What electrocardiographic signs are useful in a heart failure patient?

The electrocardiogram (ECG) is rarely normal in heart failure. Abnormalities can point to electrolyte disturbances, drug effects, or specific cardiac changes useful in the diagnosis and management of the underlying disease. Specific ECG changes commonly found in heart failure include a low QRS voltage (<0.8 mV) in the peripheral leads, a high QRS voltage in the precordial leads, and insufficient R wave progression from VI through V4. Their causes include increased extracellular fluid, myocardial fibrosis, increased myocardial mass, and frequent concomitant right ventricular dilatation. Other changes are indicative of electrolyte imbalance (Table I) or drug toxicity (Table II). Diagnosis A Q wave suggests earlier myocardial infarction, to be confirmed from the history and echocardiographic evidence of regional kinetic changes. Abnormal atrioventricular (AV) conduction in dilated cardiomyopathy requires the elimination of: Hemochromatosis (in which AV block is common), by measuring the serum ferritin and transferrin. X-linked emerin deficiency (Emery-Dreifuss muscular dystrophy with cardiac involvement). Idiopathic AV block due to a deficiency of the genes encoding the lamin A and C nuclear membrane proteins. Desmin storage disease. The ECG is particularly useful in diagnosing arrhythmia, a precipitant of heart failure, in particular if an earlier ECG is available for comparison. It can help to identify emergent tachyarrhythmia, pacemaker malfunction, reinfarction, or pulmonary embolism. Prognosis Recent evidence indicates that a long QRS is an independent predictor of poor prognosis. This feature becomes more common in advanced HF and causes desynchronization of ventricular mechanical activity, ventricular asynergy, and changes in workload and wall stress culminating in further deterioration of pump function. A long QRS is caused by Further reading Arbustini E, Morbini P, Pilotto A, Govazzi A, Tavazzi L Familial dilated cardiomyopathy: from clinical presentation to molecular genetics. Eur Heart J. 2000;21:1825-1832. Shamim W, Francis DP, Yousufuddin M, et ai. Intraventricular conduction delay: a prognostic marker in chronic heart failure. Int J Cardiol. 1999;70:171-178. loss of integrity of the myocardial collagen matrix and architectural changes in the cell structure responsible for conducting the electrical impulse. The Royal Brompton Hospital Heart Failure Unit found a graded increase in mortality with the QRS, but no definite threshold. Mortality at 3 years was 20% for patients with a QRS duration <120 ms, 36% for those with a QRS between 120 and 160 ms, and 58% for a QRS >160 ms.

Wilensky RL, Yudelman P, Cohen Al, et al. Serial electrocardiographic changes in idiopathic dilated cardiomyopathy confirmed at necropsy. Am J Cardiol. 1988;62:276-283.

Xiao HB, Roy C, Fujimoto S, Gibson DG. Natural history of abnormal conduction and its relation to prognosis in patients with dilated cardiomyopathy. Int J Cardiol. 1996;53:163-170.


instrumental finding; ECG; diagnosis; drug-induced ECG change; QRS; prognosis

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