Dressler syndrome
Dressler syndrome's disease overview
Dressler syndrome is a secondary pericarditis after a severe heart damage as follows surgery, heart injury and most commonly secondary after heart attack . This syndrome, along with some other pericardial lesions, are collectively referred to as post -heart damage syndrome.
This syndrome is characterized by the onset factor that causes pericarditis, including: pericarditis onset after myocardial muscle infarction due to anemia myocardial necrosis; Cardiac illness after heart surgery (post -deductive syndrome) and pericarditis after an accident or treatment. These lesions destroy tissue, leading to the accumulation of organized fragments and blood in the pericardium, thereby activating inflammatory reactions and immune response in place and causing pericarditis.
Moreover, this inflammation not only localizes in the pericardium but also affects the heart muscle and many other positions, such as: epidemic inflammation, pericardium, fever. Severe complications such as heart failure, ventricular arrhythmia or severe abnormalities are very rare.
In general, complications of post -heart damage syndrome are very diverse and complicated even threatening deaths such as heart compression or pericarditis, which increases hospital stay and costs. treatment.
Causes of Dressler syndrome's disease
The pathogenesis of Dressler syndrome has not been completely explained clearly, but it is found that there are many evidence related to the body's autoimmune mechanism.In 1950, Dressler gave the term "pericarditis after myocardial infarction" due to an excessive increase in body sensitivity. Depending on the individual, the increased sensitivity of releasing antigens is produced from necrotic myocardial cells, thereby onset the reactions of the immune system. Thus, according to this explanation, this is a disease syndrome caused by autoimmune mechanism.
Therefore, the clinical feature of this syndrome is the autoimmune disease with fever, increasing the concentration of substances marking inflammatory points in the blood (e.g. CRP) and leukemia; Most responded to anti -inflammatory drugs, corticoide, colchicine and tend to relapse. However, Dressler syndrome in particular and after heart damage in general not only occurs in all autoimmune patients but also in children with immunodeficiency after heart transplantation. In short, the late pericarditis after myocardial infarction (Dressler syndrome) is the condition of the body responding to autoimmune after the heart tissue is destroyed due to myocardial infarction, after cardiac arrest, after surgery or surgery or Heart injury. Both Dressler syndrome and as well as post -heart damage syndrome responded well to anti -inflammatory drugs, thus strengthening the theory of the mechanism of disease through autoimmune intermediaries.
Symptoms of Dressler syndrome's disease
Clinical
most patients with pericarditis after myocardial infarction have no symptoms. The symptoms are described by many:
Subclinical tests showing systemitis:
ECG: Provides typical evidence of pericarditis with ST difference and PR difference in multiple monks (> 20%). Straight chest X -ray: It can be seen if there is a new or severe pleural effusion, with lung infiltration. Echocardiography: Helps assess the size of the heart chamber, myocardial muscle contraction function, heart valve structure and pericardial effusion. Dressler syndrome complications The reaction of the immune system, leading to Dressler syndrome can also cause pleural effusion Dressler syndrome can cause serious complications, although rarely occur such as: Contracting pericarditis: recurrent or chronic inflammation can cause the pericardium to thicken or scars leading to the pericardium to shrink, tighten the heart to reduce the possibility of the possibility Effective blood pump of the heart Based on the combination of clinical examination and appropriate testing Diagnostic measures for Dressler syndrome's disease
Dressler syndrome's disease treatments
Aspirin treatment is the optimal choice in the pericarditis after myocardial infarction at a dose of 650mg/6 hours for at least 4 weeks with inhibition of proton pump or acid resistant to protect the stomach. NSAID or corticosteroids should be avoided by reducing the healing of myocardial scar and spreading the infarction. NSAIDs should avoid coronary artery disease due to increasing the risk of drugs due to drugs. Non -steroid anti -inflammatory drugs (Ibuprofen or Naproxen/Naprosyn), acetaminophen (Tylenol) help reduce inflammation or relieve pain. Colchicine can be treated from the beginning but it is more appropriate in the case of chronic pericarditis or recurrence if the application of Aspirin is not effective
If the amount of liquid around the heart weakens the heart function, it is necessary to remove by suction. Severe cases may require surgery to remove part of the pericardium.
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