Strategies for the use of cardioselective beta blockers in cv continuum
β-Adrenoreceptor blockers
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blockers Severe hy'pertrlglyceridaemia and acute pancreatitis It is well known that severe hypertriglyceridaemia precipitates acute pancreatitis. A 64-year-old-man with a 20 year history of peripheral and coronary artery disease, was admitted with prolonged angina at rest He was on metoprolol (I OOmg bid) but had a sinus tachycardia of I 30 beats/min. IV propranolol (Smg) relieved his angina and reduced the heart rate. Atenolol (100mg/day) was initiated. Laboratory tests on the 5th hospital day indicated hypertriglyceridaemia (56.0mmol/L; normal less than I. 7mmol/U and elevated serum cholesterol (18.0mmoI/L; normal less than 7 ,OmmoJ/ U. Ultracentrifugation confirmed hyperIipoproteinaemia. On metoprolol, serum did not exceed \ 3mmol/l. The patient developed cel'llral abdominal and back pain well as hypotension on the 8th hospital day. A serum amylase of 4460U/L confirmed pancreatitis. Treatment was conservative consisting of and IV fluids. As the patient's condition improved, he was introduced Lo a low fat diet (20g fatl and serum triglyceride and cholesterol concentrations within 2 weeks were 3. 7mmol/L and 7.0mmol/L respecllvely. blockade was continued for recurrent angina and tachycardia, The patient was subsequently given atenolol ( I OOmgl day fOT 2 week) and metoprolol (I OOmg bid for 2 weeks), Triglyceride clearance measured by IV administration of a 10% lipid solution (I mg/kg)showed that with the elimination half-life of triglyceride was increased from a normal 16.5 min to 24.5 and 27 with metoprolol and atenolol respectively. The rise in the serum concentration of triglyceride is attributed to inhibition of lipoprotein lipase by blockers. Lipoprotein lipase removes tr(glycerides from both chylomicrons and low density lipoproteins. It is also known that catecholamine secretion during stress increases blood free fatty acids resulting in increased hepatic production of triglycerides. In this patient. the stress of angina together with impaired triglyceride clearance to such an extent thaI pancreatitis was precipitated. Physicians should be alert to this dangerous complication when prescribing for acute coronary insum;,;iency. Durrington, P N. and Cairns, S..'\ .. British Med,cal Joumal284, 1016 (3 Apr 1982) 0157-7271/82/0528-0003/0$01,0010 © ADIS Press Reactions 28 May 1982 3
Transcript of β-Adrenoreceptor blockers
~-Adrenoreceptor blockers
Severe hy'pertrlglyceridaemia and acute pancreatitis It is well known that severe hypertriglyceridaemia precipitates acute pancreatitis. A 64-year-old-man with a 20 year history of peripheral and coronary artery disease, was admitted with prolonged angina at rest He was on metoprolol (I OOmg bid) but had a sinus tachycardia of I 30 beats/min. IV propranolol (Smg) relieved his angina and reduced the heart rate. Atenolol (100mg/day) was initiated. Laboratory tests on the 5th hospital day indicated hypertriglyceridaemia (56.0mmol/L; normal less than I. 7mmol/U and elevated serum cholesterol (18.0mmoI/L; normal less than 7 ,OmmoJ/ U. Ultracentrifugation confirmed hyperIipoproteinaemia. On metoprolol, serum triglyceride~ did not exceed \ 3mmol/l. The patient developed cel'llral abdominal and back pain a~ well as hypotension on the 8th hospital day. A serum amylase of 4460U/L confirmed acul~ pancreatitis. Treatment was conservative consisting of nasoga~tric a~piration and I V fluids. As the patient's condition improved, he was introduced Lo a low fat diet (20g fatl and serum triglyceride and cholesterol concentrations within 2 weeks were 3. 7mmol/L and 7.0mmol/L respecllvely. ~blockade was continued for recurrent angina and tachycardia, The patient was subsequently given atenolol ( I OOmgl day fOT
2 week) and metoprolol (I OOmg bid for 2 weeks), Triglyceride clearance measured by IV administration of a 10% lipid solution (I mg/kg)showed that with ~-blockade the elimination half-life of triglyceride was increased from a normal 16.5 min to 24.5 and 27 with metoprolol and atenolol respectively. The rise in the serum concentration of triglyceride is attributed to inhibition of lipoprotein lipase by ~blockers. Lipoprotein lipase removes tr(glycerides from both chylomicrons and low density lipoproteins. It is also known that catecholamine secretion during stress increases blood free fatty acids resulting in increased hepatic production of triglycerides. In this patient. the stress of angina together with ~-blockers, impaired triglyceride clearance to such an extent thaI pancreatitis was precipitated. Physicians should be alert to this dangerous complication when prescribing ~-blockers for acute coronary insum;,;iency.
Durrington, P N. and Cairns, S . .'\ .. British Med,cal Joumal284, 1016 (3 Apr 1982)
0157-7271/82/0528-0003/0$01,0010 © ADIS Press Reactions 28 May 1982 3
