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A myocardial bridge (MB) is a common congenital heart anomaly in which one of the coronary arteries tunnels through the heart muscle itself.. In most people, the coronary arteries rest on top of the heart muscle and feed blood down into smaller vessels (e.g. the septal arteries) which then carry blood to the heart muscle itself (i.e. populate throughout the myocardium).
Sinoatrial arrest is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes. [1]
Fibrinous pericarditis is an exudative inflammation.The pericardium is infiltrated by the fibrinous exudate. This consists of fibrin strands and leukocytes.Fibrin describes an amorphous, eosinophilic (pink) network.
As a result, the myocardium continues to demand oxygen but is not adequately supplied by the coronary artery. This imbalance leads to ischemia, damage, and in some cases can lead to death of the myocardium tissue, causing a heart attack (myocardial infarction). A proposed disease hypothesis for SCAD
It can be seen in approximately 4% of cases of acute myocardial infarction [citation needed] It is the most common type of intraventricular conduction defect seen in acute anterior myocardial infarction, and the left anterior descending artery is usually the culprit vessel. It can be seen with acute inferior wall myocardial infarction.
Nonbacterial thrombotic endocarditis (NBTE) is a form of endocarditis in which small sterile vegetations are deposited on the valve leaflets. Formerly known as marantic endocarditis, which comes from the Greek marantikos, meaning "wasting away". [1]
Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or pericardial effusion.
An inferior wall myocardial infarction may cause damage to the AV node, causing third-degree heart block. In this case, the damage is usually transitory. Studies have shown that third-degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks. [4]
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