Initiation of ventricular extrasystoles by myocardial stretch in chronically dilated and failing canine left ventricle.

Wang, Z; Taylor, Luke; Denney, W D; Hansen, David E.

doi:10.1161/01.cir.90.4.2022

Cited by 60 publications

(27 citation statements)

References 47 publications

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“…A failing, chronically dilated left ventricle might be more susceptible to initiation of ventricular beats 7,8) triggered by stretch-induced depolarization. 9) Relatively high plasma BNP concentrations have been reported in patients with echocardiographic abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Brain Natriuretic Peptide, Myocardial Wall Stress, and Ventricular Arrhythmia Severity

et al. 2004

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SUMMARYWe previously demonstrated that the severity of arrhythmias is reflected by circulating brain natriuretic peptide (BNP) concentrations in patients without signs of congestive heart failure. In the present study, we evaluated the relationships between the severity of the arrhythmia, BNP concentration, and echocardiographic findings.The subjects consisted of 52 patients with ventricular premature contractions (VPC) but no manifestations of heart failure and no digoxin or beta-blocker therapy. Patients underwent Holter monitoring, plasma sampling for BNP measurement, and transthoracic echocardiography (TTE). We scored the motion of 16 left ventricular segments, deriving a wall-motion score index (WMSI) by totaling the scores and dividing by the number of segments scored.Twenty-three patients with Lown grade I to II arrhythmias constituted group A while group B consisted of 29 Lown III to IV patients. Group B had BNP concentrations triple those in group A (57.2 versus 18.1 pg/mL, P < 0.01). Left ventricular ejection fraction (LVEF) was similar in groups A and B (65.2% versus 62.1%, NS). Although left ventricular end-diastolic dimension (LVEDD) was normal in both groups, group B exhibited a larger LVEDD than group A (50 versus 46 mm, P < 0.005). The correlation (r) between BNP and interventricular septum thickness (IVST) was 0.27 (P = 0.013) in group A and 0.37 (P < 0.0001) in group B. Between BNP and posterior wall thickness (PWT), the correlation was 0.23 (P = 0.014) in group A versus 0.33 (P < 0.0001) in group B. The WMSI in group B was higher than in group A (1.34 versus 1.11, P < 0.05).We believe that besides the changes in echocardiographic parameters, the BNP elevation in group B could be a response to abnormal wall stress from the severe ventricular arrhythmias. (Jpn Heart J 2004; 45: 771-777)

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Section: Discussionmentioning

confidence: 99%

Relationship Between Brain Natriuretic Peptide, Myocardial Wall Stress, and Ventricular Arrhythmia Severity

et al. 2004

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“…Intrinsic mechanical pulses and perturbations can trigger arrhythmias or extrasystoles, and may be especially important in diseases where wall mechanics become altered such as ischemia and heart failure. Transiently increased hemodynamic loading of failing ventricles has been observed to give rise to extrasystolic beats and ventricular tachycardia [33,34]. In a positive counterexample, precordial thump or precordial percussion offers a rapid though low efficiency method for resuscitation of a victim of witnessed cardiac arrest, though the window for benefit versus harm is small [35][36][37][38].…”

Section: Organ Scale: Cardiac Electromechanical Interactionsmentioning

confidence: 99%

Biomechanics of Cardiac Electromechanical Coupling and Mechanoelectric Feedback

Pfeiffer

Tangney

Omens

et al. 2014

Journal of Biomechanical Engineering

103

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Cardiac mechanical contraction is triggered by electrical activation via an intracellular calcium-dependent process known as excitation-contraction coupling. Dysregulation of cardiac myocyte intracellular calcium handling is a common feature of heart failure. At the organ scale, electrical dyssynchrony leads to mechanical alterations and exacerbates pump dysfunction in heart failure. A reverse coupling between cardiac mechanics and electrophysiology is also well established. It is commonly referred as cardiac mechanoelectric feedback and thought to be an important contributor to the increased risk of arrhythmia during pathological conditions that alter regional cardiac wall mechanics, including heart failure. At the cellular scale, most investigations of myocyte mechanoelectric feedback have focused on the roles of stretch-activated ion channels, though mechanisms that are independent of ionic currents have also been described. Here we review excitation-contraction coupling and mechanoelectric feedback at the cellular and organ scales, and we identify the need for new multicellular tissue-scale model systems and experiments that can help us to obtain a better understanding of how interactions between electrophysiological and mechanical processes at the cell scale affect ventricular electromechanical interactions at the organ scale in the normal and diseased heart.

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“…10,11 Volume overload of the ventricles and increased pressure within them are both stimuli for enhanced BNP production 12 and are reported to cause electrophysiological abnormalities. [13][14][15][16][17][18][19] Thus, a relationship between BNP levels and arrhythmic activity is suggested. This study tests the value of BNP levels for prediction of sudden death in a large ambulant patient population with a LVEF Ͻ35%.…”

Section: See P 2328mentioning

confidence: 99%

B-Type Natriuretic Peptide Predicts Sudden Death in Patients With Chronic Heart Failure

et al. 2002

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Background-Given the high incidence of sudden death in patients with chronic heart failure (CHF) and the efficacy of implantable cardioverter-defibrillators, an appropriate tool for the prediction of sudden death is desirable. B-type natriuretic peptide (BNP) has prognostic significance in CHF, and the stimuli for its production cause electrophysiological abnormalities. This study tests BNP levels as a predictor of sudden death. Methods and Results-BNP levels, in addition to other neurohormonal, clinical, and hemodynamic variables, were obtained from 452 patients with a left ventricular ejection fraction (LVEF) Յ35%. For prediction of sudden death, only survivors without heart transplantation (HTx) or a mechanical assist device and patients who died suddenly were analyzed. Up to 3 years, 293 patients survived without HTx or a mechanical assist device, 89 patients died, and 65 patients underwent HTx. Mode of death was sudden in 44 patients (49%), whereas 31 patients (35%) had pump failure and 14 patients (16%) died from other causes. Univariate risk factors of sudden death were log BNP (Pϭ0.0006), log N-terminal atrial natriuretic peptide (Pϭ0.003), LVEF (Pϭ0.005), log N-terminal BNP (Pϭ0.006), systolic blood pressure (Pϭ0.01), big endothelin (Pϭ0.03), and NYHA class (Pϭ0.04). In the multivariate model, log BNP level was the only independent predictor of sudden death (Pϭ0.0006). Using a cutoff point of log BNP Ͻ2.11 (130 pg/mL), Kaplan-Meier sudden death-free survival rates were significantly higher in patients below (99%) compared with patients above (81%) this cutoff point (Pϭ0.0001). Conclusion-BNP levels are a strong, independent predictor of sudden death in patients with CHF.

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Initiation of ventricular extrasystoles by myocardial stretch in chronically dilated and failing canine left ventricle.

Abstract: Altered mechanical properties and/or neurohumoral adaptations associated with chronic dilation and failure predispose the ventricle to induction of ventricular extrasystoles by transient LV diastolic stretch.

Cited by 60 publications

References 47 publications

Relationship Between Brain Natriuretic Peptide, Myocardial Wall Stress, and Ventricular Arrhythmia Severity

Relationship Between Brain Natriuretic Peptide, Myocardial Wall Stress, and Ventricular Arrhythmia Severity

Biomechanics of Cardiac Electromechanical Coupling and Mechanoelectric Feedback

B-Type Natriuretic Peptide Predicts Sudden Death in Patients With Chronic Heart Failure

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