Tacrolimus Induced Severe Cerebral and Coronary Vasospasm after Heart Transplantation

Abstract

IntroductionTacrolimus has several cardiovascular adverse events. We report case of tacrolimus-induced severe cerebral and coronary vasospasm after heart transplantation.Case ReportA 62-year-old female underwent orthotropic heart transplantation due to dialted cardiomyopathy. Her postoperative course was benign. At 2 months, she complained of severe pulsatile headache. CTA of the brain showed diffuse cerebral artery constriction with multifocal beaded features at nearly all distal cranial arteries and scant SAH in the right parietal area (Figure 1). We diagnosed reversible cerebral vasospasm syndrome (RCVS) induced by tacrolimus and planned to switch tacrolimus to sirolimus using the vasodilator. She inevitably maintained a low level of tacrolimus due to sirolimus induced diarrhea. Using nimodipine, her symptoms disappeared, and follow-up CTA of the brain showed relieved cerebral vasoconstriction and absorption of hemorrhage (Figure 1). At 5 months after surgery, she was admitted from acute rejection. After 2 weeks of treatment, she was stabilized with biopsy improvement. We maintained a triple regimen. She soon complained of chest pain. Telemetry revealed transient ST segment elevation (Figure 2). We assumed that this event was associated with elevated tacrolimus levels; thus, tacrolimus was reduced, and oral diltiazem was administered. Using a vasodilator, a coronary vasospasm provocation test was performed. During the test, severe coronary spasm was noted. Intracoronary and intravascular nitroglycerin was administered aggressively. The study was completed after confirming a normalized coronary artery(Figure 3). Twenty minutes later, she collapsed with squeezing chest pain. On-site CPR and ECMO insertion were performed. Two days later, she died of cardiogenic shock even with ECMO support.SummaryEarly detection of disease and withholding tacrolimus are important strategies. Tacrolimus has several cardiovascular adverse events. We report case of tacrolimus-induced severe cerebral and coronary vasospasm after heart transplantation. A 62-year-old female underwent orthotropic heart transplantation due to dialted cardiomyopathy. Her postoperative course was benign. At 2 months, she complained of severe pulsatile headache. CTA of the brain showed diffuse cerebral artery constriction with multifocal beaded features at nearly all distal cranial arteries and scant SAH in the right parietal area (Figure 1). We diagnosed reversible cerebral vasospasm syndrome (RCVS) induced by tacrolimus and planned to switch tacrolimus to sirolimus using the vasodilator. She inevitably maintained a low level of tacrolimus due to sirolimus induced diarrhea. Using nimodipine, her symptoms disappeared, and follow-up CTA of the brain showed relieved cerebral vasoconstriction and absorption of hemorrhage (Figure 1). At 5 months after surgery, she was admitted from acute rejection. After 2 weeks of treatment, she was stabilized with biopsy improvement. We maintained a triple regimen. She soon complained of chest pain. Telemetry revealed transient ST segment elevation (Figure 2). We assumed that this event was associated with elevated tacrolimus levels; thus, tacrolimus was reduced, and oral diltiazem was administered. Using a vasodilator, a coronary vasospasm provocation test was performed. During the test, severe coronary spasm was noted. Intracoronary and intravascular nitroglycerin was administered aggressively. The study was completed after confirming a normalized coronary artery(Figure 3). Twenty minutes later, she collapsed with squeezing chest pain. On-site CPR and ECMO insertion were performed. Two days later, she died of cardiogenic shock even with ECMO support. Early detection of disease and withholding tacrolimus are important strategies.