Effect of preload and afterload on ventricular arrhythmogenesis

Sideris, Dimitris A.; Pappas, S.; Siongas, Kostas; Grekas, Georgios; Argyri-Greka, Ourania; Koundouris, Evangelos; Foussas, Stefanos

doi:10.1016/s0022-0736(05)80285-7

Cited by 11 publications

(5 citation statements)

References 18 publications

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“…Metaraminol infusion without pressure elevation is not arrhythmogenic, however. Reducing aortic pressure by arterial bleeding22 or by sucking the ventricles into a cup27 in experiments where the animal was on a continuous metaraminol drip was associated with disappearance of ventricular arrhythmias that had appeared during the metaraminol induced blood pressure elevation. Given that no patient developed ECG disturbances suggesting myocardial ischaemia during metaraminol infusion, and that the incidence of a positive exercise test did not differ between the two groups (with and without induced ventricular ectopy), myocardial ischaemia does not seem to be the explanation for the metaraminol induced arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Segmental wall motion abnormalities alter vulnerability to ventricular ectopic beats associated with acute increases in aortic pressure in patients with underlying coronary artery disease

Siogas

Pappas

Graekas

et al. 1998

Heart

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Objective-To evaluate whether patients with coronary artery disease are susceptible to pressure related ventricular arrhythmias, and if so to identify possible risk factors. Design-Interventional study. Methods-Metaraminol was given to 43 patients undergoing coronary arteriography for ischaemic heart disease to increase their aortic pressure, provided their systolic blood pressure was < 160 mm Hg and they were in sinus rhythm, without any ventricular ectopic activity (or with fewer than six ventricular ectopic beats a minute) during a five minute control period. Results-During the metaraminol infusion, systolic aortic pressure rose from 131 (15) to 199 (12) mm Hg (mean (SD)). Ventricular ectopy appeared (or ventricular ectopic beats increased by > 100%) in 13/43 patients. Ventricular ectopy was not related to age, sex, presence of hypertension, history of myocardial infarction, use of blockers, positive exercise test, number of vessels diseased, or heart rate change during metaraminol infusion. There was a strong relation between the appearance of ventricular arrhythmia and segmental wall motion abnormalities: 1/19 (5.3%, 95% confidence interval 0.1% to 26.0%) without abnormality; 2/12 (16.7%, 2.1% to 48.4%) with hypokinesia; and 10/12 (83.3%, 51.6% to 97.1%) with akinesia or dyskinesia, 2 = 22.7, p < 0.001). Ejection fraction was also a significant but not independent risk factor. Conclusions-Patients with segmental wall motion abnormalities are predisposed to ventricular ectopic beats during an increase in systolic aortic pressure. This could be explained by associated electrophysiological inhomogeneity. The presence of mechanical inhomogeneity, as may occur in postinfarction akinesia or dyskinesia, may aVect the aortic pressure above which ventricular arrhythmias appear. (Heart 1998;79:268-273)

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Section: Discussionmentioning

confidence: 99%

Segmental wall motion abnormalities alter vulnerability to ventricular ectopic beats associated with acute increases in aortic pressure in patients with underlying coronary artery disease

Siogas

Pappas

Graekas

et al. 1998

Heart

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“…Reduced afterload reduces the workload and O 2 demand of the heart, which is mechanically favorable, especially in a diseased heart. An acute increase in afterload (29), as well as chronically high afterload post-AMI (24), has been associated with increased ventricular arrhythmias. However, arterial hypertension was not different between patients experiencing AMI with and without VF in a clinical study looking at risk factors for AMI-induced VF (14).…”

Section: Cardiac Workmentioning

confidence: 99%

Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction

Lubberding

Sattler

Flethøj

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open chest) to minimally invasive techniques, including balloon occlusion (closed chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regard to hemodynamics, electrophysiology, and arrhythmia development. Forty-two female Danish Landrace pigs (20 open chest, 22 closed chest) were anesthetized, and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (Δ −22 mmHg, Δ −1.5 L/min from baseline, both P < 0.001 intragroup). Heart rate decreased with opening of the chest but increased with balloon placement ( P < 0.001). AMI-induced ST elevation was lower in the open-chest group ( P < 0.001). Premature ventricular contractions occurred in two distinct phases (0–15 and 15–40 min), the latter of which was delayed in the open-chest group ( P = 0.005). VF occurred in 7 out of 20 and 12 out of 22 pigs in the open-chest and closed-chest groups, respectively ( P = 0.337), with longer time-to-VF in the open-chest group (23.4 ± 1.2 min in open chest and 17.8 ± 1.4 min in closed chest; P = 0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models. NEW & NOTEWORTHY We demonstrated pronounced differences in hemodynamic parameters and time course of ventricular arrhythmias in regard to mode of infarct induction. Inducing myocardial infarction by thoracotomy and subsequent ligation decreased blood pressure and cardiac output and delayed the onset of ventricular arrhythmia, whereas balloon occlusion resulted in higher heart rates during infarct.

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“…Additionally, the heart is part of a hydrodynamic system: a mechanical, hydraulically mediated mechanism for MMI, using pressure–volume changes in a system containing incompressible blood provides the MMI. Systemic arterial pressure and/or venous volume changes can influence cardiac electrophysiology and function 5, 69–74 . This would invoke the variety of cellular mechanisms covered above.…”

Section: In the Intact Heart—regulation Of Cardiac Functionmentioning

confidence: 99%

“…Systemic arterial pressure and/or venous volume changes can influence cardiac electrophysiology and function. 5,[69][70][71][72][73][74] This would invoke the variety of cellular mechanisms covered above.…”

Section: In the Intact Heart-regulation Of Cardiac Functionmentioning

confidence: 99%

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

Lab

2006

Annals of the New York Academy of Sciences

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This review covers aspects of the cardiac mechanotransduction field at different levels, and advocates the possibility that mechanoelectro-chemical transduction forms part of a network of mechanically linked integration in heart-mechanically mediated integration (MMI). It assembles evidence and observations in the literature to promote this hypothesis. Mechanical components can provide the bond between interactions at molecular, cellular, and macro levels to enable the integration. Stretch-activated channels (SACs) exist in the heart, but stresses and strains can affect other membrane channels or receptors. A cellular mechanical change can thus promote several ionic or downstream changes. Cell signal cascades have been implicated and can affect membrane electrophysiology. MMI could shape intracellular and downstream signals using the cytoskeleton and intracellular Ca(2+). MMI also spans other regulatory systems and processes such as the autonomic nervous system (ANS) and operates throughout the whole heart as an integrative system. Finally, supporting the hypothesis, if elements of the normal integration become deranged it contributes to cardiovascular disease and, potentially, lethal arrhythmia.

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Effect of preload and afterload on ventricular arrhythmogenesis

Cited by 11 publications

References 18 publications

Segmental wall motion abnormalities alter vulnerability to ventricular ectopic beats associated with acute increases in aortic pressure in patients with underlying coronary artery disease

Segmental wall motion abnormalities alter vulnerability to ventricular ectopic beats associated with acute increases in aortic pressure in patients with underlying coronary artery disease

Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

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