Management |
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ADMISSION to hospital is recommended for patients with suspected myocarditis in order to establish the diagnosis, to rule out acute coronary syndrome and to assess left ventricular function and its high-risk features( severe left ventricular dysfunction and ventricular arrhythmia).
In most cases, the clinical course is self-limiting and patients do not require therapy. Immunosuppression, interferon, IV immune globulin and immune-adsorption therapy are sometimes used to treat myocardial inflammation but cannot be generally recommended. Evidence of the benefits of these treatments is lacking. 35 For patients with fulminant myocarditis whose condition deteriorates despite optimal pharmacological management, there is a role for mechanical circulatory support.
Conventional treatment Because of the high incidence of left ventricular dysfunction, standard heart failure regimens should be initiated according to current guidelines. These include ACEIs or ARBs, diuretics, beta blockers and aldosterone antagonists. By early initiation of renin – angiotensin blockade, either with ACEIs or ARBs, chronic maladaptive cardiac remodelling can be attenuated or the progression to dilated cardiomyopathy reduced. 9
Loop and distal tubular diuretics are adjuncts in the medical therapy when symptoms are the result of sodium and water retention. 36 Beta blockers reverse the neurohumoral effects of the sympathetic nervous system, prevent catecholamine elevation, reduce heart rate and reduce the proapoptotic and cardiotoxic effects of cyclic adenosine
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Cardiac pacemaker.
monophosphate-mediated calcium overload. 37
In randomised trials, beta blockers have been shown to prolong survival, prevent arrhythmia and improve left ventricular ejection fraction. Clinical trials have demonstrated that metoprolol succinate, bisoprolol, carvedilol and nebivolol are able to improve ventricular function and heart failure symptoms, as well as reduce mortality and hospitalisations. 38
Beta blocker treatment should be avoided in the acute phase and is initiated after optimisation of volume status. Aldosterone antagonists improve left ventricular structural remodelling and performance by increasing left ventricular ejection fraction. They are added to ACEIs in patients with symptomatic New York Heart Association class III-IV heart failure with left ventricular systolic dysfunction. 39
NSAIDs and colchicine as‘ nonspecific’ anti-inflammatory therapy in pericarditis are not indicated in the treatment of patients with myocarditis. 9 Anecdotal evidence suggests NSAIDs may actually
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enhance the degree of inflammation and increase mortality.
Specific treatment Several treatments are based on expert consensus since the effect of a specific causative therapy has only been confirmed in a few studies. Response to immunosuppressive therapy has been reported in chronic virus-negative myocarditis, giant-cell myocarditis, cardiac sarcoidosis and autoimmune myocarditis. Immunosuppression should not be started with active infection. 3
In giant-cell myocarditis, combined treatment with immunosuppressants( cyclosporine and corticosteroids, with or without azathioprine or muromonab-CDs) may improve the poor prognosis and yield a median survival time of 12 months. 9 Early immunosuppressive therapy with high-dose corticosteroids has been associated with improved cardiac function in cardiac sarcoidosis. 9
Mechanical circulatory supports For patients with cardiogenic
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shock caused by acute fulminant myocarditis who deteriorate despite optimal medical treatment, mechanical circulatory support may be required. Despite the severe initial presentation, patients with fulminant myocarditis have an excellent prognosis and a high rate of recovery of ventricular function if aggressive treatment with mechanical circulatory support is initiated early. 9, 40 The threshold for mechanical circulatory support use in fulminant myocarditis is lower than that in cases of acute heart failure with cardiogenic shock from other causes.
Extracorporeal membrane oxygenation, intra-aortic balloon pump, transient or permanent left-ventricular-assisted device or biventricular-assisted device implantation, together with an implantable cardioverter defibrillator implantation, have been lifesaving as a bridge to either recovery or heart transplantation. 41 Although such support cannot cure myocarditis itself, the devices allow avoidance of fatality and increase the survival longevity of patients, especially in those with cardiogenic shock. 42
Cardiovascular implantable electronic device Temporary pacemaker insertion is required in patients with symptomatic atrioventricular block II or III. When these arrhythmias become persistent, which is rare, it necessitates permanent pacing. 9
An implantable device is indicated as secondary prophylaxis in patients with myocarditis following a cardiac arrest due to ventricular fibrillation or after symptomatic ventricular tachycardia.. A biventricular implantable cardioverter defibrillator is recommended for
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patients with left ventricular ejection fraction ≤35 % and left bundle block in New York Heart Association functional class II to IV per current guidelines.
Premature implantation of these devices should be avoided in the majority of cases as patients may improve significantly with guideline-directed heart failure therapy. These devices are considered early when indicated in patients with sarcoidosis or giant-cell myocarditis because of the poor prognosis. 9
Heart transplantation One to 8 % of patients with myocarditis ultimately proceed to heart transplantation. 43 The survival rate after heart transplantation for these patients is similar to patients with other forms of idiopathic dilated cardiomyopathy. Recurrent disease has been reported in giant-cell
43, 44
myocarditis and sarcoidosis. Therefore, close surveillance for recurrence post-transplantation, with echocardiography and EMB, is recommended in these patients.
Physical activity According to the European and American guidelines, it is strongly recommended that patients with myocarditis avoid any competitive and leisure-time sport activity for six months. 3, 8
Following a full reassessment at this stage, if the left ventricular dimension and function have normalised on echocardiography and no significant arrhythmias are present on exercise testing and 24-hour ECG Holter monitoring, they can
45, 46
resume their usual training. Sports confer a considerable risk of sudden death on these patients because of electrical instability of the inflamed myocardium. 45
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Prognosis |
Case studies |
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CLINICAL markers to predict cardiovascular death or heart transplantation in patients with suspected myocarditis include advanced New York Heart Association functional class, left ventricular and / or right ventricular dysfunction, elevated pulmonary artery pressure, syncope, systolic and diastolic hypotension, tachyarrhythmia and a QRS duration ≥120ms. 9
In patients with suspected myocarditis who have undergone EMB, immunohistological features of inflammation in the specimens have been found to be potent risk factors for identifying the patients likely to develop clinical deterioration, leading to cardiovascular death or heart transplantation. 47
The data show that neither the evidence of viral genome nor the histopathological Dallas criteria can reliably predict the outcome.
Patients with late gadolinium enhancement on CMR seem to have a higher risk of sudden cardiac death because it is a substrate for potential lethal arrhythmia. 48
The absence of beta blocker treatment is another marker for poor prognosis.
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Case study one ELLE, aged 17, presents to the ED with severe, gripping retrosternal pain four days after returning from a trip to Germany. The pain has been present for more than three hours. During the past week, she has experienced a dry cough, sore throat and nausea.
Physical examination reveals a BP of 110 / 70mmHg, a heart rate of 72bpm and a temperature of 37.3 ° C. A pleural rub is heard on the left posterior side of the chest, and a chest X-ray confirms a small left-sided pleural effusion. Elle is admitted to hospital.
Initial cardiac enzyme testing shows a low-level troponin leak of 47ng / mL. Inflammatory markers are also elevated, with a CRP of 25mg / mL, neutrophil count 12 x 109 / L and ESR of 70mm / hour. A 12-lead ECG shows concave STsegment elevation in the inferior leads( II, III and aVF) and frequent monomorphic ventricular ectopics.
Urgent echocardiogram demonstrates normal left ventricular size and function, with no features of underlying structural or valvular heart disease. On the day after
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admission, her temperature is elevated to 38.9 ° C in the morning and 39.5 ° C in the afternoon.
Scattered, small red dots appear on Elle’ s hands and feet, and the
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following day, the rash extends to her arms and legs. Both Elle’ s cheeks appear significantly flushed, raising the suspicion of an acute viral infection. An autoimmune |
screen is negative, excluding acute SLE. Repeat PCR testing for common viruses reveals acute IgM titer elevation for parvovirus B19.
The patient continues to receive 4g / day of paracetamol and 800mg ibuprofen four times daily. She is pain free after 48 hours of treatment and is discharged on day three. Both the 12-lead ECG and serial troponin levels remain normal, and a repeat echocardiogram after six months is unremarkable. The final diagnosis is peri-myocarditis and pleuritis caused by an acute parvovirus B19 infection.
Case study two Allan, 27, and previously healthy and fit, presents to his GP with a history of severe palpitations while playing tennis. He has no significant cardiovascular risk factors for coronary disease or a family history of sudden cardiac death.
Initial evaluation reveals a heart rate of approximately 180bpm, with a normal BP of 130 / 80mmHg and no symptoms of heart failure. A 12-lead ECG shows a broadcomplex tachycardia with right bundle-branch block morphology cont’ d next page
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