One of the possible causes of dilated cardiomyopathy is considered to be a sequel to myocarditis. Two mechanisms have been proposed in the process of progression of myocarditis into dilated cardiomyopathy: one is a persistent viral infection, and the other is an autoimmune myocardial injury. To clarify the possible part played by the autoimmune mechanism in the process, using an animal model, we investigated whether autoimmune myocarditis, exclusively not related to viral infection, might develop into dilated cardiomyopathy. Experimental autoimmune myocarditis was elicited in Lewis rats by immunization with cardiac myosin fraction. Rats of the control group were immunized with ovalbumin. The clinical course was observed over 4 months. Six rats from the myosin-immunized group died during the acute phase and the healing phase, and all those rats had severe myocarditis. All rats that survived until the end of the study showed enlarged and discolored hearts. Aneurysmal changes were observed in the right ventricle during thoracotomy. The ratio of heart weight to body weight of the myosin-immunized group was significantly higher than that of the control group (3.36 +/- 0.49 versus 2.69 +/- 0.06 g/kg, respectively; P < .005). The lengths of the anterior interventricular fissure and the posterior interventricular fissure of the hearts of the myosin-immunized group were significantly longer than those of the control group. The external diameter of the left ventricle of the myosin-immunized group was also significantly larger than that of the control group. Diffuse myocardial muscle loss and replacement fibrosis were the prominent histological findings of the rats of the myosin-immunized group.(ABSTRACT TRUNCATED AT 250 WORDS)
Holter ECG in addition to ECG on admission is important for detecting persistent AF or PAF in patients with ischemic stroke, especially with cardioembolism as diagnosed by neuroimaging.
SUMMARYA 58-year-old Japanese woman was admitted to our hospital because of chest pain. A continuous murmur was detected at the left parasternal area. Electrocardiogram showed ST elevation in leads V 2 , V 3 and V 4 . Chest computed tomography and echocardiography demonstrated pericardial effusion and a large mass which was adjacent to the pulmonary artery. An abnormal blood flow was detected in the mass by Doppler echocardiography. Coronary angiography confirmed that the mass was a giant aneurysm of coronary arteriovenous fistula arising from both the left and right coronary arteries. This patient had no symptoms until rupture of the fistula. Rupture of a coronary arteriovenous fistula is very rare but can be a cause of chest pain and pericardial effusion. 1) Therapeutic strategies for coronary arteriovenous fistulas have not been clearly defined because the natural histories of the disorder are still uncertain.2) The majority of coronary arteriovenous fistulas are small and asymptomatic, especially in young patients. In older patients, both symptoms and fistula-related complications increase.3) Surgical repair for coronary arteriovenous fistulas is generally recommended in the presence of symptoms of heart failure or large left-to-right shunts.
4)On the other hand, the management for asymptomatic patients with a coronary arteriovenous fistula is controversial. We report the rupture of a giant aneurysm of a coronary arteriovenous fistula presented by chest pain with pericardial effusion. The patient had no fistula-related symptoms until the rupture.
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