Nimodipine-induced junctional bradycardia in an elderly patient with subarachnoid hemorrhage.

Abstract

Subarachnoid hemorrhage is a devastating form of stroke with often detrimental outcomes for patients. Here we describe a patient with subarachnoid hemorrhage treated with nimodipine, which resulted in marked bradycardia with junctional atrioventricular heart block. Nimodipine is metabolized predominantly by the cytochrome P450 3A subfamily, and its use is often associated with adverse events, such as hypotension and bradycardia, which can be exacerbated by advanced age. Our patient had the CYP3A5*3/*3 genotype, possibly predisposing her to poor metabolism of this drug. Our case report demonstrates the potential for pharmacogenomics in patients with subarachnoid hemorrhage to help predict their response to nimodipine, minimize adverse drug reactions, and potentially individualize dosing to improve future clinical outcomes.

• Authors: Courtney L James, Marion T Turnbull, William D Freeman
• Journal: Pharmacogenomics (Pharmacogenomics) Vol. 21 Issue 6 Pg. 387-392 (04 2020) ISSN: 1744-8042 [Electronic] England
• PMID: 32284009 (Publication Type: Case Reports, Journal Article)

Chemical References

• Antihypertensive Agents
• Nimodipine
• CYP3A5 protein, human
• Cytochrome P-450 CYP3A

Topics

• Aged, 80 and over
• Antihypertensive Agents (adverse effects)
• Bradycardia (chemically induced, diagnostic imaging, genetics)
• Cytochrome P-450 CYP3A (genetics)
• Female
• Humans
• Nimodipine (adverse effects)
• Subarachnoid Hemorrhage (chemically induced, diagnostic imaging, genetics)