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Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis
International Journal of Cardiology 98 (2005) 351 – 354 www.elsevier.com/locate/ijcard
Letter to the Editor
Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis Dhanunjaya R. Lakkireddy a, Ashok K. Kondur b, Ellie J. Chediak b, Chandra K. Nair a, Ijaz A. Khan a,* a
Division of Cardiology, Creighton University School of Medicine, 3006 Webster Street, Omaha, NE 68131 2044, USA b Harper University Hospital, Detroit, MI, USA Received 26 June 2003; accepted 28 October 2003 Available online 23 April 2004
Abstract Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness. D 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Cardiac troponins; Diphtheria; Corynebacterium diphtheriae; Myocarditis; Toxic myocarditis; Cardiac toxins; Reversible myocardial injury; Left ventricular dysfunction; Heart
1. Introduction Cardiac troponins are highly specific markers of myocardial injury [1]. It has been postulated that, unlike other markers of myocardial injury, troponins could be elevated in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes [1 – 3]. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae [4]. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility,
* Corresponding author. Tel.: +1-402-280-4573; fax: +1-402-2804938. E-mail address: [email protected] (I.A. Khan). 0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2003.10.062
which could be reversible with successful treatment [5]. We report a case of diphtheric myocarditis in a 20-year-old female who had markedly elevated serum levels of cardiac troponin I with completely reversible severe left ventricular systolic.
2. Case report A 20-year-old woman presented with complaints of 4 days of dysphagia, dysphonia, fatigue, and generalized malaise. Her symptoms had progressively worsened and she developed severe dyspnea upon admission. Physical examination revealed a severely ill looking patient who was febrile, tachycardic, and tachypneic with normal blood pressure and blood oxygen saturation of 94% at room air. Patient became stridorous during the examination. Orophar-
352
D.R. Lakkireddy et al. / International Journal of Cardiology 98 (2005) 351–354
ynx showed greenish uvula with desquamative pseudomembranuous type tissue extending to the tonsillar pillars and posterior pharyngeal wall (Fig. 1). Neck was tender without obvious lymphadentis. Nasopharyngoscopic examination not only confirmed these above plain-eye findings but also showed inflammation and edema involving nasal, oral, hypopharyngeal and supraglottic regions, extending up to the vocal cords with impending upper airway obstruction. Jugular venous pressure was elevated at 5 cm above clavicle. Examination of the heart revealed tachycardia with summation gallop and no murmur or rub. An emergent tracheostomy was done to secure the airway. Laboratory evaluation showed an elevated white cell count at 12,000 per mm3 with 20% bands, hemoglobin of 9.6 g/dl and platelets of 178,000 per mm3. At admission serum cardiac troponin I was 4.5 ng/ml, which subsequently rose to 16.4 ng/ml at 8 h and 48.5 ng/ml at 12 h after the initial measurement. Electrocardiogram revealed sinus tachycardia with diffuse non-specific ST-T wave changes. A 2D-echo with Doppler showed severely impaired left ventricular systolic function with ejection fraction of 10%. Left ventricular cavity size and wall thickness was normal. A working diagnosis of desquamative pharyngitis complicated by acute myocarditis and congestive heart failure was made. She was promptly treated with 100,000 units of antidiphtheria toxin through intravenous infusion and intravenous ampicillin with sulbactam based on clinical suspicion of diphtheria. Throat swabs were sent for stains and cultures. Cultures grew pneumococcus and pseudomonads but no Corynebacterium diphtheriae. The pseudomembrane biopsy was sent for polymerase chain reaction screen of diphtheria toxin, which was positive. Her heart failure was successfully treated with digoxin, furosemide, and angiotensin converting enzyme inhibitors. On the third day of admission, patient developed diplopia from a right occulomotor neuropathy. A follow up 2D-echo 4 days into treatment revealed improvement in the left ventricular systolic function and ejection fraction rose to 20%. Patient continued to improve on medical treatment a repeat 2Decho a week later showed a complete restoration of left ventricular systolic function with ejection fraction at 60%.
The serum cardiac troponin I level measured at that time was 1.1 ng/ml. Her diplopia resolved spontaneously. A repeat 2D-echo 6 months later continued to show a normal left ventricular systolic function.
3. Discussion Diphtheria toxin is a polypeptide exotoxin that inhibits elongation factor-2 activity in protein synthesis and causes DNA fragmentation and cyotolysis causing both local and systemic manifestations [6]. Absorbed toxin can cause myocarditis, neuritis and focal necrosis in various organs, including the kidneys, liver and adrenal glands. Early changes in diphtheric myocarditis include cloudy swelling of muscle fibers and interstitial edema. These changes are followed within weeks by hyaline and granular degeneration of muscle fibers progressing to myolysis and finally to the replacement of lost muscle with fibrosis causing permanent cardiac damage [7]. The myocardial changes could be completely reversible if treatment is instituted early. Myocarditis may develop during the acute phase of illness or when the local disease is resolving or it may begin insidiously after several weeks [5]. One half to two-thirds of the patients with diphtheria infection have subtle evidence of cardiac dysfunction, but clinically significant myocarditis develops in only 10– 25% of patients and is more severe when the onset is early. Electrocardiographic changes include non-specific ST-T wave changes, heart blocks, and arrhythmias including atrial fibrillation, ventricular premature complexes and ventricular tachyarrhythmias [8]. Clinical signs include diminished heart sounds, gallop rhythm and systolic murmurs. Isolating the organism from the local lesions makes definite diagnosis of diphtheria, but in 40% cases cultures could be negative or grow other organisms [9]. High index of clinical suspicion is a key to the diagnosis and should prompt immediate treatment with antitoxin [10]. Polymerase chain reaction can be used subsequently to screen the Corynebacterium diphtheriae isolates for toxinogenecity [11]. The dose of antitoxin is dependent on the duration
Fig. 1. Swelling, gray coloring, and friability of posterior commissure (left) and epiglottis (right) seen through rigid laryngoscope.
D.R. Lakkireddy et al. / International Journal of Cardiology 98 (2005) 351–354
and the extent of the disease. Primary nasopharyngeal diphtheria with myocarditis should be treated with at least 80,000 –100,000 U of antitoxin by infusion over 60 min to neutralize the unbound toxin rapidly. Possible allergies to horse serum should be ruled out and always tested and rapidly desensitized, if present, prior to the full dose treatment. Continuous monitoring and supportive care including fluids, airway protection, ventilation support, temporary pacemakers, and heart failure treatment are crucial, if indicated. Serial echocardiograms to evaluate cardiac function are important. The primary goal of antibiotics use is to eradicate Corynebacterium diphtheriae and prevent its transmission from the patient to susceptible contacts. Cardiac troponins are highly specific markers of myocardial injury [1]. Serum cardiac troponin I elevation was initially reported with ischemic myocardial necrosis, but subsequently it has been reported with reversible ischemic myocardial injury such as in unstable angina, pulmonary embolism and sepsis; reversible non-ischemic myocardial injury such as in myocarditis, cardiac contusion and chemotherapy-induced myocardial injury; and in non-cardiac diseases such as in end-stage renal failure [2,3,12 – 15]. Changes in myocyte membrane related to reversibly injury are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of myocytes. Myocarditis associated cardiac troponin I release has been reported with various etiologies including idiopathic, viral, autoimmune, toxic venom related, and bacterial infection related myocarditis [16 – 22]. Cardiac troponin I release associated with myocarditis related to bacterial infection is exceptionally rare; Wanby and Olsen have reported such a case with Salmonella heidelberg and Campylobacter jejunii [20]. Serum cardiac troponin I in their patient reached a maximum level of 58 Ag/l (ng/ml). In cases of reversible myocardial injury associated with acute myocarditis, the recovery of myocardial function is independent of the serum cardiac troponin I levels [21,22]. Alter et al. reported a case of endomyocardial biopsyconfirmed varicella myocarditis in an adult where the serum cardiac troponin I level was markedly elevated at 63.4 Ag/ l (ng/ml) but there was a complete recovery from myocarditis in the due course of time [21]. Ammann at al. recently studied 22 patients with acute myocarditis [22]. Coronary angiography was performed in all patients to rule out significant coronary artery disease. Seventeen of 22 patients (77%) had elevated cardiac troponin I levels but no correlation was found between cardiac troponin I levels and subsequent recovery of left ventricular systolic function. The mean follow up period was of 119 F 163 days during which left ventricular ejection fraction improved from 47 F 17% during acute phase of myocarditis to 60 F 9% upon recovery. In this paper we have reported a case of diphtheria related severe acute myocarditis where there was a marked
353
elevation of serum cardiac troponin I, the level of which dropped as the left ventricular function recovered completely after successful treatment of diphtheria. This case supports the notion that the cardiac troponin I could be released in reversible myocardial injury and that the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.
References [1] Chu WW, Dieter RS, Stone CK. Evolving clinical applications of cardiac markers: a review of the literature. Wisc Med J 2002;101: 49 – 55. [2] Herrmann J, Volbracht L, Haude M, Eggebrecht H, Malyar N, Mann K, et al. Biochemical markers of ischemic and non-ischemic myocardial damage. Med Klin 2001;96:144 – 56. [3] Chen YN, Luo ZR, Zeng LJ, Wu MY, Wu YZ, Lin ZY. Cardiac troponin I: a marker for post-burn cardiac injury. Ann Clin Biochem 2000;37:447 – 51. [4] Coyle MB, Lipsky BA. Coryneform bacteria in infectious diseases: clinical and laboratory aspects. Clin Microbiol 1990;3:227 – 46. [5] Hoyne A, Welford N. Diphtheric myocarditis: a review of 496 cases. J Pediatr 1934;5:642 – 53. [6] Collier RJ. Diphtheria toxin: mode of action and structure. Bacteriol Rev 1975;39:54 – 85. [7] Hadfield TL, McEvoy P. The pathology of diphtheria. J Infect Dis 2000;181:S116 – 20. [8] Ledbetter MK, Benson CA. The electrocardiogram in diphtheric myocarditis. Am Heart J 1964;68:599 – 611. [9] Kadirova R, Kartoglu HU. Clinical characteristics and management of 676 hospitalized diphtheria cases. J Infect Dis 2000;181:S110 – 5. [10] Havaldar PV, Sankpal MN. Diphtheric myocarditis: clinical and laboratory parameters of prognosis and fatal outcome. Ann Trop Pediatr 2000;20:209 – 15. [11] Aravena-Roman M, Bowman R. Polymerase chain reaction for the detection of toxigenic corynebacterioum diphtheriae. Pathology 1995; 27:71 – 3. [12] Khan IA, Tun A, Wattanasauwan N, Win MT, Hla TA, Hussain A, et al. Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes. Am J Emerg Med 1999;17:225 – 9. [13] Mehta NJ, Jani K, Khan IA. Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism. Am Heart J 2003;145:821 – 5. [14] Tun A, Khan IA, Win MT, Hussain A, Hla TA, Wattanasuwan N, et al. Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers. Cardiology 1998;90:280 – 5. [15] Khan IA, Wattanasuwan N, Mehta NJ, Tun A, Singh N, Singh HK, et al. Prognostic value of serum cardiac troponin I in ambulatory patients with chronic renal failure undergoing long-term hemodialysis: a 2-year outcome analysis. J Am Coll Cardiol 2001;38:991 – 8. [16] Briassoulis G, Papadopoulos G, Zavras N, Pailopoulos V, Hatzis T, Thanopoulos V. Cardiac troponin I in fulminant adenovirus myocarditis treated with a 24-h infusion of high-dose intravenous immunoglobulin. Pediatr Cardiol 2000;21:391 – 4. [17] Kim M, Kim K. Elevation of cardiac troponin I in the acute stage of Kawasaki disease. Pediatr Cardiol 1999;20:184 – 8. [18] Meki AR, Mohamed ZM, Mohey El-deen HM. Significance of assessment of serum cardiac troponin I and interleukin-8 in scorpion envenomed children. Toxicon 2003;41:129 – 37. [19] Bertinchant JP, Polge A, Juan JM, Oliva-Lauraire MC, Giuliani I,
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D.R. Lakkireddy et al. / International Journal of Cardiology 98 (2005) 351–354
Marty-Double C, et al. Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings. Clin Chim Acta 2003;329:39 – 51. [20] Wanby P, Olsen B. Myocarditis in a patient with Salmonella and campylobacter enteritis. Scand J Infect Dis 2001;33:860 – 2.
[21] Alter P, Grimm W, Maisch B. Varicella myocarditis in an adult. Heart 2001;85:E2. [22] Ammann P, Naegeli B, Schuiki E, Straumann E, Frielingsdorf J, Rickli H, et al. Long-term outcome of acute myocarditis is independent of cardiac enzyme release. Int J Cardiol 2003;89:217 – 22.
Letter to the Editor
Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis Dhanunjaya R. Lakkireddy a, Ashok K. Kondur b, Ellie J. Chediak b, Chandra K. Nair a, Ijaz A. Khan a,* a
Division of Cardiology, Creighton University School of Medicine, 3006 Webster Street, Omaha, NE 68131 2044, USA b Harper University Hospital, Detroit, MI, USA Received 26 June 2003; accepted 28 October 2003 Available online 23 April 2004
Abstract Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness. D 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Cardiac troponins; Diphtheria; Corynebacterium diphtheriae; Myocarditis; Toxic myocarditis; Cardiac toxins; Reversible myocardial injury; Left ventricular dysfunction; Heart
1. Introduction Cardiac troponins are highly specific markers of myocardial injury [1]. It has been postulated that, unlike other markers of myocardial injury, troponins could be elevated in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes [1 – 3]. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae [4]. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility,
* Corresponding author. Tel.: +1-402-280-4573; fax: +1-402-2804938. E-mail address: [email protected] (I.A. Khan). 0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2003.10.062
which could be reversible with successful treatment [5]. We report a case of diphtheric myocarditis in a 20-year-old female who had markedly elevated serum levels of cardiac troponin I with completely reversible severe left ventricular systolic.
2. Case report A 20-year-old woman presented with complaints of 4 days of dysphagia, dysphonia, fatigue, and generalized malaise. Her symptoms had progressively worsened and she developed severe dyspnea upon admission. Physical examination revealed a severely ill looking patient who was febrile, tachycardic, and tachypneic with normal blood pressure and blood oxygen saturation of 94% at room air. Patient became stridorous during the examination. Orophar-
352
D.R. Lakkireddy et al. / International Journal of Cardiology 98 (2005) 351–354
ynx showed greenish uvula with desquamative pseudomembranuous type tissue extending to the tonsillar pillars and posterior pharyngeal wall (Fig. 1). Neck was tender without obvious lymphadentis. Nasopharyngoscopic examination not only confirmed these above plain-eye findings but also showed inflammation and edema involving nasal, oral, hypopharyngeal and supraglottic regions, extending up to the vocal cords with impending upper airway obstruction. Jugular venous pressure was elevated at 5 cm above clavicle. Examination of the heart revealed tachycardia with summation gallop and no murmur or rub. An emergent tracheostomy was done to secure the airway. Laboratory evaluation showed an elevated white cell count at 12,000 per mm3 with 20% bands, hemoglobin of 9.6 g/dl and platelets of 178,000 per mm3. At admission serum cardiac troponin I was 4.5 ng/ml, which subsequently rose to 16.4 ng/ml at 8 h and 48.5 ng/ml at 12 h after the initial measurement. Electrocardiogram revealed sinus tachycardia with diffuse non-specific ST-T wave changes. A 2D-echo with Doppler showed severely impaired left ventricular systolic function with ejection fraction of 10%. Left ventricular cavity size and wall thickness was normal. A working diagnosis of desquamative pharyngitis complicated by acute myocarditis and congestive heart failure was made. She was promptly treated with 100,000 units of antidiphtheria toxin through intravenous infusion and intravenous ampicillin with sulbactam based on clinical suspicion of diphtheria. Throat swabs were sent for stains and cultures. Cultures grew pneumococcus and pseudomonads but no Corynebacterium diphtheriae. The pseudomembrane biopsy was sent for polymerase chain reaction screen of diphtheria toxin, which was positive. Her heart failure was successfully treated with digoxin, furosemide, and angiotensin converting enzyme inhibitors. On the third day of admission, patient developed diplopia from a right occulomotor neuropathy. A follow up 2D-echo 4 days into treatment revealed improvement in the left ventricular systolic function and ejection fraction rose to 20%. Patient continued to improve on medical treatment a repeat 2Decho a week later showed a complete restoration of left ventricular systolic function with ejection fraction at 60%.
The serum cardiac troponin I level measured at that time was 1.1 ng/ml. Her diplopia resolved spontaneously. A repeat 2D-echo 6 months later continued to show a normal left ventricular systolic function.
3. Discussion Diphtheria toxin is a polypeptide exotoxin that inhibits elongation factor-2 activity in protein synthesis and causes DNA fragmentation and cyotolysis causing both local and systemic manifestations [6]. Absorbed toxin can cause myocarditis, neuritis and focal necrosis in various organs, including the kidneys, liver and adrenal glands. Early changes in diphtheric myocarditis include cloudy swelling of muscle fibers and interstitial edema. These changes are followed within weeks by hyaline and granular degeneration of muscle fibers progressing to myolysis and finally to the replacement of lost muscle with fibrosis causing permanent cardiac damage [7]. The myocardial changes could be completely reversible if treatment is instituted early. Myocarditis may develop during the acute phase of illness or when the local disease is resolving or it may begin insidiously after several weeks [5]. One half to two-thirds of the patients with diphtheria infection have subtle evidence of cardiac dysfunction, but clinically significant myocarditis develops in only 10– 25% of patients and is more severe when the onset is early. Electrocardiographic changes include non-specific ST-T wave changes, heart blocks, and arrhythmias including atrial fibrillation, ventricular premature complexes and ventricular tachyarrhythmias [8]. Clinical signs include diminished heart sounds, gallop rhythm and systolic murmurs. Isolating the organism from the local lesions makes definite diagnosis of diphtheria, but in 40% cases cultures could be negative or grow other organisms [9]. High index of clinical suspicion is a key to the diagnosis and should prompt immediate treatment with antitoxin [10]. Polymerase chain reaction can be used subsequently to screen the Corynebacterium diphtheriae isolates for toxinogenecity [11]. The dose of antitoxin is dependent on the duration
Fig. 1. Swelling, gray coloring, and friability of posterior commissure (left) and epiglottis (right) seen through rigid laryngoscope.
D.R. Lakkireddy et al. / International Journal of Cardiology 98 (2005) 351–354
and the extent of the disease. Primary nasopharyngeal diphtheria with myocarditis should be treated with at least 80,000 –100,000 U of antitoxin by infusion over 60 min to neutralize the unbound toxin rapidly. Possible allergies to horse serum should be ruled out and always tested and rapidly desensitized, if present, prior to the full dose treatment. Continuous monitoring and supportive care including fluids, airway protection, ventilation support, temporary pacemakers, and heart failure treatment are crucial, if indicated. Serial echocardiograms to evaluate cardiac function are important. The primary goal of antibiotics use is to eradicate Corynebacterium diphtheriae and prevent its transmission from the patient to susceptible contacts. Cardiac troponins are highly specific markers of myocardial injury [1]. Serum cardiac troponin I elevation was initially reported with ischemic myocardial necrosis, but subsequently it has been reported with reversible ischemic myocardial injury such as in unstable angina, pulmonary embolism and sepsis; reversible non-ischemic myocardial injury such as in myocarditis, cardiac contusion and chemotherapy-induced myocardial injury; and in non-cardiac diseases such as in end-stage renal failure [2,3,12 – 15]. Changes in myocyte membrane related to reversibly injury are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of myocytes. Myocarditis associated cardiac troponin I release has been reported with various etiologies including idiopathic, viral, autoimmune, toxic venom related, and bacterial infection related myocarditis [16 – 22]. Cardiac troponin I release associated with myocarditis related to bacterial infection is exceptionally rare; Wanby and Olsen have reported such a case with Salmonella heidelberg and Campylobacter jejunii [20]. Serum cardiac troponin I in their patient reached a maximum level of 58 Ag/l (ng/ml). In cases of reversible myocardial injury associated with acute myocarditis, the recovery of myocardial function is independent of the serum cardiac troponin I levels [21,22]. Alter et al. reported a case of endomyocardial biopsyconfirmed varicella myocarditis in an adult where the serum cardiac troponin I level was markedly elevated at 63.4 Ag/ l (ng/ml) but there was a complete recovery from myocarditis in the due course of time [21]. Ammann at al. recently studied 22 patients with acute myocarditis [22]. Coronary angiography was performed in all patients to rule out significant coronary artery disease. Seventeen of 22 patients (77%) had elevated cardiac troponin I levels but no correlation was found between cardiac troponin I levels and subsequent recovery of left ventricular systolic function. The mean follow up period was of 119 F 163 days during which left ventricular ejection fraction improved from 47 F 17% during acute phase of myocarditis to 60 F 9% upon recovery. In this paper we have reported a case of diphtheria related severe acute myocarditis where there was a marked
353
elevation of serum cardiac troponin I, the level of which dropped as the left ventricular function recovered completely after successful treatment of diphtheria. This case supports the notion that the cardiac troponin I could be released in reversible myocardial injury and that the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.
References [1] Chu WW, Dieter RS, Stone CK. Evolving clinical applications of cardiac markers: a review of the literature. Wisc Med J 2002;101: 49 – 55. [2] Herrmann J, Volbracht L, Haude M, Eggebrecht H, Malyar N, Mann K, et al. Biochemical markers of ischemic and non-ischemic myocardial damage. Med Klin 2001;96:144 – 56. [3] Chen YN, Luo ZR, Zeng LJ, Wu MY, Wu YZ, Lin ZY. Cardiac troponin I: a marker for post-burn cardiac injury. Ann Clin Biochem 2000;37:447 – 51. [4] Coyle MB, Lipsky BA. Coryneform bacteria in infectious diseases: clinical and laboratory aspects. Clin Microbiol 1990;3:227 – 46. [5] Hoyne A, Welford N. Diphtheric myocarditis: a review of 496 cases. J Pediatr 1934;5:642 – 53. [6] Collier RJ. Diphtheria toxin: mode of action and structure. Bacteriol Rev 1975;39:54 – 85. [7] Hadfield TL, McEvoy P. The pathology of diphtheria. J Infect Dis 2000;181:S116 – 20. [8] Ledbetter MK, Benson CA. The electrocardiogram in diphtheric myocarditis. Am Heart J 1964;68:599 – 611. [9] Kadirova R, Kartoglu HU. Clinical characteristics and management of 676 hospitalized diphtheria cases. J Infect Dis 2000;181:S110 – 5. [10] Havaldar PV, Sankpal MN. Diphtheric myocarditis: clinical and laboratory parameters of prognosis and fatal outcome. Ann Trop Pediatr 2000;20:209 – 15. [11] Aravena-Roman M, Bowman R. Polymerase chain reaction for the detection of toxigenic corynebacterioum diphtheriae. Pathology 1995; 27:71 – 3. [12] Khan IA, Tun A, Wattanasauwan N, Win MT, Hla TA, Hussain A, et al. Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes. Am J Emerg Med 1999;17:225 – 9. [13] Mehta NJ, Jani K, Khan IA. Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism. Am Heart J 2003;145:821 – 5. [14] Tun A, Khan IA, Win MT, Hussain A, Hla TA, Wattanasuwan N, et al. Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers. Cardiology 1998;90:280 – 5. [15] Khan IA, Wattanasuwan N, Mehta NJ, Tun A, Singh N, Singh HK, et al. Prognostic value of serum cardiac troponin I in ambulatory patients with chronic renal failure undergoing long-term hemodialysis: a 2-year outcome analysis. J Am Coll Cardiol 2001;38:991 – 8. [16] Briassoulis G, Papadopoulos G, Zavras N, Pailopoulos V, Hatzis T, Thanopoulos V. Cardiac troponin I in fulminant adenovirus myocarditis treated with a 24-h infusion of high-dose intravenous immunoglobulin. Pediatr Cardiol 2000;21:391 – 4. [17] Kim M, Kim K. Elevation of cardiac troponin I in the acute stage of Kawasaki disease. Pediatr Cardiol 1999;20:184 – 8. [18] Meki AR, Mohamed ZM, Mohey El-deen HM. Significance of assessment of serum cardiac troponin I and interleukin-8 in scorpion envenomed children. Toxicon 2003;41:129 – 37. [19] Bertinchant JP, Polge A, Juan JM, Oliva-Lauraire MC, Giuliani I,
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D.R. Lakkireddy et al. / International Journal of Cardiology 98 (2005) 351–354
Marty-Double C, et al. Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings. Clin Chim Acta 2003;329:39 – 51. [20] Wanby P, Olsen B. Myocarditis in a patient with Salmonella and campylobacter enteritis. Scand J Infect Dis 2001;33:860 – 2.
[21] Alter P, Grimm W, Maisch B. Varicella myocarditis in an adult. Heart 2001;85:E2. [22] Ammann P, Naegeli B, Schuiki E, Straumann E, Frielingsdorf J, Rickli H, et al. Long-term outcome of acute myocarditis is independent of cardiac enzyme release. Int J Cardiol 2003;89:217 – 22.