‘Ally McBeal heart?’– Drug induced cardiomyopathy in a young woman

Abstract

Dilated cardiomyopathy is relatively uncommon in women of child bearing age. When it does occur, it is most commonly as a sequela of pregnancy, viral myocarditis or excessive alcohol intake. However, individuals in this age group are also amongst the most likely to consume other recreational drugs. We present the case of a young woman whose long-term amphetamine habit resulted in severe impairment of left ventricular function. Mrs X was a 30-year-old mother of two children who was referred from her general practitioner with a four month history of ankle swelling, together with increased abdominal distension and breathlessness over the previous 3 days. Past medical history included an episode of pneumonia 7 years earlier, mild asthma (never requiring hospitalization), and regular panic attacks. Symptomatic enquiry revealed that she had been experiencing a sensation of panic most nights in the last 2 months when she found she had been waking from sleep breathless. These symptoms were eased by sitting forward and she was adamant that they were quite distinct from the symptoms she would typically experience during a traditional panic attack. She had a 20-pack year smoking history but professed only very occasional alcohol consumption. She did, however, admit to having taken amphetamines on a daily basis for the last 4 years. Her motivation for this habit was a desire to stay thin – and indeed she had initially begun to abuse the drug at a time when she was trying to give up smoking and subsequently gained weight. She purchased the drug illegally, consuming approximately one tablespoon per day. She estimated that she would utilize 15 g of amphetamine per month at a price of roughly 10 pounds sterling per gram. On examination she was thin with a BMI of 19 kg m−2. Respiratory rate was increased and saturations on air were low at 92%. A sinus tachycardia of 120 bpm was present. Blood pressure was 125/90. The apex beat was displaced and the jugular venous pressure was elevated 8 cm. Auscultation revealed a gallop rhythm and a left basal effusion. There was hepatomegaly, mild ascites and peripheral pitting oedema. ECG demonstrated biphasic P waves in keeping with left atrial enlargement, a left ventricular hypertrophy and strain pattern, and Q waves in the anteroseptal leads. CXR showed cardiomegaly, interstitial pulmonary oedema and a small left pleural effusion. Full blood count with MCV of 84, urea and electrolytes normal. Liver function tests were marginally abnormal with bilirubin 22 mmol l−1[4–20], alkaline phosphatase 83 (30–100 IU l−1), ALT 70 (5–31 IU l−1) and albumin 28 g l−1[35–50]. A diagnosis of amphetamine-related cardiomyopathy was made and she was commenced on a diuretic, warfarin and an ACE inhibitor. Subsequent echocardiography confirmed a significantly dilated left ventricle (systolic and diastolic dimensions 6.1/6.9 cm, respectively; normal upper limits 3.5/5.7 cm). There was global impairment of contraction with an estimated ejection fraction of 26%. Left atrium was 4.1 cm (1.9–4.0 cm). During a 7 day stay she made a dramatic improvement on therapy with both clinical and radiographic resolution of her pulmonary oedema. At that stage her left ventricular dimensions had improved to 5.7/6.8 cm and left atrium to 2.9 cm with an ejection fraction of 33%. She expressed a firm wish to stay off amphetamines for good and coped well with minor withdrawal symptoms, requiring only occasional small doses of diazepam.