A heart attack is caused by necrosis (death) through lysis (membrane rupture) of the cells of part of the human heart muscle (myocardium) following a prolonged lack (hence the ischaemia) of blood and oxygen.
The majority of myocardial infarctions occurs around 30 minutes after the occlusion of one or more coronary arteries as a result of blood clots formed at the atherosclerotic plaques: plaques made up of accumulations of bad fat (cholesterol) and cellular waste products.
When it becomes very brittle and ruptures, the plaque elicits a reaction inside the arterial vessel and thus the birth of thromboses which, increasing progressively in volume, end up obstructing the entire coronary lumen and giving rise to heart attack.
But let’s go back to the papillaries: these muscle appendages face inside the ventricular cavity and the chordae tendineae (tendinous chords), i.e. the tissue filaments that ensure the stability of the mitral valve leaflets and prevent them - allow us the term - to “stray” (prolapse) into the atrium during cardiac activity, are grafted on them. There are 2 papillary muscles in the left ventricle (anterior and posterior muscle) and they can have a cleft structure.
The damage to the papillary muscles due to acute myocardial infarction (often associated with inferoposterior infarction caused by right coronary artery blockage), aided also by the intervened instability of the chordae tendineae, can lead, as we mentioned above, to valvular insufficiency with presence of blood regurgitation in the left atrium and - if not treated properly - to true heart failure.