This month’s ECG was recorded from a 42-year old male who was complaining of gradually increasing exertional dyspnoea over several months. He was also experiencing breathlessness when lying flat. He had not had any chest pain. Physical examination revealed swollen ankles and feet and a raised jugular venous pressure. Blood pressure was135/90mmHg. There was an apical pansystolic murmur.
Does the ECG provide any clues as to the probable clinical diagnosis?
Let’s begin with a systematic description of the ECG, then go on to discuss what it might all mean.
- There is sinus rhythm with a heart rate of about 92 bpm.
- The QRS axis is about 0 degrees, which is within normal limits.
- All the QRS complexes in the limb leads are of low amplitude: none has a total amplitude of more than 0.5mV.
- In the chest leads the QRS amplitudes do not meet the Sokolow-Lyon criterion for LVH, ie S(V1) + R(V5/V6) greater or equal to 3.5mV, but the S waves in V2 and V3 are quite deep. There is also a poor R wave progression in the chest leads with a late transition (V5) to positivity.
- There is widespread, non-specific T wave flattening in the limb leads, and ST depression with low amplitude T waves in V5 and V6.The broad, slightly notched P waves in lead II and biphasic P wave with dominant terminal negative deflection suggest left atrial abnormality.
Let’s consider some of the possible causes of some of these abnormalities:
Highish resting heart rate: heart failure, fever, anaemia, pulmonary embolism, anxiety.
Left atrial abnormality: hypertension, LV systolic dysfunction, mitral valve disease
Widespread ST/T wave abnormalities: myocardial ischaemia, old MI, hypothyroidism, cardiac amyloidosis and dilated cardiomyopathy.
Poor R wave progression: old anterior MI, cardiac amyloidosis and dilated cardiomyopathy.
Now, let’s bring the clinical details of the case into the discussion. The history is not suggestive of coronary artery disease, so old MI or ongoing myocardial ischaemia in this case are unlikely. The blood pressure is normal, ruling out hypertensive heart disease. Although the pansystolic murmur is most likely due to mitral regurgitation, this is not necessarily caused by primary mitral valve disease: it may be secondary to left ventricular systolic dysfunction. Cardiac amyloidosis is a possible cause of several of the abnormalities listed, as well as the clinical features, but such deep S waves in V2 and V3 are not typical of the condition.
As Max pointed out, the combination of low-amplitude QRS complexes in the limb leads (all complexes not more than 0.8mV); dominant S wave in V4; and S(V1/V2) + R(V5/V6) at least 3.5mV is known as Goldberger’s triad, and this is reported to be highly suggestive of a dilated cardiomyopathy.
First described in 1982, Goldberger’s triad is generally reported to have high specificity but low sensitivity(1). This means that most patients with these features will have a dilated cardiomyopathy but the absence of the triad certainly does not exclude the diagnosis.
As we have seen, all the abnormal features of this ECG individually have several possible explanations. However, the total combination of features, whilst not absolutely diagnostic of any condition, is, especially when considered in the presenting clinical context, highly suggestive of a dilated cardiomyopathy. Well done to all those who worked this out. In this case dilated cardiomyopathy was suspected and subsequently confirmed by echocardiography.
- Goldberger A L. A specific ECG triad associated with congestive heart failure. Pacing Clin Electrophysiol 1982;5:593-9.