Heart & Lung 44 (2015) 178
Contents lists available at ScienceDirect
Heart & Lung journal homepage: www.heartandlung.org
Letter to the Editor
Ivabradine in cardiogenic shock: Fact or fiction? We read with great interest the recent article by Bonadei et al. documenting the role ivabradine in a patient with cardiogenic shock.1 Although management of the patient was successful, we want to address some points that merit more attention. Cardiogenic shock usually presents with low systolic blood pressure and clinical signs of hypoperfusion. Hypoperfusion causes release of catecholamines, which increase contractility and peripheral blood flow, but also increase myocardial oxygen demand and have proarrhythmic and myocardiotoxic effects.2 Next to an early revascularization strategy and optimal drug therapy including vasopressors and positive inotropic agents, intraaortic baloon pump (IABP) is considered as an additional option to achieve initial hemodynamic stabilization and improve clinical outcome. Inotropic agents and vasoconstrictors temporarily improve cardiac output and peripheral perfusion but do not interrupt vicious circle.2,3 Rapid IABP support may temporarily relieve ischemia and support the circulation. Relief of coronary occlusion interrupts the vicious circle and results better hemodynamic response like increase in blood pressure and decrease in heart rate.3 In the current case report the heart rate of the patient decreased from 130 bpm to 105 bpm after successful intervention (left main coronary artery stenting and IABP) and administration of furosemide. However, heart rate reduction after 48 h of ivabradine therapy was higher than the clinical trials’ results (105 bpm to 80 bpm). For instance, after 1 month of ivabradine therapy, an uncorrected heart rate reduction was 15 bpm in the SHIfT trial, and 13 bpm in the INTENSIfY trial.4,5 Therefore, we think that, the reduction of the heart rate is an expected result of clinical stabilization, IABP support, and decompensation after diuretic therapy rather than an ivabradine effect. Cavusoglu et al have recently shown in a randomized, placebo-controlled trial that the dobutamine induced increase in heart rate was blunted by ivabradine treatment in patients hospitalized with acute decompensated heart failure.6 After dobutamine administration at incremental doses of 5, 10 and 15 mg/kg/min, dose dependent increase in heart rate was 5 bpm, 13 bpm, 18 bpm, respectively in the control group of their study population. However, in this study there is no data on the dosage of inotropics and early effects of ivabradine in heart rate reduction.
0147-9563/$ e see front matter Ó 2015 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.hrtlng.2014.11.004
We think that it could not be postulated that better hemodynamic response or clinical improvement of the patient was not solely due to ivabradine as Bonadei et al mentioned. In conclusion, we think that while the patient was fortunatedshe did not suffer any detectable complicationsda good outcome in one patient certainly does not prove that the approach the authors used is broadly applicable. References 1. Bonadei I, Sciatti E, Vizzardi E, D’Aloia A, Metra M. Ivabradine during cardiogenic shock: a clinical case and review of the literature. Heart Lung. 2015;44:57e58. 2. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117:686e697. 3. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. J Am Med Assoc. 2006;295:2511e2515. 4. Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT) a randomised placebo-controlled study. Lancet. 2010;376: 875e885. 5. Zugck C, Martinka P, Stöckl G. Ivabradine treatment in a chronic heart failure patient cohort: symptom reduction and improvement in quality of life in clinical practice. Adv Ther. 2014;31:961e974. 6. Cavusoglu Y, Mert U, Nadir A, Mutlu F, Morrad B, Ulus T. Ivabradine treatment prevents dobutamine-induced increase in heart rate in patients with acute decompensated heart failure. J Cardiovasc Med (Hagerstown); 2014 Jun 11 [Epub ahead of print] PubMed PMID: 24922198).
ur Mert, MD* Kadir Ug Gurbet Özge Mert, MD _ Ibrahim Altun, MD Murat Biteker, MD la Sıtkı Koçman University Mug Faculty of Medicine Department of Cardiology Turkey la Sıtkı Koçman Üniversitesi Tıp * Corresponding author. Mug la, Turkey. Fakültesi, Orhaniye Mah. Haluk Özsoy Cad. 48000/Mug Tel.: þ90 252 214 13 26. E-mail address: [email protected] (K.U. Mert)
Contents lists available at ScienceDirect
Heart & Lung journal homepage: www.heartandlung.org
Letter to the Editor
Ivabradine in cardiogenic shock: Fact or fiction? We read with great interest the recent article by Bonadei et al. documenting the role ivabradine in a patient with cardiogenic shock.1 Although management of the patient was successful, we want to address some points that merit more attention. Cardiogenic shock usually presents with low systolic blood pressure and clinical signs of hypoperfusion. Hypoperfusion causes release of catecholamines, which increase contractility and peripheral blood flow, but also increase myocardial oxygen demand and have proarrhythmic and myocardiotoxic effects.2 Next to an early revascularization strategy and optimal drug therapy including vasopressors and positive inotropic agents, intraaortic baloon pump (IABP) is considered as an additional option to achieve initial hemodynamic stabilization and improve clinical outcome. Inotropic agents and vasoconstrictors temporarily improve cardiac output and peripheral perfusion but do not interrupt vicious circle.2,3 Rapid IABP support may temporarily relieve ischemia and support the circulation. Relief of coronary occlusion interrupts the vicious circle and results better hemodynamic response like increase in blood pressure and decrease in heart rate.3 In the current case report the heart rate of the patient decreased from 130 bpm to 105 bpm after successful intervention (left main coronary artery stenting and IABP) and administration of furosemide. However, heart rate reduction after 48 h of ivabradine therapy was higher than the clinical trials’ results (105 bpm to 80 bpm). For instance, after 1 month of ivabradine therapy, an uncorrected heart rate reduction was 15 bpm in the SHIfT trial, and 13 bpm in the INTENSIfY trial.4,5 Therefore, we think that, the reduction of the heart rate is an expected result of clinical stabilization, IABP support, and decompensation after diuretic therapy rather than an ivabradine effect. Cavusoglu et al have recently shown in a randomized, placebo-controlled trial that the dobutamine induced increase in heart rate was blunted by ivabradine treatment in patients hospitalized with acute decompensated heart failure.6 After dobutamine administration at incremental doses of 5, 10 and 15 mg/kg/min, dose dependent increase in heart rate was 5 bpm, 13 bpm, 18 bpm, respectively in the control group of their study population. However, in this study there is no data on the dosage of inotropics and early effects of ivabradine in heart rate reduction.
0147-9563/$ e see front matter Ó 2015 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.hrtlng.2014.11.004
We think that it could not be postulated that better hemodynamic response or clinical improvement of the patient was not solely due to ivabradine as Bonadei et al mentioned. In conclusion, we think that while the patient was fortunatedshe did not suffer any detectable complicationsda good outcome in one patient certainly does not prove that the approach the authors used is broadly applicable. References 1. Bonadei I, Sciatti E, Vizzardi E, D’Aloia A, Metra M. Ivabradine during cardiogenic shock: a clinical case and review of the literature. Heart Lung. 2015;44:57e58. 2. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117:686e697. 3. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. J Am Med Assoc. 2006;295:2511e2515. 4. Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT) a randomised placebo-controlled study. Lancet. 2010;376: 875e885. 5. Zugck C, Martinka P, Stöckl G. Ivabradine treatment in a chronic heart failure patient cohort: symptom reduction and improvement in quality of life in clinical practice. Adv Ther. 2014;31:961e974. 6. Cavusoglu Y, Mert U, Nadir A, Mutlu F, Morrad B, Ulus T. Ivabradine treatment prevents dobutamine-induced increase in heart rate in patients with acute decompensated heart failure. J Cardiovasc Med (Hagerstown); 2014 Jun 11 [Epub ahead of print] PubMed PMID: 24922198).
ur Mert, MD* Kadir Ug Gurbet Özge Mert, MD _ Ibrahim Altun, MD Murat Biteker, MD la Sıtkı Koçman University Mug Faculty of Medicine Department of Cardiology Turkey la Sıtkı Koçman Üniversitesi Tıp * Corresponding author. Mug la, Turkey. Fakültesi, Orhaniye Mah. Haluk Özsoy Cad. 48000/Mug Tel.: þ90 252 214 13 26. E-mail address: [email protected] (K.U. Mert)
