lisinopril and Bradycardia

A case of severe bradycardia and hypotension associated with concomitant tizanidine and lisinopril therapy is reported.. An 85-year-old man with a chief complaint of profound weakness was admitted to the hospital with a blood pressure reading of 60/32 mm Hg and a heart rate of 37 beats/min. His medical history included type 2 diabetes mellitus, congestive heart failure, gastroesophageal reflux disease, chronic obstructive pulmonary disease, osteoarthritis, restless leg syndrome, benign prostatic hyperplasia, generalized anxiety disorder with depression, and severe chronic back pain for which he was receiving treatment at a pain clinic. Two days before hospital admission, he had been seen at the pain clinic and started on ti-zanidine. Additional medications included acetaminophen, chlorpromazine, citalopram, finasteride, lidocaine patch, lisinopril, metformin, pramipexole, omeprazole, simvastatin, theophylline, diclofenac topical gel, hydrocodone-acetaminophen, and ondansetron. After taking three doses of the newly prescribed tizanidine, he developed severe hypotension and bradycardia. Notable laboratory test values included a serum creatinine concentration of 1.90 mg/dL, a blood urea nitrogen concentration of 21 mg/dL, a serum potassium concentration of 5.5 meq/L, and a serum sodium concentration of 128 meq/L. Upon admission, tizanidine, lisinopril, theophylline, omeprazole, and simvastatin were withheld, and i.v. fluids were administered. The patient's vital signs began to gradually improve. Within 24 hours, the patient's blood pressure and heart rate had improved, as had the previously abnormal laboratory test values. Tizanidine was discontinued, and all of his other preadmission medications were restarted at discharge.. The addition of tizanidine in a patient receiving long-term treatment with lisinopril was associated with severe hypotension and bradycardia.

Topics: Adrenergic alpha-2 Receptor Agonists; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitors; Bradycardia; Clonidine; Drug Interactions; Humans; Hypotension; Lisinopril; Male; Severity of Illness Index

There is a small body of literature on the interactions between lithium and angiotensin-converting enzyme inhibitors (ACEIs), but little data documenting the differences between these agents in their impact on serum lithium levels. We present the case of a 46-year-old male who sustained a five-fold increase in his serum lithium level after switching from fosinopril to lisinopril, with a peak serum lithium level of 3.4 meq/l. There was also an increase in serum creatinine from 1.1 on fosinopril to 1.4 after switching to lisinopril. The patient was hospitalized, and intravenously hydrated with 0.5 normal saline, with a reduction of the serum lithium level to 0.7 meq/l by 72 h after admission. The hospital course was marked by two episodes of bradycardia, but was otherwise uneventful, and the patient was discharged without any neurological sequelae. This case demonstrates that ACEIs may have differential effects on renal function, and the potential for significant alterations in lithium clearance that may not be clinically evident for several weeks. Lithium-treated patients who have a change in ACEI, especially those who are older or have below average renal function, must have diligent monitoring for the first 4-6 weeks after switching to detect potentially serious changes in serum lithium levels.

Topics: Angiotensin-Converting Enzyme Inhibitors; Antimanic Agents; Bipolar Disorder; Bradycardia; Fosinopril; Heart Rate; Humans; Lisinopril; Lithium; Male; Middle Aged; Psychotic Disorders

To determine whether the cardiovascular effects of chronic treatment with lisinopril are age related, we compared baroreflex sensitivity and pressor responsiveness in 4-mo- and 21-mo-old male rats that had been given oral lisinopril daily for 4 wk. Reflex bradycardia elicited by elevating blood pressure with phenylephrine was stronger in 4-mo-old rats than it was in 21-mo-old rats and also stronger in lisinopril-treated rats than it was in untreated rats of the same age. Pressor responses to angiotensin or norepinephrine were recorded after combined cholinergic and beta-adrenergic blockade and then analyzed not only as absolute but also as percent increases in mean pressure. Although pressor responses seemed to be slightly reduced by lisinopril when expressed as absolute increases in mean pressure, corresponding percent increases were always larger in 4-mo-old rats than they were in 21-mo-old rats and were clearly enhanced by lisinopril more in younger rats. The stronger overall enhancement of pressor responsiveness and reflex bradycardia in younger rats suggests that the cardiovascular effects of lisinopril diminish with advancing age.

Topics: Aging; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Baroreflex; Blood Pressure; Body Weight; Bradycardia; Consciousness; Drinking; Lisinopril; Male; Norepinephrine; Phenylephrine; Rats; Rats, Sprague-Dawley; Sympathomimetics; Vasoconstrictor Agents

To determine how short-term treatment with an angiotensin-converting enzyme (ACE) inhibitor affects drug-induced reflex bradycardia at different ages in conscious rats, we compared the magnitude of drug-induced reflex bradycardia before and after injecting bolus intravenous doses of lisinopril, 1 mg/100 g, in male Sprague-Dawley rats aged 4 (young) or 19 (old) months. Anesthetic artifacts were avoided by recording all drug-induced cardiovascular responses from femoral arterial cannulas implanted 1 week earlier. For eliciting reflex bradycardia, blood pressure was increased by graded intravenous infusion of angiotensin or phenylephrine. Impairment of reflex bradycardia in old rats occurred only during pressor responses to angiotensin but not when blood pressure was equally increased with phenylephrine. Subsequent administration of lisinopril affected neither pressor and reflex bradycardic responses to phenylephrine nor pressor responses to angiotensin. However, contrary to the baroreflex enhancement described previously by others, the reflex bradycardia induced by angiotensin was reduced by lisinopril treatment but only in old and not in young rats. Thus our results indicate that whereas angiotensin-induced reflex bradycardia was already impaired in old rats before lisinopril was given, it was reduced further after short-term lisinopril treatment.

Topics: Aging; Angiotensin II; Animals; Antihypertensive Agents; Bradycardia; Lisinopril; Male; Phenylephrine; Rats; Rats, Sprague-Dawley