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Cardiomyopathy and Myocarditis

Cardiomyopathy and Myocarditis. 林少琳 高雄榮民總醫院. Pathology of DCM. Dilation of all 4 chambers, the ventricles are more dilated than atria. Scars are occasionally found in RV or LV. Thrombi were found at the ventricular apex in about 60% of autopsy cases.

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Cardiomyopathy and Myocarditis

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  1. Cardiomyopathy and Myocarditis 林少琳 高雄榮民總醫院

  2. Pathology of DCM Dilation of all 4 chambers, the ventricles are more dilated than atria. Scars are occasionally found in RV or LV. Thrombi were found at the ventricular apex in about 60% of autopsy cases. Microscopy: extensive areas of interstitial and perivascular fibrosis, cellular infiltrates, cellular hypertrophy, and myocardial cell degeneration. Coronary arteries are usually normal.

  3. Factors with reduced survival in dilated CM S3Depressed serum LV conduction delay sodium levelsElevation of filling pr. Elevated serum Age>55 years epinephrine levels Cardiac enlargementVentricular arrhythmia Depressed cardiac Large thallium defect output Myocardial biopsyDepressed ejection findings fraction Ventricularshape-more Functional class 3-4 spherical

  4. Medical Treatment for DCM For CHF : bed-rest, salt restrictio, diuretics, digitalis, vasodilator, converting enzyme, etc. Anticoagulation:I.v. heparin for 7-10 days followed by lifelone warfarin in DCM patients who has AF. Addition of antiplatelet may be helpful to prevent recurrent embolic episodes. Antiarrhythmics: low dose aminodarone may be healful to patients with VT, VF or who survival from sudden cardiac death.

  5. Surgery for DCM Mitral valvuloplasty or replacementin DCM patients who have severe MR. Cardiac transplantation in young individual who has refractory heart failure. One year survival is about 81% and 5-year survival 58%.

  6. Alcoholic Cardiomyopathy 1.Chronic excessive consumption of alcohol may be associated with CHF, hypertension, arrhythmia and sudden death. It is the major cause of secondary nonischemic dilated cardiomyopathy (DCM). 2. Ceasing consumption of alcohol may halt the progression of alcoholic DCM.

  7. Alcoholic Cardiomyopathy 3.Three machnism may result inmyocardial damage: (1) a direct toxic effect of alcohol or its metabolities (2) nutritional effect. Eg. Thiamine deficiency may lead to beriberi heart disease. (3) toxic effect due to additives (cobalt). 4. It has been speculated that alcohol caused myocardial damage only through dietary deficiencies, but now is clear that alcoholic DCM may occur in the absence of nutritional deficiencies. (N Engl J. Med 320:409.1989)

  8. Peripartum Cardiomyopathy (PPCM) 1. Most patients developed symptoms during the last month of pregnancy or immediately postpartum, although it may occur at any time during the last 3 months of pregnancy or the first 6 month postpartum. 2. The incidence is about 1/1500 in the U.S. but has a higher incidence (1/100) in certain part of Africa.

  9. Peripartum Cardiomyopathy (PPCM) 3.The incidence of PPCM is greater in women with twin pregnancy, multiparous, >30years of age, and black. 4.Patients usually have symptoms of CHF, chest pain, palptitation, and occasional peripheral or pulmonary embolization.

  10. Peripartum Cardiomyopathy (PPCM) 5. The PPCM may be due to myocarditis, nutritional deficiency, small-vessel coronary artery abnormalities, hormonal effects, toxemia, or maternal immunologiical response to fetal antigen. 6. About 50% may demonstrate deterioration, persistent LV dysfunction, chronic CHF, or early death.

  11. Treatment of PPCM 1.Acute CHF should be treated vigorously with O2diureties, inotropic support with digitalis and vasodilators. The hydralazine is safe for CHF during pregnancy. 2.Nitroprusside may have fetal toxicity in animals. Angiotensin-converting enzyme inhibitors have deleterious effect on B.P. control and renal function in the fetus, and therefore are not recommened for antepartum therapy.

  12. Treatment of PPCM 3.Immunosuppressive therapy is not recommended at the present time. 4.Subsequent pregnosis in women with PPCM are often associated with relapses and a high risk for maternal mortality. Thus, subsequent pregnancy should be discouraged in patients with PPCM.

  13. HCM-General Consideration Hypertrophic cardiomyopathy (HCM) is defined as ventricular hypertrophy without identifible cause that is associated with normal ventricular cavity size, and usually has myocardial fiber disarray. LV is the predominant site of involvement, RV involvement may occur in apparent isolation or in association with left-sided involvement. LV contraaction is usually normal or hyperdynamic but with diastoolic dysfunction.

  14. Management strategies in HCM Alcohol septal ablation Surgical therapy • Myectomy to relieve LVOT obstruction • Mitral valve replacement and myectomy with severe mitral regurgitation unrelated to LVOT obstruction • Permanent pacemaker insertion (currently experimental) • Appropriate AV delay to minimize LVOT gradient. AV=atrioventricular; LVOT=left ventricular out flow track.

  15. Recommendations for athletic activity of patients with hypertrophic cardiomyopathy (HCM) 1. Athletes with HCM should not ordinarily participate in competitive sports. 2. In low-risk HCM patients(>30 years old), consideration may be given to athletes without: a. Ventricular tachycardia on Holter monitoring b. Family history of sudden death c. History of syncope or episode of impaired consciousness

  16. Recommendations for athletic activity of patients with hypertrophic cardiomyopathy d.Severe hemodynamic abnormalities, including a LV outflow gradient  50 mmHg e.Exercise-induced hypotension f. Moderate or severe mitral regurgitation g.Enlarged left atrium ( 50 mm) h.Paroxysmal atrial fibrillation i. Abnormal myocardial perfusion (J Am Coll Cardiol 24:845, 1994)

  17. Endomyocardial fibrosis(EMF)--general consideration(2) 2. A young adult who presents with cardiac restriction and heart failure, with or without thromboembolism, and who has significant hyper-eosinophilia should be considered to have hypereosinophilic EMF until proved otherwise.

  18. Myocarditis 1. Myocarditis, i.e., cardiac inflammation, is most commonly the result of an infectious process. 2. Myocarditis also may result from a hyper-sensitivity to drugs or may be caused by radiation, chemicals, or physical agents.

  19. Viral Myocarditis Clinical Manifestation 1. Significant acute myocarditis in the United States is caused most commonly by viruses, especially coxsackievirus B. 2. The clinical manifestations range from an asymptomatic state, with transient ECG findings of ST-T abnormalities, to a fulminant condition with arrhythmias, heart failure, and death. 3. Viral myocarditis is most often self-limited and without sequelae, severe involvement may recur.

  20. Viral Myocarditis Clinical Manifestation 4. Viral myocarditis occasionally progresses to a chronic form and to dilated cardiomyopathy 5. Patients often give a history of upper respira-tory febrile illness, and viral nasopharyngitis or tonsillitis may be evident clinically. 6. The isolation of virus from the stool, pharyngeal washings, or other body fluids and changes in specific antibody titers are diagnostic.

  21. Viral Myocarditis Clinical Manifestation 7. Strenuous activity should be proscribed until the ECG has returned to normal. 8. Congestive heart failure may respond to the usual measures (digitalis, diuretics, salt restriction). Arrhythmias are common and are occasionally difficult to manage. 9. Deaths attributed to heart failure, tachy-arrhythmias, and heart block have been reported.

  22. HIV Myocarditis 1. Human immunodeficiency virus (HIV) infected patients usually have subclinical cardiac involve-ment, including pericardial effusion, right-sided chamber enlargement and neoplastic involvement. 2. The most common finding (10 % of HIV patients) is LV dysfunction, which appears to be due to infiltration of the myocardium by the virus itself or by other infections such as toxoplasmosis, and by cardiac metastasis in Kaposi’s sarcoma 3.The dilated cardiomyopathy of HIV infection may respond to standard therapy with digitalis, diuretics , and vasodilators.

  23. Bacterial myocarditis 1. Bacterial involvement of the heart is un- common, but it does occur, it is usually as a complication of bacterial endocarditis (typically due to Staphylococcus aureus and enterococci). 2. Myocardial abscess formation may involve the valve rings and interventricular septum. 3. Diphtheritic myocarditis develops in over one- quarter of the patients with diphtheria, and is the most common cause of death due to diphtheria.

  24. Bacterial myocarditis 4. Cardiac damage is due to the liberation of a toxin that leads to a dilated, hypocontractile heart; the conducting system is frequently involved. 5. Cardiomegaly and severe congestive heart failure typically appear after the first week of illness. 6. Prompt therapy with antitoxin is crucial; antibiotic therapy is also indicated but is of less urgency.

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