prolonging the duration of spontaneous depolarization in the sinus node. The activity of ivabradine under conditions of enhanced sympathoadrenergic activity has been addressed by investigating the effects of repeated oral administration in mice with sympathoadrenergic activation due to either stress, cardiac-restricted overexpression of b 2 -adrenergic receptors (b 2 AR), or b-agonist administration. HR and left ventricular fractional shortening (FS) were determined by echocardiography.2 Initial experiments showed that the conscious restrained state was associated with stress-mediated sympathetic activation, while sympathetic withdrawal occurred under anaesthetized conditions. In wild-type mice, ivabradine reduced HR under both conscious and anaesthetized states, with a similar degree in absolute reduction under both states. FS was unchanged by the treatment. 3 Ivabradine was similarly effective in reducing HR in the b 2 AR transgenic mice. Further, ivabradine at 10 mg kg À1 day À1 reduced the maximal HR increase in response to the b-agonist isoproterenol, without modifying the response of contractile parameters. 4 These data indicate that oral administration of ivabradine in mice reduces HR while ventricular performance is maintained. This specific HR-reducing action of ivabradine is well preserved under conditions that are associated with significant activation of the sympathoadrenergic system.

show abstract

“…Left ventricular systolic function, measured by left ventricular ejection fraction (LVEF), improves or normalizes and symptoms resolve if tachycardia is controlled with medication 1,2 or ablation. [3][4][5][6][7][8][9][10][11] TIC has been described in patients of all ages, in heart transplant patients, 12 and even in utero. 13 Rhythms causing TIC include atrial fibrillation, 14 -16 atrial flutter, 17 supraventricular tachycardia, 3,4,8,10,12,18 ventricular tachycardia, [5][6][7]19,20 fascicular tachycardia, 2 ventricular ectopy, 21 and even persistent rapid DDD pacing.…”

mentioning

confidence: 99%

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

et al. 2004

View full text Add to dashboard Cite

Background-Tachycardia-induced cardiomyopathy is a reversible cause of heart failure. We hypothesized that although left ventricular ejection fraction measurements normalize after heart rate or rhythm control in patients with tachycardia-induced cardiomyopathy, recurrent tachycardia may have abrupt and deleterious consequences. Methods and Results-Patients with tachycardia-induced cardiomyopathy that developed over years were evaluated and treated. Tachycardia episodes and outcomes were assessed. Twenty-four patients were identified. All had NYHA functional class III heart failure or greater on presentation. One third were heart transplant candidates. There were 17 men and 7 women with a mean age of 46Ϯ16 years and mean left ventricular ejection fraction of 0.26Ϯ0.09 at the index visit. The cause was atrial fibrillation (nϭ13), atrial flutter (nϭ4), atrial tachycardia (nϭ3), idiopathic ventricular tachycardia (nϭ1), permanent junctional reciprocating tachycardia (nϭ2), and bigeminal ventricular premature contractions (nϭ1). Within 6 months of rate control or correction of the rhythm, left ventricular ejection fraction improved or normalized and symptoms abated in all. Five patients had tachycardia recur. In these patients, left ventricular ejection fraction dropped precipitously and heart failure ensued within 6 months, even though the initial impairment took years. Rate control eliminated heart failure and improved or normalized ejection fraction in 6 months. Three of 24 patients died suddenly and unexpectedly. Conclusions-Tachycardia-induced cardiomyopathy develops slowly and appears reversible by left ventricular ejection fraction improvement, but recurrent tachycardia causes rapid decline in left ventricular function and development of heart failure. Sudden death is possible.

show abstract

Tachycardia-induced cardiomyopathy: A reversible form of left ventricular dysfunction

Cited by 482 publications

References 37 publications

Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology

Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology

I_f channel inhibitor ivabradine lowers heart rate in mice with enhanced sympathoadrenergic activities

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

Contact Info

Product

Resources

About

Tachycardia-induced cardiomyopathy: A reversible form of left ventricular dysfunction

Cited by 482 publications

References 37 publications

Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology

Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology

If channel inhibitor ivabradine lowers heart rate in mice with enhanced sympathoadrenergic activities

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

Contact Info

Product

Resources

About

I_f channel inhibitor ivabradine lowers heart rate in mice with enhanced sympathoadrenergic activities