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Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction
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MODEL
Hellenic Journal of Cardiology (2017) xx, 1e3
Available online at www.sciencedirect.com
ScienceDirect journal homepage: http://www.journals.elsevier.com/ hellenic-journal-of-cardiology/
LETTER TO THE EDITOR
Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction
KEYWORDS Ischemic cardiomyopathy; preserved ejection fraction; programmed ventricular stimulation; noninvasive risk stratification
A 68-year old asymptomatic coronary artery disease (CAD) patient was referred to the Electrophysiology Laboratory for assessment following a recording of nonsustained ventricular tachycardia (nsVT) in a follow-up 24-hour ambulatory ECG recording (Holter) after a recent episode of atrial fibrillation. The patient suffered an acute inferior wall myocardial infarction (MI) in 2007 with angiography, demonstrating total right coronary artery occlusion that was not amenable to revascularization. The left ventricular ejection fraction (LVEF) was 55%, with mild posteroinferior wall hypokinesia. He was on optimal medical therapy and otherwise enjoying a healthful and active lifestyle (NYHA class I). Several indices of electrical instability, namely, deceleration capacity (DC) and late potentials (LP) (Figure 1A), were also abnormal. Repeat angiography revealed onevessel disease, with chronic total occlusion of the right coronary artery. Based on the above findings, the patient was submitted to programmed ventricular stimulation (PVS), and a sustained monomorphic VT was readily inducible at the right ventricular apex with morphology suggesting an origin from the inferior left ventricular wall (Figure 1B). A quadripolar catheter subsequently placed at the inferior left ventricular wall recorded prominent LPs (Figure 1C). Peer review under responsibility of Hellenic Cardiological Society.
A well-preserved LVEF was confirmed echocardiographically, and mechanical dispersion of the peak longitudinal strain among the 16 ventricular segments was calculated at 74 msec (Figure 2A). Magnetic resonance imaging (MRI) revealed fibrosis with late Gadolinium enhancement (LGE) in the posterior wall (Figure 2B). Our case represents a typical CAD patient e asymptomatic with a preserved left ventricular ejection fraction ewho was excluded a priori from ICD protection and who nonetheless exhibited an arrhythmogenic potential, culminating in the induction of VT upon PVS. Several noninvasive and imaging modalities also detected this underestimated arrhythmogenic potential. DC is a measure of autonomic nervous system function, and a decreased DC has been proposed to be an independent risk factor beyond EF for sudden and total death.1 Similarly, the presence of LPs represents the existence of disarrayed myocardial cell bundles, leading to anisotropic impulse propagation and potentially creating the substrate for re-entry. LPs are associated with an increased sudden cardiac death (SCD) risk. On the other hand, TWA, an index of repolarization dispersion and an abnormal action potential duration restitution curve,1 was normal (25 mV). The imaging modalities revealed subtle alterations associated with arrhythmogenesis. MRI detected LGE, denoting fibrosis at the infarcted area, which has been related to SCD or ventricular tachyarrhythmia occurrence in a meta-analysis.2 Mechanical dispersion of the peak longitudinal strain (74 msec) was extremely close to the cutoff value proposed for differentiating patients with arrhythmic events (75 msec).3 Notably, EF was not an independent predictor of events in either study. Although noninvasive features may detect electrical instability or an arrhythmia-prone histological substrate, they cannot establish the presence of functional circuits. Induction of monomorphic VT in the remote post-MI period is highly suggestive of the presence of established circuits. Studies have favourably reported on PVS values for the positive selection of patients with a relatively preserved (>35%) EF.4 In this context, the decision to implant an ICD
http://dx.doi.org/10.1016/j.hjc.2017.03.002 1109-9666/ª 2017 Hellenic Cardiological Society. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Gatzoulis KA, et al., Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction, Hellenic Journal of Cardiology (2017), http://dx.doi.org/10.1016/ j.hjc.2017.03.002
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MODEL
Letter to the Editor
Figure 1 Surface ECG and PVS findings. A. Late potentials from a signal-averaged electrocardiogram. Abnormal late depolarization currents are noted (arrow) at the end of the QRS complex and confirmed by the highly abnormal parameters of the filtered QRS duration (148 msec), low amplitude signal duration (73 msec) and RMS40 (4 mV). B. VT induction at PVS. Morphology (superior axis e RBBB) localizes the exit site at the inferior wall. II, III, aVF, V1: Surface ECG leads, RVA: Right ventricular apex, S1-3: Drive train, first, and second extrastimuli. C. LPs detected at the left ventricular inferior wall (arrows).
Figure 2 Echocardiography and MRI findings. A. Left ventricular longitudinal strain as a function of time and as a bullseye. Note the reduced peak strain in the posterior wall (pink-colored area) and mechanical dispersion of 74 msec. B. MRI short axis image with LGE evident at the inferoposterior wall (white arrow). Right ventricular dilatation and extensive wall fibrosis are also appreciated (black arrow).
Please cite this article in press as: Gatzoulis KA, et al., Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction, Hellenic Journal of Cardiology (2017), http://dx.doi.org/10.1016/ j.hjc.2017.03.002
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MODEL
Letter to the Editor appears to be justified, especially given the favourable anticipated cost-benefit ratio. The reported case stresses the need for clinicians to more rigorously assess all post-MI patients for SCD risk. When noninvasive indices and imaging modalities demonstrate a propensity for malignant arrhythmogenesis, PVS could be a final means for assessment and treatment guidance, especially given the possibility of complications following ICD insertion (rare but potentially devastating).5 Unfortunately, an uneventful short follow-up period (w3 months from risk stratification) precludes us from definitely concluding that this arrhythmogenic potential will eventually translate into clinical ventricular tachyarrhythmias. Completion of the currently underway PRESERVE-EF study,6 which seeks high-risk post-MI patients with a wellpreserved EF receiving an ICD, is expected to provide answers regarding these issues.
Conflict of interest None declared.
References 1. Arsenos P, Gatzoulis K, Dilaveris P, et al. Arrhythmic sudden cardiac death: substrate, mechanisms and current risk stratification strategies for the post-myocardial infarction patient. Hellenic J Cardiol. 2013;54:301e315. 2. Disertori M, Rigoni M, Pace N, et al. Myocardial Fibrosis Assessment by LGE Is a Powerful Predictor of Ventricular Tachyarrhythmias in Ischemic and Nonischemic LV Dysfunction: A MetaAnalysis. JACC Cardiovascular Imaging. 2016;9:1046e1055. 3. Haugaa KH, Grenne BL, Eek CH, et al. Strain echocardiography improves risk prediction of ventricular arrhythmias after
3 myocardial infarction. JACC Cardiovascular Imaging. 2013;6: 841e850. 4. Gatzoulis KA, Tsiachris D, Arsenos P, et al. Prognostic value of programmed ventricular stimulation for sudden death in selected high risk patients with structural heart disease and preserved systolic function. Int J Cardiol. 2014;176: 1449e1451. 5. Fanourgiakis J, Simantirakis E, Maniadakis N, et al. Complications Related to Cardiac Rhythm Management Device Therapy and Their Financial Implication: A Prospective Single-Center TwoYear Survey. Hellenic J Cardiol. 2016;57:33e38. 6. Gatzoulis KA, Tsiachris D, Arsenos P, et al. Post myocardial infarction risk stratification for sudden cardiac death in patients with preserved ejection fraction: PRESERVE-EF study design. Hellenic J Cardiol. 2014;55:361e368.
Konstantinos A. Gatzoulis* Christos-Konstantinos Antoniou Polychronis Dilaveris Christina Chrysohoou Petros Arsenos Konstantinos Trachanas Dimitrios Tousoulis First Division of Cardiology, Athens Medical School, Hippokration General Hospital, 114 Vasilissis Sofias Ave. 11527, Athens, Greece *Corresponding author. Konstantinos A. Gatzoulis, 181 Dorieon St., Mail box 175, 19009 Drafi Attikis, Athens, Greece. Tel.: þ30 6944580369. E-mail address: [email protected] (K.A. Gatzoulis) 22 February 2017
Please cite this article in press as: Gatzoulis KA, et al., Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction, Hellenic Journal of Cardiology (2017), http://dx.doi.org/10.1016/ j.hjc.2017.03.002
MODEL
Hellenic Journal of Cardiology (2017) xx, 1e3
Available online at www.sciencedirect.com
ScienceDirect journal homepage: http://www.journals.elsevier.com/ hellenic-journal-of-cardiology/
LETTER TO THE EDITOR
Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction
KEYWORDS Ischemic cardiomyopathy; preserved ejection fraction; programmed ventricular stimulation; noninvasive risk stratification
A 68-year old asymptomatic coronary artery disease (CAD) patient was referred to the Electrophysiology Laboratory for assessment following a recording of nonsustained ventricular tachycardia (nsVT) in a follow-up 24-hour ambulatory ECG recording (Holter) after a recent episode of atrial fibrillation. The patient suffered an acute inferior wall myocardial infarction (MI) in 2007 with angiography, demonstrating total right coronary artery occlusion that was not amenable to revascularization. The left ventricular ejection fraction (LVEF) was 55%, with mild posteroinferior wall hypokinesia. He was on optimal medical therapy and otherwise enjoying a healthful and active lifestyle (NYHA class I). Several indices of electrical instability, namely, deceleration capacity (DC) and late potentials (LP) (Figure 1A), were also abnormal. Repeat angiography revealed onevessel disease, with chronic total occlusion of the right coronary artery. Based on the above findings, the patient was submitted to programmed ventricular stimulation (PVS), and a sustained monomorphic VT was readily inducible at the right ventricular apex with morphology suggesting an origin from the inferior left ventricular wall (Figure 1B). A quadripolar catheter subsequently placed at the inferior left ventricular wall recorded prominent LPs (Figure 1C). Peer review under responsibility of Hellenic Cardiological Society.
A well-preserved LVEF was confirmed echocardiographically, and mechanical dispersion of the peak longitudinal strain among the 16 ventricular segments was calculated at 74 msec (Figure 2A). Magnetic resonance imaging (MRI) revealed fibrosis with late Gadolinium enhancement (LGE) in the posterior wall (Figure 2B). Our case represents a typical CAD patient e asymptomatic with a preserved left ventricular ejection fraction ewho was excluded a priori from ICD protection and who nonetheless exhibited an arrhythmogenic potential, culminating in the induction of VT upon PVS. Several noninvasive and imaging modalities also detected this underestimated arrhythmogenic potential. DC is a measure of autonomic nervous system function, and a decreased DC has been proposed to be an independent risk factor beyond EF for sudden and total death.1 Similarly, the presence of LPs represents the existence of disarrayed myocardial cell bundles, leading to anisotropic impulse propagation and potentially creating the substrate for re-entry. LPs are associated with an increased sudden cardiac death (SCD) risk. On the other hand, TWA, an index of repolarization dispersion and an abnormal action potential duration restitution curve,1 was normal (25 mV). The imaging modalities revealed subtle alterations associated with arrhythmogenesis. MRI detected LGE, denoting fibrosis at the infarcted area, which has been related to SCD or ventricular tachyarrhythmia occurrence in a meta-analysis.2 Mechanical dispersion of the peak longitudinal strain (74 msec) was extremely close to the cutoff value proposed for differentiating patients with arrhythmic events (75 msec).3 Notably, EF was not an independent predictor of events in either study. Although noninvasive features may detect electrical instability or an arrhythmia-prone histological substrate, they cannot establish the presence of functional circuits. Induction of monomorphic VT in the remote post-MI period is highly suggestive of the presence of established circuits. Studies have favourably reported on PVS values for the positive selection of patients with a relatively preserved (>35%) EF.4 In this context, the decision to implant an ICD
http://dx.doi.org/10.1016/j.hjc.2017.03.002 1109-9666/ª 2017 Hellenic Cardiological Society. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Gatzoulis KA, et al., Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction, Hellenic Journal of Cardiology (2017), http://dx.doi.org/10.1016/ j.hjc.2017.03.002
+ 2
MODEL
Letter to the Editor
Figure 1 Surface ECG and PVS findings. A. Late potentials from a signal-averaged electrocardiogram. Abnormal late depolarization currents are noted (arrow) at the end of the QRS complex and confirmed by the highly abnormal parameters of the filtered QRS duration (148 msec), low amplitude signal duration (73 msec) and RMS40 (4 mV). B. VT induction at PVS. Morphology (superior axis e RBBB) localizes the exit site at the inferior wall. II, III, aVF, V1: Surface ECG leads, RVA: Right ventricular apex, S1-3: Drive train, first, and second extrastimuli. C. LPs detected at the left ventricular inferior wall (arrows).
Figure 2 Echocardiography and MRI findings. A. Left ventricular longitudinal strain as a function of time and as a bullseye. Note the reduced peak strain in the posterior wall (pink-colored area) and mechanical dispersion of 74 msec. B. MRI short axis image with LGE evident at the inferoposterior wall (white arrow). Right ventricular dilatation and extensive wall fibrosis are also appreciated (black arrow).
Please cite this article in press as: Gatzoulis KA, et al., Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction, Hellenic Journal of Cardiology (2017), http://dx.doi.org/10.1016/ j.hjc.2017.03.002
+
MODEL
Letter to the Editor appears to be justified, especially given the favourable anticipated cost-benefit ratio. The reported case stresses the need for clinicians to more rigorously assess all post-MI patients for SCD risk. When noninvasive indices and imaging modalities demonstrate a propensity for malignant arrhythmogenesis, PVS could be a final means for assessment and treatment guidance, especially given the possibility of complications following ICD insertion (rare but potentially devastating).5 Unfortunately, an uneventful short follow-up period (w3 months from risk stratification) precludes us from definitely concluding that this arrhythmogenic potential will eventually translate into clinical ventricular tachyarrhythmias. Completion of the currently underway PRESERVE-EF study,6 which seeks high-risk post-MI patients with a wellpreserved EF receiving an ICD, is expected to provide answers regarding these issues.
Conflict of interest None declared.
References 1. Arsenos P, Gatzoulis K, Dilaveris P, et al. Arrhythmic sudden cardiac death: substrate, mechanisms and current risk stratification strategies for the post-myocardial infarction patient. Hellenic J Cardiol. 2013;54:301e315. 2. Disertori M, Rigoni M, Pace N, et al. Myocardial Fibrosis Assessment by LGE Is a Powerful Predictor of Ventricular Tachyarrhythmias in Ischemic and Nonischemic LV Dysfunction: A MetaAnalysis. JACC Cardiovascular Imaging. 2016;9:1046e1055. 3. Haugaa KH, Grenne BL, Eek CH, et al. Strain echocardiography improves risk prediction of ventricular arrhythmias after
3 myocardial infarction. JACC Cardiovascular Imaging. 2013;6: 841e850. 4. Gatzoulis KA, Tsiachris D, Arsenos P, et al. Prognostic value of programmed ventricular stimulation for sudden death in selected high risk patients with structural heart disease and preserved systolic function. Int J Cardiol. 2014;176: 1449e1451. 5. Fanourgiakis J, Simantirakis E, Maniadakis N, et al. Complications Related to Cardiac Rhythm Management Device Therapy and Their Financial Implication: A Prospective Single-Center TwoYear Survey. Hellenic J Cardiol. 2016;57:33e38. 6. Gatzoulis KA, Tsiachris D, Arsenos P, et al. Post myocardial infarction risk stratification for sudden cardiac death in patients with preserved ejection fraction: PRESERVE-EF study design. Hellenic J Cardiol. 2014;55:361e368.
Konstantinos A. Gatzoulis* Christos-Konstantinos Antoniou Polychronis Dilaveris Christina Chrysohoou Petros Arsenos Konstantinos Trachanas Dimitrios Tousoulis First Division of Cardiology, Athens Medical School, Hippokration General Hospital, 114 Vasilissis Sofias Ave. 11527, Athens, Greece *Corresponding author. Konstantinos A. Gatzoulis, 181 Dorieon St., Mail box 175, 19009 Drafi Attikis, Athens, Greece. Tel.: þ30 6944580369. E-mail address: [email protected] (K.A. Gatzoulis) 22 February 2017
Please cite this article in press as: Gatzoulis KA, et al., Ventricular arrhythmogenic potential assessment in an asymptomatic ischemic cardiomyopathy patient with a normal ejection fraction, Hellenic Journal of Cardiology (2017), http://dx.doi.org/10.1016/ j.hjc.2017.03.002