Overview Of Acute Coronary Syndrome (Acs)

(Unstable angina, acute MI, myocardial infarction)

Acute coronary syndrome results from an acute obstruction of a coronary artery. The consequences depend on the degree of narrowing and the location, ranging from unstable angina to a non-ST segment elevation myocardial infarction (NSTEMI, syn. Non-STEMI), ST segment elevation myocardial infarction (STEMI) and sudden cardiac death. The symptoms of these syndromes are similar (except sudden death). These include discomfort in the chest area with or without dyspnea, nausea and sweating and cold sweats. The diagnosis results from the ECG and the presence or absence of serological markers. The therapy consists of the administration of antiplatelet agents, anticoagulants, nitrates and beta-blockers. In a STEMI an emergency even reperfusion by fibrinolytic agents, percutaneous coronary intervention (PCI), or is sometimes performed by coronary bypass surgery.

(See also Overview of coronary heart disease.)

Acute coronary syndrome results from an acute obstruction of a coronary artery. The consequences depend on the degree of narrowing and the location, ranging from unstable angina to a non-ST segment elevation myocardial infarction (NSTEMI, syn. Non-STEMI), ST segment elevation myocardial infarction (STEMI) and sudden cardiac death. The symptoms of these syndromes are similar (except sudden death). These include discomfort in the chest area with or without dyspnea, nausea and sweating and cold sweats. The diagnosis results from the ECG and the presence or absence of serological markers. The therapy consists of the administration of antiplatelet agents, anticoagulants, nitrates and beta-blockers. In a STEMI an emergency even reperfusion by fibrinolytic agents, percutaneous coronary intervention (PCI), or is sometimes performed by coronary bypass surgery. (See also Overview of coronary heart disease.) Classification to acute coronary syndrome ghören Unstable angina non-ST-elevation myocardial infarction (NSTEMI) ST-segment elevation myocardial infarction (STEMI) These syndromes include all acute coronary ischemia and differ based on symptoms, ECG findings and cardiac markers -Mirror. It is helpful to distinguish the syndrome because prognosis and treatment may vary. Unstable angina (acute coronary insufficiency, Präinfarktangina, Intermediärsyndrom) is defined as one or more of the following in patients whose cardiac biomarkers do not meet the criteria for MI: Prolonged rest angina pectoris (usually> 20 min) Emerging angina a symptomatology that at least grade 3 CCS (Canadian Cardiac Society-) corresponds classification (see Table: classification system of the Canadian cardiovascular Society for angina pectoris) crescendo angina, d. H. a previously diagnosed angina (increasing z. B. ?1 to CCS degrees or until at least CCS grade 3) with pectoris now noticeably more frequent and more serious symptoms of longer duration or a lesser load threshold. During the attack, unstable angina pectoris and ECG changes, such as ST-segment depression, ST-segment elevation or an inversion of the T wave may occur. However, these changes are temporary. Among the cardiac markers CK is not increased, but cardiac troponin, especially when measured with highly sensitive troponin test (hs-cTn) may be slightly increased. This unstable angina pectoris is clinically unstable and often the harbinger of a myocardial infarction or arrhythmia, or, but less frequently, sudden cardiac death. The non-ST segment elevation myocardial infarction (NSTEMI, subendocardial infarction) is a myocardial necrosis (evidence of cardiac markers in the blood, troponin I or troponin T and CK are increased) without acute ST-segment elevation or Q waves. ECG changes, such as ST-segment depression, inversion of the T wave, or both may be present. ST segment elevation myocardial infarction (STEMI, transmural myocardial infarction) is a myocardial necrosis with ECG changes, showing a ST segment elevation, which is not rapidly removed by the administration of nitroglycerin, or a newly occurring left bundle branch block. The cardiac markers troponin I or troponin T and CK are elevated. Both types of MI may or may not produce Q waves in the ECG (Q wave MI, non-Q-wave MI). Etiology The most common cause of acute coronary syndrome is an acute thrombus in an atherosclerotic coronary artery atheromatous plaques are sometimes unstable or inflamed, tear open or shatter and put thrombogenic material free. This in turn activates platelets and sets the coagulation cascade in motion, causing acute thrombus is produced. This leads to a conformational change of the glycoprotein IIb / IIIa, which is the receptor for fibrinogen, on the membrane and thus to cross-linking (cross-linking) of the platelet (and thus to aggregation). Also atheromas that cause minimal obstruction can rupture and cause thrombosis. In> 50% of cases, the stenosis is <40% before the event. Thus, although the degree of stenosis helps with symptom forecast, it is not always says thrombotic events before. The resulting thrombus suddenly obstructs the blood flow to some areas of the myocardium. A spontaneous thrombolysis occurs in about two-thirds of patients. After 24 hours, a thrombotic obstruction is only about 30% of patients. Almost always, however, the obstruction lasts long enough to cause tissue necrosis. Less common causes of acute coronary syndromes are embolism of the coronary arteries coronary spasm Coronary arterial embolism can occur in mitral or aortic stenosis, infective endocarditis or maran genetic endocarditis. A cocaine use and other causes of coronary spasms can in some cases lead to a myocardial infarction. A triggered by coronary artery spasm myocardial infarction may occur in normal or atherosclerotic coronary arteries. Pathophysiology The initial impact will depend on the extent, location and duration of the obstruction and range from transient ischemia to a heart attack. The measurement of newer, more sensitive cardiac markers shows that it probably comes even in mild forms of cell necrosis. Ischemic events are therefore often held and a division into sub-groups appear so, even if it would be useful, a little arbitrary. Sequelae after an acute event depend primarily on how large and the nature of the infarcted cardiac tissue. Myocardial dysfunction in ischemic (but not infarcted) tissue contractility and relaxation are affected. This results in hypokinetic or akinetic segments, which expand during systole or bulge out (so-called. Paradoxical movement). The extent of the affected area determines the effect, ranging from a minimal to mild heart failure to cardiogenic shock; usually large parts of the myocardium ischemic must be to cause significant myocardial dysfunction. About two-thirds of hospital patients with acute myocardial infarction there is a certain failure, you will be referred to as ischemic cardiomyopathy, when the low cardiac output and heart failure persist. Ischemia involving the papillary muscles can lead to mitral regurgitation. Dysfunctional wall movement can thrombus formation ermöglichen.Myokardinfarkt (MI), myocardial infarction is an ischemic myocardial necrosis due to an abrupt decrease in coronary blood flow in a myocardial portion. The infarcted tissue is permanently damaged, but the ischemic dysfunction of the surrounding tissue is potentially reversible. Myocardial infarction refers mainly to the left ventricle (LV), however, the damaged area to the right ventricle (RV) or the atria may extend. A heart attack may be transmural or non-transmural. Transmural infarcts involve all layers of the wall of the myocardium from epicardium to endocardium and are usually characterized to by pathological Q waves on ECG. Nontransmural or subendocardial infarcts do not extend through the ventricular wall and cause only out of changes in the ST segment and the T wave (ST-T). Because the transmural depth of necrosis can not be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI, if a ST-segment elevation or Q waves are present in the ECG or not. Necrosis of a substantial part of the septum or ventricular wall can rupture, with dire consequences. It can form a ventricular aneurysm or pseudoaneurysm, Electrophysiological dysfunction Electrical malfunction may be significant in any form of ACS. Ischemic and necrotic cells have lost their ability to a normal electrical activity. This is reflected in different ECG -changes (primarily in ST-T abnormalities), arrhythmias and conduction disturbances. The ST-T abnormalities in ischemia (often drop from the J-point) are located in a ST-segment depression, inversion of the T-wave, ST-segment elevation (often referred to as a current of injury) and pointed in a high T-wave in the hyperacute infarction phase. Conduction disturbances can reflect the damage of the sinus node, the AV node or the specialized conduction tissue. Most of the changes are temporary, but some remain. Symptoms and signs The symptoms of acute coronary syndrome depend on the extent and location of the obstruction and can be quite different. Painful stimuli of thoracic organs, including the heart, can cause discomfort, which can be painful, stinging and sometimes perceived as a sharp pain as pressure, tearing the air with a Aufstoßdrang, upset stomach, burning. Many patients deny that they have and pain just this simply as "discomfort" off. The assessment of the extent of ischemia solely on the basis of symptoms, with the exception of a massive heart attack, very difficult. Symptoms of ACS are similar to those of angina pectoris and are discussed more pectoris and acute myocardial infarction in sections unstable angina. After the acute event, many complications can occur. Usually they involve electrical dysfunction z. B. (conduction failure, arrhythmias) Malfunctions of the myocardium (for. Example, heart failure, rupture of the ventricular septum, or rupture of the free wall, ventricular aneurysm, pseudoaneurysm, murale thrombus formation or cardiogenic shock) Valvulare dysfunction (typically mitral insufficiency) with any form of ACS can be significant electrical noise, but large areas of myocardial ischemia must be to cause significant myocardial dysfunction. Other complications of ACS include recurrent ischemia and pericarditis. Pericarditis which occurs 2-10 weeks after an MI is referred to as post-MI syndrome or Dressler's syndrome. Diagnosis Serial ECGs Serial cardiac markers Immediate coronary angiography in patients with STEMI or complications (eg. As persistent chest pain, hypotension, significantly increased cardiac markers, unstable arrhythmias) Delayed angiography (24-48 h) pectoris in patients with NSTEMI or unstable angina without the above mentioned side effects an ACS> 30 years and in women> 40 years should then be drawn (in patients with diabetes mellitus even in younger people) are considered among men when the main symptoms are pain or discomfort in the chest area. The pain must be from other pain associated with pneumonia, pulmonary embolism, pericarditis, rib fracture, rib cartilage separation, esophageal spasm, acute aortic dissection, kidney stones, or splenic infarction are distinguished in various abdominal complaints. In patients with a previously diagnosed hiatal hernia, peptic ulcer or gall bladder disorders caution should suddenly be allocated to these diseases new symptoms. (For approach to diagnosis, see also chest pain.) In a suspected ACS, the procedure is always the same: initial ECG and other serial ECG analysis, serial measurements of cardiac enzymes that make a distinction unstable angina from a NSTEMI or STEMI possible. Each emergency facility should have a triage system to identify patients with chest pain to quickly and be able to initiate the specific survey instruments, and ECG. The measures the pulse oximetry and include chest X-ray (v. A. To detect an extension of the mediastinum, which indicates an aortic dissection). ECG The ECG is the most important investigation and should be done within the first 10 minutes. The ECG findings is the trend for the next steps. Fibrinolysis can help with STEMI may, while increasing the risk in NSTEMI. In addition, an urgent cardiac catheterization in patients with acute STEMI is indicated, but not in those with NSTEMI. (Editor’s note: The Kutkoronarangiographie is also not used, it is the Revaskularisationsstrategie the first choice The Akutkoronarangiographie is indicated in patients with acute STEMI, but not in those with NSTEMI!). A STEMI is usually due to the initial ECG -Befundes diagnosed. Here, a ST-segment elevation ? 1 mm in 2 or more contiguous leads that detect the damaged tissue shows (obtained Acute lateral LV infarction (tracing within a few hours of onset of disease).). Clinical calculator: M.I. “Prediction Decision TreeCalc” Acute lateral LV infarction (tracing within a few hours of onset of the disease condition). There is a striking hyperacute ST-segment elevation in leads I, aVL, V4 and V6 and reciprocal depression in other derivatives. (Editor’s note:.. The ECG changes that are listed here are typical (for the sides = lateral) wall infarction and not for anterior infarction in acute anterior myocardial infarction it raises in V1-V4) Clinical Calculator: prediction of myocardial infarction without Q wave pathological Q waves are not necessary for diagnosis. The ECG analysis must be done very carefully because an ST-segment elevation, v. a. in the inferior leads (II, III, aVF), can be very subtle. Sometimes the attention can be incorrectly drawn to derivatives with an ST-segment depression. At a characteristic symptomatology the ST-segment elevation in the ECG has a specificity of 90% and a sensitivity of 45% for the diagnosis of myocardial infarction. The first diagnosis can confirm when at repeated recordings (every 8 h on the first day, then 1 times a day) shows a gradual movement towards stable, more normal pattern or in the following days (Inferior (diaphragmatic) LV infarction develop (after the first 24 h) pathological.) Q waves. Inferior (diaphragm) LV infarction (after the first 24 h). Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF. Since nontransmural infarction (non-Q-wave myocardial infarction) is usually play in the subendocardial or middle myocardial layers, they do not occur together with pioneering Q waves or a unique ST-segment elevation in the ECG. Instead, they usually lead only to ST-segment and T-wave changes of varying amounts that are less conspicuous, variable or non-specific and sometimes difficult to interpret (NSTEMI). Disappearance of these deviations (or enhance it yourself) in repeated ECG recordings, ischemia is very likely. In repeated unchanged ECG findings acute myocardial infarction is unlikely. However, there is still clinically suspected, the diagnosis has to be proven otherwise. A normal ECG in a pain-free patient does not rule out unstable angina pectoris. A normal ECG, recorded during an attack of pain does not rule out angina, but suggests that the pain is not due to ischemia. If you suspect a right ventricular infarction is usually an ECG with 15 derivations with additional leads in V4R and, for the diagnosis of posterior wall infarction, in V8 and V9 is recorded. (Editor’s note: If you suspect a RV infarction (especially in the context of an extended rear wall infarction) is written an ECG with right precordial leads V1R-V6R usually being especially ST-segment elevation in V4R relevant if there are signs of a. extended side wall infarction (ST elevation in I, aVL, V5, V6, ST depression in V1 and V2) is recorded for the diagnosis of a large rear wall infarct expansion of the left-precordial leads to V7 to V9.) the ECG diagnosis of myocardial infarction more difficult because this rather changes in a similar STEMI with a simultaneous left bundle branch block configuration (left bundle branch block.). An ST segment elevation, which coincides with the QRS complex, is a significant indication of myocardial infarction, as well as an ST-segment elevation> 5 mm in at least 2 precordial leads. In general, however, each patient with suspicious symptoms and a left bundle branch block emerging (or left bundle branch block, one of the does not know whether he was already present) treated like a STEMI. Clinical Calculator: M.I. Criteria for the likelihood of chest pain in LBBB LBBB. Cardiac markers cardiac markers (serum markers of myocardial cell injury) are cardiac enzymes (eg. B., CK-MB) Cell content (for. Example troponin I, troponin T, myoglobin) These markers are released into the blood stream after myocardial cell necrosis. The markers appear after an injury at different times and levels increase gradually varies from. Sensitivity and specificity of Myokardzellenverletzungen vary between these markers significantly, but the troponins (cTn) are the most sensitive and specific, and are now the markers of choice. Recently, several new, highly sensitive assays of cardiac troponin are (hs-cTn), which are also very accurate, has become available. These assays can measure reliably Tn levels (T or I), which are as low as 0.003-0.006 ng / ml (3-6 pg / ml); some research assays go as low as 0.001 ng / ml (1 pg / ml). Previously it had been unlikely with less sensitive cTn assays that Tn was discovered, except in patients who had an acute cardiac disease. Thus, a “positive” was Tn (i. E. Above the detection limit) very specific. However, the new hs-cTn-tests can detect small amounts of Tn in many healthy people. Therefore, hs-CTN mirrors must be based on a normal range and will only be “increased” as defined, if they are higher than 99% of the reference population. Even if an elevated troponin levels indicating a Myokardzellenverletzung, it does not cover the cause of the injury on (although any troponin elevation increases the risk of unwanted patterns in many diseases). In addition to ACS, many other cardiac and non-cardiac diseases hs-cTn levels may increase (see table: causes elevated troponin). Not all increased hs-CTN represent mirror MI and not every myocardial necrosis resulting from an acute coronary event, even if the etiology is ischemic. However, by lower Tn levels are detected, hs-cTn assays enable earlier identification of MI than other assays and they have in many centers replacing tests for other cardiac markers. In patients with suspected ACS, a hs CTN levels at presentation and 3 h later should be included (at 0 and 6 h using a standard TN assays). A hs-cTn levels must be interpreted based on the pretest probability of disease in a patient, which can be clinically estimated based on: risk factors for ACS symptoms ECG A high pretest probability plus an elevated hs-cTn levels are highly suggestive of ACS, whereas it is unlikely that a low pretest probability plus normal hs-cTn ACS represents. The diagnosis is difficult when the test results are in contradiction with the pretest probability. In this case, serial hs-cTn levels often help. A patient with a low pretest probability and initially slightly elevated hs-cTn that remains stable at a repetition of the test has probably a non-ACS cardiac disease (eg. As heart failure, stable coronary artery disease). If the mirror, however, significantly increases with repetition (d. H.> 20-50%), the probability of ACS is much higher. If a patient has a high pretest probability has a normal hs-cTn levels, which when repeated> 50% increase, ACS is likely. Persistent normal levels (often at 6 h and later, if the suspicion is difficult) suggest the need to consider a different diagnosis into consideration. Causes elevated troponin type conditions MI (ischemic) ACS Classic AMI STEMI NSTEMI non-ACS (coronary) Increased demand (stable CHD lesion) coronary artery -embolie, or dissection in connection with interventions (PCI, CABG) cocaine or methamphetamine non-ACS (coronary) hypoxia ischemia Global Hypoperfusion Kardiothorakale Operation Sudden cardiac death – direct myocardial damage (nichtischämisch) heart disease heart failure cardiomyopathy (eg. B. hypertrophic, viral) hypertension myocarditis, pericarditis injury (ablation, cardiac contusion, cardioversion, electrical shock) cancer infiltrative diseases (eg. As amyloidosis) Systemic diseases pulmonary embolism toxicity (z. B. anthracyclines) trauma (severe burns) Extreme exertion kidney failure sepsis stroke subarachnoid hemorrhage analytical assay based on Poor performance calibration error on sample based Heterophilic Antikör acute by interference from substances ACS = coronary syndrome; AMI = acute MI; CABG = coronary artery bypass surgery; NSTEMI = non-ST-segment elevation MI; PCI = percutaneous coronary intervention; STEMI = ST-segment elevation MI. Coronary angiography Coronary angiography is often a combination of diagnostic and percutaneous coronary intervention ((PCI-z. B. angioplasty, stent insert). If possible, an emergency coronary angiography and PCI be as soon as possible (after the occurrence of an acute MI primary PCI) is performed. In many tertiary centers, this approach has significantly reduced morbidity and mortality and long-term results improved. often the infarction course is actually stopped when the time of pain to PCI is short (<3-4 hours angiography). is at patients with STEMI, patient urgently carried out with persistent chest pain despite maximum medical therapy, and patients with complications (eg. B. significantly increased cardiac markers, presence of cardiogenic shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias.) patients with uncomplicated NSTEMI or unstable angina whose symptoms sic have improved h, will angiography usually within the first 24-48 hours of hospitalization to locate lesions require treatment. After initial diagnosis and treatment, a coronary angiography in patients with evidence of ongoing ischemia (ECG or because of symptoms), with hemodynamic instability, recurrent ventricular tachyarrhythmias and other deviations that indicate recurrent ischemic events, are performed. Some experts also recommend that an angiography prior to hospital discharge in STEMI patients with inducible ischemia in stress imaging or an ejection fraction of <40% performed wird.Andere Tests Routine laboratory tests are inconclusive, however, show non-specific deviations leading to a tissue necrosis fit (z. B. elevated ESR, moderately elevated white blood cell count with a left shift). A lipid profile Fasting should be received within the first 24 hours in all patients with ACS in the hospital. (Editor's note: The sobriety is no longer required today, the lipid profile should be performed at recording immediately.) An additional imaging of the myocardium (cardiac imaging tests) is not necessary if already been provided by cardiac markers or ECG diagnosis. In patients with myocardial infarction but a bedside echocardiography is invaluable meaningful to detect mechanical complications. Before or shortly after discharge a load test with an imaging method (display means radionuclide or echocardiography with drugs or physically induced stress) should be performed in patients with symptoms of ACS in not a meaningful ECG findings and did not increase cardiac enzymes. Imaging abnormalities in such patients show an increased risk of complications in the next 3-6 months and suggest a need for angiography close that should be performed before discharge or soon after, with PCI or CABG as just necessary. The right heart catheterization with a-tipped pulmonary artery catheter having a balloon can be performed to measure the pressure in the right heart, in the pulmonary artery, the occlusion pressure in the pulmonary artery and cardiac output. This test is not routinely recommended and should only be performed when the patient significant complications (eg. As severe heart failure, hypoxia, hypotension) have and then by physicians who are experienced in catheter placement and management protocols. Forecast A global risk should be estimated through formal clinical risk scores (thrombosis in myocardial infarction [TIMI] Global Registry of Acute Coronary Events [GRACE], platelet glycoprotein IIb / IIIa in Unstable Angina: Rezeptorsuppression in use of Integrilin therapy [PURSUIT] ) or with a combination of the following high-risk factors: Recurrent angina / ischemia at rest or during activity low intensity heart failure worsening Mitralklappeninsuffizienz high-risk stress test result (test ?5 minutes stopped due to symptoms, significant ECG abnormalities, hypotension or complex ventricular arrhythmias) Hemodynamic instability Sustained ventricular tachycardia diabetes mellitus PCI over the last 6 months Previous CABG LV ejection fraction <0.40 Clinical Calculator: TIMI (thrombolysis in myocardial infarction) credit score for unstable angina or non-ST-segment elevation myocardial infarction Clinical Calculator: TIMI (thrombolysis in myocardial infarction) scores for acute ST-segment elevation myocardial infarction therapy Preclinical supply: oxygen, aspirin, nitrates and / or opioids for pain and presentation at an appropriate medical facility drug treatment: antihrombozytäre drugs, antianginal drugs, anticoagulants and in some cases, other drugs often angiography to assess the anatomy of the coronary arteries Oft Reperfusionstherapie: Fibrinolytische, perkutane Koronarintervention oder eine Koronararterien-Bypass-Operation Unterstützende Behandlung "Post discharge rehabilitation" und andauernde Behandlung der koronaren Herzkrankheit Ziele der Therapie, einschließlich einer medikamentösen Behandlung sind die Beseitigung der Schmerzen, Unterbrechung der Thrombose, Beendigung der Ischämie, Begrenzung der Infarktgröße, Senkung der Herzarbeit, Vorbeugung und Behandlung von Komplikationen. Das ACS ist ein medizinischer Notfall und das Resultat wird wesentlich von einer sofortigen Diagnostik und Behandlung beeinflusst. Die Behandlung erfolgt parallel zur Diagnostik. Krankheitsbilder, die zur Verschlimmerung des Zustands beitragen (z. B. Anämie oder Herzinsuffizienz), werden aggressiv behandelt. Da der Brustschmerz bei einem Myokardinfarkt in der Regel in den ersten 12–24 h abklingt, sollte jedem anha

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