ACUTE MYOCARDITIS.pptx

ACUTE MYOCARDITIS Acute Myocarditis clinical syndrome characterized by inflammation of myocytes resulting from infectious, toxic, and autoimmune etiologies. Ongoing viral infection, myocardial destruction, and adverse remodeling can lead to persistent ventricular dysfunction and dilated cardiomyop...

ACUTE MYOCARDITIS Acute Myocarditis clinical syndrome characterized by inflammation of myocytes resulting from infectious, toxic, and autoimmune etiologies. Ongoing viral infection, myocardial destruction, and adverse remodeling can lead to persistent ventricular dysfunction and dilated cardiomyopathy. the clinical presentation may range from nearly asymptomatic to overt heart failure requiring transplantation; Acute myocarditis causes focal or diffuse inflammation of the myocardium Most causes are infectious, caused by viral, bacterial, rickettsial, spirochetal, fungal, or parasitic agents; Toxins, drugs and immunologic reaction can also cause myocarditis. Mortality/Morbidity Rarely, myocarditis is fulminant and leads rapidly to cardiovascular collapse and shock. Mortality for clinically significant and biopsy-proven myocarditis varies widely. - Patients who initially have and then subsequently clear virus as demonstrated by polymerase chain reaction of endomyocardial biopsy tissue have excellent recovery with a return to normal or near-normal left ventricular function and overall mortality less than 4%. - Patients with persistent viral genome expression and/or antimyosin auto antibodies show limited recovery of left ventricular (LV) function. Essential of diagnosis  Often follows an upper respiratory infection or GI infection  May present with chest pain (pleuritic or nonspecific) or signs of heart failure  ECG may show sinus tachycardia, other arrhythmias, nonspecific repolarization changes, intraventricular conduction abnormalities  Echocardiogram documents cardiomegaly and contractile dysfunction  Myocardial biopsy may reveal a characteristic inflammatory pattern. General considerations Viral myocarditis: most common form, usually caused by coxsackieviruses. Rickettsial myocarditis. Diphteric myocarditis: caused by the toxin and often is manifested by conduction abnormalities as well as heart failure. Chagas’ diseas: caused by the insect-borne protozoar Trypanosoma cruzi, is a common form of myocarditis in Central and South America; the major clinical manifestations appear after a latent period of more than a decade. At this stage, patients present with cardiomyopathy, conduction disturbances and sudden death. General considerations Toxoplasmosis. Among parasitic infections, trichinosis is the common cause of cardiac involvement. The potential for the HIV virus to cause myocarditis is well recognized. In addition, other infectious myocarditis are more common in patients with AIDS. Covid-19 related myocarditis History nonspecific illness characterized by fever>38°C within the preceding 30 days, fatigue, mild dyspnea, and myalgias. A few patients present acutely with fulminant congestive heart failure (CHF) secondary to widespread myocardial involvement. Small, focal inflammation in electrically sensitive areas may be the etiology of patients whose initial presentation is sudden death. History Most cases of myocarditis are subclinical; therefore, the patient rarely seeks medical attention during acute illness. These subclinical cases may have transient ECG abnormalities. An antecedent viral syndrome is present in more than one half of patients with myocarditis. The appearance of cardiac-specific symptoms occurs primarily in the subacute virus-clearing phase; therefore, patients commonly present 2 weeks after the acute viremia. History Chest pain – Chest discomfort is reported in 35% of patients. – The pain is most commonly described as a pleuritic, sharp, stabbing precordial pain. Pericarditis may be associated in many cases and may cause some of the clinical presentation of pain. Dyspnea on exertion is common. Orthopnea and shortness of breath at rest may be noted if CHF is present. Palpitations are common. Syncope in a patient with a presentation consistent with myocarditis may signal high-grade atrioventricular (AV) block and risk for sudden death. Physical Tachypnea and tachycardia are common. Tachycardia is often out of proportion to fever. Classic signs of ventricular dysfunction including the following: – – – – Jugular venous distention Bibasilar crackles Ascites Peripheral edema S3 may be noted with significant ventricular involvement. Cyanosis may occur. Murmurs of mitral or tricuspid regurgitation may be present due to ventricular dilation. Pericardial effusion, without tamponade, and pericardial and pleural friction rub Laboratory Studies Cardiac troponin Erythrocyte sedimentation rate (ESR), CRP is elevated in many patients with acute myocarditis Other serum biomarkers: cytokines, complement, and antiheart antibodies have been shown in studies to be routinely elevated in immune-mediated myocarditis. Leukocytosis is present in 25% of cases ECG Sinus tachycardia is the most frequent finding. Decreased QRS amplitude and transitory Q-wave development is very suggestive of myocarditis. Conduction delay, including Mobitz I, Mobitz II, or complete heart block Left or right bundlebranch block i Chest radiography A chest radiograph can reveal cardiomegaly. Pulmonary stasis: interstitial and alveolar edema Pleural effusion Echocardiography Impairment of left ventricular systolic and diastolic function Segmental wall motion abnormalities Impaired ejection fraction A pericardial effusion may be present, although findings of tamponade are rare. Ventricular thrombus has been identified in 15% of patients studied with echocardiography MRI MRI is capable of showing abnormal signal intensity in the affected myocardium. – MRI can demonstrate nodular and patchy areas of inflammation, can be used to guide later biopsy. – Especially consider MRI in patients with chest pain and positive cardiac enzyme level results with normal coronary anatomy. Diagnostic studies Serum viral titers and serologic tests for other agents may indicate the cause. Endomyocardial biopsy: round cell inflammatory response with necrosis, but the patchy distribution of abnormalities makes the test relatively insensitive. This picture defines an “active” inflammatory stage and may persist for many months. Treatment and prognosis Specific antimicrobial therapy is indicated when an infecting agent is identified. Immunosuppressive therapy with corticosteroids: when the process is acute (<6 months) and if the biopsy suggests ongoing inflammation; immunosuppressive therapy without histological confirmation is unwise. treatment of heart failure and arrhythmias. Many cases resolve spontaneously, but in others cardiac function deteriorates progressively and may lead to dilated cardiomyopathy. Many cases of dilated cardiomyopathy may represent the end stage of viral myocarditis!!! Management of Patients with Life-Threatening Acute Myocarditis Patients with life-threatening presentation should be supervised in ICU with hemodynamic monitoring, cardiac catheterisation (to exclude ACS) Endomyocardial biopsy In patients with hemodynamic instability a mechanical cardio-pulmonary assist device may be needed as a bridge to recovery or to heart transplantation ICD implantation for complex arrhythmias should be deferred until resolution of the acute episode Drug induced & toxic myocarditis Doxorubicin and other cytotoxic agents, and cathecolamines (especially with pheocromocytoma) can produce a pathologic picture of inflammation and necrosis;. The phenothiazines, lithium, chloroquine, disopyramide, antimony containing compounds, and arsenicals can also cause electrocardiographic changes, arrhythmias or heart failure. Hypersensitivity reactions to sulfonamides, penicillins, and amino salicylic acid Radiation can cause an acute inflammatory reaction as well as a chronic fibrosis, usually in conjunction with pericarditis. Cocaine cardiotoxicity : Cocaine can cause coronary artery spasm, myocardial infarction, arrhythmias and myocarditis. The Cardiomyopathies The cardiomyopathies :  a heterogeneous group of entities affecting the myocardium primarily and not associated with the major causes of cardiac disease, i.e., ischemic heart disease, hypertension, valvular disease, or congenital defects.  while some have specific causes, many cases are idiopathic. Classification of Cardiomyopathies 1. Dilated Cardiomyopathies 2. Hypertrophic Cardiomyopathies 3. Restrictive Cardiomyopathies Dilated Cardiomyopathy Essential of Diagnosis Symptoms and signs of heart failure ECG may show: atrial and ventricular hypertrophy; sometimes low QRS voltage in the limb leads due to difuse myocardial fibrosis, nonspecific repolarization abnormalities, intraventricular conduction abnormalities. X-ray shows cardiomegaly Echocardiogram confirms LV dilation, thinning and global myocardial dysfunction with reduced contractility, systolic dysfunction . General Considerations Dilated cardiomyopathies usually present with symptoms and signs of congestive heart failure (most commonly dyspnoea). Occasionally, symptomatic ventricular arrhythmias are the presenting event. Often no cause can be identified, but chronic alcohol abuse and myocarditis are probably frequent causes. Histologically, the picture is one of extensive fibrosis. Clinical Findings A. Symptoms and Signs:  The initial presentation may be severe biventricular failure.  The physical examination reveals cardiomegaly, S3 gallop rhythm, and often a murmur of functional mitral regurgitation.  Signs of left- and right-sided failure may be present on initial examination. Electrocardiography Cardiac MRI Treatment Few cases of cardiomyopathy are amenable to specific therapy. Alcohol use should be discontinued. There is often marked recovery of cardiac function following a period of abstinence in alcoholic cardiomyopathy. Endocrine causes (thyroid dysfunction, acromegaly, pheocromocytoma) should be treated. Immunosuppressive therapy is not indicated in chronic dilated cardiomyopathy. Classical diet and drug management of congestive heart failure( diuretics, ACE –inhibitors, low dose betablockers, consider chronic anticoagulation if cavities are much enlarged). Prognosis variable, with some patients remaining stable, some deteriorating gradually, and others declining rapidly. Once heart failure is manifest, the natural history is similar to that of other causes of heart failure. Arterial and pulmonary emboli are more common in dilated cardiomyopathy than in ischemic cardiomyopathy; suitable candidates may benefit from chronic anticoagulation especially when atrial fibrillation appears. Treatment of DCM Various surgical options are available for patients with disease refractory to medical therapy. These include the following: Left ventricular assist devices Cardiac resynchronization therapy (biventricular pacing) Automatic implantable cardioverter-defibrillators Ventricular restoration surgery Heart transplantation Hypertrophic Cardiomyopathy Essentials of Diagnosis May present with dyspnea, chest pain, syncope. Examination shows sustained apical impulse, S4 gallop, systolic ejection murmur. ECG shows LV hypertrophy, occasionally septal Q waves in the absence of infarction Echocardiogram shows hypertrophy, which may be asymmetric: usually shows normal or enhanced contractility and signs of dynamic obstruction. General Considerations Myocardial hypertrophy unrelated to any pressure or volume overload The interventricular septum may be disproportionately involved (asymmetric septal hypertrophy), but in some cases the hypertrophy is localized at the apex. The left ventricular outflow tract is often narrowed during systole between the bulging septum and an anteriorly displaced anterior mitral valve leaflet, causing a dynamic obstruction (hence the name of idiopathic hypertrophic sub aortic stenosis). The obstruction is worsened by factors that increase myocardial contractility (sympathetic stimulation, digoxin) or that decrease LV filling (Valsalva maneuver, peripheral vasodilators). General Considerations Hypertrophic cardiomyopathy is in some cases inherited as an autosomal dominant trait with variable penetrance caused by mutations of a number of genes, most of which code for myosin heavy chains. These patients usually present in early childhood. Except in late stages, hypertrophic cardiomyoparthy is characterized by a small, hypercontractile LV. Clinical Findings Symptoms and Signs:  The most frequent symptoms are dyspnea and chest pain.  Syncope is also common and is typically postexertional, when diastolic filling diminishes and outflow obstruction increases.  Arrhythmias are an important problem. Atrial fibrillation is a poor prognostic sign. Ventricular arrhythmias are also common, and sudden death may occur, often in athletes after extraordinary exertion. Clinical Findings Physical examination:  loud S4.  In cases with outflow obstruction, a loud systolic murmur is present that increases with upright posture or Valsalva’s maneuver and decreases with squatting. Clinical Findings Electrocardiography and Chest X-Ray:  LV hypertrophy is nearly universal.  Exagerated septal Q waves inferolaterally may suggest myocardial infarction. Diagnostic studies:  The echocardiogram is diagnostic, revealing asymmetric LV hypertrophy, systolic anterior motion of the mitral valve, a small and hyper contractile LV and delayed relaxation and filling of the LV during diastole.  Doppler ultrasound : dynamic obstruction of left ventricular outflow tract, mitral regurgitation. Treatment Beta-blockers should be the initial drug in symptomatic individuals, especially when dynamic outflow obstruction is noted on the echocardiogram. Dyspnea, angina and arrhythmias respond in about 50% of patients. Treatment Excision of part of the myocardial septum has been successful in patients with severe symptoms . Dual-chamber pacing may diminish left ventricular outflow tract obstruction. Patients with malignant ventricular arrhythmias and unexplained syncope in the presence of a positive family history for sudden death are probably best managed with an implantable defibrillator. Prognosis The natural history of hypertrophic cardiomyopathy is highly variable. Several specific mutations are associated with a higher incidence of early malignant arrhythmias and sudden death. Some patients remain asymptomatic for many years or for life. Sudden death, especially during exercise, may be the initial event. Hypertrophic cardiomyopathy is the pathologic feature most frequently associated with sudden death in athletes. Restrictive Cardiomyopathy characterized by impaired diastolic filling with preserved contractile function. This condition is relatively uncommon, with the most frequent causes being amyloidosis, radiation, and myocardial fibrosis after open heart surgery. In Africa, endomyocardial fibrosis, a specific entity in which there is severe fibrosis of the endocardium, often with eosinophilia (Loffler’s syndrome) is common. Restrictive Cardiomyopathy Other causes of a restrictive picture are infiltrative cardiomyopathies (eg, sarcoidosis, hemochromatosis, carcinoid syndrome) and connective tissue diseases (e.g., scleroderma). Almost invariably, conduction disturbances are present. Low voltage on the ECG combined with ventricular hypertrophy by echo are suggestive. Rectal, abdominal fat or gingival biopsies- as well as myocardial biopsy- can be diagnostic. ECG Echocardiography Restrictive Cardiomyopathy Differential diagnosis with constrictive pericarditis. Myocardial biopsies are usually negative with pericarditis but not in restrictive cardiomyopathy. In some cases, only surgical exploration can make the diagnosis. Diuretics can help, but excessive diuresis can produce worsening symptoms. Steroids may be helpful in sarcoidosis