Zusammenfassung
Während in den vergangenen Jahren die dokumentierte Infarktsterblichkeit durch die Einführung der Intensivüberwachung, der Thrombolyse, effektiver antithrombotischer Therapien sowie der Koronarangioplastie von ca. 30% in den 60er Jahren auf derzeit 6–7% deutlich gesenkt werden konnte, ist die historisch zwischen 70% und 80% angesiedelte Sterblichkeit bei kardiogenem Schock infolge eines akuten Myokardinfarkts trotz moderner Therapiemaßnahmen kaum verbessert worden. Unverändert stellt das myokardiale Pumpversagen mit nachfolgendem kardiogenem Schock und daraus resultierendem Multiorganversagen die Hauptursache der Infarktsterblichkeit im Krankenhaus dar. Die medikamentöse Therapie in Form von Katecholaminen hat den großen Nachteil, dass der myokardiale Sauerstoffverbrauch aufgrund der Steigerung der Herzfrequenz erhöht und damit möglicherweise das Infarktareal vergrößert wird. Eine Reduktion der Herzfrequenz durch den Einsatz von β-Blockern ist aufgrund der blutdrucksenkenden und der negativ inotropen Wirkung dieser Substanzklasse kontraindiziert. Theoretisch ist vorstellbar, dass eine isolierte Herzfrequenzreduktion bei gleichzeitig fehlenden negativ inotropen Effekten sich positiv auf die Hämodynamik bei Patienten mit kardiogenem Schock auswirken kann. In dieser Übersicht sollen aktuelle Konzepte der Diagnostik und Therapie des kardiogenen Schocks kurz besprochen und im zweiten Teil auf den neuen If-Kanal-Inhibitor Ivabradin als einen möglichen therapeutischen Ansatz eingegangen werden.
Abstract
Documented mortality from acute myocardial infarction (AMI) has significantly decreased from around 30% in the 1960s to currently 6–7%, following the introduction of intensive-care treatment, thrombolysis, effective antithrombotic therapy, and coronary angioplasty. However, the approximate mortality of 70–80% of patients with cardiogenic shock following AMI has hardly improved despite the introduction of modern treatment strategies. The major cause of in-hospital AMI mortality remains myocardial failure with consecutive cardiogenic shock and multiorgan failure. Reduction of heart rate is one of the most important energy-saving maneuvers, which can be achieved by administration of β-receptor-blocking agents. In patients with clinical signs of hypotension, however, the guidelines recommend to stabilize the patient before administering an oral β-receptor blocker, mainly because of the hypotensive effects of the substance class. In this situation, selective heart rate reduction, e.g., via administration of ivabradine without side effects of hypotension may be advantageous and better tolerated in patients with cardiogenic shock. The aim of the present review is to briefly summarize the treatment options of cardiogenic shock and the mechanisms of action of ivabradine as well as to present a case report of a patient with cardiogenic shock due to main trunk occlusion, where treatment with ivabradine seemed to beneficially influence the outcome.
Literatur
Topalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Crit Care Med 2008;36:Suppl:S66–74.
Fox KA, Anderson FAJr, Dabbous OH, et al. Intervention in acute coronary syndromes: do patients undergo intervention on the basis of their risk characteristics? The Global Registry of Acute Coronary Events (GRACE). Heart 2007;93:177–82.
Hasdai D, Harrington RA, Hochman JS, et al. Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic shock complicating acute coronary syndromes without persistent ST-segment elevation. J Am Coll Cardiol 2000;36:685–92.
Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008;117:686–97.
Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 2008;29:2909–45.
Sanborn TA, Sleeper LA, Webb JG, et al. Correlates of one-year survival in patients with cardiogenic shock complicating acute myocardial infarction: angiographic findings from the SHOCK trial. J Am Coll Cardiol 2003;42:1373–9.
Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA 2006;295:2511–5.
Heer T, Zeymer U, Juenger C, et al. Beneficial effects of abciximab in patients with primary percutaneous intervention for acute ST segment elevation myocardial infarction in clinical practice. Heart 2006;92:1484–9.
Chen EW, Canto JG, Parsons LS, et al. Relation between hospital intra-aortic balloon counterpulsation volume and mortality in acute myocardial infarction complicated by cardiogenic shock. Circulation 2003;108:951–7.
Moiseyev VS, Poder P, Andrejevs N, et al. Safety and efficacy of a novel calcium sensitizer, levosimendan, in patients with left ventricular failure due to an acute myocardial infarction. A randomized, placebo-controlled, double-blind study (RUSSLAN). Eur Heart J 2002;23:1422–32.
Fuhrmann JT, Schmeisser A, Schulze MR, et al. Levosimendan is superior to enoximone in refractory cardiogenic shock complicating acute myocardial infarction. Crit Care Med 2008;36:2257–66.
Alexander JH, Reynolds HR, Stebbins AL, et al. Effect of tilarginine acetate in patients with acute myocardial infarction and cardiogenic shock: the TRIUMPH randomized controlled trial. JAMA 2007;297: 1657–66.
Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet 2005;366:1622–32.
Califf RM, Bengtson JR. Cardiogenic shock. N Engl J Med 1994;330: 1724–30.
Brown H, Difrancesco D, Noble S. Cardiac pacemaker oscillation and its modulation by autonomic transmitters. J Exp Biol 1979;81:175–204.
Schipke JD, Buter I, Hohlfeld T, et al. Selective If channel inhibition: an alternative for treating coronary artery disease? Herz 2006;31:55–74.
DiFrancesco D, Tortora P. Direct activation of cardiac pacemaker channels by intracellular cyclic AMP. Nature 1991;351:145–7.
Tardif JC, Ford I, Tendera M, et al. Efficacy of ivabradine, a new selective If inhibitor, compared with atenolol in patients with chronic stable angina. Eur Heart J 2005;26:2529–36.
Ruzyllo W, Tendera M, Ford I, et al. Antianginal efficacy and safety of ivabradine compared with amlodipine in patients with stable effort angina pectoris: a 3-month randomised, double-blind, multicentre, noninferiority trial. Drugs 2007;67:393–405.
Fox K, Garcia MA, Ardissino D, et al. Guidelines on the management of stable angina pectoris: executive summary: the Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. Eur Heart J 2006;27:1341–81.
Heusch G. Pleiotropic action(s) of the bradycardic agent ivabradine: cardiovascular protection beyond heart rate reduction. Br J Pharmacol 2008;155:970–1.
Dedkov EI, Zheng W, Christensen LP, et al. Preservation of coronary reserve by ivabradine-induced reduction in heart rate in infarcted rats is associated with decrease in perivascular collagen. Am J Physiol Heart Circ Physiol 2007;293:H590–8.
DiFrancesco D, Camm JA. Heart rate lowering by specific and selective If current inhibition with ivabradine: a new therapeutic perspective in cardiovascular disease. Drugs 2004;64:1757–65.
Heusch G, Skyschally A, Gres P, et al. Improvement of regional myocardial blood flow and function and reduction of infarct size with ivabradine: protection beyond heart rate reduction. Eur Heart J 2008; 29:2265–75.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Post, F., Münzel, T. Ivabradin – eine neue Therapieoption bei kardiogenem Schock?. Herz 34, 224–229 (2009). https://doi.org/10.1007/s00059-009-3231-8
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00059-009-3231-8