Case Report Decompensation of Chronic Heart Failure Associated With Pregabalin in Patients With Neuropathic Pain

Pregabalin (Lyrica) is a new anticonvulsant used for peripheral neuropathic pain. We report 3 patients with known chronic heart failure and left ventricular systolic dysfunction who had an exacerbation of heart failure after commencing on Pregabalin for neuropathic pain. Patient 1 was a 69-year-old man with ischemic cardiomyopathy and a documented left ventricular ejection fraction of 40%. His heart failure status had been stable for 6 months and his standard medication prescription was frusemide 40 mg, bisoprolol 5 mg, glyceryl trinitrate patch 10 mg, and eplerenone 25 mg. He was previously intolerant of ACEI and ARB therapy. He was also taking atorvastatin, lansoprazole, insulin, diltiazem, and nicorandil, the last 2 for the management of refractory angina. He was started on Pregabalin for neuropathic pain related to diabetes. Over the next 4 weeks, he became increasingly short of breath and noticed a weight gain. On examination, he had raised jugular venous pressure, pitting ankle edema, and clear lung fields. His Btype natriuretic peptide (BNP) level increased to 611 pg/ mL from a baseline of 293 pg/mL. An increase in oral diuretic was prescribed and Pregabalin was discontinued. However, 3 days later, he continued to be dyspneic and had developed paroxysmal nocturnal dyspnea. He was given a stat dose of intravenous frusemide 60 mg. He had a good symptomatic improvement and a 5.8-kg weight loss over the ensuing days and remains well. Patient 2 is a 59-year-old man with nonischemic dilated cardiomyopathy with severe left ventricular systolic dysfunction. His heart failure status had been stable for 1 year and his standard daily medication included bumetanide 2 mg, perindopril 4 mg, metoprolol 25 mg, and digoxin 0.125 mg. He was also taking warfarin, pravastatin, insulin, and metformin. He was started on Pregabalin for a peripheral neuropathy related to diabetes. Over the next 2 months, he became increasingly dyspneic and noticed weight gain. On examination, there was confirmatory evidence of heart failure with elevated jugular venous pressure, ankle edema, and bibasal lung crackles. There was no significant change in BNP (266 pg/mL from 247 pg/ mL at baseline). Pregabalin was discontinued with no improvement. Oral diuretics were increased with improvement in symptoms, a 3-kg weight loss, and resolution of all clinical signs of heart failure. Patient 3 was a 72-year-old man with a nonischemic cardiomyopathy and an ejection fraction of 38%. His heart failure status had been stable for 4 months and his standard medication included losartan 50 mg, carvedilol 12.5 mg BD, digoxin 0.125 mg, nitrate patch 10 mg, frusemide 40 mg, and warfarin. He was started on Pregabalin for paraesthesia in his feet. Over the next 4 weeks, his clinical status deteriorated. He developed symptoms of biventricular heart failure with shortness of breath, fatigue, ankle edema, orthopnea, and paroxysmal nocturnal dyspneadall associated with a significant weight gain. He also complained of ataxia and dry mouth. On examination, his jugular venous pressure was raised, ascites were present, and lung crackles were audible. His BNP rose to 2110 pg/mL from a baseline of 461 pg/mL. Pregabalin was discontinued and he was treated with intravenous diuretics and an increase in oral diuretics. He had a good response with improvement in symptoms, a weight loss of 5.8 kg, and a fall in BNP to 561 pg/mL over the next 2 weeks.