Acute myocardial infarction is a myocardial necrosis, which is caused by an acute obstruction of a coronary artery. Symptoms 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. Treatment is with platelet inhibitors, anticoagulants, nitrates, beta blockers, statins and reperfusion therapy. In a ST-segment elevation myocardial infarction stretching (STEMI), an emergency even reperfusion by fibrinolytic agents, percutaneous coronary intervention (PCI), or occasionally performed by coronary bypass surgery. In myocardial infarction without ST-segment elevation, reperfusion is performed by percutaneous intervention or coronary bypass surgery.
(See also Procedure for acute coronary syndromes.)
Acute myocardial infarction is a myocardial necrosis, which is caused by an acute obstruction of a coronary artery. Symptoms 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. Treatment is with platelet inhibitors, anticoagulants, nitrates, beta blockers, statins and reperfusion therapy. In a ST-segment elevation myocardial infarction stretching (STEMI), an emergency even reperfusion by fibrinolytic agents, percutaneous coronary intervention (PCI), or occasionally performed by coronary bypass surgery. In myocardial infarction without ST-segment elevation, reperfusion is performed by percutaneous intervention or coronary bypass surgery. (See also Procedure for acute coronary syndromes.) In the US, about 1.5 million people suffer a myocardial infarction per year. This has a fatal outcome at 400,000 to 500,000 people. (.. Editor’s note .: In Germany, the incidence is about 300 infarctions / 100,000; cardiac arrest). Acute myocardial infarction (MI), along with unstable angina, called acute coronary syndrome. include acute myocardial infarction both non-ST-segment elevation infarction (NSTEMI) and ST-segment elevation infarction (STEMI). The distinction between NSTEMI and STEMI is crucial since treatment strategies for these two units are different. Pathophysiology of myocardial infarction is defined as myocardial necrosis in a clinical setting, which is consistent with a myocardial ischemia (1). These conditions may be due to an increase in cardiac biomarkers (preferably cardiac troponin; [cTn]) above the 99th. Percentile of the upper target value (URL) are satisfied; and plus at least one of the following symptoms: Symptoms of ischemia ECG changes indicative of a new ischemia (significant ST / T-bills or left bundle branch block) development of pathological Q waves imaging evidence new Myokardverlusts or new regional wall motion abnormalities angiography or autopsy evidence another for intracoronary thrombus Some criteria are used to diagnose MI during and after percutaneous coronary intervention or coronary artery bypass surgery and as a cause of sudden death. MI can be classified based on etiology and circumstances in 5 types: Type 1: Spontaneous MI by ischemia due to a primary coronary event (e.g., rupture, erosion, or cracking of plaque, coronary dissection.) Type 2: ischemia (due to increased oxygen demand . eg hypertension) or decreased supply (eg coronary artery spasm or embolism, arrhythmias, hypotension) type 3:. contiguously with sudden, unexpected cardiac death type 4a: In connection with percutaneous coronary intervention (signs and symptoms of myocardial infarction with cTn values> 5 x 99th percentile URL) type 4b with documented stent thrombosis associated type 5: In connection with a coronary artery bypass graft surgery (signs and symptoms of myocardial infarction with CTN values> 10 x 99th percentile URL) location infarction myocardial infarction refers mainly to the lin ken ventricle (LV), however, the damaged area to the right ventricle (RV) or the atria may extend. An RV infarction usually arises due to an obstruction of the right coronary or a dominant RCX. The RV infarction is characterized by high right ventricular filling pressures and is often associated with severe tricuspid regurgitation and reduced cardiac output. A right ventricular dysfunction up to a certain extent occurs in about half of patients with a posterior myocardial infarction and leads in 10-15% of cases hemodynamic abnormalities. A dysfunction of the RV should be considered in any patient with a posterior myocardial infarction and elevated jugular venous pressure in combination with hypotension or shock considered. An RV infarction as a complication of left ventricular infarction can significantly increase the risk of death. Front wall infarcts are usually larger and have a worse prognosis than posterior wall infarction. They usually arise as a result of obstruction of the left coronary artery, v here. a. the RIVA, while rear wall infarcts an occlusion of the right coronary artery or the dominant RCX widerspiegeln.Infarktausmaß infarction may Transmural not transmural Transmural infarcts involve all layers of the wall of the myocardium from epicardium to endocardium and are usually characterized on the ECG by pathological Q waves. 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). Subendocardial infarcts usually involve the inner third of the myocardium where wall tension is highest and myocardial blood flow is most sensitive to changes in blood flow. These infarcts can occur after a prolonged hypotension. Because the transmural depth of necrosis can not be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI, depending on whether a ST-segment elevation or Q waves are present in the ECG or not. The volume of myocardium destroyed can be roughly estimated by the extent and duration of CK-rise or the maximum level of the common measured troponin. The non-ST segment Elevationsmyokardinfarkt (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. 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) is a myocardial necrosis with ECG changes, a ST segment elevation, which do not readily canceled by the administration of nitroglycerin. The cardiac markers troponin I or troponin T and CK are erhöht.Hinweis the pathophysiology first Thygesen K, Alpert JS, Jaffe AS, et al.the Writing Group on behalf of the Joint ESC / ACCF / AHA / WHF Task Force for the Universal definition of Myocardial Infarction: ESC / ACCF / AHA / WHF Expert Consensus Document Third Universal definition of Myocardial Infarction. Circulation 126: 2020-2035, 2012. doi: 10.1161 / CIR.0b013e31826e1058 symptoms and complaints The symptoms of NSTEMI and STEMI are the same. Days to weeks before the infarction of patients show up at about two-thirds of symptoms, the harbingers of infarction events are. These include an unstable or crescendo angina, shortness of breath and fatigue. The first symptom of acute myocardial infarction is usually a deep, substernal visceral pain that is often described by patients as pressure or burning and to the back, to the jaw, radiating to the left and right arms, shoulders or in all of these areas can , The pain similar to angina pectoris of, but are usually more intense and last longer. The patients often also suffer from dyspnea, nausea and vomiting and sweating. The symptoms can be to little or only briefly at rest or during administration of nitroglycerin. However, it can also only mild discomfort. About 20% of acute myocardial infarctions run silently (d. H. Asymptomatic or vague symptoms that are not recognized by the patient as a disease), a phenomenon that is more common in patients with diabetes. Often the symptoms are interpreted as indigestion, v. a. because a spontaneous relief is falsely attributed to a belching or taking an antacid. Some patients have syncope. In women rather atypical chest discomfort occur. Elderly patients give more of a dyspnea as ischemic chest pain. In severe ischemic attacks, patients often suffer from severe pain, are restless and anxious. Nausea and vomiting may v. a. occur in an inferior myocardial infarction. Dyspnea and weakness as a result of LV failure, pulmonary edema, shock or significant arrhythmia can dominate the clinical picture. Patients may have a pale and clammy skin. A peripheral or central cyanosis can be seen. The pulse may be swaying thready and blood pressure, although many patients have initially during pain attacks more or less hypertonic values. The heart sounds are usually somewhat attenuated; a fourth heart sound is almost always in front. In the area of ??the apex a soft, blowing systolic may be present, indicative of a papillary muscle. A friction sound or noticeable noise in the first study may indicate an existing pre-existing conditions of the heart or other diagnosis. The finding of a rubbing noise within a few hours after the onset of myocardial infarction symptoms rather indicates an acute pericarditis as a myocardial infarction. Friction sounds, usually temporary, but are often found on the 2nd and 3rd day after a STEMI. When scanning the chest wall is sensitive at about 15% of patients. In a right-(RV) infarction increased filling pressures diagnostic serial ECGs Serial show in the RV, jammed jugular veins (often with Kussmaul sign free lung fields and hypotension. Cardiac markers Immediate coronary angiography (seidenn there are fibrinolytic administered) in patients with STEMI or complications (z. B. ongoing chest pain, hypotension, significantly increased cardiac markers, unstable arrhythmias) begins Delayed coronary angiography (within 24-48 hours) for patients with NSTEMI without complications (See also algorithm approach to acute myocardial infarction). The evaluation with start and serial ECG and serial measurements of cardiac markers, to help between unstable angina pectoris, ST-segment elevation myocardial infarction, and nic ht to distinguish ST-segment elevation myocardial infarction. The distinction is the way 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 generally 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!.) ECG The ECG is the most important test and should be within the first 10 minutes are carried out. A STEMI is usually diagnosed due to the initial ECG findings. Here, a ST-segment elevation ? 1 mm in 2 or more contiguous leads that detect the damaged tissue shows (Acute lateral LV infarction (tracing within a few hours of onset of the disease condition)., A lateral left ventricular infarction (after the first 24 h)., Lateral left ventricular infarction (several days later)., acute inferior (diaphragmatic) LV infarction (tracing collected within a few hours of onset of the disease)., inferior (diaphragmatic) LV infarction (after the first 24 h) (diaphragm)., and Inferior LV infarction (several days later).). 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..) Lateral left ventricular infarction (after the first 24 h ). ST segment are less increased; significant Q waves develop and R waves in leads I, aVL, V4 and V6 are lost. Lateral left ventricular infarction (several days later). Significant Q-waves and R-loss continues. ST segments are now isoelectric substantially. The ECG is in the course of the following months likely to change only slowly. Acute inferior (diaphragm) LV infarction (tracing applicable within a few hours of onset of disease). There is a hyperacute ST-segment elevation in leads II, III, and aVF, and reciprocal depression in other derivatives. Inferior (diaphragm) LV infarction (after the first 24 h). Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF. Inferior (diaphragmatic) LV infarction (several days later). The ST segments are now isoelectric. Abnormal Q waves in leads II, III, and aVF show that the myocardial scars continue. 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 be confirmed when in repeated recordings (on the first day every 8 h, then 1 times a day) shows a gradual movement towards stable, more normal pattern or develop pathological Q waves in the following days. If you suspect a right ventricular infarction is usually an ECG with 15 derivations with additional leads in V4-6R 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 with a simultaneous left bundle branch block configuration because this is more like changes in a STEMI. 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 probability of breast pain in LBBB Cardiac markers Cardiac markers (serum markers of Myokardzellenverletzungen) are cardiac enzymes (eg. B. CK-MB) and cellular components (for. Example, troponin I, troponin T and myoglobin), according to a necrosis of myocardial cells are released into the bloodstream. 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 an acute coronary syndrome (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 suspected of having a myocardial infarction 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 strongly suggest myocardial infarction down whereas it is unlikely that a low pretest probability plus normal hs-cTn represents a myocardial infarction. 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 a myocardial infarction is much higher. If a patient has a high pretest probability has a normal hs-cTn levels, which increases> 50% when hs-cTc is re-measured, a myocardial infarction is likely. Persistent normal levels (often at 6 h and later, if the suspicion is difficult) indicate the need for a different diagnosis to consider ziehen.Koronarangiographie Coronary angiography is often a combination of diagnostic and percutaneous coronary intervention (PCI-z. B . angioplasty, stent insert). If possible, be an emergency coronary angiography and PCI performed as soon as possible after the occurrence of an acute MI (primary PCI). In many tertiary centers, this approach has significantly reduced morbidity and mortality and long-term results improved. Often the course of infarction is actually stopped when the time of pain to PCI is short (<3-4 hours). Angiography is used in patients with STEMI patients urgently performed 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 whose symptoms have improved, 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 is performed with inducible ischemia in stress imaging or an ejection fraction of <40%. Forecast A global risk should be estimated through formal clinical risk scores (thrombosis in myocardial infarction [TIMI] or 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 in ?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 six months previous CABG LV ejection fraction <0.40 Clinical calculator: TIMI (thrombolysis in myocardial infarction) scores f r unstable angina or non-ST-segment elevation myocardial infarction Clinical calculator: TIMI (thrombolysis in myocardial infarction) scores for acute ST-segment elevation myocardial infarction The overall mortality rate of approximately 30%. Die from 25-30% of patients before reaching a hospital (usually due to ventricular fibrillation). The mortality rate at the hospital is about 10% (usually as a result of cardiogenic shock). However, it depends significantly on the severity of left ventricular insufficiency (see Table: Killip classification and mortality rates of acute myocardial infarction *). In patients who received reperfusion (fibrinolysis or PCI), the in-hospital mortality is 5-6% compared with 15% in patients who may receive reperfusion, but are currently not treated. In centers with established primary PCI programs reported in-hospital mortality was <5%. Most patients who die as a result of cardiogenic shock have a heart attack or a combination of a scarred tissue infarction and a new infarct area in which ?50% of the left ventricular mass are affected. In patients with STEMI five clinical features for a mortality of 90% predictively (see Table: Mortalitätssrisiko in 30 days at STEMI): old age (31% of total mortality), low systolic blood pressure (24%), Killip classification> 1 (15%), increased heart rate (12%) and localization in the front wall (6%). Mortality rates for women and patients with diabetes tend to be higher. The mortality rate is in patients who have survived the initial hospital phase, during the first year after the acute heart attack at 8-10%. Most deaths occur in the first 3-4 months. Persistent ventricular arrhythmias, heart failure, poor ventricular function and recurrent ischaemia represent a high risk. Many experts recommend a stress test prior to hospital discharge or within 6 weeks thereafter. A good exercise capacity without ECG -deviations is a hallmark of a favorable prognosis. Further evaluation is not usually required. Reduced exercise capacity is a sign of poor prognosis. The cardiac functioning after recovery depends to a large extent on how much functional myocardium remains after acute infarction. Acute damages are in addition to scarring from previous heart attacks. In a damage of> 50% of the left ventricular mass longer survival is unlikely. Killip classification and mortality rates of acute myocardial infarction * Class PAO2 Clinical description mortality rate in the hospital 1 Normal No clinical evidence of left ventricular (LV) failure 3-5% 2 Slightly reduced Light to moderate LV failure 6-10% 3 Heavy abnormal LV failure, pulmonary edema 20-30% 4 Highly abnormal cardiogenic shock: hypotension, tachycardia, mental Obtundation, cool extremities, oliguria hypoxia> 80% * Determined by repeated examination of the patient in the course of the disease. Determines while the patient is breathing room air. Adapted from Killip T, Kimball JT: Treatment of myocardial infarction in a coronary care unit. A two-year experience with 250 patients. The American Journal of Cardiology 20: 457-464, 1967. Mortalitätssrisiko in 30 days in STEMI score points risk factor aged ?75 3 Age 65-74 2 diabetes mellitus, hypertension or angina pectoris 1 Systolic blood pressure <100 mmHg 3 heartbeat> 100 beats / min 2 Killip Class II-IV 2 weight <67 kg 1 Anterior ST elevation or left bundle branch block 1 time for treatment> 4 h 1 Total score possible risk 0-14 Points Total mortality rate at 30 days (%) 0 0.8 1 1.6 2 2.2 3 4.4 4 7.3 5 12.4