Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to dissemintate knowledge & skills of Acute Cardiovascular Care
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Mr Javier Balaguer Recena
Dr. Sara Moreno Reviriego
Experimental, electrocardiographic, echocardiographic and electrophysiologic studies show that patients with RBBB may have an additional delay in left ventricular activation because of the pathological substrate of the associated heart disease. Therefore, they could benefit from CRT.
Despite many advances in its treatment over the past decades, heart failure remains a problem of high prevalence, morbidity and mortality worldwide (1). Since its appearance in the 80's (2) and its clinical application in 90 years(3), cardiac resynchronisation therapy (CRT) has become an essential therapeutic tool in the treatment of heart failure patient today. Its aim is to restore electrical synchrony, commonly impaired in these patients, and thus the cardiac function. Its results have been excellent. According to a recent meta-analysis of McAlister et al (4), CRT provides significant improvement in functional class, left ventricular ejection fraction (LVEF), the distance walked at 6 minutes, quality of life and a reduction in hospitalisation for heart failure and overall mortality, mainly due to a reduction in mortality from progressive heart failure. Moreover, these benefits occur in a stable and progressive manner. However, there are still 20-30% of patients who do not respond to therapy (5). Therefore, it is essential to make a careful selection of candidates. Several randomised trials have suppported its recommendation in patients in sinus rhythm, NYHA functional class III-IV, left ventricular ejection fraction (LVEF ) ≤ 35% and QRS ≥ 120 ms (1,6,7,8) . Subsequent studies have recommended the use of CRT in patients ins sinus rhythm, NYHA functional class II, LVEF ≤ 30% and QRS ≥ 130 ms (9) (figure 1). While these indications are clear (Recommendation Class I, Level A), there is less consensus about various sub-populations underrepresented in clinical trials.
Figure 1. Recommendations for the use of CRT where the evidence is strong from the 2012 guidelines for the diagnosis and treatment of acute and chronic heart failure (9).
Figure legend:Class I recommendation. CRT-P: Cardiac resynchronization device. CRT-D device for cardiac resynchronization and defibrillation. HF: heart failure. SR: Sinus rhythm. LBBB: left bundle branch block. LVEF: Left ventricular ejection fraction. *:For patients who are expected to survive with good functional status for > 1 year. **: Despite optimal pharmacological therapy.
Activation of the interventricular septum and right ventricle in left bundle branch block (LBBB) occurs at an early stage through the right branch. As a result, the left ventricle is activated from the septoapical to the posterolateral region and from the endocardium to the epicardium (figure 2) in a slow manner because of the absence of conduction tissue (cell to cell conduction). Together, these particularities lead to uncoordinated and ineffective myocardial contraction. On the one hand, early septal contraction does not increase pressure in the left ventricular cavity due to the absence of opposition from the posterolateral wall. Subsequently, lateral contraction occurs during late systole so that the intraventricular maximum pressure is reached at the beginning of diastole. The result is a reduction in stroke volume that, together with mitral regurgitation secondary to late activation of papillary muscle, causes a significant decrease in cardiac output. The purpose of cardiac resynchronisation therapy in these patients is to eliminate this delay in activation by simultaneous stimulation of the septum and left ventricular wall, and thus, allowing for more efficient mechanical contraction. Figure 2. Pathophysiology of intraventricular conduction disorders. On the left side, ventricular myocardial activation vector in patients with LBBB. On the right, ventricular myocardial activation vector in patients with RBBB.
Conclusion: With respect to the pathophysiolgic basis of cardiac resinchronisation therapy in patients with advanced heart failure and right bundle branch block, we should consider that:
(1) ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Dickstein K, Cohen-Solal A, Filippatos G et al Eur Heart J 2008;29:2388–442. (2) An even more physiological pacing. Changing the sequence of activation. En: Steinbach K, Glogar D, Laszkovics A, editores. De Teresa E, Chamorro JL, Pulpón LA. Cardiac Pacing. Proceedings of the VIIth World Symposium on Cardiac Pacing. Darmstadt, Alemania: Steinkoopff Verlag, 1983; 395-400. (3) Four chamber pacing in dilated cardiomyopahy. Cazeau S, Ritter P, Bakdach S. PACE 1994; 17: 1974-1979. (4) Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction. McAlister FA, Ezekowitz J, Hooton N, et al. A systematic review. JAMA. 2007;297:2502-2514. (5) Registro Español de Desfibrilador Automático Implantable. V Informe Oficial del Grupo de Trabajo de Desfibrilador Automático Implantable de la Sociedad Española de Cardiología (2008) Peinado R, Torrecilla EG, Ormaetxe J, et al. Rev Esp Cardiol 2009; 62: 1435-1449. (6) Focused update of the European Society of Cardiology guidelines on device therapy in heart failure. An update of the 2008 European Society of Cardiology guidelines for the diagnosis and treatment of acute and chronic heart failure and the 2007 European Society of Cardiology guidelines for cardiac and resynchronization therapy. Dickstein K, Vardas PE, Auricchio A, et al. 2010. Eur Heart J 2010; 31: 2677-2687. (7) Guidelines for cardiac pacing and cardiac resynchronization therapy. Vardas PE, Auricchio A, Blanc JJ, et al. The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association. Eur Heart J 2007; 28: 2256–2295. (8) ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities: A Report of the American College Of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline update for implantation of cardiac pacemakers and antiarrhythmia devices). Epstein AE, Di Marco JP, Ellenbogen KA, et al. J Am Coll Cardiol 2008; 51: e1–6. (9) ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012 McMurray JJV, Adamopoulos S, Anker SD, et al. The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur Heart J 2012; 33: 1787-1847. (10) Significance of QRS complex duration in patients with heart failure. Kashani A, Barold SS. J Am Coll Cardiol 2005 20; 46: 2183-92. (11) Right and left ventricular activation sequence in patients with heart failure and right bundle branch block: a detailed analysis using three-dimensional non-fluoroscopic electro- anatomic mapping system. Fantoni C, Kawabata M, Massaro R, et al. J Cardiovasc Electrophysiol 2005; 16: 112–119. (12) Left bundle branch block masquerading as right bundle branch block. Richman JL, Wolff L. Am Heart J. 1954; 47: 383–393. (13) Right bundle branch block and impaired left ventricular function as evidence of a left ventricular conduction delay. Takamatsu H, Tada H, Okaniwa H, et al. Circ J. 2008; 72: 120-6. (14) Endocardial activation of left bundle branch block. Vassallo JA, Cassidy DM, Marchlinski FE, et al. Circulation 1984; 69: 914–923. (15) Diminished left ventricular dyssynchrony and impact of resynchronization in failing hearts with right versus left bundle branch block. Byrne MJ, Helm RH, Daya S, et al. J Am Coll Cardiol 2007; 50:1484–90. 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Sara Moreno Reviriego, Javier Balaguer Recena Arrhythmia and Electrophysiology Unit, Cardiology Service, University Hospital of Guadalajara, Guadalajara (Spain) Authors' disclosures: None declared.