Atrial Fibrillation (AF) and Congestive Heart Failure (CHF) are widespread cardiac disorders that are often concurrent. In fact, AF is found in 15 – 30% of patients with CHF, patients who experience these coexisting disorders also have a worse prognosis than CHF sufferers alone. Additionally, as patients New York Heart Association (NYHA) class increase, so does the prevalence of AF, from <10% in NHYA I to nearly 50% in NHYA IV sufferers. (1)
If there is such a prevalence of CHF and AF sufferers, then it makes sense that a number of patients receiving Cardiac Resynchronisation Therapy (CRT) will also experience AF at some point after implantation of a device. This insinuates patients will continue to be at risk of an increased mortality, a decreased quality of life and further hospitalisations. The number is actually quite significant, in patients who are suitable for CRT, nearly 30% experience AF post implantation. If such a high number are going to experience AF, is there anyway we can help this patient group?
It has been shown by large randomized trials that CRT therapy in itself can benefit these patient’s, the possible reasons for this include reduction in the degree of Mitral regurgitation, improvements in LV systolic function and remodelling of the atria and ventricles including many more. However, there is conflicting data to support this claim.
The CARE-HF study demonstrated that the incidence of AF for patients treated with CRT (16%) was comparable to the patient group receiving optimal pharmacological therapy and no CRT therapy (14%).(2) Another large heart failure trial, COMPANION produced data to show the incidence of pre-implantation AF (17%) was contrasted with a post implantation incidence rate (16%). (3)
Hoppe U.C et al reported from the CARE-HF study that although CRT improved the patients outcome regardless of whether AF developed, CRT did not reduce the incidence of AF from the evidence we have seen. (5) (Figure 1)
A study by Kies. P et al reported that although CRT pacing resulted in significant clinical benefit and significant left atrial and left ventricular remodelling in 74 CRT patients with chronic AF, 93% of patients did not reverted to Sinus Rhythm. (4)
It appears likely that up to 30% of CRT patients are going to experience AF and the associated added complications such as adverse hemodynamics changes, stroke, the loss of atrial contribution and the loss of AV synchrony at some point. Not only that, but persistent and permanent AF patients are unlikely to revert to Sinus Rhythm. (4) Is there a way that technology can help?
The main goal of CRT is to establish Bi-ventricular pacing as near to 100% as possible to establish resynchronisation, this is normally achieved by programming an optimised, shortened AV delay that is less than the patients’ intrinsic PR interval (Figure 2).
Under certain circumstances however, 100% Bi-ventricular pacing is unachievable, one such condition is if a patient is in fast AF. For those CRT patients that have not received AV node ablation, fast, irregular conduction through to the ventricle is a possibility. To manage such an issue one important function of CRT pacing is the ability to “Trigger” on intrinsic complexes.
The triggering function enables resynchronisation to occur by pacing the left ventricle (via the coronary sinus) in response to an intrinsic complex sensed by the right ventricular lead. Additionally, in latest model devices, the triggering function can be employed to resynchronise on right ventricular Ectopy for those patients suffering from extra systoles. One possible scenario would be patients experiencing Ventricular Bigeminy where resynchronisation can be cut to 50%. The function can also be programmed to actually continue to trigger above the upper tracking rate to again produce 100% resynchronisation under all circumstances. (Figure 3).
Often, AF goes undetected. Some data sources quote figures as high as 75% of atrial arrhythmias are asymptomatic. It is therefore advantageous for CRT devices to have advanced diagnostics for the identification and recording of AF episodes.
Ideally, the following data should be available:
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Atrial Burden (% per day)
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Mean ventricular rate during episodes
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Max. ventricular rate during episodes
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No of mode switching episodes per day
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Holter recording capability
Today, the majority of CRT devices available have many of the above mentioned capabilities. Whilst this proves to be a good diagnostic aid there are limitations to there use. Generally, patients with CRT devices are followed up on a 3 or 6 monthly basis where their devices will be interrogated and the data is retrieved.
However, what happens between follow up’s? How can we assess a patients’ atrial rhythm unless they report it. The answer is Home Monitoring.
With the capability of early detection of AF and transmission of data the clinician can be informed of all the above stated information on a daily basis, or if they wish, as they happen on an event basis.
High definition IEGM’s of an atrial arrhythmia will be transmitted after detection containing marker channel, far-field, atrial, RV and LV electrogram for CRT devices. (Figure 4)
The transmitted data will also contain information regarding episode type, initial detection, termination and episode duration. (Figure 5)
| General | |
| Episode Number | 6 |
| Episode Type | Atr. Monitoring |
| Detection | 31-Aug-2006 17:14:39 |
| Termination | 31-Aug-2006 17:53:05 |
| Duration | 38min 26sec |
Figure 5: Atrial Monitoring Episode Details
From the data available it seems inevitable that at some point up to 30% of patients receiving CRT therapy will encounter Atrial Fibrillation, even for those patients accepting the relevant rhythm and rate control.
If technology can help to deliver resynchronisation therapy under the majority of circumstances using the triggering functionality then this must be a prerequisite.
If technology can help in identifying and informing the clinician of an atrial arrhythmia using a prompt, automatic method and provides all the necessary data, this is obviously going to be beneficial in tailoring and optimising medication, possibly using internal cardio-version through the device to terminate an episode or planning patient care.
References:
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Maisel W.H, Stevenson L.W – Atrial Fibrillation in Heart Failure. Epidemiology, pathophysiology and rationale for therapy. Am J Cardio 2003;91:2D-8D
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John G.F. Cleland, M.D., Jean-Claude Daubert, M.D., Erland Erdmann, M.D., Nick Freemantle, Ph.D., Daniel Gras, M.D., Lukas Kappenberger, M.D., and Luigi Tavazzi, M.D., for the Cardiac Resynchronization — Heart Failure (CARE-HF) Study Investigators. - The Effect of Cardiac Resynchronization on Morbidity and Mortality in Heart Failure. N Engl J Med 2005;352.
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Michael R. Bristow, M.D., Leslie A. Saxon, M.D., John Boehmer, M.D.,Steven Krueger, M.D., David A. Kass, M.D., Teresa De Marco, M.D.,Peter Carson, M.D., Lorenzo DiCarlo, M.D., David DeMets, Ph.D.,Bill G. White, Ph.D., Dale W. DeVries, B.A., and Arthur M. Feldman, M.D., Ph.D.,for the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) InvestigatorsKies . – Cardiac Resynchronization Therapy with or without an Implantable Defibrillator in Advanced Chronic Heart Failure. N Engl J Med 2004;350:2140-50.
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P et al. – Cardiac Resynchronisation Therapy in chronic atrial fibrillation: impact on left atrial size and reversal to sinus rhythm. Heart 2006;92:490-494
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Uta C.Hoppe, Jaime M. Casares, Hans Eiskjaer, Arne Hagemann, John G.F. Cleland, Nick Freemantle and Erland Erdmann. – Effect of Cardiac Resynchronisation on the Incidence of Atrial Fibrillation in Patients with Severe Heart Failure. Circulation 2006;114:18-25

