Fragile heart: an unusual cause of chest pain

A. Mohammed Rashid*

MRCEM Resident – 1st year, Kauvery Hospital, Chennai, India

*Correspondence: doctorrashid1992@gmail.com

Introduction

Eosinophilic Myocarditis (EM) is an acute life-threatening inflammatory disease of the heart. It is often an elusive diagnosis but treatment is straight forward. Very few cases of eosinophilic myocarditis have been reported in literature. Peripheral blood eosinophilia associated with cardiac symptomatology should always raise suspicion of EM.

Diagnosis of Eosinophilic myocarditis is usually made when patient has

  1. Eosinophilia (>0.5 K/mm3),
  2. Symptoms of chest pain, dyspnea, or palpitations,
  3. Elevated cardiac biomarkers,
  4. ECG changes, particularly ST-segment elevation (≈50% of cases) and pathological Q waves (≈20% of cases), and
  5. LV wall thickening and abnormal wall motion on echocardiography.

Case Presentation

A 33 years old male with no comorbidities presented at our emergency department with history of abdominal pain in the epigastric region that was colicky in nature, non-radiating, aggravated on changing posture, and relieved on taking rest, for the past seven days. He had no history of fever with rash/chills and rigor, cough, cold, vomiting, loose stools, decreased urine output, palpitations, breathlessness, headache, back pain, excessive sweating or giddiness. He was neither a smoker nor consumed alcohol. He had not taken any medications for the above complaints.

No history of any allergy in the past.

On receiving him in Emergency department he was conscious, oriented, afebrile with blood pressure of 110/70mmhg, pulse:105 beats/min, respiration of 20/min and a temperature of 98.4°F. He had no pallor, icterus, cyanosis, clubbing, lymphadenopathy or pedal edema.

On systemic examination: Chest was clear, no added sounds. Cardiac: S1S2 heard, no murmur. Abdomen revealed diffuse abdominal tenderness predominant in epigastric region, right hypochondrium and umbilical region with guarding rigidity. Bowel sounds heard. Per rectum: soft stools, no blood stains, fissure. Routine investigations were done.

Investigations

White blood cells 11,700
Red blood cells 4.27
Haemoglobin 12.6
C Reactive Protein 7
Procalcitonin 0.05
Platelet 4,32,000
Absolute lymphocyte count 4210
Absolute eosinophil count 1110
ESR 15
Total bilirubin 1.68
Direct bilirubin 0.47
Indirect bilirubin 1.21
SGOT 26.4
SGOT 39.2
Total protein 7.21
Albumin 4.29
Globulin 2.92

CT Chest

Mild right sided pleural effusion with bilateral basal dependent atelectatic changes. Cardiomegaly

CT Abdomen

Gall bladder was moderately distended with mild diffuse edematous wall thickening. Mild inflammation along the second part of duodenum, right paracolic gutter with mild thickening of right anterior renal and lateral conal fascia.

Capture

ECHO demonstrated: Global hypokinesia of LV

Severe LV Systolic Dysfunction (LVEF=30%)

Grade II AR, Mild MR

Grade II TR(RVSP-41mmHg)

Tachycardia noted during study(HR:103)

Dilated IVC -Non collapsing

 

ECG

Heart rate:100/min, sinus rhythm, normal axis, normal interval,

No significant ST/T changes

ECG-changes

 

Management

In view of persisting abdominal pain he was administered proton pump inhibitor, antipyretics and antiemetic.

In view of poor ejection fraction (30%) and tachycardia he was shifted to coronary care unit.

Cardiology evaluation

In view of Trop I: Negative, NTproBNP:6121 and ECG showing no significant MI changes, CAG was not done. Loading doses of Tab. Clopilet, Tab. Aspirin, Tab. Aztor and Tab. Flavedon mr were given as prophylaxis, and Inj. Lasi x 20 mg.

Gastroenterologist opinion suggested possibilities of eosinophilic enteritis and colitis. Advised to do mucosal biopsy and myocardial biopsy for further evaluation which the patient declined to undergo

He was managed on corticosteroid injection and fluid restriction < 1 L/day.

Repeated CBC showed increasing trend of eosinophil Count, hence provisional diagnosis was made of eosinophilic myocarditis. He was maintained on tapering doses of corticosteroid. He felt symptomatically better and was discharged on Tab. Wysolone 15 mg od and was advised review after 1 month.

On follow up, he was found to be asymptomatic and hemodynamically stable.

Discussion

Although no controlled trial data or guidelines exist, observational studies suggest a benefit from early immunosuppression with agents such as corticosteroids, cyclophosphamide, intravenous immunoglobulin, or antithymocyte globulin. Recently, Brambatti et al found a lower incidence of in-hospital death among those treated with corticosteroids (9.9%) versus those who were not (65.7%) [5].

EM is an inflammation of the heart muscle that is caused by the infiltration and inflammation from the eosinophils. Research has been focused on eosinophilic heart disease ever since 1936 when Löffler described two cases of endocarditis parietalis fibroplastica [1]. It was identified in 0.5% of cases in an unselected autopsy series of patients with heart failure and in 0.1% of cases among a cohort of patients biopsied for suspected myocarditis. The prevalence of EM in patients undergoing heart transplantation has been reported to be 3 to 7% [2,3].

Eosinophilia is considered to be reactive in lung, GIT, and urogenital tumors as well as in certain types of hematologic disorders such as T-cell and Hodgkin lymphomas.

Microbial agents that may provoke EM are the following:

  1. Viruses: Hepatitis B and C; Parvovirus, Adenovirus, Herpes simplex virus, Epstein-Barr virus and Rubella.
  2. Bacteria: Staphylococcus, Streptococcus, C-Diphtheria and tick-borne bacterias.
  3. Parasites: Trypanosoma cruzi, Toxoplasma, Trichinella and Entamoeba.
  4. Fungi: Yeast infections, such as candida; molds such as Aspergillus; and other fungi, such as Histoplasma, often found in bird droppings, can sometimes cause myocarditis [7].
  5. Vasculitis: Churg-strauss syndrome, a disorder marked by blood vessel inflammation. This inflammation can restrict blood flow to organs and tissues, sometimes permanently damaging them. This condition is also known as eosinophilic granulomatosis with polyangiitis (EGPA).
  6. Hematologic disorder: Idiopathic hypereosinophilia syndrome [9].

Conclusion

  1. Diagnosis of Eosinophilic myocarditis is usually made when patient has
  1. Eosinophilia (>0.5 K/mm3);
  2. Symptoms of chest pain, dyspnea, or palpitations;
  3. Elevated cardiac biomarkers;
  4. ECG changes, particularly ST-segment elevation (≈50% of cases) and pathological Q waves (≈20% of cases); and
  5. LV wall thickening and abnormal wall motion on echocardiography [11].
  1. Peripheral blood eosinophilia associated with cardiac symptomatology should always raise suspicion for EM.

It is often a forgotten cause of myocarditis, hopefully not anymore.

Acknowledgments

I would like to thank, Drs. S. Vadivel Kumaran, Medical  Gastroenterologist, K.P. Suresh Kumar, Senior Consultant Cardiologist, Dr. Vishnu, Consultant Cardiologist, Dr. Aslesha, Head of Emergency Department, Dr. Vidya, Emergency Physician for guiding me to prepare this article.

Reference

  1. Oakley CM, Olsen EGJ. Eosinophilia and heart disease. Brit Heart J. 1977;39(3):233-7.
  2. Ali AM, Straatman LP, Allard MF, et al. Eosinophilic myocarditis: case series and review of literature. Can J Cardiol. 2006;22:1233-7.
  3. Sugiyama Kato T, Mancini D, Marboe C. Characteristics of patients with advanced heart failure having eosinophilic infiltration of the myocardium in the recent era. Int Heart J. 2013;54:146-8.
  4. Working Group. Guidelines for diagnosis and treatment of myocarditis (JCS 2009): digest version. Circ J. 2011;75:734-43.
  5. Brambatti M, Matassini MV, Adler ED, et al. Eosinophilic myocarditis: characteristics, treatment, and outcomes. J Am Coll Cardiol. 2017;70:2363-75.
  6. Marzano AV, Lorini M, Carbonelli V, et al. Enhanced tissue factor expression by blood eosinophils from patients with hypereosinophilia: a possible link with thrombosis. PLoS ONE. 2014;9(11).
  7. Baandrup U. Eosinophilic myocarditis. Herz. 2012;37(8):849-53.
  8. Masi AT, Hunder GG, Lie JT, et al. The American college of rheumatology 1990 criteria for the classification of churg-strauss syndrome (allergic granulomatosis and angiitis) Arthr Rheumat. 1990;33(8):1094-100.
  9. Ogbogu PU, Bochner BS, Butterfield JH, et al. Hypereosinophilic syndrome: a multicenter, retrospective analysis of clinical characteristics and response to therapy. J Allergy Clin Immunol. 2009;124(6):1319.e3-25.e3.
  10. Friedrich MG, Sechtem U, Schulz-Menger J, et al. Cardiovascular magnetic resonance in myocarditis: a JACC white paper. J Am Coll Cardiol. 2009;53(17):1475-87.
  11. Caforio ALP, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2013;34(33):2636-48.
Dr-A-Mohammed-Rashid

Dr. A. Mohammed Rashid

MRCEM Resident

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