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ScienceDirect Journal of Electrocardiology 47 (2014) 273 www.jecgonline.com
Letter to the Editor Nina Hakacova, MD, PhD Children's Heart Centre Skane University Hospital Lund, Sweden E-mail address: [email protected]
Right and left ventricular pressure overload as imaged by electrocardiogram Electrical changes in the heart evolve as pressure load of either the right (RV) or the left ventricle (LV) changes [1]. So called “electro-mechanical feedback” has been studied mostly in the left ventricle, with pressure overloads caused by aortic stenosis or systemic hypertension [2,3]. Regarding the RV, electro-mechanical changes have been described with pressure overloads caused by pulmonary stenosis or pulmonary hypertension [4–6]. Currently however, electrocardiography (ECG) is used rarely, in prediction and/or follow-up of changing ventricular pressure overloading conditions in clinical practice. Only the mechanical change of heart function, and the anatomical change of increase in mass are being followed by imaging modalities such as ultrasound or MRI [7]. Even though “electrical instability” is mentioned as an important predictive factor of lifethreatening events in patients with pressure overload of the ventricles, the ECG has become obsolete as a clinical tool, except to detect arrhythmias [8,9]. In clinical practice, many abnormalities imposed by acquired or congenital heart disease can lead to pressure overload of the right and/or left ventricle and can subsequently lead to heart failure, when the compensatory mechanisms become inadequate. Can clinicians monitor these conditions by ECG, to identify changes that can detect the severity of pressure overload non-invasively? How does pressure overloading or unloading change electrical potentials and how rapidly does this evolve? Can clinicians then guide the therapy by responding to these “clinical electrophysiologic” changes? There are compelling data to suggest that appreciation and understanding of electrophysiologic changes can facilitate recognition of pathophysiological processes in the heart [1,6,10]. Appreciation of both right–left heart interactions and electro-mechanical interactions may be possible by using the clinically available standard ECG as a non-invasive “electrophysiologic imaging” technology. The Journal of Electrocardiology is preparing a symposium on right and/or left ventricular pressure overload as imaged by the ECG in its September–October 2014 issue. Papers concerning both adult and pediatric cardiology will be included after emerging from the Journal's peer-review process. The purpose of this letter is to invite contributions from those who can share their understanding on this topic. Not only strengths, but also vulnerabilities of the ECG should be discussed, and thus potentially lead to innovations in use of the ECG as a method of monitoring the clinical course of these patients. 0022-0736/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Galen Wagner, MD Duke Clinical Research Institute Durham, NC, USA Ljuba Bacharova, MD, PhD International Laser Center Bratislava, Slovakia http://dx.doi.org/10.1016/j.jelectrocard.2014.01.006 References [1] Lab MJ. Mechanoelectric feedback (transduction) in heart: concepts and implications. Cardiovasc Res 1996;32:3–14. [2] Sarubbi B, Calvanese R, Cappelli Bigazzi M, Santoro G, Giovanna Russo M, Calabro R. Electrophysiological changes following balloon valvuloplasty and angioplasty for aortic stenosis and coartaction of aorta: clinical evidence for mechano-electrical feedback in humans. Int J Cardiol 2004;93:7–11. [3] Wang Z, Kutschke W, Richardson KE, Karimi M, Hill JA. Electrical remodeling in pressure-overload cardiac hypertrophy: role of calcineurin. Circulation 2001;104:1657–63. [4] Zeltser I, Gaynor JW, Petko M, Myung RJ, Birbach M, Waibel R, et al. The roles of chronic pressure and volume overload states in induction of arrhythmias: an animal model of physiologic sequelae after repair of tetralogy of Fallot. J Thorac Cardiovasc Surg 2005;130:1542–8. [5] Katholi RE, Couri DM. Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications. Int J Hypertens 2011;2011:1–10. [6] Gatzoulis MA, Till JA, Somerville J, Redington AN. Mechanoelectrical interaction in tetralogy of Fallot. QRS prolongation relates to right ventricular size and predicts malignant ventricular arrhythmias and sudden death. Circulation 1995;92:231–7. [7] Koestenberger M, Nagel B, Avian A, Ravekes W, Sorantin E, Cvirn G, et al. Systolic right ventricular function in children and young adults with pulmonary artery hypertension secondary to congenital heart disease and tetralogy of Fallot: tricuspid annular plane systolic excursion (TAPSE) and magnetic resonance imaging data. Congenit Heart Dis 2012;7:250–8. [8] Dean JW, Lab MJ. Arrhythmia in heart failure: role of mechanically induced changes in electrophysiology. Lancet 1989;1:1309–12. [9] Hansen DE, Craig CS, Hondeghem LM. Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. Circulation 1990;81: 1094–105. [10] Bacharova L, Estes EH, Bang LE, Hill JA, Macfarlane PW, Rowlandson I, Schillaci G. Second statement of the Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy. J Electrocardiol 2011;44:568–70.
ScienceDirect Journal of Electrocardiology 47 (2014) 273 www.jecgonline.com
Letter to the Editor Nina Hakacova, MD, PhD Children's Heart Centre Skane University Hospital Lund, Sweden E-mail address: [email protected]
Right and left ventricular pressure overload as imaged by electrocardiogram Electrical changes in the heart evolve as pressure load of either the right (RV) or the left ventricle (LV) changes [1]. So called “electro-mechanical feedback” has been studied mostly in the left ventricle, with pressure overloads caused by aortic stenosis or systemic hypertension [2,3]. Regarding the RV, electro-mechanical changes have been described with pressure overloads caused by pulmonary stenosis or pulmonary hypertension [4–6]. Currently however, electrocardiography (ECG) is used rarely, in prediction and/or follow-up of changing ventricular pressure overloading conditions in clinical practice. Only the mechanical change of heart function, and the anatomical change of increase in mass are being followed by imaging modalities such as ultrasound or MRI [7]. Even though “electrical instability” is mentioned as an important predictive factor of lifethreatening events in patients with pressure overload of the ventricles, the ECG has become obsolete as a clinical tool, except to detect arrhythmias [8,9]. In clinical practice, many abnormalities imposed by acquired or congenital heart disease can lead to pressure overload of the right and/or left ventricle and can subsequently lead to heart failure, when the compensatory mechanisms become inadequate. Can clinicians monitor these conditions by ECG, to identify changes that can detect the severity of pressure overload non-invasively? How does pressure overloading or unloading change electrical potentials and how rapidly does this evolve? Can clinicians then guide the therapy by responding to these “clinical electrophysiologic” changes? There are compelling data to suggest that appreciation and understanding of electrophysiologic changes can facilitate recognition of pathophysiological processes in the heart [1,6,10]. Appreciation of both right–left heart interactions and electro-mechanical interactions may be possible by using the clinically available standard ECG as a non-invasive “electrophysiologic imaging” technology. The Journal of Electrocardiology is preparing a symposium on right and/or left ventricular pressure overload as imaged by the ECG in its September–October 2014 issue. Papers concerning both adult and pediatric cardiology will be included after emerging from the Journal's peer-review process. The purpose of this letter is to invite contributions from those who can share their understanding on this topic. Not only strengths, but also vulnerabilities of the ECG should be discussed, and thus potentially lead to innovations in use of the ECG as a method of monitoring the clinical course of these patients. 0022-0736/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Galen Wagner, MD Duke Clinical Research Institute Durham, NC, USA Ljuba Bacharova, MD, PhD International Laser Center Bratislava, Slovakia http://dx.doi.org/10.1016/j.jelectrocard.2014.01.006 References [1] Lab MJ. Mechanoelectric feedback (transduction) in heart: concepts and implications. Cardiovasc Res 1996;32:3–14. [2] Sarubbi B, Calvanese R, Cappelli Bigazzi M, Santoro G, Giovanna Russo M, Calabro R. Electrophysiological changes following balloon valvuloplasty and angioplasty for aortic stenosis and coartaction of aorta: clinical evidence for mechano-electrical feedback in humans. Int J Cardiol 2004;93:7–11. [3] Wang Z, Kutschke W, Richardson KE, Karimi M, Hill JA. Electrical remodeling in pressure-overload cardiac hypertrophy: role of calcineurin. Circulation 2001;104:1657–63. [4] Zeltser I, Gaynor JW, Petko M, Myung RJ, Birbach M, Waibel R, et al. The roles of chronic pressure and volume overload states in induction of arrhythmias: an animal model of physiologic sequelae after repair of tetralogy of Fallot. J Thorac Cardiovasc Surg 2005;130:1542–8. [5] Katholi RE, Couri DM. Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications. Int J Hypertens 2011;2011:1–10. [6] Gatzoulis MA, Till JA, Somerville J, Redington AN. Mechanoelectrical interaction in tetralogy of Fallot. QRS prolongation relates to right ventricular size and predicts malignant ventricular arrhythmias and sudden death. Circulation 1995;92:231–7. [7] Koestenberger M, Nagel B, Avian A, Ravekes W, Sorantin E, Cvirn G, et al. Systolic right ventricular function in children and young adults with pulmonary artery hypertension secondary to congenital heart disease and tetralogy of Fallot: tricuspid annular plane systolic excursion (TAPSE) and magnetic resonance imaging data. Congenit Heart Dis 2012;7:250–8. [8] Dean JW, Lab MJ. Arrhythmia in heart failure: role of mechanically induced changes in electrophysiology. Lancet 1989;1:1309–12. [9] Hansen DE, Craig CS, Hondeghem LM. Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. Circulation 1990;81: 1094–105. [10] Bacharova L, Estes EH, Bang LE, Hill JA, Macfarlane PW, Rowlandson I, Schillaci G. Second statement of the Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy. J Electrocardiol 2011;44:568–70.
