Myocarditis is defined as inflammation of the myocardium.
The most common cause is Coxsackie B virus infection. But it can also be due to other viruses(e.g. HIV, cytomegalo virus), bacterial, protozoal, metazoal and fungal infections. Rarely it could be due to hypersensitivity, or a toxic agent.
Few other specific causes are:
i) Rheumatic Carditis. (See section on rheumatic fever)
ii) Chagas Disease. It is seen in central and south America and is due to infection with trypanosome cruzi.
iii) Toxoplasmosis and cytomegalo virus myocarditis are usually seen in cardiac transplant recipients.
iv) Lyme disease (due to spirochete), eosinophilic myocarditis, giant cell myocarditis are other entities.
Pathology
Infection usually viral is responsible for cardiac injury. The infective agents induce adverse immunologic responses that persist despite eradication of the infective agent. The heart usually shows foci of active inflammation with necrosis. In toxoplasmosis, toxoplasma cysts are seen in myocytes. In eosinophilic and giant cell myocarditis, the predominant cells infiltrating myocardial interstitium are eosinophils and giant cells respectively.
Clinical Menifestation
There is H/O antecedent viral syndromes with flu like symptoms Patient may be totally asymptomatic and may have no signs.The clinical symptoms and signs are due to:
i) depressed LV function (both systolic and diastolic) viz. dyspnoea, cardiac failure and S3.
ii) arrhythmias-usually ventricular viz. palpitations. Syncope and sudden death is known to occur.
iii) Heart blocks, may occur. Sometimes patient may present as dilated cordiomyopathy with failure. Patients with peripartum cardiomyopathy have high frequency of myocarditis. The severity of myocarditis is judged by degree of LV dysfunction, presence of cardiac failure,arrhythmias and heart block. Clinically, a classification of primary myocarditis is proposed viz. Fulminant, subacute, chronic active and chronic persistent (Table ).
The most common cause is Coxsackie B virus infection. But it can also be due to other viruses(e.g. HIV, cytomegalo virus), bacterial, protozoal, metazoal and fungal infections. Rarely it could be due to hypersensitivity, or a toxic agent.
Few other specific causes are:
i) Rheumatic Carditis. (See section on rheumatic fever)
ii) Chagas Disease. It is seen in central and south America and is due to infection with trypanosome cruzi.
iii) Toxoplasmosis and cytomegalo virus myocarditis are usually seen in cardiac transplant recipients.
iv) Lyme disease (due to spirochete), eosinophilic myocarditis, giant cell myocarditis are other entities.
Pathology
Infection usually viral is responsible for cardiac injury. The infective agents induce adverse immunologic responses that persist despite eradication of the infective agent. The heart usually shows foci of active inflammation with necrosis. In toxoplasmosis, toxoplasma cysts are seen in myocytes. In eosinophilic and giant cell myocarditis, the predominant cells infiltrating myocardial interstitium are eosinophils and giant cells respectively.
Clinical Menifestation
There is H/O antecedent viral syndromes with flu like symptoms Patient may be totally asymptomatic and may have no signs.The clinical symptoms and signs are due to:
i) depressed LV function (both systolic and diastolic) viz. dyspnoea, cardiac failure and S3.
ii) arrhythmias-usually ventricular viz. palpitations. Syncope and sudden death is known to occur.
iii) Heart blocks, may occur. Sometimes patient may present as dilated cordiomyopathy with failure. Patients with peripartum cardiomyopathy have high frequency of myocarditis. The severity of myocarditis is judged by degree of LV dysfunction, presence of cardiac failure,arrhythmias and heart block. Clinically, a classification of primary myocarditis is proposed viz. Fulminant, subacute, chronic active and chronic persistent (Table ).
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| Pathologic Classification of Myocarditis |
Blood studies are nonspecific. There may be rise in ESR, CPK-MB. There may be abnormalities in T and B-lymphocyte counts CD 4/ CD8 ratios may be abnormal. Elevated IgM antibody titer to enterovirus may suggest previous infection.
X-Ray Chest
May show cardiomegaly and signs of pulmonary venous congestion.
Electrocardiography
Sinus tachycardia, diffuse ST.T. changes and prolonged QTc suggest myocarditis in setting of viral infection. Occasionally pattern of myocardial infarction is seen. LBBB and complete heart block can occur, but they are usually transient both supraventricular and ventricular arrhythmias are seen. The former occurs usually in presence of cardiac failure. The latter at times may be theonly manifestation of myocarditis. Holter shows episodes of unsustained ventricular tachycardia in almost 25 per cent of cases even with mild symptoms.
Echocardiography
It will usually show LV systolic dysfunction. Rarely segmental wall abnormalities may occur. LV size is normal or only slightly dilated Ventricular thrombi are seen in 15 per cent. Cardiac catheterization and hemodynamic studies are rarely done. The important diagnostic tool is endomyocardial biopsy. The diagnosis is based on Dallas criteria which define active myocarditis, as presence of inflammatory infiltrate and areas of necrosis (not typical of ischaemic changes). Imaging with radioisotopes which are inflammation avid e.g. gallium 67 or iridium III- antimyosin monoclonal antibody and MRI imaging are promising tools for the future.
Diagnosis
The diagnosis of myocarditis should be suspected under following circumstances.
1) In the setting of antecedent viral infection, diffuse ST.T Changes on EKG and/or presence of LV dysfunction on clinical examination or echo or cardiac failure.
2) In cardiac failure of no obvious etiology, if heart size is normal or only slightly dilated, in the young population.
3) Peripartum cardiomyopathy. At least 20 per cent are due to myocarditis.
4) Ventricular tachyarrhythmia in absence of any obvious cause. This needs to be confirmed by endomyocardial biopsy.
5) Sudden death in absence of any other cause.
Prognosis
1) Vast majority may remain asymptomatic at onset and have no residual evidence of LV dysfunction.
2) About 1/3rd of patients recover completely.
3) Severe forms of myocarditis may lead to dilated cardiomyopathy. However the frequency of progression is unknown. Sudden death is a rare event.
Management
Specific Therapy
A number of uncontrolled and nonrandomized studies suggested usefulness of immunosuppressant agents viz. prednisolone and azathioprine or more aggressively with interferon and anti-CD3. They remain unproven on multicentric, randomized trials. Similarly immune modulatory therapy with a single infusion of high dose immunoglobulin (29mg/kg) has
shown no benefit.
Symptomatic Therapy
This includes treatment of LV dysfunction and cardiac failure. Ventricular arrhythmias need to be treated with amiodarone and complete heart block with temporary pacing. Permanent pacemaker,AICD implantation or cardiac transplant are not indicated in acute phase. All need anticoagulant therapy in view ventricular thrombi.
X-Ray Chest
May show cardiomegaly and signs of pulmonary venous congestion.
Electrocardiography
Sinus tachycardia, diffuse ST.T. changes and prolonged QTc suggest myocarditis in setting of viral infection. Occasionally pattern of myocardial infarction is seen. LBBB and complete heart block can occur, but they are usually transient both supraventricular and ventricular arrhythmias are seen. The former occurs usually in presence of cardiac failure. The latter at times may be theonly manifestation of myocarditis. Holter shows episodes of unsustained ventricular tachycardia in almost 25 per cent of cases even with mild symptoms.
Echocardiography
It will usually show LV systolic dysfunction. Rarely segmental wall abnormalities may occur. LV size is normal or only slightly dilated Ventricular thrombi are seen in 15 per cent. Cardiac catheterization and hemodynamic studies are rarely done. The important diagnostic tool is endomyocardial biopsy. The diagnosis is based on Dallas criteria which define active myocarditis, as presence of inflammatory infiltrate and areas of necrosis (not typical of ischaemic changes). Imaging with radioisotopes which are inflammation avid e.g. gallium 67 or iridium III- antimyosin monoclonal antibody and MRI imaging are promising tools for the future.
Diagnosis
The diagnosis of myocarditis should be suspected under following circumstances.
1) In the setting of antecedent viral infection, diffuse ST.T Changes on EKG and/or presence of LV dysfunction on clinical examination or echo or cardiac failure.
2) In cardiac failure of no obvious etiology, if heart size is normal or only slightly dilated, in the young population.
3) Peripartum cardiomyopathy. At least 20 per cent are due to myocarditis.
4) Ventricular tachyarrhythmia in absence of any obvious cause. This needs to be confirmed by endomyocardial biopsy.
5) Sudden death in absence of any other cause.
Prognosis
1) Vast majority may remain asymptomatic at onset and have no residual evidence of LV dysfunction.
2) About 1/3rd of patients recover completely.
3) Severe forms of myocarditis may lead to dilated cardiomyopathy. However the frequency of progression is unknown. Sudden death is a rare event.
Management
Specific Therapy
A number of uncontrolled and nonrandomized studies suggested usefulness of immunosuppressant agents viz. prednisolone and azathioprine or more aggressively with interferon and anti-CD3. They remain unproven on multicentric, randomized trials. Similarly immune modulatory therapy with a single infusion of high dose immunoglobulin (29mg/kg) has
shown no benefit.
Symptomatic Therapy
This includes treatment of LV dysfunction and cardiac failure. Ventricular arrhythmias need to be treated with amiodarone and complete heart block with temporary pacing. Permanent pacemaker,AICD implantation or cardiac transplant are not indicated in acute phase. All need anticoagulant therapy in view ventricular thrombi.
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