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Delayed Presentation of Amiodarone Induced Thyrotoxicosis Following Heart Transplant
The 19th Annual Scientific Meeting
HFSA
S73
(n524), and left ventricular hypertrophy (n510). Average initial LVEF by echocardiogram was 42 6 16%, cardiac index 2.39 6 0.77 L/min/m2, mean PA pressure 26 6 10 mmHg and PCWP 17 6 7 mmHg. EMB was diagnostic in 30% (n522) and effected management in 44% (n532) of patients. The most common effects on clinical care included a change in diagnostic strategy (n510) and change in medical therapy (n518) with 5 patients being started on immunosuppression. CMR provided a single diagnosis in 36% (n526), multiple diagnoses in 18% (n513) and no diagnosis in 47% (n534). CMR suggested nonischemic cardiomyopathy in 27 cases, with most common etiologies listed in the differential being myocarditis (n515), amyloid (n511), infiltrative cardiomyopathy (n59), and sarcoid (n56). Delayed gadolinium enhancement was present in 33 patients. CMR results influenced management in 44% (n532), most frequently with a change in diagnostic strategy (n523) that primarily involved proceeding with EMB. When EMB followed CMR (n553), it provided additional clinical utility (marked by change in management/diagnostic strategy) 40% of the time. EMB confirmed diagnosis of amyloid in 7 cases, myocarditis in 4 cases, and sarcoid in 1 case. Conclusion: EMB and CMR provided a single diagnosis and effected management at similar rates. Despite development of noninvasive diagnostic strategies in HF, CMR did not preclude the need for EMB, which provided supplementary information and critically affected diagnostic and clinical strategy in a significant number of cases. Thus EMB continues to play an important role in a select subset of unexplained cardiomyopathy patients.
160 Delayed Presentation of Amiodarone Induced Thyrotoxicosis Following Heart Transplant LaVone Smith, Jamie Kennedy, Anthony McCall, Jennifer Kirby, Sula Mazimba; University of Virginia, Charlottesville, VA Introduction: Amiodarone is commonly used in the advanced heart failure population for treatment of arrhythmias. Three to five percent of patients treated with amiodarone develop hyperthyroidism, most commonly Type II Amiodarone Induced Thyrotoxicosis (AIT) from destructive thyroiditis. There is little data available evaluating the prevalence of AIT in the transplant population or related morbidity and mortality. Case Series: Approximately half of the patients transplanted at our center are treated with amiodarone prior to cardiac transplant. In the last 20 years, 87 patients received amiodarone prior to or immediately post transplant, and 5 patients developed thyroiditis following transplant (5.7 %). Four patients were treated with amiodarone for an average of 1.6 years prior to transplant, then discontinued at the time of transplant. One patient started amiodarone 5 days after transplant for atrial fibrillation and continued for 1.8 years. On average, thyroid dysfunction was diagnosed 366 days after discontinuation of amiodarone. The mechanism of dysfunction was thought to be thyroiditis in each patient. Two patients underwent coronary angiography around the time of their diagnosis, so the iodine load may have contributed to an iodine induced thyrotoxicosis in addition to amiodarone. Patients received steroids as part
Table 1. Patient characteristics
Age at transplantation Sex
Average daily dose of amiodarone
Duration of Time to diagnosis steroids prior to Duration of of hyperthyroidism diagnosis of amiodarone after amiodarone hyperthyroidism treatment (days) exposure (days) (days)
Time between steroid completion and diagnosis of hyperthyroidism (days)
57 52
M M
400 mg 400 mg
299 741
194 390
195 390
0 0
70 51
M M
200 mg 200 mg
628 682
336 401
336 320
0 81
46
F
400 mg
660
511
665
511
of their post-transplant immunosuppression regimen and were treated on average for more than 1 year prior to the diagnosis of thyroiditis. At the time of diagnosis, 4 of the 5 patients had either recently completed their steroid course or had been tapered to a low dose (5 mg/ day or lower). To date, none of our patients have experienced serious morbidity as a result of thyroiditis. Hyperthyroidism was not observed in transplant patients who had not been treated with amiodarone. We hypothesize that treatment with steroids may mask early diagnosis due to partial treatment of thyroiditis. We observed a higher prevalence of AIT in our transplant population than predicted, but the significance of this observation in a relatively small patient population is unclear. Conclusion: Patients remain at risk for development of AIT for a prolonged time after discontinuation of amiodarone. This risk may persist up to 1 year after amiodarone discontinuation. Larger studies are needed to address the temporal relationship of AIT following heart transplant and the effect of steroids. A prolonged period of thyroid function monitoring should be considered in post-transplant patients with prior amiodarone therapy.
Type II AIT Presumed Type II AIT vs. Iodine induced thyrotoxicosis Type II AIT Iodine induced thyrotoxicosis Thyroiditis
162 Heart Failure Preserved Ejection Fraction Patients Benefit From Heart Failure Reduced Ejection Fraction Guidelines Gregg Steahr, Linda Kelly, Meredith Moore, Brenda Hott; Northside Hospital, Cumming, GA Background: Optimal treatment for Heart Failure preserved Ejection Fraction (HFpEF) has yet to be defined. The condition comprises nearly half the heart failure (HF) population. Recent studies have shown cost and outcomes of patients (pts) with
161 Incremental Diagnostic and Clinical Utility of Endomyocardial Biopsy Over Cardiac Magnetic Resonance Imaging Alone in Patients with Unexplained Heart Failure Nisha A. Gilotra1, Mosi K. Bennett2, Van-Khue Ton1, Nicole Minkove1, Adam Shpigel1, Nishant Shah1, Kristina Montemayor1, Allison Hays1, Marc K. Halushka1, Stuart D. Russell1; 1Johns Hopkins Hospital, Baltimore, MD; 2 Minneapolis Heart Institute, Minneapolis, MN Background: The timely identification of heart failure (HF) etiology can have important therapeutic and prognostic implications. Endomyocardial biopsy (EMB) remains the gold standard for diagnosing several myocardial disorders, however it is not without risk. Cardiac magnetic resonance (CMR) imaging has emerged as a means to characterize specific HF subtypes, however its effect on clinical management is unknown and its diagnostic utility in relation to EMB is poorly understood. Hypothesis: We hypothesized that EMB has added clinical utility to CMR in the diagnosis and management of unexplained HF. Methods: Seventy three patients with unexplained HF were identified who underwent both EMB and CMR within six months of each other between 2010 and 2014. Two physicians retrospectively reviewed clinical records and EMB/CMR findings in each case to determine the diagnostic utility and impact on clinical management of each test. Results: The study population consisted of 40% blacks and 40% females, with a median age of 51 years, including four children (two infants). The most common EMB indications included: new acute HF with hemodynamic compromise (n515), restrictive cardiomyopathy
Mechanism of hyperthyroidism
Figure 1.
HFSA
S73
(n524), and left ventricular hypertrophy (n510). Average initial LVEF by echocardiogram was 42 6 16%, cardiac index 2.39 6 0.77 L/min/m2, mean PA pressure 26 6 10 mmHg and PCWP 17 6 7 mmHg. EMB was diagnostic in 30% (n522) and effected management in 44% (n532) of patients. The most common effects on clinical care included a change in diagnostic strategy (n510) and change in medical therapy (n518) with 5 patients being started on immunosuppression. CMR provided a single diagnosis in 36% (n526), multiple diagnoses in 18% (n513) and no diagnosis in 47% (n534). CMR suggested nonischemic cardiomyopathy in 27 cases, with most common etiologies listed in the differential being myocarditis (n515), amyloid (n511), infiltrative cardiomyopathy (n59), and sarcoid (n56). Delayed gadolinium enhancement was present in 33 patients. CMR results influenced management in 44% (n532), most frequently with a change in diagnostic strategy (n523) that primarily involved proceeding with EMB. When EMB followed CMR (n553), it provided additional clinical utility (marked by change in management/diagnostic strategy) 40% of the time. EMB confirmed diagnosis of amyloid in 7 cases, myocarditis in 4 cases, and sarcoid in 1 case. Conclusion: EMB and CMR provided a single diagnosis and effected management at similar rates. Despite development of noninvasive diagnostic strategies in HF, CMR did not preclude the need for EMB, which provided supplementary information and critically affected diagnostic and clinical strategy in a significant number of cases. Thus EMB continues to play an important role in a select subset of unexplained cardiomyopathy patients.
160 Delayed Presentation of Amiodarone Induced Thyrotoxicosis Following Heart Transplant LaVone Smith, Jamie Kennedy, Anthony McCall, Jennifer Kirby, Sula Mazimba; University of Virginia, Charlottesville, VA Introduction: Amiodarone is commonly used in the advanced heart failure population for treatment of arrhythmias. Three to five percent of patients treated with amiodarone develop hyperthyroidism, most commonly Type II Amiodarone Induced Thyrotoxicosis (AIT) from destructive thyroiditis. There is little data available evaluating the prevalence of AIT in the transplant population or related morbidity and mortality. Case Series: Approximately half of the patients transplanted at our center are treated with amiodarone prior to cardiac transplant. In the last 20 years, 87 patients received amiodarone prior to or immediately post transplant, and 5 patients developed thyroiditis following transplant (5.7 %). Four patients were treated with amiodarone for an average of 1.6 years prior to transplant, then discontinued at the time of transplant. One patient started amiodarone 5 days after transplant for atrial fibrillation and continued for 1.8 years. On average, thyroid dysfunction was diagnosed 366 days after discontinuation of amiodarone. The mechanism of dysfunction was thought to be thyroiditis in each patient. Two patients underwent coronary angiography around the time of their diagnosis, so the iodine load may have contributed to an iodine induced thyrotoxicosis in addition to amiodarone. Patients received steroids as part
Table 1. Patient characteristics
Age at transplantation Sex
Average daily dose of amiodarone
Duration of Time to diagnosis steroids prior to Duration of of hyperthyroidism diagnosis of amiodarone after amiodarone hyperthyroidism treatment (days) exposure (days) (days)
Time between steroid completion and diagnosis of hyperthyroidism (days)
57 52
M M
400 mg 400 mg
299 741
194 390
195 390
0 0
70 51
M M
200 mg 200 mg
628 682
336 401
336 320
0 81
46
F
400 mg
660
511
665
511
of their post-transplant immunosuppression regimen and were treated on average for more than 1 year prior to the diagnosis of thyroiditis. At the time of diagnosis, 4 of the 5 patients had either recently completed their steroid course or had been tapered to a low dose (5 mg/ day or lower). To date, none of our patients have experienced serious morbidity as a result of thyroiditis. Hyperthyroidism was not observed in transplant patients who had not been treated with amiodarone. We hypothesize that treatment with steroids may mask early diagnosis due to partial treatment of thyroiditis. We observed a higher prevalence of AIT in our transplant population than predicted, but the significance of this observation in a relatively small patient population is unclear. Conclusion: Patients remain at risk for development of AIT for a prolonged time after discontinuation of amiodarone. This risk may persist up to 1 year after amiodarone discontinuation. Larger studies are needed to address the temporal relationship of AIT following heart transplant and the effect of steroids. A prolonged period of thyroid function monitoring should be considered in post-transplant patients with prior amiodarone therapy.
Type II AIT Presumed Type II AIT vs. Iodine induced thyrotoxicosis Type II AIT Iodine induced thyrotoxicosis Thyroiditis
162 Heart Failure Preserved Ejection Fraction Patients Benefit From Heart Failure Reduced Ejection Fraction Guidelines Gregg Steahr, Linda Kelly, Meredith Moore, Brenda Hott; Northside Hospital, Cumming, GA Background: Optimal treatment for Heart Failure preserved Ejection Fraction (HFpEF) has yet to be defined. The condition comprises nearly half the heart failure (HF) population. Recent studies have shown cost and outcomes of patients (pts) with
161 Incremental Diagnostic and Clinical Utility of Endomyocardial Biopsy Over Cardiac Magnetic Resonance Imaging Alone in Patients with Unexplained Heart Failure Nisha A. Gilotra1, Mosi K. Bennett2, Van-Khue Ton1, Nicole Minkove1, Adam Shpigel1, Nishant Shah1, Kristina Montemayor1, Allison Hays1, Marc K. Halushka1, Stuart D. Russell1; 1Johns Hopkins Hospital, Baltimore, MD; 2 Minneapolis Heart Institute, Minneapolis, MN Background: The timely identification of heart failure (HF) etiology can have important therapeutic and prognostic implications. Endomyocardial biopsy (EMB) remains the gold standard for diagnosing several myocardial disorders, however it is not without risk. Cardiac magnetic resonance (CMR) imaging has emerged as a means to characterize specific HF subtypes, however its effect on clinical management is unknown and its diagnostic utility in relation to EMB is poorly understood. Hypothesis: We hypothesized that EMB has added clinical utility to CMR in the diagnosis and management of unexplained HF. Methods: Seventy three patients with unexplained HF were identified who underwent both EMB and CMR within six months of each other between 2010 and 2014. Two physicians retrospectively reviewed clinical records and EMB/CMR findings in each case to determine the diagnostic utility and impact on clinical management of each test. Results: The study population consisted of 40% blacks and 40% females, with a median age of 51 years, including four children (two infants). The most common EMB indications included: new acute HF with hemodynamic compromise (n515), restrictive cardiomyopathy
Mechanism of hyperthyroidism
Figure 1.