Heart Failure
Cardiac Resynchronisation Therapy – Evolving Strategies to Enhance Response
Jagmeet P Singh
Associate Professor of Medicine, and Director, Cardiac Resynchronization Therapy Program, Cardiac Arrhythmia Service, Massachusetts General Hospital Heart Center, Harvard Medical School
Abstract
Cardiac resynchronisation therapy (CRT) has gained widespread acceptance as a safe and effective therapeutic strategy for congestive heart failure (CHF) refractory to optimal medical therapy. The use of implantable devices has substantially altered the natural history of systolic heart failure. These devices exert their physiological impact through ventricular remodelling, associated with a reduction in left ventricular (LV) volumes and an improvement in ejection fraction (EF). Several prospective randomised studies have shown that this in turn translates into long-term clinical benefits such as improved quality of life, increased functional capacity and reduction in hospitalisation for heart failure and overall mortality. Despite these obvious benefits, there remain more than a few unresolved concerns, the most important being that up to one-third of patients treated with CRT do not derive any detectable benefit. There are several determinants of successful delivery and response to CRT, including selecting the appropriate patient, patient-specific optimal LV pacing lead placement and appropriate post-implant device care and follow-up. This article highlights the importance of collectively working on all of these aspects of CRT to enhance and maximise response.
Keywords
Cardiac resynchronisation therapy, heart failure, biventricular pacemaker, cardiomyopathy
jsingh@partners.org
Cardiac resynchronisation therapy (CRT) has achieved widespread approval as a safe and efficient therapeutic strategy for medically refractory congestive heart failure (CHF). The standard indications for CRT include patients with advanced heart failure and evidence of systolic dysfunction (ejection fraction [EF] ≤35%), conduction tissue disease (QRS duration ≥120ms) and marked cardiac symptoms (New York Heart Association [NYHA] class III and IV), despite optimal medical therapy.1
CRT and CRT with defibrillator
therapy (CRT-D) involve placement of right atrial (RA), right ventricular (RV) and left ventricular (LV) leads, and exert their physiological impact via synchronising ventricular contraction. This in turn results in improved pumping efficiency, improved LV filling and a reduction in the extent of mitral regurgitation.2,3
These
implantable devices have substantially altered the natural history of patients with heart failure and exert their physiological impact through ventricular remodelling, which occurs over time with a reduction in LV volumes and improvement in EF.
Several
prospective randomised studies have shown that this in turn translates into long-term clinical benefits such as improved quality of life, increased functional capacity, reduction in hospitalisation for heart failure and reduction in overall mortality.1,4
Despite these
palpable benefits, there remain more than a few unresolved concerns, the most important being that up to one-third of patients treated with CRT do not derive any detectable benefit.5
Given the
high prevalence, morbidity and mortality of CHF and the substantial price tag to society both from CHF as a disease and from CRT as a therapy, the importance of maximising the response of all patients
© T O UCH BRIEFINGS 2010
to CRT is evidently immense. There are several determinants of successful delivery and response to device therapy, which include selecting the appropriate patient, patient-specific appropriate LV lead placement and optimal post-implant device care and follow- up. This article highlights the importance of collectively working on all of these fronts to enhance the response to CRT.
Patient Selection
Surface Electrocardiogram and Mechanical Dyssynchrony
After meeting the criteria of compromised LV function and medically refractory heart failure (NYHA >3), patient selection is still driven by the presence of a wide QRS on the surface electrocardiogram (ECG). It is noteworthy that ECG evidence of an intra-ventricular conduction defect, although a surrogate for ventricular dyssynchrony, is not predictive of acute and long-term response to CRT. The imprecision in the ability of surface QRS to predict response is explained by the complexity and multiple levels of electrical and mechanical dyssynchrony in the myopathic heart. This dyssynchrony can exist at numerous levels and can be inter-atrial, ventricular,
atrio-ventricular, intra-ventricular or intramural.6 inter- Most studies have
emphasised the importance of intra-ventricular dyssynchrony as the main contributing factor to progressive heart failure and determination of CRT response.7
Although a QRS width >120ms is an accepted selection criterion, there is evidence that the degree of change in the QRS duration
83
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92