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  • Acute Myocarditis Presenting as Cardiac Tamponade: DISCUSSION

The precise pathogenesis of myocarditis is unknown. Available evidence suggest a multifactorial process involving direct cell damage, autoimmunity and microvascular spasms with vascular damage.

Myocarditis has a varied presentation, from asymptomatic to heart failure and cardiogenic shock sometimes culminating in death. A clinical diagnosis is suggested by an antecedent history of viral illness with flu-like symptoms coupled with features of cardiac disease. The majority of patients have features consistent with prior viral illness. This subsides by the time myocarditis develops but usually occurs within two weeks of presentation. Symptoms include fatigue, malaise, myalgia, arthralgia, and fever. Patients may also have shortness of breath, palpitations, and chest pain.

Our patient’s history on presentation was consistent with a viral upper respiratory tract infection. In such patients with nonspecific symptoms, it is notunusual for the diagnosis of myocarditis to be missed. A high sense of awareness and clinical suspicion is necessary for a diagnosis to be made when a viral prodrome precedes symptoms of cardiac illness. Severe myalgia in the course of a viral syndrome has been suggested to be a pointer to those patients who may subsequently develop myocardial disease.

Usually the signs of disease include fever, tachycardia, cyanosis, hypotension, elevated JVD, and systolic murmurs. Tachycardia out of proportion to the degree of pyrexia suggests cardiac disease in the patient with a history of viral illness. Acute cardiac failure and cardiogenic shock are rare presentations of myocarditis. Even with such presentation, all the clinical features consistent with severe myopericardial disease may not be demonstrable. The main findings in our patient were tachycardia and hypotension. She did not have S3 gallop, JVD, or crackles on lung examination. However, the hemodynamic instability and the widened mediastinum on chest x-ray on presentation prompted the consideration of aortic dissection. TEE performed at the bedside in the emergency room excluded this possibility and revealed the presence of pericardial effusion and cardiac tamponade.
Abnormal results of laboratory tests, such as leuco-cytosis, and elevated erythrocyte sedimentation rate are usually nonspecific serving essentially as markers of inflammatory disease. Cardiac enzymes tend to be elevated. Serological tests support viral etiology when a four-fold increase in viral neutralizing antibody is demonstrable in paired sera or a positive culture is obtained from blood, stool, urine, or pharyngeal secretions. CXR findings indicative of cardiac involvement include an enlarged cardiac silhouette and prominent pulmonary veins. Electrocardiographic changes include low voltage complexes, ST changes, and possible arrhythmia. Myocardial infarction is a differential diagnosis in patients with chest pain. Q-waves may occur but are unusual in myocarditis. As observed in our patient, systolic function is usually depressed, and there may be evidence of pericardial effUsion on 2-D echocardiogram. silagra 100

Endomyocardial biopsy has served as the gold standard for the diagnosis of acute myocarditis with utilization of the “Dallas criteria”. A biopsy was not performed on our patient, and her diagnosis was made on clinical grounds. We did not insist on biopsy because of its limitations, such as significant interobserver variability and sampling error since the disease may be patchy or focal with multiple samples of biopsy being required. Moreover, there is still no clear consensus on therapeutic use of the biopsy results.

The management of acute myocarditis usually consists of general supportive measures, management of complications, and specific treatment when possible.

Management of complications of myocarditis is essentially directed at treating acute heart failure and arrhythmia if present. Angiotensin converting enzyme inhibitors (ACE inhibitors) and diuretics with or without digoxin are useful. Patients with significant reduction in left ventricular ejection fraction should receive ACE inhibitors unless contraindications exist, in which case a combination of hydralazine and isosorbide dinitrate, or the angiotensin-2 receptor blockers are acceptable alternatives. Diuretics, sodium, and water restriction are utilized when there is volume overload. Digoxin is given to patients with atrial fibrillation and rapid ventricular response and to those with impaired systolic function not adequately responsive to ACE-inhibitors and diuretics. B-blockers are not recommended in this acute phase. In patients with severe heart failure, hypotension, or shock as observed in the case reported admission to an intensive care unit with hemodynamic monitoring and the short-term use of ionotropic support may be beneficial. Complications not directly related to myocarditis may occur and need to be vigorously managed. Our patient required treatment for nosocomial pneumonia and pleural effusion.
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Specific treatment of viral myocarditis has concentrated mainly on the benefit or otherwise of immunosuppression. Our patient received no immunosuppressive therapy. The Myocarditis Treatment Trial demonstrated no survival difference or significant difference in left ventricular ejection fraction in patients treated with immunosuppressive therapy, compared with patients who received only conventional therapy.

The long-term prognosis of myocarditis is varied. While some reports suggest a good prognosis, albeit in individuals who on presentation had mild symptoms and normal left ventricular function, others indicate a poor outcome in those patients whose presentation is characterized by features of dilated cardiomyopathy. The majority of patients with less-than-desirable outcome reportedly had severe symptoms and impaired left ventricular fimction on presentation. Several clinical variables have been identified as predictors of a good outcome. These include normal left ventricular function, less-intensive conventional therapy, and a short duration of disease. A depressed right ventricular function has also been identified as an independent predictor of death or progression to cardiac transplant. suhagra 100

Our patient on presentation had reduced left ventricular function and required intensive treatment, thus indicating a poor outcome according to the above prediction model. Despite these negative indicator variables and fulminant presentation, she had a good outcome. We recommend a low index of suspicion for viral myocarditis in patients presenting with symptoms of a viral illness and cardiac dysfunction since complete resolution is attainable.

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