In coronary heart disease (CHD) it comes to impaired blood flow to the coronary arteries. In most cases, atheroma are responsible. Clinically, CHD as silent ischemia, angina pectoris, acute coronary syndrome presented (unstable angina, myocardial infarction), and sudden cardiac death. The diagnosis results from the symptoms, ECG, stress testing, and sometimes from the coronary angiography. Prevention includes reducing modifiable risk factors (eg. As hypercholesterolemia, hypertension, lack of exercise, obesity and smoking). The treatment involves the administration of drugs and measures to reduce ischemia and to restore or improve coronary blood flow.

In industrialized countries, the CHD is the leading cause of death in both sexes and about making one-third of all deaths. The mortality rate is in fair-skinned men in the age group of 25 to 34-year-olds is about 1 / 10,000 and in the age group of 55 to 64-year-olds almost 1/100. The mortality rate of light-skinned men in the age group of 35- to 44-year-olds is 6.1 times higher than the light-skinned women of the same age group. For unknown reasons, the difference between the sexes in the non-fair-skinned population is less pronounced and in patients with diabetes mellitus. The death rate among women increases after menopause, and corresponds to an age of 75 years of men or is even higher.

In coronary heart disease (CHD) it comes to impaired blood flow to the coronary arteries. In most cases, atheroma are responsible. Clinically, CHD as silent ischemia, angina pectoris, acute coronary syndrome presented (unstable angina, myocardial infarction), and sudden cardiac death. The diagnosis results from the symptoms, ECG, stress testing, and sometimes from the coronary angiography. Prevention includes reducing modifiable risk factors (eg. As hypercholesterolemia, hypertension, lack of exercise, obesity and smoking). The treatment involves the administration of drugs and measures to reduce ischemia and to restore or improve coronary blood flow. In industrialized countries, the CHD is the leading cause of death in both sexes and about making one-third of all deaths. The mortality rate is in fair-skinned men in the age group of 25 to 34-year-olds is about 1 / 10,000 and in the age group of 55 to 64-year-olds almost 1/100. The mortality rate of light-skinned men in the age group of 35- to 44-year-olds is 6.1 times higher than the light-skinned women of the same age group. For unknown reasons, the difference between the sexes in the non-fair-skinned population is less pronounced and in patients with diabetes mellitus. The death rate among women increases after menopause, and corresponds to an age of 75 years of men or is even higher. Normally etiology is coronary heart disease before due to a rule arises coronary arterial atherosclerosis due subintimaler deposits of atheroma in the large and medium-sized coronary arteries. Rare coronary heart disease due to coronary artery spasm (see Variant angina) Vascular endothelial dysfunction may promote atherosclerosis and contribute to coronary artery spasm. Of increasing importance is now the endothelial dysfunction as a cause of angina without epicardial coronary artery spasm or (see syndrome X). Rare causes are Koronarembolien, dissection, aneurysms (eg. As in a Kawasaki syndrome) and vasculitis (z. B. in systemic lupus erythematosus or syphilis). Pathophysiology The various vessels are often unevenly affected by coronary artery disease. Typically, they can be found at points of turbulence (z. B. to vascular bifurcations). When the atheromatous plaque increases, the arterial vascular lumen becomes progressively smaller until it (often with angina pectoris) comes to ischemia. The degree of stenosis, which leads to ischemia, varies with the Sauersoffvedarf the heart muscle. Occasionally ruptures or disintegrates atheromatous plaque. The reasons are unclear, but are probably the plaque morphology, the calcium content of the plaque and the softening of plaque due to an inflammatory process together. Due to the rupture of collagen and other thrombogenic material free, the platelets and the coagulation cascade are activated. The result is an acute thrombus that breaks the coronary blood flow and requires a certain degree of myocardial ischemia. The consequences of acute ischemia, which are grouped under the term “acute coronary syndrome” (ACS), depend on the location and degree of obstruction and range from unstable angina pectoris over a transmural infarction to sudden death. A coronary spasm is a temporary focal increase in vascular tone, which leads to a significant narrowing of the vessel lumen and reduced blood flow and can cause symptomatic ischemia (Prinzmetal’s angina). A noticeable narrowing can promote the formation of thrombus and cause a infarction or life-threatening arrhythmias. The spasms can occur in arteries with or without atheroma. In arteries without atheroma of basal coronary tone is probably increased and the response to the vasoconstrictor stimuli probably increased. The exact mechanism is not clear, however, endothelial cell nitric oxide synthesis or variations in an imbalance between endothelial constricting and dilating factors may be involved. In arteries with atheroma atheroma causes endothelial dysfunction, possibly leading to a local hypercontractility. Among the mechanisms discussed include a loss of sensitivity to intrinsic vasodilators (eg. As acetylcholine) and an increased production of vasoconstrictors (z. B. Angiotensin II, Endothelin, leukotrienes, serotonin, thromboxane) in the region of the atheroma. Recurrent spasms can damage the intima and lead to the formation of atheroma further. The use of vasoconstrictive drugs (eg. As cocaine, nicotine) and emotional stress can also trigger coronary Spamsen. Risk Factors presence of risk factors for coronary heart disease are the same as risk factors for atherosclerosis: high blood levels of low density lipoprotein (LDL) cholesterol (see dyslipidemia) High blood levels of lipoprotein A Low blood levels of high-density lipoprotein (HDL) cholesterol diabetes mellitus (especially type 2) Smoking obesity Physical inactivity High levels of apo B (Apo B) High blood levels of C-reactive protein (CRP) Possibly, smoking among women at particularly high risk of myocardial infarction is (especially in women <45 years ). Genetic factors play a role and various systemic diseases (eg. As hypertension and hypothyroidism) and metabolic disorders (eg. As hyperhomocysteinemia) are additional risk factors. High levels of Apo B is a major risk factor, it can be an indication of an increased risk, even if the total cholesterol or LDL cholesterol are normal. A high serum concentration of C-reactive protein (CRP) is a sign of plaque instability and inflammation and may be a major indicator of the risk of an ischemic event as a high LDL levels. A high serum concentration of triglycerides and insulin (a sign of insulin resistance) may be risk factors, but this is not clearly understood. The risk of coronary artery disease increases by smoking, a fatty and high calorie diet, which, however, poor in phytochemicals (found in fruits and vegetables), fiber, and vitamin C, D and E is a diet relatively low in omega-3 (n -3) -mehrfach-unsaturated fatty acids (PUFA, at least in some people) and poor stress. Anatomieder coronary artery, the right and left coronary artery originate from the right or left sinus aortae in the aortic root just above the opening of the aortic valve (arteries of the heart). The coronary arteries are divided into large and medium arteries that run along the surface of the heart (epicardial coronary arteries). This branch out below in smaller arterioles that supply the myocardium. The left coronary artery begins as the left main trunk artery (LCA, left coronary artery) and divided immediately into the left anterior descending artery (LAD, Syn. LAD, left A. anterior descending) and sometimes the main trunk divides into three vessels, the medium is then referred to as the ramus intermedius. The RIVA usually follows the interventricular sulcus anterior and runs in some people over the Herzapex on. This artery supplies the anterior septum (to the proximal conduction system) and the anterior free wall of the left ventricle (LV). The RCX is usually smaller than the RIVA and supplies the lateral free wall of the left ventricle. Most people have a dominant right side: the right coronary artery (RCA, right coronary artery) runs in the sulcus posterior interventricular the right side of the heart. It supplies the sinus node (55%), the right ventricle (RV), and usually the AV node and the inferior myocardial wall. About 10-15% of people show a left dominance: The RCX is larger and extends to the supply of the rear wall and the AV node along the interventricular groove posterior. Arteries of the heart treatment drug therapy, including antiplatelet drugs, lipid-lowering agents (eg., Statins) and beta blockers percutaneous coronary intervention in acute thrombosis sometimes fibrinolytic drugs Coronary artery bypass surgery Treatment is aimed usually starting on the cardiac workload by reducing the oxygen demand and an improvement in coronary blood flow to reduce and stop the atherosclerotic process in the long run and reverse. The coronary blood flow can be improved by a percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). An acute coronary thrombosis can sometimes be dissolved by fibrinolytic drugs. Drug treatment The medical treatment of patients with coronary heart disease depends on the symptoms of cardiac function and the presence of other diseases. Among the recommended treatments include antiplatelet medications to prevent clot formation and statins to reduce LDL cholesterol levels (improving the short-term and long-term results likely by improving the atheromatous plaque stability and endothelial function). Beta blockers are effective in reducing the symptoms of angina pectoris (by decreasing the heart rate and contractility, which reduces the oxygen demand), and for the reduction of mortality after an infarction, v. a. when an LV dysfunction is present after myocardial infarction (MI). Calcium channel blockers are also helpful, often combined with beta-blockers in the treatment of angina and hypertension, but it could not be shown to reduce mortality. Nitrates widen the coronary arteries light and decrease venous return, reducing cardiac work and relieve the angina. Longer-acting nitrate drugs do not help in reducing angina events, but reduce the mortality. ACE inhibitors and angiotensin II receptor antagonists are most effective in CHD patients with LV dysfunction. There are little evidence to guide therapy for patients with endothelial dysfunction. The treatment is generally similar for typical atherosclerosis of large vessels, but it is feared that the use of beta-blockers increase the endothelial dysfunction kann.Perkutane coronary intervention (PCI) First PCI was performed only with balloon angioplasty. However, about 30-40% of the patients developed within 6 months restenosis and 1 of 3 needed ultimately angioplasty or bypass surgery. The insertion of a simple metal stents after angioplasty reduces the restenosis rate, but still many patients require repeated treatment. Drug-eluting stents that secrete an antiproliferative drug (z. B. sirolimus, paclitaxel, everolimus) over a period of several weeks have the restenosis rate is reduced to <10%. As controversies surrounding drug-eluting stents and abrupt stent thrombosis in 2016 came up, the use of new drug-eluting stents declined in most centers. Subsequent investigations have shown that the risk of acute thrombosis is much lower than previously thought. With the development of new platforms for drug-eluting stents, the incidence of in-stent thrombosis was significantly reduced. Today PCI is usually performed with stents and about three quarters of all stents used in the US are drug-putting. Patients without significant infarction or significant complications can accommodate relatively quickly their work and their normal activities after the insertion of a stent. However, strenuous activity should be avoided for 6 weeks. In-stent thrombosis occurs due to the inherent thrombogenicity of metal stents. Most cases occur within the first 24-48 hours. However, a late stent thrombosis (rare) occurs after 30 days and up to ?1 year occur both with simple metal stents as well as drug-eluting stents, v. a. after the treatment was stopped antiplatelet. A progressive endothelialization simple metal stents occurs in the first few months and reduces the risk of thrombosis. However, the anti-proliferative drugs that are secreted by drug-eluting stents inhibit this process and prolong the risk of thrombosis. Therefore, patients who undergo stent implantation, treated with various antiplatelet agents. The current standard therapy for patients with a simple metal or a drug-eluting stent is made of unlimited aspirin, plus clopidogrel, prasugrel or ticagrelor for at least 6-12 months and intraprocedural anticoagulation with heparin or a similar agent (z. B. bivalirudin , especially for those who have a high risk of bleeding). The best results are achieved when the newer antiplatelet agents are started before the procedure. Angioplasty stent var model = {thumbnailUrl: '/-/media/manual/professional/images/angioplasty_stent_01_high_blausen_de.jpg?la=de&thn=0&mw=350' imageUrl: '/ - / media / manual / professional / images / angioplasty_stent_01_high_blausen_de. ? lang = en & jpg thn = 0 ', title:' angioplasty stent ', description:' 'credits'', hideCredits: false, hideTitle: false, hideFigure: false, hideDescription: true}; var panel = $ (MManual.utils.getCurrentScript ()) Closest ( 'image-element-panel.'). ko.applyBindings (model, panel.get (0)); The glycoprotein IIb / IIIa inhibitors are but are not routinely given also in acute (i. E. No co-morbidities, no acute coronary syndrome), where elective stent to be implanted. Although they are controversial, they can be useful with an acute coronary syndrome in some patients, but should not be considered as routine into consideration. It is unclear whether it is advantageous to give glycoprotein IIb / IIIa inhibitors before arriving in the cath lab, but most national organizations do not recommend their use in this situation. After stent implantation, a statin is added if it is not already used. Patients receiving a statin before surgery, have a lower risk of periprocedural MI. The overall risk of PCI is comparable to that of coronary bypass surgery. The mortality rate is <1%, the Q-wave MI rate <2%. In <1% occurs due to Intimaeinrissen in an obstruction that makes then an emergency even bypass surgery required. The risk of stroke in PCI is significantly lower than with CABG (0.34% vs. 1.2%). PCI heals alone or the progression of coronary heart disease is not prevented, so statins part of a post-PCI treatment should be. For such treatment has been shown to be the long-term event-free survival verbessert.Koronararterielle bypass surgery (CABG) Coronary artery bypass graft (CABG) uses arteries (z. B. internal mammary, radial artery) whenever this is possible and portions of autologous veins (eg. saphena BV), if necessary, to bypass diseased segments of the coronary arteries. 1 year after the operation 85% of the venous bypasses are still open and, after 5 years, a third or more are completely blocked. All thing are after 10 years up to 97% of internal mammary grafts remain open. Arteries may hypertrophy to accommodate the increased blood flow. CABG is PCI is superior in patients with diabetes and in patients with multivessel disease who are susceptible to transplant. A coronary artery bypass surgery is usually performed with a heart-lung machine while the heart is stopped. This bypass machine pumps blood and enriches this with oxygen. The risks of this procedure include stroke and myocardial infarction. the risk is for patients with normal heart size without Myokardinfarktanamnese, good ventricular function and no additional risk factors for perioperative myocardial infarction in <5% of stroke at 1-2% and the risk of death at ? 1% (n. d. Talk .: depending on the success rate of heart surgery center). The risk increases with age and the presence of underlying disease. The operative mortality in a second bypass surgery is 3 to 5 times higher than in the first operation. After the use of a heart-lung machine about 25-30% of patients develop cognitive impairment or behavioral changes that may be caused by micro emboli within the cardiopulmonary bypass. Cognitive or behavioral changes are more common in older patients, which raises the suspicion that these changes are most likely due to decreased "neural reserve" is triggered, making the elderly more prone to minor injuries during the use of cardiopulmonary bypass. It may be this is mild to serious disorders that can persist for weeks or years. To minimize this risk, some cardiac surgical centers use a "Beating Heart" technique (CABG without the use of the heart-lung machine), in which a device mechanically stabilizes the complex of the heart, on which the surgeon operates. However, long-term studies have shown no lasting benefits of this approach compared to conventional coronary bypass surgery with heart-lung machine. CHD can also progress despite a bypass surgery. Postoperatively, the rate of proximal obstruction of the bypassed vessels increases. thrombus formation, it comes to a premature closure of the vein bypasses. A subsequent closure (several years later) is due to a slow atherosclerotic degeneration of the intima and media. Aspirin prolonged the patency of the vein bypasses. Smokes a patient after coronary bypass surgery on, this has serious adverse effects on the patency of the bypass. After CABG administration of a statin doses are required to achieve a recommended target LDL levels be commenced or continued should. Prevention The prevention of coronary heart disease involves modifying the atherosclerotic risk factors: smoking cessation weight loss healthy diet Regular exercise change of serum lipid levels reduction in salt intake adjustment of hypertension and diabetes antihypertensive drugs should be used to achieve a target blood pressure of <130/80 mmHg. Lowering blood lipid levels (especially with statins) can slow the progression of coronary heart disease or even reverse partially again. LDL targets are ? 100 mg / dl (? 2.59 mmol / L) in patients with known CAD 70-80 mg / dL (1.81 to 2.07 mmol / l) for those with history of an ischemic event. Nicotinic acid or fibrate can be added with an HDL <40 mg / dl (<1.03 mmol / l) in patients, although some recent studies have shown no less ischemic risk or slowed progression of atherosclerosis when drugs are used to to increase HDL (1). Note to prevent the first AIM-HIGH Investigators, soil WE, Probst Field JL, Anderson T, et al. Niacin in patients with low HDL cholesterol levels received intensive statin therapy. N Engl J Med 365 (24): 2255-2267, 2011. doi: 10.1056 / NEJMoa1107579.

Health Life Media Team

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