Adrenergic myocarditis: Difference between revisions

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{{Myocarditis}}
{{Myocarditis}}
{{SK}} Adrenergic crisis, pheochromocytoma, Neurogenic Stunned Myocardium, Catecholamine induced cardiomyopathy, catecholamine mediated myocarditis
{{SK}} Adrenergic crisis, pheochromocytoma, Neurogenic Stunned Myocardium, Catecholamine induced cardiomyopathy, catecholamine mediated myocarditis. focal myocardial necrosis, nor-epinephrin myocarditis.


==Overview==
==Overview==
Adrenergic myocarditis is a reversible phenomenon of  catecholamine mediated myocardial inflammation seen in pheochromocytoma.  Pheochromocytoma is a tumour of adrenal medulla which produces excess amount of catecholamines.  Wide spectrum of myocardial dysfunctions are present in pheochromocytoma which include acute myocardial infarction (both ST elevation and non ST elevation), cardiomyopathy, tako-tsubo cardiomyopathy, congestive heart failure, acute pulmonary edema, cardiac arrythmias.  Direct myocardial injury by catecholamines is the most popular theory among other proposed causes.<ref name="pmid15703419">{{cite journal| author=Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G et al.| title=Neurohumoral features of myocardial stunning due to sudden emotional stress. | journal=N Engl J Med | year= 2005 | volume= 352 | issue= 6 | pages= 539-48 | pmid=15703419 | doi=10.1056/NEJMoa043046 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15703419  }} </ref>
Adrenergic myocarditis is a reversible phenomenon of  catecholamine mediated myocardial inflammation seen in pheochromocytoma.  Pheochromocytoma is a tumour of adrenal medulla which produces excess amount of catecholamines.  Wide spectrum of myocardial dysfunctions are present in pheochromocytoma which include acute myocardial infarction (both ST elevation and non ST elevation), cardiomyopathy, tako-tsubo cardiomyopathy, congestive heart failure, acute pulmonary edema and cardiac arrythmias.  Direct myocardial injury caused by catecholamines is the most popular theory among other proposed causes.<ref name="pmid15703419">{{cite journal| author=Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G et al.| title=Neurohumoral features of myocardial stunning due to sudden emotional stress. | journal=N Engl J Med | year= 2005 | volume= 352 | issue= 6 | pages= 539-48 | pmid=15703419 | doi=10.1056/NEJMoa043046 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15703419  }} </ref>


==Clinical presentation==
==Clinical presentation==
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Pheochromocytoma classically presents with episodic hypertension, sweating, tremors and palpitations, 12% of patients have cardiac symptoms as their initial manifestation.<ref name="pmid22297057">{{cite journal| author=Yu R, Nissen NN, Bannykh SI| title=Cardiac complications as initial manifestation of pheochromocytoma: frequency, outcome, and predictors. | journal=Endocr Pract | year= 2012 | volume= 18 | issue= 4 | pages= 483-92 | pmid=22297057 | doi=10.4158/EP11327.OR | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22297057  }} </ref>  For the first time in 1987, Mc-Ginley etal described catecholamine induced myocarditis as the presenting manifestation of pheochromocytoma.<ref name="pmid2881206">{{cite journal| author=Imperato-McGinley J, Gautier T, Ehlers K, Zullo MA, Goldstein DS, Vaughan ED| title=Reversibility of catecholamine-induced dilated cardiomyopathy in a child with a pheochromocytoma. | journal=N Engl J Med | year= 1987 | volume= 316 | issue= 13 | pages= 793-7 | pmid=2881206 | doi=10.1056/NEJM198703263161307 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2881206  }} </ref>  Pheochromocytoma patients with myocarditis present with chest pain, breathless, dizziness, palpiations which are very similar to clinical features of acute coronary syndrome (ACS), therefore ruling out ACS is the priority.  In one study done by Sardesai etal five out of six patients with pheochromocytoma presented with acute pulmonary edema and died with in 24 hours.<ref name="pmid2337495">{{cite journal| author=Sardesai SH, Mourant AJ, Sivathandon Y, Farrow R, Gibbons DO| title=Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure. | journal=Br Heart J | year= 1990 | volume= 63 | issue= 4 | pages= 234-7 | pmid=2337495 | doi= | pmc=PMC1024438 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2337495  }} </ref>  Four out of those five patients had evidence of focal myocardial necrosis on autopsy.
Pheochromocytoma classically presents with episodic hypertension, sweating, tremors and palpitations, 12% of patients have cardiac symptoms as their initial manifestation.<ref name="pmid22297057">{{cite journal| author=Yu R, Nissen NN, Bannykh SI| title=Cardiac complications as initial manifestation of pheochromocytoma: frequency, outcome, and predictors. | journal=Endocr Pract | year= 2012 | volume= 18 | issue= 4 | pages= 483-92 | pmid=22297057 | doi=10.4158/EP11327.OR | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22297057  }} </ref>  For the first time in 1987, Mc-Ginley etal described catecholamine induced myocarditis as the presenting manifestation of pheochromocytoma.<ref name="pmid2881206">{{cite journal| author=Imperato-McGinley J, Gautier T, Ehlers K, Zullo MA, Goldstein DS, Vaughan ED| title=Reversibility of catecholamine-induced dilated cardiomyopathy in a child with a pheochromocytoma. | journal=N Engl J Med | year= 1987 | volume= 316 | issue= 13 | pages= 793-7 | pmid=2881206 | doi=10.1056/NEJM198703263161307 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2881206  }} </ref>  Pheochromocytoma patients with myocarditis present with chest pain, breathless, dizziness, palpiations which are very similar to clinical features of acute coronary syndrome (ACS), therefore ruling out ACS is the priority.  In one study done by Sardesai etal five out of six patients with pheochromocytoma presented with acute pulmonary edema and died with in 24 hours.<ref name="pmid2337495">{{cite journal| author=Sardesai SH, Mourant AJ, Sivathandon Y, Farrow R, Gibbons DO| title=Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure. | journal=Br Heart J | year= 1990 | volume= 63 | issue= 4 | pages= 234-7 | pmid=2337495 | doi= | pmc=PMC1024438 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2337495  }} </ref>  Four out of those five patients had evidence of focal myocardial necrosis on autopsy.
==Pathophysiology==
==Pathophysiology==
M
A number of mechanisms have been proposed to define cause of catecholamine mediated myocardial necrosis and inflammation:
* Direct toxic effect of catecholamines on cardiomyocytes mediated by cyclic-AMP results in increased calcium inside cells. This in turn impair their structure and function.<ref name="pmid1370925">{{cite journal| author=Mann DL, Kent RL, Parsons B, Cooper G| title=Adrenergic effects on the biology of the adult mammalian cardiocyte. | journal=Circulation | year= 1992 | volume= 85 | issue= 2 | pages= 790-804 | pmid=1370925 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1370925  }} </ref>
* Increased free radical production by catecholamines also contributes to cell damage.<ref name="pmid7151008">{{cite journal| author=Singal PK, Kapur N, Dhillon KS, Beamish RE, Dhalla NS| title=Role of free radicals in catecholamine-induced cardiomyopathy. | journal=Can J Physiol Pharmacol | year= 1982 | volume= 60 | issue= 11 | pages= 1390-7 | pmid=7151008 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7151008  }} </ref>
* Vasospasm caused by catecholamines.


===Microscopic Features===
Initially focal lesions of necrosis have edema and myofibril degeneration, which leads to striation loss in cardiomyocytes.  This initial necrosis results in inflammatory infilteration with monocytes. Histologic changes include focal degeneration, contraction band necrosis, thickening of small and medium sized coronary arteries and interstitial fibrosis.<ref name="pmid2337495">{{cite journal| author=Sardesai SH, Mourant AJ, Sivathandon Y, Farrow R, Gibbons DO| title=Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure. | journal=Br Heart J | year= 1990 | volume= 63 | issue= 4 | pages= 234-7 | pmid=2337495 | doi= | pmc=PMC1024438 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2337495  }} </ref><ref name="pmid5932021">{{cite journal| author=Van Vliet PD, Burchell HB, Titus JL| title=Focal myocarditis associated with pheochromocytoma. | journal=N Engl J Med | year= 1966 | volume= 274 | issue= 20 | pages= 1102-8 | pmid=5932021 | doi=10.1056/NEJM196605192742002 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5932021  }} </ref>


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Revision as of 05:47, 16 September 2013

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Synonyms and keywords: Adrenergic crisis, pheochromocytoma, Neurogenic Stunned Myocardium, Catecholamine induced cardiomyopathy, catecholamine mediated myocarditis. focal myocardial necrosis, nor-epinephrin myocarditis.

Overview

Adrenergic myocarditis is a reversible phenomenon of catecholamine mediated myocardial inflammation seen in pheochromocytoma. Pheochromocytoma is a tumour of adrenal medulla which produces excess amount of catecholamines. Wide spectrum of myocardial dysfunctions are present in pheochromocytoma which include acute myocardial infarction (both ST elevation and non ST elevation), cardiomyopathy, tako-tsubo cardiomyopathy, congestive heart failure, acute pulmonary edema and cardiac arrythmias. Direct myocardial injury caused by catecholamines is the most popular theory among other proposed causes.[1]

Clinical presentation

Clinically significant myocarditis is rare in pheochromocytoma, however, studies have shown that 50% of patients who died with pheochromocytoma had evidence of acute myocarditis on autopsy.[2] Pheochromocytoma classically presents with episodic hypertension, sweating, tremors and palpitations, 12% of patients have cardiac symptoms as their initial manifestation.[3] For the first time in 1987, Mc-Ginley etal described catecholamine induced myocarditis as the presenting manifestation of pheochromocytoma.[4] Pheochromocytoma patients with myocarditis present with chest pain, breathless, dizziness, palpiations which are very similar to clinical features of acute coronary syndrome (ACS), therefore ruling out ACS is the priority. In one study done by Sardesai etal five out of six patients with pheochromocytoma presented with acute pulmonary edema and died with in 24 hours.[5] Four out of those five patients had evidence of focal myocardial necrosis on autopsy.

Pathophysiology

A number of mechanisms have been proposed to define cause of catecholamine mediated myocardial necrosis and inflammation:

  • Direct toxic effect of catecholamines on cardiomyocytes mediated by cyclic-AMP results in increased calcium inside cells. This in turn impair their structure and function.[6]
  • Increased free radical production by catecholamines also contributes to cell damage.[7]
  • Vasospasm caused by catecholamines.

Microscopic Features

Initially focal lesions of necrosis have edema and myofibril degeneration, which leads to striation loss in cardiomyocytes. This initial necrosis results in inflammatory infilteration with monocytes. Histologic changes include focal degeneration, contraction band necrosis, thickening of small and medium sized coronary arteries and interstitial fibrosis.[5][2]

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References

  1. Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G; et al. (2005). "Neurohumoral features of myocardial stunning due to sudden emotional stress". N Engl J Med. 352 (6): 539–48. doi:10.1056/NEJMoa043046. PMID 15703419.
  2. 2.0 2.1 Van Vliet PD, Burchell HB, Titus JL (1966). "Focal myocarditis associated with pheochromocytoma". N Engl J Med. 274 (20): 1102–8. doi:10.1056/NEJM196605192742002. PMID 5932021.
  3. Yu R, Nissen NN, Bannykh SI (2012). "Cardiac complications as initial manifestation of pheochromocytoma: frequency, outcome, and predictors". Endocr Pract. 18 (4): 483–92. doi:10.4158/EP11327.OR. PMID 22297057.
  4. Imperato-McGinley J, Gautier T, Ehlers K, Zullo MA, Goldstein DS, Vaughan ED (1987). "Reversibility of catecholamine-induced dilated cardiomyopathy in a child with a pheochromocytoma". N Engl J Med. 316 (13): 793–7. doi:10.1056/NEJM198703263161307. PMID 2881206.
  5. 5.0 5.1 Sardesai SH, Mourant AJ, Sivathandon Y, Farrow R, Gibbons DO (1990). "Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure". Br Heart J. 63 (4): 234–7. PMC 1024438. PMID 2337495.
  6. Mann DL, Kent RL, Parsons B, Cooper G (1992). "Adrenergic effects on the biology of the adult mammalian cardiocyte". Circulation. 85 (2): 790–804. PMID 1370925.
  7. Singal PK, Kapur N, Dhillon KS, Beamish RE, Dhalla NS (1982). "Role of free radicals in catecholamine-induced cardiomyopathy". Can J Physiol Pharmacol. 60 (11): 1390–7. PMID 7151008.


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