Advertisement
ECG education

Alcoholic cardiomyopathy

Vivienne Miller

Figures

Abstract

Jim, aged 67 years, had a stroke one year ago. He was admitted to hospital at the time under the care of a neurologist, but discharged himself against medical advice the next morning and was lost to follow up. Jim presented to a new GP complaining of increased shortness of breath over the past week, which had stopped him walking to the local shops 300 metres away. This was a particularly signi cant problem to Jim as he did not drive.

The GP noted that Jim smelt of alcohol, had mild foot and ankle oedema, a mildly raised jugulovenous pressure and decreased bibasal air entry on examination. Jim was not short of breath at rest, his blood pressure was 157/98 mmHg and his heart rate was 90 beats per minute and regular with occasional ectopics. He had grade 4/5 weakness of the right upper limb and a very mild facial droop that Jim said was from the stroke the year before. Jim was taking no medications. The GP took the opportunity to perform an ECG, which is shown in the Figure.

Key Points

  • The toxic effects of alcohol may cause supraventricular arrhythmias, sudden death, hypertensive heart disease and stroke. Acute, untreated alcohol withdrawal has been associated with takotsubo cardiomyopathy.
  • The prognosis for a patient with alcoholic cardiomyopathy depends largely on whether they can abstain completely from alcohol, how long they have been drinking and whether there are any other contributing causes of heart disease.
  • There is now evidence against the routine implantation of automatic implantable cardiac de brillators for nonischaemic cardiomyopathy.
  • The condition is termed ‘dry beriberi’ if the presentation is predominantly neurological.
  • ‘Wet beriberi’ tends to signi cantly involve the heart.
  • It is important that the affected patient have carefully administered treatment for beriberi. Cardiac complications may be worsened by the administration of thiamine due to consequent vasoconstriction and the inability of the damaged heart to cope with pumping against the increased arterial vascular pressure.

Figures