Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. Post-myocardial complications occur after a period of ischemia, these changes can be seen in gross tissue changes and microscopic changes. Necrosis begins after 20 minutes of an infarction. Under 4 hours of ischemia, there are no gross or microscopic changes noted. From 4-24 hours coagulative necrosis begins to be seen, which is characterized by the removal of dead cardiomyocytes through heterolysis and the nucleus through karyorrhexis, karyolysis, and pyknosis. On gross examination, coagulative necrosis shows darkened discoloration of the infarcted tissue. The most common complication during this period is arrhythmias. Day 1-7 is marked by the inflammatory phase. Days 1-3 are marked by “acute inflammation”, in which neutrophils infiltrate the ischemic tissue. A major complication during this period is fibrinous pericarditis, particularly in transmural ventricular wall damage (an infarct that impacted all 3 layers of the heart, the epicardium, myocardium, and endocardium). This leads to inflammation, such as swelling, leading to rubbing of the heart on the pericardium. Day 4 through 7 are marked by “chronic inflammation”, on histology macrophages will be seen infiltrating the tissue. 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. Weeks 1-3 are marked on histology by abundant capillaries, and fibroblast infiltration. Fibroblasts start replacing the lost cardiomyocytes with collagen type 1 and leads to the granulation of tissue. After several weeks fibrosis occurs and heavy collagen formation. Collagen is not as strong or compliant as the myocardium that it replaced, this instability could lead to a ventricular aneurysm, and the stasis of blood in an aneurysm can lead to a mural thrombus. A rarer complication that also occurs during this time is Dressler's syndrome and is thought to have autoimmune origins. Congestive heart failure A myocardial infarction may compromise the function of the heart as a pump for the circulation,