The impact of changing oedematous states on the QRS duration: implications for cardiac resynchronization therapy and implantable cardioverter/defibrillator implantation.
Increased ECG QRS duration (QRSd) in patients with dilated cardiomyopathy (DCM) or heart failure (HF) is a well-known phenomenon. The QRSd is not a static ECG measurement but shows fluctuations, and its recent inclusion among the parameters used in referring patients for implantable cardioverter/defibrillators (ICDs) or cardiac resynchronization therapy (CRT) has led to renewed interest in its natural course and its determinants. Although clinical deterioration has been traditionally associated with increasing QRSd, its changes often are left unexplained. Also, the recent description of a decrease in QRSd, well correlated with attenuated amplitude of QRS complexes in patients with peripheral oedema (PERO) in the context of a variety of illnesses, has added complexity to the matter. This communication aims at calling attention to the importance of a few clinical and ECG parameters when documenting changes in the QRSd in serial ECGs. Thus, presence or absence of PERO and change in the patients' weight, along with alteration in the amplitude of QRS complexes and shifts to/from incomplete/complete bundle branch block patterns, all should be considered when assessing changes in QRSd for meaningful follow-up of patients with DCM or CHF, or referral for ICD or CRT. Evaluation of the QRSd as a selection parameter for referring patients suitable for device implantation should continue along with the employment of mechanical analysis of ventricular dyssynchrony. Although reference here is made to QRSd particularly in connection with DCM and HF, the above apply to other oedematous states (i.e. patients with chronic renal failure, or those undergoing haemodialysis).
Madias
John E
JE
D002304:Cardiac Pacing, Artificial; D017147:Defibrillators, Implantable; D004487:Edema / Q000503:physiopathology*; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D006801:Humans