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Acute myocarditis secondary to Campylobacter jejuni enterocolitis
Resuscitation (2008) 79, 165—167
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/resuscitation
CASE REPORT
Acute myocarditis secondary to Campylobacter jejuni enterocolitis夽 A.J. Turley a,∗, J.G. Crilley b, J.A. Hall a a b
The James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, United Kingdom Darlington Memorial Hospital, Hollyhurst Road, Darlington, Co Durham DL3 6HX, United Kingdom
Received 8 January 2008; received in revised form 14 April 2008; accepted 24 April 2008
KEYWORDS Campylobacter jejuni; Enterocolitis; Myocarditis; Myocardial infarction; Prognosis
Summary Myocarditis is a rare condition that can mimic an acute coronary syndrome (ACS). We present the case of a 24-year-old male with Noonan syndrome who presented with a diarrhoeal pro-dromal illness, acute onset chest pain, elevated cardiac biomarkers and an abnormal ECG with ST elevation in the absence of obstructive coronary artery disease. The patient had acute myocarditis secondary to Campylobacter jejuni enterocolitis. Infective myocarditis is most commonly due to a viral infection. Myocarditis is very rarely due to a bacterial infection with only isolated reports of myocarditis induced by Campylobacter jejuni infection. At follow-up he remains well. Myocarditis should be considered in all patients presenting with acute onset chest pain and elevated cardiac biomarkers. © 2008 Elsevier Ireland Ltd. All rights reserved.
Introduction Myocarditis is a rare condition that can mimic an acute coronary syndrome (ACS). Infective myocarditis is most commonly due to a viral infection. Myocarditis due to a bacterial infection is extremely rare. We present the case of a 24year-old male with Noonan syndrome who presented with
夽 A Spanish translated version of the summary of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2008.04.021. ∗ Corresponding author at: Cardiothoracic Division, The James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, United Kingdom. Tel.: +44 1642 854623; fax: +44 1642 854190. E-mail addresses: [email protected] (A.J. Turley), [email protected] (J.G. Crilley), [email protected] (J.A. Hall).
a diarrhoeal pro-dromal illness, acute onset chest pain, elevated cardiac biomarkers and an abnormal ECG with ST elevation in the absence of obstructive coronary artery disease. The patient had acute myocarditis secondary to Campylobacter jejuni enterocolitis. Myocarditis should be considered in the differential diagnosis of all patients presenting with acute onset chest pain and elevated cardiac biomarkers.
Case history A 24-year-old male with Noonan syndrome was admitted acutely unwell with chest pain. Two days prior he had a single short-lived episode of dull heavy left-sided chest discomfort which occurred at rest and resolved spontaneously. Several episodes of chest pain lasting no longer than 30-min had occurred in the 24-h before admission. Non-steroidal
0300-9572/$ — see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2008.04.021
166
A.J. Turley et al.
Fig. 1
12-Lead ECG demonstrating widespread anterior ST segment elevation.
anti-inflammatory drugs had eased but not resolved his symptoms. The day of admission he experienced 4 h of continuous central chest pain associated with vomiting. His GP called paramedics after performing a 12-lead ECG, interpreted as being diagnostic of a ST elevation myocardial infarction in the context of the patients symptoms. The patient received aspirin and pre-hospital thrombolysis. Furthermore he gave a 6-day history of diarrhoea, fevers and profuse sweating which started after he had attended a wedding where he ate a buffet meal. He was on no regular medication, denied illicit drug use and had no risk factors for ischaemic heart disease. On arrival at his local emergency department, his 12lead ECG remained unchanged (Fig. 1). He received opiates for ongoing chest discomfort and clopidogrel. He was transferred to the regional cardiothoracic centre for further evaluation. On arrival he was pain-free, pyrexial (38.5 ◦ C) and normotensive with a sinus tachycardia. Heart sounds were normal with no murmurs or rubs heard. Serial ECGs remained unchanged and a transthoracic echocardiogram demonstrated a small pericardial effusion (<1 cm) with an akinetic left ventricular apical segment and an abnormal appearance of the left ventricular apex. A diagnostic coronary angiogram demonstrated normal coronary arteries and antiplatelet agents were discontinued. A stool specimen isolated Campylobacter jejuni. The patient was diagnosed as suffering from acute myocarditis secondary to Campylobacter jejuni infection given the history of recent diarrhoea infection, normal coronary arteries, elevated troponin T 1.4 ng/ml (reference < 0.01 ng/ml), signs of inflammation (fever and CRP 125 nmol/l) and an echocardiogram demonstrating regional wall abnormalities. The patient was commenced on erythromycin following microbiological advice (he had an allergy to ciprofloxacin) and started on an ACE-inhibitor and beta-blocker for his left ventricular systolic dysfunction. The patient’s condition improved. His temperature settled and his inflammatory markers fell. He remained haemodynamically stable throughout admission and serial
echocardiograms showed improvement in LV systolic function. He was discharged home after 14 days and instructed not to work for 3 months. A Cardiac MR scan 4 weeks later showed patchy gadolinium enhancement consistent with recent myocarditis (Fig. 2). At follow-up he remains asymptomatic with a normal exercise tolerance and good LV systolic function.
Discussion Myocarditis is defined as inflammation of the heart muscle. Its true prevalence is unknown although evidence of myocardial inflammation is found in 5% of post-mortem
Fig. 2 Delayed enhancement cardiac MR scan in the short axis view demonstrates patchy enhancement of gadolinium in the anterolateral wall and less markedly in the inferoseptal wall. This diffuse pattern of enhancement is typical of myocarditis.
Acute myocarditis secondary to Campylobacter jejuni enterocolitis examinations.1 Myocarditis can progress to a chronic cardiomyopathy and is a leading cause of sudden death in patients under 40 years old.2 In the majority of patient’s enterovirus and adenovirus infections are the most likely cause of myocarditis although parvovirus B19 and herpes virus 6 are also increasingly implicated.3 Myocarditis is very rarely due to bacterial infection with only three previous reports of myocarditis induced by Campylobacter jejuni infection.4—6 The most frequently reported causes of bacterial myocarditis being salmonellosis and shigellosis.7 The clinical manifestation is variable with symptoms such as acute onset chest pain and dyspnoea often mistaken for an ACS. Other presentations range from a pro-dromal illness of fever, malaise and arthralgia/myalgia that can last several weeks to cardiogenic shock or sudden death. The diagnosis is primarily clinical and reached after a process of exclusion of other causes of the clinical signs and symptoms. Biochemical tests can demonstrate elevation in acute phase reactants and elevation in cardiac biomarkers as seen in our patient. The 12-lead ECG may mimic the changes of an ACS or it may show tachy or bradyarrhythmias. In patients presenting with chest pain, ECG abnormalities and a raised cardiac biomarker, diagnostic coronary angiography needs to be undertaken to exclude obstructive coronary artery disease. There is no clear relationship between the clinical, laboratory and ECG findings in patients with myocarditis and no validated diagnostic criteria are used in daily clinical practice. The endomyocardial biopsy is regarded by some as the gold standard investigation although is limited by sampling error of inflammation, its low sensitivity and specificity and the degree of inter-observer variability in applying the diagnostic (Dallas) criteria.8 Cardiac magnetic resonance imaging (CMR) can be extremely useful in cases of suspected myocarditis. This non-invasive investigation helps identify the extent of inflammation in patients with myocarditis and clearly identifies its patchy distribution throughout the myocardium. It also identifies co-existent pericardial involvement and demonstrates the extent of regional wall abnormalities.6,9 The underlying pathophysiology of myocarditis secondary to Campylobacter jejuni is unclear. Campylobacter jejuni is known to cause other conditions including acute motor axonal neuropathy (Guillain-Barré syndrome) through the process of ganglioside mimicry, supporting an autoimmune pathophysiology. Other theories include a direct effect of
167
the bacterium or its toxin on the myocardium. The latter theory would seem more plausible given the short timescale between diarrhoea symptom onset and myocarditis that ourselves and others have observed.10 No established treatment regimen exists and treatment relates to the patients haemodynamic status. Bed rest should be considered during the acute phase of the illness and patients placed on telemetry. If patients are severely ill then treatment with intravenous inotropes and left ventricular mechanical assist devices may be required. The condition followed a self-limiting course as seen by others and the patient was discharged home 14 days after admission on beta-blockers and ACE-inhibition.6
Conflict of interest None.
References 1. Burlo P, Comino A, Di Gioia V, Passarino G, Mollo F. Adult myocarditis in a general hospital: observations on 605 autopsies. Pathologica 1995;87(6):646—9. 2. Drory Y, Turetz Y, Hiss Y, Lev B, Fisman EZ, Pines A, et al. Sudden unexpected death in persons less than 40 years of age. Am J Cardiol 1991;68(13):1388—92. 3. Mahrholdt H, Wagner A, Deluigi CC, Kispert E, Hager S, Meinhardt G, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation 2006;114(15):1581—90. 4. Pena LA, Fishbein MC. Fatal myocarditis related to Campylobacter jejuni infection: a case report. Cardiovasc Pathol 2007;16(2):119—21. 5. Cunningham C, Lee CH. Myocarditis related to Campylobacter jejuni infection: a case report. BMC Infect Dis 2003;3:16. 6. Cox ID, Fluck DS, Joy MD. Campylobacter myocarditis: loose bowels and a baggy heart. Eur J Heart Fail 2001;3(1):105—7. 7. Wanby P, Olsen B. Myocarditis in a patient with salmonella and Campylobacter enteritis. Scand J Infect Dis 2001;33(11): 860—2. 8. Heymans S. Myocarditis and heart failure: need for better diagnostic, predictive, and therapeutic tools. Eur Heart J 2007;28(11):1279—80. 9. Yelgec NS, Dymarkowski S, Ganame J, Bogaert J. Value of MRI in patients with a clinical suspicion of acute myocarditis. Eur Radiol 2007;17(9):2211—7. 10. Yuki N. Carbohydrate mimicry: a new paradigm of autoimmune diseases. Curr Opin Immunol 2005;17(6):577—82.
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/resuscitation
CASE REPORT
Acute myocarditis secondary to Campylobacter jejuni enterocolitis夽 A.J. Turley a,∗, J.G. Crilley b, J.A. Hall a a b
The James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, United Kingdom Darlington Memorial Hospital, Hollyhurst Road, Darlington, Co Durham DL3 6HX, United Kingdom
Received 8 January 2008; received in revised form 14 April 2008; accepted 24 April 2008
KEYWORDS Campylobacter jejuni; Enterocolitis; Myocarditis; Myocardial infarction; Prognosis
Summary Myocarditis is a rare condition that can mimic an acute coronary syndrome (ACS). We present the case of a 24-year-old male with Noonan syndrome who presented with a diarrhoeal pro-dromal illness, acute onset chest pain, elevated cardiac biomarkers and an abnormal ECG with ST elevation in the absence of obstructive coronary artery disease. The patient had acute myocarditis secondary to Campylobacter jejuni enterocolitis. Infective myocarditis is most commonly due to a viral infection. Myocarditis is very rarely due to a bacterial infection with only isolated reports of myocarditis induced by Campylobacter jejuni infection. At follow-up he remains well. Myocarditis should be considered in all patients presenting with acute onset chest pain and elevated cardiac biomarkers. © 2008 Elsevier Ireland Ltd. All rights reserved.
Introduction Myocarditis is a rare condition that can mimic an acute coronary syndrome (ACS). Infective myocarditis is most commonly due to a viral infection. Myocarditis due to a bacterial infection is extremely rare. We present the case of a 24year-old male with Noonan syndrome who presented with
夽 A Spanish translated version of the summary of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2008.04.021. ∗ Corresponding author at: Cardiothoracic Division, The James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, United Kingdom. Tel.: +44 1642 854623; fax: +44 1642 854190. E-mail addresses: [email protected] (A.J. Turley), [email protected] (J.G. Crilley), [email protected] (J.A. Hall).
a diarrhoeal pro-dromal illness, acute onset chest pain, elevated cardiac biomarkers and an abnormal ECG with ST elevation in the absence of obstructive coronary artery disease. The patient had acute myocarditis secondary to Campylobacter jejuni enterocolitis. Myocarditis should be considered in the differential diagnosis of all patients presenting with acute onset chest pain and elevated cardiac biomarkers.
Case history A 24-year-old male with Noonan syndrome was admitted acutely unwell with chest pain. Two days prior he had a single short-lived episode of dull heavy left-sided chest discomfort which occurred at rest and resolved spontaneously. Several episodes of chest pain lasting no longer than 30-min had occurred in the 24-h before admission. Non-steroidal
0300-9572/$ — see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2008.04.021
166
A.J. Turley et al.
Fig. 1
12-Lead ECG demonstrating widespread anterior ST segment elevation.
anti-inflammatory drugs had eased but not resolved his symptoms. The day of admission he experienced 4 h of continuous central chest pain associated with vomiting. His GP called paramedics after performing a 12-lead ECG, interpreted as being diagnostic of a ST elevation myocardial infarction in the context of the patients symptoms. The patient received aspirin and pre-hospital thrombolysis. Furthermore he gave a 6-day history of diarrhoea, fevers and profuse sweating which started after he had attended a wedding where he ate a buffet meal. He was on no regular medication, denied illicit drug use and had no risk factors for ischaemic heart disease. On arrival at his local emergency department, his 12lead ECG remained unchanged (Fig. 1). He received opiates for ongoing chest discomfort and clopidogrel. He was transferred to the regional cardiothoracic centre for further evaluation. On arrival he was pain-free, pyrexial (38.5 ◦ C) and normotensive with a sinus tachycardia. Heart sounds were normal with no murmurs or rubs heard. Serial ECGs remained unchanged and a transthoracic echocardiogram demonstrated a small pericardial effusion (<1 cm) with an akinetic left ventricular apical segment and an abnormal appearance of the left ventricular apex. A diagnostic coronary angiogram demonstrated normal coronary arteries and antiplatelet agents were discontinued. A stool specimen isolated Campylobacter jejuni. The patient was diagnosed as suffering from acute myocarditis secondary to Campylobacter jejuni infection given the history of recent diarrhoea infection, normal coronary arteries, elevated troponin T 1.4 ng/ml (reference < 0.01 ng/ml), signs of inflammation (fever and CRP 125 nmol/l) and an echocardiogram demonstrating regional wall abnormalities. The patient was commenced on erythromycin following microbiological advice (he had an allergy to ciprofloxacin) and started on an ACE-inhibitor and beta-blocker for his left ventricular systolic dysfunction. The patient’s condition improved. His temperature settled and his inflammatory markers fell. He remained haemodynamically stable throughout admission and serial
echocardiograms showed improvement in LV systolic function. He was discharged home after 14 days and instructed not to work for 3 months. A Cardiac MR scan 4 weeks later showed patchy gadolinium enhancement consistent with recent myocarditis (Fig. 2). At follow-up he remains asymptomatic with a normal exercise tolerance and good LV systolic function.
Discussion Myocarditis is defined as inflammation of the heart muscle. Its true prevalence is unknown although evidence of myocardial inflammation is found in 5% of post-mortem
Fig. 2 Delayed enhancement cardiac MR scan in the short axis view demonstrates patchy enhancement of gadolinium in the anterolateral wall and less markedly in the inferoseptal wall. This diffuse pattern of enhancement is typical of myocarditis.
Acute myocarditis secondary to Campylobacter jejuni enterocolitis examinations.1 Myocarditis can progress to a chronic cardiomyopathy and is a leading cause of sudden death in patients under 40 years old.2 In the majority of patient’s enterovirus and adenovirus infections are the most likely cause of myocarditis although parvovirus B19 and herpes virus 6 are also increasingly implicated.3 Myocarditis is very rarely due to bacterial infection with only three previous reports of myocarditis induced by Campylobacter jejuni infection.4—6 The most frequently reported causes of bacterial myocarditis being salmonellosis and shigellosis.7 The clinical manifestation is variable with symptoms such as acute onset chest pain and dyspnoea often mistaken for an ACS. Other presentations range from a pro-dromal illness of fever, malaise and arthralgia/myalgia that can last several weeks to cardiogenic shock or sudden death. The diagnosis is primarily clinical and reached after a process of exclusion of other causes of the clinical signs and symptoms. Biochemical tests can demonstrate elevation in acute phase reactants and elevation in cardiac biomarkers as seen in our patient. The 12-lead ECG may mimic the changes of an ACS or it may show tachy or bradyarrhythmias. In patients presenting with chest pain, ECG abnormalities and a raised cardiac biomarker, diagnostic coronary angiography needs to be undertaken to exclude obstructive coronary artery disease. There is no clear relationship between the clinical, laboratory and ECG findings in patients with myocarditis and no validated diagnostic criteria are used in daily clinical practice. The endomyocardial biopsy is regarded by some as the gold standard investigation although is limited by sampling error of inflammation, its low sensitivity and specificity and the degree of inter-observer variability in applying the diagnostic (Dallas) criteria.8 Cardiac magnetic resonance imaging (CMR) can be extremely useful in cases of suspected myocarditis. This non-invasive investigation helps identify the extent of inflammation in patients with myocarditis and clearly identifies its patchy distribution throughout the myocardium. It also identifies co-existent pericardial involvement and demonstrates the extent of regional wall abnormalities.6,9 The underlying pathophysiology of myocarditis secondary to Campylobacter jejuni is unclear. Campylobacter jejuni is known to cause other conditions including acute motor axonal neuropathy (Guillain-Barré syndrome) through the process of ganglioside mimicry, supporting an autoimmune pathophysiology. Other theories include a direct effect of
167
the bacterium or its toxin on the myocardium. The latter theory would seem more plausible given the short timescale between diarrhoea symptom onset and myocarditis that ourselves and others have observed.10 No established treatment regimen exists and treatment relates to the patients haemodynamic status. Bed rest should be considered during the acute phase of the illness and patients placed on telemetry. If patients are severely ill then treatment with intravenous inotropes and left ventricular mechanical assist devices may be required. The condition followed a self-limiting course as seen by others and the patient was discharged home 14 days after admission on beta-blockers and ACE-inhibition.6
Conflict of interest None.
References 1. Burlo P, Comino A, Di Gioia V, Passarino G, Mollo F. Adult myocarditis in a general hospital: observations on 605 autopsies. Pathologica 1995;87(6):646—9. 2. Drory Y, Turetz Y, Hiss Y, Lev B, Fisman EZ, Pines A, et al. Sudden unexpected death in persons less than 40 years of age. Am J Cardiol 1991;68(13):1388—92. 3. Mahrholdt H, Wagner A, Deluigi CC, Kispert E, Hager S, Meinhardt G, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation 2006;114(15):1581—90. 4. Pena LA, Fishbein MC. Fatal myocarditis related to Campylobacter jejuni infection: a case report. Cardiovasc Pathol 2007;16(2):119—21. 5. Cunningham C, Lee CH. Myocarditis related to Campylobacter jejuni infection: a case report. BMC Infect Dis 2003;3:16. 6. Cox ID, Fluck DS, Joy MD. Campylobacter myocarditis: loose bowels and a baggy heart. Eur J Heart Fail 2001;3(1):105—7. 7. Wanby P, Olsen B. Myocarditis in a patient with salmonella and Campylobacter enteritis. Scand J Infect Dis 2001;33(11): 860—2. 8. Heymans S. Myocarditis and heart failure: need for better diagnostic, predictive, and therapeutic tools. Eur Heart J 2007;28(11):1279—80. 9. Yelgec NS, Dymarkowski S, Ganame J, Bogaert J. Value of MRI in patients with a clinical suspicion of acute myocarditis. Eur Radiol 2007;17(9):2211—7. 10. Yuki N. Carbohydrate mimicry: a new paradigm of autoimmune diseases. Curr Opin Immunol 2005;17(6):577—82.