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Papillary muscle rupture can be caused by a myocardial infarction, and dysfunction can be caused by ischemia. Rarely, blunt chest trauma can be the cause of papillary muscle rupture, resulting from the sudden deceleration or compression of the heart. [4] Complications may lead to worsening of mitral regurgitation. [5]
The trabeculae carneae and the papillary muscles make up a significant percentage of the ventricular mass in the heart (12-17% in normal human adult hearts), and are correlated with ventricular end diastolic volume. [5] Trabeculae ratios of capillary-to myocyte differ between the walls of the right and left ventricle.
The moderator band (also known as septomarginal trabecula [1]) is a band of cardiac muscle found in the right ventricle of the heart. [2] [3] [4] It is well-marked in sheep and some other animals, including humans. It extends from the base of the anterior papillary muscle of the tricuspid valve to the ventricular septum. [2]
There are three types of these muscles. The third type, the papillary muscles, give origin at their apices to the chordae tendinae which attach to the cusps of the tricuspid valve and to the mitral valve. The mass of the left ventricle, as estimated by magnetic resonance imaging, averages 143 g ± 38.4 g, with a range of 87–224 g. [2]
The anterolateral papillary muscle more frequently receives two blood supplies: left anterior descending (LAD) artery and the left circumflex artery (LCX). [5] It is therefore more frequently resistant to coronary ischemia (insufficiency of oxygen-rich blood). On the other hand, the posteromedial papillary muscle is usually supplied only by the ...
The papillary muscles extend from the walls of the heart to valves by cartilaginous connections called chordae tendinae. These muscles prevent the valves from falling too far back when they close. [24] During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight.
Papillary muscles are finger-like projections from the wall of the left ventricle. When the left ventricle contracts, the pressure in the ventricle forces the valve to close, while the tendons keep the leaflets coapting together and prevent the valve from opening in the wrong direction (thus preventing blood flowing back to the left atrium).
The role of these macrophages is the removal of necrotic myocytes. However, these cells are directly involved in the weakening of the tissue, leading to complications such as a ventricular free wall rupture, intraventricular septum rupture, or a papillary muscle rupture. At a gross anatomical level, this staged is marked by a yellow pallor.