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43. Acute Myocarditis: “I Thought My Soul Was Weak, but My Heart??”
Keywords
MyocarditisCongestive heart failureAdenovirusParvovirus B-19Human herpesvirus 6 Coxsackie BLymeCase
“I’m having trouble catching my breath!”
Pertinent History
A previously healthy 19-year-old male presented to the emergency department with a chief complaint of progressive shortness of breath and fatigue. He was seen by his family doctor 3 weeks ago for an upper respiratory infection and was treated symptomatically with acetaminophen/diphenhydramine combination. He has had improvement of his rhinorrhea, congestion, and sore throat; yet, for the past 3 days, he has had progressive difficulty walking a flight of stairs due to shortness of breath, and he has noticed swelling in bilateral lower legs. He reports intermittent palpitations and “heaviness” in his chest.
He denies recent travel, productive cough, hemoptysis, unilateral extremity swelling, and syncope. He endorses intermittent low-grade fever (Tmax 100.6 °F/38.1 °C yesterday), and a 12 lb. weight gain over the past week with no change in his diet.
PMH
No significant medical history. No medications other than Tylenol PM as needed No vitamins or supplements.
Social History
Drinks 2–3 alcoholic beverages per week
Smokes marijuana occasionally. No tobacco products.
Family History
Noncontributory
Pertinent Physical Exam
HR 122, RR 32, BP 120/65, Temperature 99.3 °F/37.4 °C, SpO2 95% on room air
Except as noted below, the findings of the physical exam are within normal limits.
ENT: Thyroid has no palpable nodules and is normal in size. JVD present (11 cm H2O) with a positive hepatojugular reflex.
Cardiovascular: Regular tachycardic rhythm, S3 gallop present.
Pulmonary: Tachypnea with bibasilar crackles. Speaking in 5–6-word sentences at a time.
Abdomen: No hepatosplenomegaly, abdomen soft and nontender in all quadrants with normal bowel sounds.
Extremities: Bilateral 2+ pitting edema to mid-shin. Equal, symmetric pulses in all extremities.
Skin: Diaphoretic and cool to the touch. No rashes, ecchymoses, or erythema.
Pertinent Test Results
ECG showed sinus tachycardia with new LBBB, but did not meet Sgarbossa criteria.
Chest X-ray showed bilateral interstitial edema and cardiomegaly.
Lab Results | |||
|---|---|---|---|
Test | Results | Units | Normal Range |
Troponin | 6.3 | ng/ml | <0.04 |
BNP | 800 | pg/ml | <100 |
TSH/T4, Chemistry, CBC, and D-dimer were all within normal limits.
Emergency Department Management
He was placed on continuous telemetry. Bedside ultrasound was performed, which demonstrated a LV with thickened walls with global decrease in cardiac contractility and evidence of interstitial pulmonary edema bilaterally. The inferior vena cava was plethoric and showed <50% collapsibility. The patient was given 40 mg IV furosemide, 325 mg aspirin and started on CPAP for work of breathing and to decrease his preload and afterload. Nitroglycerin was held initially as patient was normotensive.
Updates on Emergency Department Course
Upon initial reassessment, it was noted that patient was tolerating CPAP well and was less tachypneic. He reported feeling that his dyspnea had subjectively improved. ECG and troponin were repeated without significant change from previous findings. He was admitted to the cardiology service for suspected myocarditis with acute decompensated heart failure.
Learning Points
Priming Questions
- 1.
What are the important historical and clinical features of myocarditis?
- 2.
What diagnostic studies should you order to evaluate a patient for myocarditis?
- 3.
What are your first steps in treating a patient with acute myocarditis?
Introduction/Background
- 1.
Myocarditis is defined as an inflammatory disease of the myocardium that is diagnosed by defined histological, immunological, and immunohistochemical criteria according to the current WHO classification [1].
- 2.
Myocarditis has a wide spectrum of illness severity: it may be a mild and self-limiting condition, or it can be fulminant and life threatening [2].
- 3.
There are multiple etiologies of myocarditis, the most common of these is viral infections. Adenovirus, parvovirus B-19, and human herpesvirus 6 are the most common viruses attributed to the development of myocarditis. Enteroviruses, notably Coxsackie B, were the most common etiology up until the 1990s [2].
Other notable etiologies of myocarditis include bacterial (associated with Lyme disease), autoimmune diseases such as Churg–Strauss syndrome or Crohn’s Disease, hypersensitivity reactions to drugs (some examples include clozapine, penicillins, sulfonamides, and mesalamine), and toxic reaction to drugs (sympathomimetics, alcohol) [3].
- 4.
While it is difficult to ascertain the natural history of myocarditis, as many cases may be subclinical, the US Myocarditis Treatment trial enrolled adults with biopsy proven myocarditis, the mortality in a group of 111 patients was 20% at 1 year and 56% at 4.3 years [4].
Physiology/Pathophysiology
- 1.
The pathophysiology of acute myocarditis manifests in three distinct phases: the acute phase, the subacute phase, and the chronic phase [3].
The acute phase occurs in the first 1–3 days and consists of viral entry into the cardiac myocytes through a specific receptor: the coxsackie virus and adenovirus receptor [CAR]. Studies on explanted hearts with dilated cardiomyopathy have demonstrated higher CAR expression than in the myocardium of patients who do not have dilated cardiomyopathy [7]. Interestingly, when CAR is eliminated in rodent models, neither infection with coxsackievirus nor histologic evidence of myocarditis occurs [8].
During the acute phase, viral entry into myocytes induces cellular injury and eventual myocyte necrosis leading to exposure of intracellular antigens (myosin) and activation of the host’s innate immune system [3].
The subacute phase can last a few weeks to several months, and it includes activated virus-specific T cells that target the host myocardium. This leads to T-cell-induced myocardial injury with subsequent myocardial necrosis. In addition, high levels of cytokines, particularly TNF, and antibodies are produced during this phase [9].
In most patients, the host immune response subsides following viral elimination, and LV function is able to recover without sequelae; however, in some patients, the cardiomyopathy enters a chronic and irreversible stage [1].
The chronic phase develops if there is a persistent inflammatory response—cytokines activate matrix metalloproteinases, which destroy the natural interstitial collagen and elastin framework of the heart [10].
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