From the Research
Lithium can cause myocarditis in chronic toxicity through disruption of cellular ion transport systems, induction of oxidative stress, and alteration of cardiac conduction, with significant risk at serum levels exceeding 2.0 mEq/L. The exact mechanisms of lithium-induced myocarditis are complex and multifaceted, involving alterations in sodium-potassium ATPase pumps, calcium handling in cardiac myocytes, and triggering of inflammatory responses 1. Additionally, lithium can induce oxidative stress in cardiac tissue, leading to free radical damage and cell death, as well as affect cardiac conduction by altering membrane potentials and interfering with normal electrical activity 2, 3.
Key Findings
- Lithium disrupts cellular ion transport systems, particularly sodium-potassium ATPase pumps, leading to altered calcium handling in cardiac myocytes 1
- Lithium can induce oxidative stress in cardiac tissue, leading to free radical damage and cell death 4
- The medication may also affect cardiac conduction by altering membrane potentials and interfering with normal electrical activity 2, 3
- Chronic lithium toxicity typically occurs at serum levels above 1.5 mEq/L, with significant risk at levels exceeding 2.0 mEq/L 1
- Patients on long-term lithium therapy should have regular monitoring of serum lithium levels, renal function, and cardiac status, including ECGs 5, 1
Clinical Implications
- Early symptoms of lithium-induced myocarditis may include chest pain, arrhythmias, and heart failure signs 2, 3
- The risk increases with advanced age, pre-existing cardiac disease, and concurrent use of other cardiotoxic medications 5, 4
- Frequent monitoring of patients on lithium therapy can ensure the medication's safe use and minimize the risk of cardiac complications 1