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Cause of atrioventricular block in patients after heart transplantation
Guanggen Cui1, Jon Kobashigawa, Armen Margarian
1Department of Medicine, UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1679, USA.
Insights
Atrioventricular block (AVB) after heart transplant is often linked to rejection and transplant coronary artery disease (TCAD). Most severe AVB types result from surgical or catheterization procedures, not rejection.
Area of Science:
- Cardiology
- Transplant Surgery
- Electrophysiology
Background:
- The precise incidence and etiology of atrioventricular block (AVB) following heart transplantation are not well-established.
- Understanding AVB causes is crucial for post-transplant patient management.
Purpose of the Study:
- To determine the incidence and causes of atrioventricular block (AVB) after heart transplantation.
- To correlate AVB with clinical, laboratory, rejection, and imaging findings.
Main Methods:
- Retrospective review of electrocardiograms from 1047 heart transplant recipients.
- Correlation of AVB occurrence with clinical symptoms, laboratory data, rejection grade, echocardiography, and coronary angiography.
Main Results:
- 10.8% of patients (113/1047) developed AVB.
- First-degree AVB was linked to cellular rejection and transplant coronary artery disease (TCAD).
- Second-degree and complete AVB (CAVB) were primarily associated with surgical or catheter-based interventions.
Conclusions:
- First-degree AVB is causally related to cellular rejection and TCAD-induced atrial conduction disturbances.
- More severe AVB (Mobitz I, Mobitz II, CAVB) predominantly results from surgical injury or catheter interventions.
- Distinguishing AVB causes is vital for targeted post-heart transplant care.
Background:
The precise incidence and cause of atrioventricular block (AVB) after heart transplantation remain uncertain.
Methods And Results:
After surgery, immediate and follow-up electrocardiograms from 1047 consecutive patients who underwent heart transplantation were reviewed for AVB and correlated with clinical symptoms, laboratory data, rejection grade, and echocardiogram and coronary angiography findings. A total of 113 patients demonstrated various kinds of AVB; the incidence was 10.8%. First-degree AVB occurred in 87 patients, 37 of whom also demonstrated persistent atrial tachyarrhythmias (ATAs). In 30 patients, first-degree AVB occurred 7 days to 120 months after heart transplantation. Among those, 88% demonstrated cellular rejection, and 20% developed transplant coronary artery disease (TCAD). Fifty patients demonstrated first-degree AVB without ATA, 32 of whom developed AVB from operative day 7 to 156 months. The incidence of cellular rejection was significantly lower (36%, P<0.01), and the rejection was less severe. In 18 patients, AVB occurred early postoperatively (0-7 days), and most were secondary to surgical injury. Second-degree AVB Mobitz I occurred in six patients (four patients with TCAD and two patients undergoing percutaneous transluminal coronary angioplasty). One patient developed Mobitz II during coronary artery stenting. Complete AVB (CAVB) occurred in 19 patients. Nine episodes of CAVB occurred during endomyocardial biopsy or coronary angiography, and four occurred immediately after heart transplantation as the result of surgical insult.
Conclusion:
These results indicate that first-degree AVB is causatively related to cellular rejection and TCAD-induced atrial conduction disturbance. Second-degree AVB and CAVB were mainly the consequences of surgical and catheter intervention injury.
