Management of hypercalcaemia-induced heart failure using mechanical circulatory support

Management of hypercalcaemia-induced heart failure using mechanical circulatory support Abstract Acute heart failure is associated with high morbidity and mortality. Heart failure is caused by various conditions, including electrolyte imbalances. We report a rare case of hypercalcaemia-induced acute heart failure complicated by cardiogenic shock. Mechanical circulatory support was used successfully in this patient until calcium homeostasis was restored. Hypercalcaemia, Acute heart failure, Mechanical circulatory support INTRODUCTION A 38-year-old woman with no medical history or regular medications presented to a community hospital with muscle weakness, lethargy, loss of appetite and abdominal pain. Laboratory tests revealed severe hypercalcaemia with a total plasma calcium level of 5.84 mmol/l (normal reference range 2.2–2.6 mmol/l, Fig. 1A). Supportive medical treatment comprising forced diuresis, administration of corticosteroids, calcitonin and bisphosphonates was started, and the patient was transferred to the intensive care unit for further treatment. On arrival, we initiated haemodialysis. Additional laboratory tests revealed elevated levels of plasma parathormone (PTH 2941 ng/l, normal reference range 15–65 ng/l) and serum cardiac biomarkers (troponin T, creatinine kinase and creatinine kinase myocardial band). Cervical sonography showed a mass inferior to the left lobe of the thyroid gland measuring 8 × 5 × 4 cm in size (Fig. 1B). The electrocardiogram showed a sinus tachycardia of 120/min and inferolateral ST-segment depression with a normal QT interval (Fig. 1C). Despite treatment, calcium levels remained high at 4.5 mmol/l (Fig. 1A). On Day 2, progressive haemodynamic instability occurred. Haemodynamic measurements using thermodilution revealed a markedly decreased cardiac output. We started mechanical ventilation and administered inotropes and vasopressors. Shortly after, cardiac arrest with asystole occurred, and the patient underwent prolonged cardiopulmonary resuscitation. As haemodynamic stability could not be achieved, the patient underwent emergency cannulation of the right atrium and the ascending aorta, and treatment using an extracorporeal left ventricular assist device (a centrifugal pump, CentriMag, Levitronix, USA connected to a membrane oxygenator, Medos, Germany) was initiated. The patient underwent an urgent parathyroidectomy, and histopathological examination of the specimen revealed an adenoma of the parathyroid gland (Fig. 1D). Thereafter, calcium and PTH levels normalized rapidly (Fig. 1A), and catecholamine therapy was gradually reduced. On Day 10, haemodynamics and gas exchange remained stable, and the patient was successfully weaned from the assist device. After a prolonged in-hospital stay of almost 2 months, the patient was discharged from our hospital without any sequelae. Figure 1: View largeDownload slide (A) Time course of normalization of calcium (Ca2+, normal reference range 2.2–2.6 mmol/l) and phosphate ( PO43−, normal reference range 0.85–1.45 mmol/l) levels. (B) Cervical sonography revealed a mass inferior to the left lobe of the thyroid gland. (C) Electrocardiogram at hospital admission (paper speed 50 mm/s). (D) Histopathological examination of the cervical mass revealed an adenoma of the parathyroid gland. Haematoxylin and eosin stain ×2.5 magnification (large image) and ×40 magnification. Figure 1: View largeDownload slide (A) Time course of normalization of calcium (Ca2+, normal reference range 2.2–2.6 mmol/l) and phosphate ( PO43−, normal reference range 0.85–1.45 mmol/l) levels. (B) Cervical sonography revealed a mass inferior to the left lobe of the thyroid gland. (C) Electrocardiogram at hospital admission (paper speed 50 mm/s). (D) Histopathological examination of the cervical mass revealed an adenoma of the parathyroid gland. Haematoxylin and eosin stain ×2.5 magnification (large image) and ×40 magnification. DISCUSSION We report a case of acute heart failure due to excessive hypercalcaemia in a patient with primary hyperparathyroidism. Calcium concentration is a function of intestinal absorption, renal excretion and turnover from skeletal calcium reservoirs, which is tightly controlled by PTH, calcitonin and vitamin D metabolites. In healthy individuals, PTH secretion from the parathyroid glands is triggered by the reduction in plasma-ionized calcium levels. PTH stimulates bone resorption, and thus calcium release and intestinal and renal calcium absorption, both directly and indirectly by promoting the renal formation of calcitriol [1]. Primary hyperparathyroidism is characterized by excessive PTH secretion by a benign parathyroid adenoma (in 80% of cases), multiglandular hyperplasia (15–20% of cases) or, rarely, parathyroid cancer (<1% of cases) [1]. Typically, primary hyperparathyroidism is associated with the triad of renal stones, osteoporosis and gastrointestinal symptoms. However, most patients are either asymptomatic or present with unspecific complaints such as muscle weakness, fatigue and lethargy [1, 2]. Cardiac involvement mainly consists of hypertension, arrhythmias, valvular or myocardial calcification and ventricular hypertrophy [2] and ultimately, although rare, heart failure. When reviewing our case, we speculate that hypercalcaemia-induced acute heart failure occurred through the following mechanisms: first, intracellular hypercalcaemia has been shown to impair myocardial repolarization–relaxation coupling and, thus, reduce diastolic relaxation capacity, contributing to the development of heart failure [3]. Second, increased intracellular calcium levels may have led to myocardial contraction band necrosis, which is characterized by excessive contraction of myofibrils and subsequent myocytolysis [4]. This may explain the release of cardiac biomarkers as observed in our patient. Finally, catecholamines are known to increase intracellular calcium levels [4], and consequently, catecholamine treatment might have worsened intracellular calcium overload contributing to the observed haemodynamic instability. CONCLUSION In summary, we present a rare case of hypercalcaemia-induced acute heart failure with cardiogenic shock. The occurrence of acute heart failure is associated with high morbidity and mortality. Heart failure can be caused by various conditions, including electrolyte imbalances [5]. Hypercalcaemia may cause acute heart failure through (i) impaired cardiac relaxation by persistent activation of the actin–myosin cross-bridge interaction and (ii) myocardial necrosis. As demonstrated in our case, the deployment of a left ventricular assist device may be a viable option in hypercalcaemia-induced cardiogenic shock until calcium homeostasis is restored. Funding Hendrik Sager is supported by the ‘European Research Coucil (ERC starting grant; grant number: STRATO 759272)’, the ‘Deutsche Forschungsgemeinschaft (grant number: SA 1668/5-1)’, the ‘Deutsches Zentrum für Herz-Kreislauf-Forschung (grant number: DZHK Rotation-Grant for Medical Doctors 2016-2017)’, the ‘Else-Kröner-Forschungskolleg Technische Universität München (grant number: clinical leave scholarship 2017-2018)’, and the ‘Deutsche Herzstiftung (grant number: F/28/17)’. Conflict of interest: none declared. REFERENCES 1 Bilezikian JP, Bandeira L, Khan A, Cusano NE. Hyperparathyroidism. Lancet  2018; 391: 168– 78. Google Scholar CrossRef Search ADS PubMed  2 Andersson P, Rydberg E, Willenheimer R. Primary hyperparathyroidism and heart disease—a review. Eur Heart J  2004; 25: 1776– 87. Google Scholar CrossRef Search ADS PubMed  3 Kho C, Lee A, Hajjar RJ. Altered sarcoplasmic reticulum calcium cycling–targets for heart failure therapy. Nat Rev Cardiol  2012; 9: 717– 33. Google Scholar CrossRef Search ADS PubMed  4 Schmittinger CA, Dunser MW, Torgersen C, Luckner G, Lorenz I, Schmid S et al.   Histologic pathologies of the myocardium in septic shock: a prospective observational study. Shock  2013; 39: 329– 35. Google Scholar CrossRef Search ADS PubMed  5 Braunwald E. Heart failure. JACC Heart Fail  2013; 1: 1– 20. Google Scholar CrossRef Search ADS PubMed  © The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Cardio-Thoracic Surgery Oxford University Press

Management of hypercalcaemia-induced heart failure using mechanical circulatory support

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Oxford University Press
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© The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
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1010-7940
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1873-734X
D.O.I.
10.1093/ejcts/ezy139
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Abstract

Abstract Acute heart failure is associated with high morbidity and mortality. Heart failure is caused by various conditions, including electrolyte imbalances. We report a rare case of hypercalcaemia-induced acute heart failure complicated by cardiogenic shock. Mechanical circulatory support was used successfully in this patient until calcium homeostasis was restored. Hypercalcaemia, Acute heart failure, Mechanical circulatory support INTRODUCTION A 38-year-old woman with no medical history or regular medications presented to a community hospital with muscle weakness, lethargy, loss of appetite and abdominal pain. Laboratory tests revealed severe hypercalcaemia with a total plasma calcium level of 5.84 mmol/l (normal reference range 2.2–2.6 mmol/l, Fig. 1A). Supportive medical treatment comprising forced diuresis, administration of corticosteroids, calcitonin and bisphosphonates was started, and the patient was transferred to the intensive care unit for further treatment. On arrival, we initiated haemodialysis. Additional laboratory tests revealed elevated levels of plasma parathormone (PTH 2941 ng/l, normal reference range 15–65 ng/l) and serum cardiac biomarkers (troponin T, creatinine kinase and creatinine kinase myocardial band). Cervical sonography showed a mass inferior to the left lobe of the thyroid gland measuring 8 × 5 × 4 cm in size (Fig. 1B). The electrocardiogram showed a sinus tachycardia of 120/min and inferolateral ST-segment depression with a normal QT interval (Fig. 1C). Despite treatment, calcium levels remained high at 4.5 mmol/l (Fig. 1A). On Day 2, progressive haemodynamic instability occurred. Haemodynamic measurements using thermodilution revealed a markedly decreased cardiac output. We started mechanical ventilation and administered inotropes and vasopressors. Shortly after, cardiac arrest with asystole occurred, and the patient underwent prolonged cardiopulmonary resuscitation. As haemodynamic stability could not be achieved, the patient underwent emergency cannulation of the right atrium and the ascending aorta, and treatment using an extracorporeal left ventricular assist device (a centrifugal pump, CentriMag, Levitronix, USA connected to a membrane oxygenator, Medos, Germany) was initiated. The patient underwent an urgent parathyroidectomy, and histopathological examination of the specimen revealed an adenoma of the parathyroid gland (Fig. 1D). Thereafter, calcium and PTH levels normalized rapidly (Fig. 1A), and catecholamine therapy was gradually reduced. On Day 10, haemodynamics and gas exchange remained stable, and the patient was successfully weaned from the assist device. After a prolonged in-hospital stay of almost 2 months, the patient was discharged from our hospital without any sequelae. Figure 1: View largeDownload slide (A) Time course of normalization of calcium (Ca2+, normal reference range 2.2–2.6 mmol/l) and phosphate ( PO43−, normal reference range 0.85–1.45 mmol/l) levels. (B) Cervical sonography revealed a mass inferior to the left lobe of the thyroid gland. (C) Electrocardiogram at hospital admission (paper speed 50 mm/s). (D) Histopathological examination of the cervical mass revealed an adenoma of the parathyroid gland. Haematoxylin and eosin stain ×2.5 magnification (large image) and ×40 magnification. Figure 1: View largeDownload slide (A) Time course of normalization of calcium (Ca2+, normal reference range 2.2–2.6 mmol/l) and phosphate ( PO43−, normal reference range 0.85–1.45 mmol/l) levels. (B) Cervical sonography revealed a mass inferior to the left lobe of the thyroid gland. (C) Electrocardiogram at hospital admission (paper speed 50 mm/s). (D) Histopathological examination of the cervical mass revealed an adenoma of the parathyroid gland. Haematoxylin and eosin stain ×2.5 magnification (large image) and ×40 magnification. DISCUSSION We report a case of acute heart failure due to excessive hypercalcaemia in a patient with primary hyperparathyroidism. Calcium concentration is a function of intestinal absorption, renal excretion and turnover from skeletal calcium reservoirs, which is tightly controlled by PTH, calcitonin and vitamin D metabolites. In healthy individuals, PTH secretion from the parathyroid glands is triggered by the reduction in plasma-ionized calcium levels. PTH stimulates bone resorption, and thus calcium release and intestinal and renal calcium absorption, both directly and indirectly by promoting the renal formation of calcitriol [1]. Primary hyperparathyroidism is characterized by excessive PTH secretion by a benign parathyroid adenoma (in 80% of cases), multiglandular hyperplasia (15–20% of cases) or, rarely, parathyroid cancer (<1% of cases) [1]. Typically, primary hyperparathyroidism is associated with the triad of renal stones, osteoporosis and gastrointestinal symptoms. However, most patients are either asymptomatic or present with unspecific complaints such as muscle weakness, fatigue and lethargy [1, 2]. Cardiac involvement mainly consists of hypertension, arrhythmias, valvular or myocardial calcification and ventricular hypertrophy [2] and ultimately, although rare, heart failure. When reviewing our case, we speculate that hypercalcaemia-induced acute heart failure occurred through the following mechanisms: first, intracellular hypercalcaemia has been shown to impair myocardial repolarization–relaxation coupling and, thus, reduce diastolic relaxation capacity, contributing to the development of heart failure [3]. Second, increased intracellular calcium levels may have led to myocardial contraction band necrosis, which is characterized by excessive contraction of myofibrils and subsequent myocytolysis [4]. This may explain the release of cardiac biomarkers as observed in our patient. Finally, catecholamines are known to increase intracellular calcium levels [4], and consequently, catecholamine treatment might have worsened intracellular calcium overload contributing to the observed haemodynamic instability. CONCLUSION In summary, we present a rare case of hypercalcaemia-induced acute heart failure with cardiogenic shock. The occurrence of acute heart failure is associated with high morbidity and mortality. Heart failure can be caused by various conditions, including electrolyte imbalances [5]. Hypercalcaemia may cause acute heart failure through (i) impaired cardiac relaxation by persistent activation of the actin–myosin cross-bridge interaction and (ii) myocardial necrosis. As demonstrated in our case, the deployment of a left ventricular assist device may be a viable option in hypercalcaemia-induced cardiogenic shock until calcium homeostasis is restored. Funding Hendrik Sager is supported by the ‘European Research Coucil (ERC starting grant; grant number: STRATO 759272)’, the ‘Deutsche Forschungsgemeinschaft (grant number: SA 1668/5-1)’, the ‘Deutsches Zentrum für Herz-Kreislauf-Forschung (grant number: DZHK Rotation-Grant for Medical Doctors 2016-2017)’, the ‘Else-Kröner-Forschungskolleg Technische Universität München (grant number: clinical leave scholarship 2017-2018)’, and the ‘Deutsche Herzstiftung (grant number: F/28/17)’. Conflict of interest: none declared. REFERENCES 1 Bilezikian JP, Bandeira L, Khan A, Cusano NE. Hyperparathyroidism. Lancet  2018; 391: 168– 78. Google Scholar CrossRef Search ADS PubMed  2 Andersson P, Rydberg E, Willenheimer R. Primary hyperparathyroidism and heart disease—a review. Eur Heart J  2004; 25: 1776– 87. Google Scholar CrossRef Search ADS PubMed  3 Kho C, Lee A, Hajjar RJ. Altered sarcoplasmic reticulum calcium cycling–targets for heart failure therapy. Nat Rev Cardiol  2012; 9: 717– 33. Google Scholar CrossRef Search ADS PubMed  4 Schmittinger CA, Dunser MW, Torgersen C, Luckner G, Lorenz I, Schmid S et al.   Histologic pathologies of the myocardium in septic shock: a prospective observational study. Shock  2013; 39: 329– 35. Google Scholar CrossRef Search ADS PubMed  5 Braunwald E. Heart failure. JACC Heart Fail  2013; 1: 1– 20. Google Scholar CrossRef Search ADS PubMed  © The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

European Journal of Cardio-Thoracic SurgeryOxford University Press

Published: Mar 30, 2018

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