Adrenergic myocarditis: Difference between revisions
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{{Myocarditis}} | {{Myocarditis}} | ||
{{SK}} | {{SK}} Neurogenic stunned myocardium, catecholamine induced cardiomyopathy, catecholamine mediated myocarditis. focal myocardial necrosis, norepinephrine 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 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> | 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> | ||
== | ==Historical Perspective== | ||
Clinically significant myocarditis is rare in pheochromocytoma, however, studies have shown that 50% of patients | Clinically significant myocarditis is rare in pheochromocytoma, however, studies have shown that 50% of patients with pheochromocytoma had evidence of acute myocarditis on autopsy.<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> | ||
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== | ||
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===Microscopic Features=== | ===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> | 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> | ||
== | ==Differentiating Adrenergic Cardiomyopathy from other Diseases== | ||
*[[Stress induced cardiomyopathy]] also known as [[Tako-tsubo cardiomyopathy]] | *[[Stress induced cardiomyopathy]] also known as [[Tako-tsubo cardiomyopathy]] | ||
It is reversible like adrenergic myocarditis and has implications of catecholamines involvement in its pathology. It occurs as a result of sudden emotional or physical stress. Hypokinesia of apex specifically results in apical ballooning of myocardium. Adrenergic myocarditis on the other hand can affect myocardium focally as well as globally and does not show apical ballooning in [[echocardiography]]. <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> | It is reversible like adrenergic myocarditis and has implications of catecholamines involvement in its pathology. It occurs as a result of sudden emotional or physical stress. Hypokinesia of apex specifically results in apical ballooning of myocardium. Adrenergic myocarditis on the other hand can affect myocardium focally as well as globally and does not show apical ballooning in [[echocardiography]]. <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> | ||
*[[Acute coronary syndrome]] (ACS) | |||
As ACS manifests very similar to Adrenergic myocarditis, it has to be ruled out with [[coronary angiography]]. Adrenergic myocarditis lacks evidence of coronary artery disease. | |||
*[[Neurogenic stunned myocardium]] | |||
This is also a type of myocardial hypokinesia which occurs in event of a stroke and sub arachnoid hemorrhage. Role of catecholamines has been implied in it. | |||
==Diagnosis== | ==Diagnosis== | ||
===History=== | |||
Majority of pheochromocytoma patients present with triad of headache, sweating and palpitaions. Weight loss, chest pain, blurring of vision and pallor are among other less common symptoms. Paroxysmal hypertension along with presence of positive family history should raise suspicion of [[Pheochromocytoma]]. Presence of myocarditis should be suspected in a diagnosed case of Pheochromocytoma with cardiac symptoms. | Majority of pheochromocytoma patients present with triad of headache, sweating and palpitaions. Weight loss, chest pain, blurring of vision and pallor are among other less common symptoms. Paroxysmal hypertension along with presence of positive family history should raise suspicion of [[Pheochromocytoma]]. Presence of myocarditis should be suspected in a diagnosed case of Pheochromocytoma with cardiac symptoms. | ||
As Adrenergic myocarditis presents with symptoms similar to [[acute coronary syndrome]], it has to be ruled out initially with coronary angiography. | As Adrenergic myocarditis presents with symptoms similar to [[acute coronary syndrome]], it has to be ruled out initially with coronary angiography. | ||
Revision as of 13:45, 16 September 2013
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Synonyms and keywords: Neurogenic stunned myocardium, catecholamine induced cardiomyopathy, catecholamine mediated myocarditis. focal myocardial necrosis, norepinephrine 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]
Historical Perspective
Clinically significant myocarditis is rare in pheochromocytoma, however, studies have shown that 50% of patients 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]
Differentiating Adrenergic Cardiomyopathy from other Diseases
- Stress induced cardiomyopathy also known as Tako-tsubo cardiomyopathy
It is reversible like adrenergic myocarditis and has implications of catecholamines involvement in its pathology. It occurs as a result of sudden emotional or physical stress. Hypokinesia of apex specifically results in apical ballooning of myocardium. Adrenergic myocarditis on the other hand can affect myocardium focally as well as globally and does not show apical ballooning in echocardiography. [1]
- Acute coronary syndrome (ACS)
As ACS manifests very similar to Adrenergic myocarditis, it has to be ruled out with coronary angiography. Adrenergic myocarditis lacks evidence of coronary artery disease.
This is also a type of myocardial hypokinesia which occurs in event of a stroke and sub arachnoid hemorrhage. Role of catecholamines has been implied in it.
Diagnosis
History
Majority of pheochromocytoma patients present with triad of headache, sweating and palpitaions. Weight loss, chest pain, blurring of vision and pallor are among other less common symptoms. Paroxysmal hypertension along with presence of positive family history should raise suspicion of Pheochromocytoma. Presence of myocarditis should be suspected in a diagnosed case of Pheochromocytoma with cardiac symptoms. As Adrenergic myocarditis presents with symptoms similar to acute coronary syndrome, it has to be ruled out initially with coronary angiography. Other tests required:
- Echocardiography: Systolic anterior motion of mitral valve, Global hypokinesis, hypokinesia of base and apex, decreased ejection fraction
- Electrocardiography: Left ventricular hypertrophy, sinus tachycardia, ischemic changes of myocardium, transient Q waves[8]
- Cardiac Magnetic Resonance
- Elevated cardiac markers.
All findings normalise after resection of tumor.
Treatment
Surgical resection of tumor is ultimate treatment to remove excess catecholamines from body. Alpha receptors need to be blocked before surgery with phenoxybenzamine to control hypertension.
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References
- ↑ 1.0 1.1 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.
- ↑ 2.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 5.0 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.
- ↑ 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.
- ↑ 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.
- ↑ Bertrand JH, Grollier G, Potier JC (1987). "[Transient Q wave in adrenergic myocarditis. Contribution of echocardiography apropos of a case]". Arch Mal Coeur Vaiss. 80 (11): 1675–80. PMID 3128212.