Intrahepatic Portosystemic Shunt In Cardiac Amyloidosis: Turning Off The Faucet Leads To Resolution Of Hepatic Encephalopathy And Improvement In Heart Failure Symptoms
HFSA ePoster Library. Sailer C. 09/10/21; 343578; 336
Christine Sailer
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Abstract
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Introduction:Vasoplegia is a well-described post-operative complication, defined as hypotension due to a decline in systemic vascular resistance in the setting of normal cardiac output and filling pressures. Angiotensin II is a vasoconstrictor with a potential for thrombosis. We present a case of vasoplegia refractory to standard therapy in a patient status post Left Ventricular Assist Device (LVAD) placement in which angiotensin II was utilized successfully.
Case Description:A 44-year-old African American man with history of stage D idiopathic dilated cardiomyopathy and chronic kidney disease status post HeartMate 3 (HM3) LVAD placement three months ago, complicated by right ventricular failure requiring home milrinone infusion, presented to clinic for follow-up. He was found to have Class IV heart failure symptoms and anasarca, despite an increase in his home diuretic regimen, requiring hospital admission. He denied fever, productive cough or infectious exposures, LVAD alarms, or changes in urine output.
Despite an increase of his milrinone and addition of dobutamine, epinephrine, bumetanide, and intravenous chlorothiazide on admission, his hemodynamics on right heart catheterization revealed elevated biventricular filling pressures and a low systemic vascular resistance (SVR) without evidence of right ventricular failure on these therapies (Table 1). The patient maintained poor urine output and required continuous dialysis. However, due to continued vasoplegia, fluid removal was not possible despite maximizing ionotropic and pressor support.
A trial of angiotensin II was attempted after discussion with the patient and family about the associated thrombotic risk to HM3. With optimized dosing of angiotensin II, SVR improved (Table 1), and fluid was successfully removed with continuous dialysis. Ionotropic and pressor support was then weaned. The patient did not develop any thromboembolic events or pump thrombosis of the LVAD. The patient was discharged home and one month later underwent a successful heart and kidney transplantation.
Conclusion: Angiotensin II use carries significant thromboembolic risk for some patients, with the ATHOS-3 trial showing 12.9% risk versus 5% for placebo. Although this can raise concerns among patients with mechanical circulatory support, significant hemodynamic improvement can be achieved with those facing refractory vasoplegia. Clinicians should be aware of the risks of angiotensin II use and be prepared to utilize the medication in the appropriate patient following a discussion of the potential risks and benefits.
Case Description:A 44-year-old African American man with history of stage D idiopathic dilated cardiomyopathy and chronic kidney disease status post HeartMate 3 (HM3) LVAD placement three months ago, complicated by right ventricular failure requiring home milrinone infusion, presented to clinic for follow-up. He was found to have Class IV heart failure symptoms and anasarca, despite an increase in his home diuretic regimen, requiring hospital admission. He denied fever, productive cough or infectious exposures, LVAD alarms, or changes in urine output.
Despite an increase of his milrinone and addition of dobutamine, epinephrine, bumetanide, and intravenous chlorothiazide on admission, his hemodynamics on right heart catheterization revealed elevated biventricular filling pressures and a low systemic vascular resistance (SVR) without evidence of right ventricular failure on these therapies (Table 1). The patient maintained poor urine output and required continuous dialysis. However, due to continued vasoplegia, fluid removal was not possible despite maximizing ionotropic and pressor support.
A trial of angiotensin II was attempted after discussion with the patient and family about the associated thrombotic risk to HM3. With optimized dosing of angiotensin II, SVR improved (Table 1), and fluid was successfully removed with continuous dialysis. Ionotropic and pressor support was then weaned. The patient did not develop any thromboembolic events or pump thrombosis of the LVAD. The patient was discharged home and one month later underwent a successful heart and kidney transplantation.
Conclusion: Angiotensin II use carries significant thromboembolic risk for some patients, with the ATHOS-3 trial showing 12.9% risk versus 5% for placebo. Although this can raise concerns among patients with mechanical circulatory support, significant hemodynamic improvement can be achieved with those facing refractory vasoplegia. Clinicians should be aware of the risks of angiotensin II use and be prepared to utilize the medication in the appropriate patient following a discussion of the potential risks and benefits.
| MAP (mmHg) | RA Pressures (mmHg) | PAP (mmHg) | PCWP (mmHg) | Cardiac Output (L/min) | Cardiac Index (L/min/m2) | SVR (Dynes/sec/cm-5) | |
| Hemodynamic Values Prior to Angiotensin II Initiation | 45 | 20 | 61/31 | 27 | 6.27 | 2.88 | 319 |
| Hemodynamic Values After Angiotensin II Initiation | 65 | 6 | 54/17 | 16 | 5.4 | 2.5 | 875 |
Introduction:Vasoplegia is a well-described post-operative complication, defined as hypotension due to a decline in systemic vascular resistance in the setting of normal cardiac output and filling pressures. Angiotensin II is a vasoconstrictor with a potential for thrombosis. We present a case of vasoplegia refractory to standard therapy in a patient status post Left Ventricular Assist Device (LVAD) placement in which angiotensin II was utilized successfully.
Case Description:A 44-year-old African American man with history of stage D idiopathic dilated cardiomyopathy and chronic kidney disease status post HeartMate 3 (HM3) LVAD placement three months ago, complicated by right ventricular failure requiring home milrinone infusion, presented to clinic for follow-up. He was found to have Class IV heart failure symptoms and anasarca, despite an increase in his home diuretic regimen, requiring hospital admission. He denied fever, productive cough or infectious exposures, LVAD alarms, or changes in urine output.
Despite an increase of his milrinone and addition of dobutamine, epinephrine, bumetanide, and intravenous chlorothiazide on admission, his hemodynamics on right heart catheterization revealed elevated biventricular filling pressures and a low systemic vascular resistance (SVR) without evidence of right ventricular failure on these therapies (Table 1). The patient maintained poor urine output and required continuous dialysis. However, due to continued vasoplegia, fluid removal was not possible despite maximizing ionotropic and pressor support.
A trial of angiotensin II was attempted after discussion with the patient and family about the associated thrombotic risk to HM3. With optimized dosing of angiotensin II, SVR improved (Table 1), and fluid was successfully removed with continuous dialysis. Ionotropic and pressor support was then weaned. The patient did not develop any thromboembolic events or pump thrombosis of the LVAD. The patient was discharged home and one month later underwent a successful heart and kidney transplantation.
Conclusion: Angiotensin II use carries significant thromboembolic risk for some patients, with the ATHOS-3 trial showing 12.9% risk versus 5% for placebo. Although this can raise concerns among patients with mechanical circulatory support, significant hemodynamic improvement can be achieved with those facing refractory vasoplegia. Clinicians should be aware of the risks of angiotensin II use and be prepared to utilize the medication in the appropriate patient following a discussion of the potential risks and benefits.
Case Description:A 44-year-old African American man with history of stage D idiopathic dilated cardiomyopathy and chronic kidney disease status post HeartMate 3 (HM3) LVAD placement three months ago, complicated by right ventricular failure requiring home milrinone infusion, presented to clinic for follow-up. He was found to have Class IV heart failure symptoms and anasarca, despite an increase in his home diuretic regimen, requiring hospital admission. He denied fever, productive cough or infectious exposures, LVAD alarms, or changes in urine output.
Despite an increase of his milrinone and addition of dobutamine, epinephrine, bumetanide, and intravenous chlorothiazide on admission, his hemodynamics on right heart catheterization revealed elevated biventricular filling pressures and a low systemic vascular resistance (SVR) without evidence of right ventricular failure on these therapies (Table 1). The patient maintained poor urine output and required continuous dialysis. However, due to continued vasoplegia, fluid removal was not possible despite maximizing ionotropic and pressor support.
A trial of angiotensin II was attempted after discussion with the patient and family about the associated thrombotic risk to HM3. With optimized dosing of angiotensin II, SVR improved (Table 1), and fluid was successfully removed with continuous dialysis. Ionotropic and pressor support was then weaned. The patient did not develop any thromboembolic events or pump thrombosis of the LVAD. The patient was discharged home and one month later underwent a successful heart and kidney transplantation.
Conclusion: Angiotensin II use carries significant thromboembolic risk for some patients, with the ATHOS-3 trial showing 12.9% risk versus 5% for placebo. Although this can raise concerns among patients with mechanical circulatory support, significant hemodynamic improvement can be achieved with those facing refractory vasoplegia. Clinicians should be aware of the risks of angiotensin II use and be prepared to utilize the medication in the appropriate patient following a discussion of the potential risks and benefits.
| MAP (mmHg) | RA Pressures (mmHg) | PAP (mmHg) | PCWP (mmHg) | Cardiac Output (L/min) | Cardiac Index (L/min/m2) | SVR (Dynes/sec/cm-5) | |
| Hemodynamic Values Prior to Angiotensin II Initiation | 45 | 20 | 61/31 | 27 | 6.27 | 2.88 | 319 |
| Hemodynamic Values After Angiotensin II Initiation | 65 | 6 | 54/17 | 16 | 5.4 | 2.5 | 875 |
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