From the Guidelines
Heart transplant patients are at an increased risk of dysrhythmias due to various factors, including rejection, decreased left ventricular ejection fraction (LVEF), coronary vasculopathy, and damage to the conduction system itself, as noted in the 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death 1. The development of disease in the transplanted heart, such as coronary vasculopathy or acute rejection, can lead to ventricular arrhythmias and sudden cardiac death (SCD), with an incidence ranging from 10% to 35% in observational studies 1. Key risk factors for dysrhythmias in heart transplant patients include:
- Rejection, both acute and chronic, which can cause inflammation and fibrosis, creating arrhythmogenic substrates
- Decreased LVEF, which is a predictor of SCD
- Coronary vasculopathy, which can lead to myocardial ischemia and ventricular arrhythmias
- Damage to the conduction system itself, which can occur during procurement and implantation of the donor heart
- Electrolyte imbalances, such as potassium and magnesium imbalances, which can occur due to immunosuppressive medications
- Medication side effects, such as QT interval prolongation, which can trigger arrhythmias. Regular monitoring of electrolytes, immunosuppressant drug levels, and surveillance for rejection through endomyocardial biopsies and echocardiograms is essential for early detection and management of these risk factors, as suggested by the 2017 AHA/ACC/HRS guideline 1.
From the Research
Risk Factors for Dysrhythmia in Heart Transplant Patients
- The risk factors for dysrhythmia, specifically torsades de pointes (TdP), in heart transplant patients include hypokalemia, female sex, drug-drug interactions, advancing age, genetic predisposition, hypomagnesemia, heart failure, bradycardia, and corrected QT (QTc) interval prolongation 2, 3, 4
- Other risk factors for TdP include QTc interval >500 ms, increase in QTc interval ≥60 ms from the pretreatment value, acute myocardial infarction, heart failure with reduced ejection fraction, hypocalcemia, treatment with diuretics, and elevated plasma concentrations of QTc interval-prolonging drugs due to drug interactions 4
- Patient-related risk factors, such as female sex, age >65 years, and uncorrected electrolyte disturbances, should also be considered when prescribing drugs associated with QT prolongation 5
Drug-Induced Arrhythmias
- Many widely used medications, including antiarrhythmic agents, antimicrobial drugs, psychotropic medications, and methadone, can prolong the QT interval and provoke TdP 3
- Pharmacokinetic drug interactions, such as those between antifungal agents, macrolide antibiotics, and drugs to treat human immunodeficiency virus, can increase the risk of TdP 4
- Pharmacists play an important role in minimizing the risk of drug-induced QTc interval prolongation and TdP through knowledge of drugs associated with a known or possible risk of TdP and individualized assessment of risk 4
Management of Drug-Induced Arrhythmias
- Management of drug-induced arrhythmias includes discontinuation of the offending medication and following treatment guidelines for the specific arrhythmia 3
- Treatment of hemodynamically stable TdP consists of discontinuation of the offending drug(s), correction of electrolyte abnormalities, and administration of intravenous magnesium sulfate 1 to 2 g 4
- A simple algorithm can be used to guide clinical management in patients who are at risk of QT prolongation/TdP, those exposed to QT-prolonging medication, or have QT prolongation 5