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LETTER TO EDITOR
Year : 2013  |  Volume : 7  |  Issue : 2  |  Page : 220-222

A case of extensive cardiac calcification


1 Department of Critical Care Medicine, SGPGIMS, Lucknow, Uttar Pradesh, India
2 Department of Radiodiagnosis, SGPGIMS, Lucknow, Uttar Pradesh, India

Correspondence Address:
Tanmoy Ghatak
Rammohan Pally, Arambagh, Hooghly, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1658-354X.114066

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Date of Web Publication26-Jun-2013
 


How to cite this article:
Ghatak T, Singh RK, Azim A, Gurjar M, Baronia AK, Hiralal. A case of extensive cardiac calcification. Saudi J Anaesth 2013;7:220-2

How to cite this URL:
Ghatak T, Singh RK, Azim A, Gurjar M, Baronia AK, Hiralal. A case of extensive cardiac calcification. Saudi J Anaesth [serial online] 2013 [cited 2020 Oct 30];7:220-2. Available from: https://www.saudija.org/text.asp?2013/7/2/220/114066

Sir,

Myocardial calcification occurs in either previously injured/necrotic myocardium with normocalcemia or healthy myocardium with hypercalcemia. [1] Though localized myocardial calcifications are common after myocardial infarction; extensive myocardial calcification is rarely reported. [1] Extensive myocardial calcification in the setting of severe acute pancreatitis (SAP) has not been described yet. We are sharing one such interesting case from our intensive care unit (ICU).

A 39-year-old businessman presented to ICU with history of acute onset severe abdominal pain and vomiting, following a binge drinking. He was a chronic alcoholic since 10 yrs and had a history of irregularly treated hypertension for two years with normal baseline creatinine values. He had no h/o chest pain suggesting myocardial infarction or chest trauma. On examination, he was conscious, restless, having distended and tender abdomen and was in shock. He had high total leukocyte count (28,000/cmm), serum creatinine (4 mg/dl) and lipase of 1500 IU/L. Screening electrocardiography (ECG) and transthoracic echocardiography (TTE) were normal. Computed tomography (CT) of abdomen confirmed our working diagnosis of SAP (pancreatic parenchymal necrosis >50%).

During his stay in ICU, he had issues like septic shock (multiple episodes), acute kidney injury, and raised intra-abdominal pressure. He was treated with broad-spectrum antibiotics, anti-fungals, vasopressor and inotropes, mechanical ventilation with tracheostomy, enteral nutrition, renal replacement therapy, and multiple percutaneous drainages followed by timely necrosectomy to drain necrotic abdominal content. TTE was repeated to re-check his cardiological status as we were facing difficulty in weaning on 12 th week of ICU stay. It showed calcification of mitral leaflet and myocardium with grade I diastolic dysfunction of left ventricle. A ring calcification around left ventricle was prominent in subsequent CT scan [Figure 1]. ECG showed non-specific ST-T changes. Cardiac enzyme markers were normal. Serum calcium (maximum 10.2 mg/dl) and phosphorus levels (maximum 5 mg/dl) since admission were within normal limit (checked repeatedly). Retrospective analysis of previous scans revealed that cardiac calcification was just started on 6 th week [Figure 2]. The patient, however, succumbed to his illness due to multi-drug-resistant complicated intra-abdominal infection and septic shock within a few weeks. Post-mortem cardiac biopsy could not be done due to non-availability of consent.
Figure 1: Computed tomography view of left ventricular ring calcification (arrowed)

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Figure 2: Computed tomography view showing initiation of left ventricular wall calcification (arrowed)

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Cardiovascular complications of SAP occur temporally in the early period of the disease with dismal clinical outcome due to proteolytic enzymes or systemic inflammatory response. [2],[3] ECG changes like non-specific ST-T changes, ST segment elevation, and sinus tachycardia are linked with SAP-related electrolyte (calcium, phosphate, and magnesium) abnormalities. [2] To the best of our knowledge and literature search, we could not find any report of SAP with myocardial calcification or structural cardiac abnormalities.

Mechanism of the myocardial calcification is believed to be either dystrophic or metastatic in nature. [1],[4] Dystrophic calcification occurs in injured or necrotic myocardium with a normal serum calcium level. On the other hand, metastatic calcification can occur in previously healthy myocardium with malignant (parathyroid carcinoma, multiple myeloma, lymphoma, leukemia) or benign conditions (like chronic renal failure, hyperparathyroidism, and vitamin D excess) with calcium homeostasis abnormality. [1],[5] In literature search, extensive cardiac calcification is reported with variety of conditions related to sepsis, septic shock, vasopressor uses, even resuscitation. [4],[5],[6],[7] Papillary muscle, valves, aneurysm, and sites of healed myocardial infarct are the common sites for myocardial calcification. Interestingly, at present, no definitive therapies are available for myocardial calcification, other than cardiac transplant. [2]

This case report is an eye-opener, that myocardial calcification can occur as a complication of SAP. At present, we cannot comment on the exact mechanism of the myocardial calcification in this patient. Most likely, disordered calcium-phosphate homeostasis resulting in deposition of calcium in normal myocardial tissue may be responsible for that metastatic calcification. Calcium homeostasis abnormality in early pancreatitis may be the culprit. But, absence of cardiac calcification in older CT scan (before 6 th week) and normal calcium with phosphorus values go against it. Vasospastic mechanisms due to vasopressor use leading to myocardial injury and sepsis-related dystrophic calcification, however, cannot be excluded.

 
  References Top

1.Van Kruijswijk RC, Heijden JJ, Uijlings R, Otterspoor LC. Sepsis-related myocardial calcification. Circ Heart Fail 2011;4:e16-8.  Back to cited text no. 1
    
2.Sokmen M, Budaci MS, Öztekn E. Electrocardiographic changes and importance of repolarization changes in cases with acute pancreatitis. Turk J Gastroenterol 2011;22:315-20.  Back to cited text no. 2
    
3.Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med 2006;354:2142-50.  Back to cited text no. 3
    
4.Simonson S, Miller WT Jr, Perl A, Torigian DA. Diffuse left ventricular myocardial calcification in the setting of sepsis on CT imaging. J Thorac Imaging 2007;22:343-5.  Back to cited text no. 4
    
5.Kempf AE, Momeni MG, Saremi F. Myocardial calcinosis in chronic renal failure. J Radiol Case Rep 2009;3:16-9.  Back to cited text no. 5
    
6.Lapatto-Reiniluoto O, Vaalamo M, Takkunen O, Mänttäri M. Left ventricular calcification following resuscitation. J Intern Med 2000;248:85-7.  Back to cited text no. 6
    
7.Schellhammer F, Ansen S, Arnold G, Brochhagen HG, Lackner K. Myocardial calcification following septic shock. Cardiology 2002;98:102-3.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2]



 

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