Myocardial infarction complications
Myocardial infarction complications may occur following a heart attack, or may need time to develop. 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 microscopic changes noted. From 4-24 hours you begin to see coagulative necrosis, characterized by the removal of dead cardiomyocytes through heterolysis and the nucleus through karyorrhexis 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". A major complication during this period is fibrinous pericarditis in transmural ventricular wall damage.
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. Weeks 1-3 are marked on histology by abundant capillaries, fibroblast infiltration. Fibroblasts start replacing the lost cardiomyocytes with collagen type 1 and leads to the granulation of tissue. After several weeks fibrosis heavy collagen formation. Collagen is not as strong or compliant as the myocardium that it replaced, this instability could lead to a ventricular aneurysm, the stasis of blood in an aneurysm can lead to a mural thrombus. A rarer complication that occurs during this time is Dressler’s syndrome and is thought to have autoimmune origins.
A myocardial infarction may compromise the function of the heart as a pump for the circulation, a state called heart failure. There are different types of heart failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles; the incidence of heart failure is high in patients with diabetes and requires special management strategies. Myocardial rupture is most common three to five days after myocardial infarction of small degree, but may occur one day to three weeks later. In the modern era of early revascularization and intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs; this may occur in the free walls of the ventricles, the septum between them, the papillary muscles, or less the atria. Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively.
The weakness may lead to ventricular aneurysm, a localized dilation or ballooning of the heart chamber. Risk factors for myocardial rupture include completion of infarction, female sex, advanced age, a lack of a previous history of myocardial infarction. In addition, the risk of rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI; the shear stress between the infarcted segment and the surrounding normal myocardium makes it a nidus for rupture. Rupture is a catastrophic event that may result a life-threatening process known as cardiac tamponade, in which blood accumulates within the pericardium or heart sac, compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart, which can lead to right ventricular failure as well as pulmonary overcirculation. Rupture of the papillary muscle may lead to acute mitral regurgitation and subsequent pulmonary edema and even cardiogenic shock.
Since the electrical characteristics of the infarcted tissue change, arrhythmias are a frequent complication. The re-entry phenomenon may cause rapid heart rates, ischemia in the electrical conduction system of the heart may cause a complete heart block; as a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may affect the heart sac; this is called pericarditis. In Dressler's syndrome, this occurs several weeks after the initial event. If pericarditis were to persist, pericardial effusion may occur which could in turn lead to cardiac tamponade if not properly treated. A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following is cardi
Cardiac muscle is one of three types of vertebrate muscles, with the other two being skeletal and smooth muscles. It is an striated muscle that constitutes the main tissue of the walls of the heart; the myocardium forms a thick middle layer between the outer layer of the heart wall and the inner layer, with blood supplied via the coronary circulation. It is composed of individual heart muscle cells joined together by intercalated discs, encased by collagen fibres and other substances that form the extracellular matrix. Cardiac muscle contracts in a similar manner to skeletal muscle, although with some important differences. An electrical stimulation in the form of an action potential triggers the release of calcium from the cell's internal calcium store, the sarcoplasmic reticulum; the rise in calcium causes the cell's myofilaments to slide past each other in a process called excitation contraction coupling. Diseases of heart muscle are of major importance; these include conditions caused by a restricted blood supply to the muscle including angina pectoris and myocardial infarction, other heart muscle disease known as cardiomyopathies.
Cardiac muscle tissue or myocardium forms the bulk of the heart. The heart wall is a three layered structure with a thick layer of myocardium sandwiched between the inner endocardium and the outer epicardium; the inner endocardium lines the cardiac chambers, covers the cardiac valves, joins with the endothelium that lines the blood vessels that connect to the heart. On the outer aspect of the myocardium is the epicardium which forms part of the pericardium, the sack that surrounds and lubricates the heart. Within the myocardium there cardiomyocytes; the sheets of muscle that wrap around the left ventricle closest to the endocardium are oriented perpendicularly to those closest to the epicardium. When these sheets contract in a coordinated manner they allow the ventricle to squeeze in several direction – longitudinally and with a twisting motion to squeeze the maximum amount of blood out of the heart with each heartbeat. Contracting heart muscle uses a lot of energy, therefore requires a constant flow of blood to provide oxygen and nutrients.
Blood is brought to the myocardium by the coronary arteries. These lie on the outer or epicardial surface of the heart. Blood is drained away by the coronary veins into the right atrium; when looked at microscopically, cardiac muscle can be likened to the wall of a house. Most of the wall is taken up by bricks, which in cardiac muscle are individual cardiac muscle cells or cardiomyocytes; the mortar which surrounds the bricks is known as the extracellular matrix, produced by supporting cells known as fibroblasts. In the same way that the walls of a house contain electrical wires and plumbing, cardiac muscle contains specialised cells for conducting electrical signals and blood vessels to bring nutrients to the muscle cells and take away waste products. Cardiac muscle cells or cardiomyocytes are the contracting cells; each cardiomyocyte needs to contract in coordination with its neighbouring cells to efficiently pump blood from the heart, if this coordination breaks down – despite individual cells contracting – the heart may not pump at all, such as may occur during abnormal heart rhythms such as ventricular fibrillation.
Viewed through a microscope, cardiac muscle cells are rectangular, measuring 100–150μm by 30–40μm. Individual cardiac muscle cells are joined together at their ends by intercalated disks to form long fibres; each cell contains myofibrils, specialised protein fibres that slide past each other. These are organised into the fundamental contractile units of muscle cells; the regular organisation of myofibrils into sarcomeres gives cardiac muscle cells a striped or striated appearance when looked at through a microscope, similar to skeletal muscle. These striations are caused by lighter I bands composed of a protein called actin, darker A bands composed of myosin. Cardiomyocytes contain T-tubules, pouches of membrane that run from the surface to the cell's interior which help to which improve the efficiency of contraction; the majority of these cells contain only one nucleus, unlike skeletal muscle cells which contain many nuclei. Cardiac muscle cells contain many mitochondria which provide the energy needed for the cell in the form of adenosine triphosphate, making them resistant to fatigue.
T-tubules are microscopic tubes. They are continuous with the cell membrane, are composed of the same phospholipid bilayer, are open at the cell surface to the extracellular fluid that surrounds the cell. T-tubules in cardiac muscle are fewer in number. In the centre of the cell they join together, running into and along the cell as a transverse-axial network. Inside the cell they lie close to the sarcoplasmic reticulum. Here, a single tubule pairs with part of the sarcoplasmic reticulum called a terminal cisterna in a combination known as a diad; the functions of T-tubules include transmitting electrical impulses known as action potentials from the cell surface to the cell's core, helping to regulate the concentration of cal
A myocardial bridge occurs when one of the coronary arteries tunnels through the myocardium rather than resting on top of it. The arteries rest on top of the heart muscle and feed blood down into smaller vessels that populate throughout the myocardium. However, if the muscle grows around one of the larger arteries a myocardial bridge is formed; as the heart squeezes to pump blood, the muscle exerts pressure across the bridge and constricts the artery. This defect is present from birth. Though affected individuals may never exhibit symptoms, clinical manifestations include asymptomatic anomaly, myocardial infarction, to sudden cardiac death; the incidence of the condition in the general population is estimated at 5% based on autopsy findings, but significance when found in association with other cardiac conditions is unknown. The condition is diagnosed on a scale based on. If there is less than 50% blockage the condition is benign. Blockage over 70% causes some pain. Small amounts of myocardial bridging are undetectable, as the blood flows through the coronary while the heart is relaxing in diastole.
This condition can cause complications such as vasospasm, angina pectoris, ventricular tachycardia. Additionally many patients express discomfort in specific positions. Surgery for symptomatic myocardial bridge of the left anterior descending artery may include myotomy, coronary artery bypass surgery, or both. Procedure selection is based on the size of the underlying artery during diastole, the presence of concomitant proximal coronary artery disease, the presence of anatomic factors that would increase the risk of myotomy. Surgical strategy for the management should be customized, the treatment of choice is myotomy but bypass surgery can be added when there is proximal coronary obstruction or anatomic anomalies that increase the risk of recurrence of the obstruction. Cardiac CT Angiography Harlan Krumholz, M. D. discusses myocardial bridging Medical definition of myocardial bridge Myocardial bridge summary by the Texas Heart Institute
The endocardium is the innermost layer of tissue that lines the chambers of the heart. Its cells are embryologically and biologically similar to the endothelial cells that line blood vessels; the endocardium provides protection to the valves and heart chambers. The endocardium underlies the much more voluminous myocardium, the muscular tissue responsible for the contraction of the heart; the outer layer of the heart is termed epicardium and the heart is surrounded by a small amount of fluid enclosed by a fibrous sac called the pericardium. The endocardium, made up of endothelial cells, controls myocardial function; this modulating role is separate from the homeometric and heterometric regulatory mechanisms that control myocardial contractility. Moreover, the endothelium of the myocardial capillaries, closely appositioned to the cardiomyocytes, is involved in this modulatory role. Thus, the cardiac endothelium controls the development of the heart in the embryo as well as in the adult, for example during hypertrophy.
Additionally, the contractility and electrophysiological environment of the cardiomyocyte are regulated by the cardiac endothelium. The endocardial endothelium may act as a kind of blood–heart barrier, thus controlling the ionic composition of the extracellular fluid in which the cardiomyocytes bathe. In myocardial infarction, ischemia of the myocardium can extend to the endocardium, disrupting the inner lining of the heart. Less extensive infarctions are "subendocardial" and do not affect the epicardium. In the acute setting, subendocardial infarctions are more dangerous than transmural infarctions because they create an area of dead tissue surrounded by a boundary region of damaged myocytes; this damaged region will conduct impulses more resulting in irregular rhythms. The damaged region may become more life-threatening. In the chronic setting, transmural infarctions are more dangerous due to the greater amount of muscular damage and the development of scar tissue leading to impaired systolic contractility, impaired diastolic relaxation, increased risk for rupture and thrombus formation.
During depolarization the impulse is carried from endocardium to epicardium, during repolarization the impulse moves from epicardium to endocardium. In infective endocarditis, the endocardium is affected by bacteria. Heart Myocardium Histology image: 64_06 at the University of Oklahoma Health Sciences Center - "Heart and AV valve" Histology image: 64_07 at the University of Oklahoma Health Sciences Center - "Heart and AV valve"