Which Patients with Dilated Cardiomyopathy May Really Benefit from Dual-chamber Pacing?

  • S. Romano
  • M. Pagani
  • P. Montanari
  • ISSC Group


Congestive heart failure is one of the leading causes of morbidity and mortality in our country. In most patients, signs and symptoms of heart failure are the result of an enlarged, poorly contractile left ventricle. Therapy has been directed toward lowering pre-load, reducing after-load, improving contractility and interfering with the detrimental neurohumoral mechanisms activated in heart failure. In 1990, dual-chamber pacing was proposed as a therapeutic alternative for relief of symptoms in patients with dilated cardiomyopathy and severe heart failure who were unresponsive to the optimal medical therapy [1]. Initial reports have demonstrated a subjective abatement in symptoms as well as an objective increase in ejection fraction and cardiac output in patients undergoing dual-chamber pacing with short atrioventricular (AV) intervals [2, 3]. Subsequently these results were partially confirmed [4] or completely contradicted [5, 6], probably because the results were derived from observational studies with small, heterogeneous patient populations. In addition, it is unknown whether all subjects with left ventricular systolic disfunction respond to dual-chamber pacing or whether the beneficial effect is limited to a select subgroup of patients. The hemodynamic mechanisms of this “electrical” therapy may be resumed in three main physiopathologic statements:
  1. 1)

    The reduction of mitral regurgitation. Sequential pacing with short AV interval leads to an activated atrium during the expulsive stage of the left ventricle, thus determining the reduction of the ventriculoatrial gradient, the diastolic mitral regurgitation and the early mitral valve closure [1, 7].

  2. 2)

    A better utilization of the Frank-Starling mechanism obtained by restoring the atrioventricular synchronization [8].

  3. 3)

    A better sequence of the activation-relaxation induced by sequential pacing compared with that realized by the normal conduction pathways [3, 4, 9]. This mechanism may reduce the apical activation delay, that it’s very pronounced in dilated hearts, and, consequently, the wall stress.



Mitral Regurgitation Dilate Cardiomyopathy Sequential Pace Hemodynamic Mechanism Group Congestive Heart Failure 
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  1. 1.
    Hochleitner M, Hortnagl H, Choi-Keung NG, Hortnagl H, Gechnitzer F, Zechmann W (1990) Usefulness of physiologic dual-chamber pacing in drug resistant idiopathic dilated cardiomyopathy. Am J Cardiol 66: 198PubMedCrossRefGoogle Scholar
  2. 2.
    Brecker SJD, Xiao HB, Sparrow J, Gibson DJ (1992) Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy. Lancet 340: 1308PubMedCrossRefGoogle Scholar
  3. 3.
    Auricchio A, Sommariva L, Salo RW et al (1993) Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual chamber pacing with shortened AV delay. PACE 16: 2034PubMedCrossRefGoogle Scholar
  4. 4.
    Nishimura RA, Hayes DL, Holmes Jr DR, Tajik AJ (1995) Mechanism of hemodynamic improvement by dual-chamber pacing for severe left ventricular dysfunction: an acute doppler and catheterization hemodynamic study. J Am Coll Cardiol 25: 281PubMedCrossRefGoogle Scholar
  5. 5.
    Gold MR, Feliciano Z, Gottlieb SS, Fisher ML (1995) Dual-chamber pacing with short atrioventricular delay in congestive heart failure: a randomized study. J Am Coll Cardiol 26: 967PubMedCrossRefGoogle Scholar
  6. 6.
    Linde C, Gadler F, Edner M, Nordlander R, Roseqvist M, Ryden L (1995) Results of atrioventricular synchronous pacing with optimized delay in patients with severe congestive heart failure. Am J Cardiol 75: 919PubMedCrossRefGoogle Scholar
  7. 7.
    Proclemer A, Morocutti G, Di Chiara A, Ziacchi V, Fracalossi C, Feruglio A (1993) Indicazione non comune alla elettrostimolazione cardiaca permanente: stimolazione bicamerale ad intervallo atrio-ventricolare breve nella cardiomiopatia dilatativa. Cardiostimolazione 11, 4: 350Google Scholar
  8. 8.
    Ishikawa T, Kimura K, Nihei T, Usui T, Kashiwaghi M, Ishii M (1991) Relationship between diastolic mitral regurgitation and PQ intervals or cardiac function in patients implanted with DDD pacemakers. PACE 14: 1797PubMedCrossRefGoogle Scholar
  9. 9.
    Rosenqvist M, Isaaz K, Borvinick EH (1991) Relative importance of activation sequence to atrioventricular synchrony in left ventricular function. Am J Cardiol 67: 148PubMedCrossRefGoogle Scholar
  10. 10.
    Capucci A, Villani GQ, Peraldo C et al (1996) Hemodynamic benefit of dual-chamber pacing with optimized A-V delay in congestive heart failure: preliminary results of a randomized study. Eur J Cardiac Pacing Electrophysiol vol 6 n 1 (suppl 5): 143Google Scholar
  11. 11.
    Pagani M, Montanari P, Seveso G et al (1996) Permanent pacing in dilated cardiomyopathy. In: Santini M (ed) Progress in clinical pacing 1996. Futura Media Services Inc, Armonk, NY, pp 53–58Google Scholar
  12. 12.
    Modena MG, Rossi R, Carcagni A, Molinari R, Mattioli G (1996) The importance of different atrioventricular delay for left ventricular filling in sequential pacing: clinical implications. PACE 19 (part I): 1595PubMedCrossRefGoogle Scholar
  13. 13.
    Ohno M, Cheng CP, Little WC (1994) Mechanism of altered patterns of left ventricular filling during the development of congestive heart failure. Circulation 89: 2241PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Italia 1998

Authors and Affiliations

  • S. Romano
    • 1
  • M. Pagani
    • 1
  • P. Montanari
    • 1
  • ISSC Group
    • 1
  1. 1.Divisione di CardiologiaUSSL 34Legnano (MI)Italy

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