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I./4.4.: Diagnostics beyond imaging
I./4.4.1.: ECG
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It can be said on a few diagnostic procedures that it has been one of the basic examinations of cardiology and remained this for more than a hundred years (since 1896) like the ECG. This is particularly true for patients with an acute myocardial infarction, where a diagnosis is based on the ECG, and a decision on the patient’s further therapy should also be made on the base of the first ECG. Different signs of ECG are seen in the two basic pathological groups. .
I./4.4.1.1.: NSTE-ACS (non-ST-elevation acute coronary syndrome)
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The ECG examination (recording with 12 leads) is one of the most important helps in making a diagnosis. A recording made in a period when the patient is free of complaints helps primarily to recognize a myocardial infarction that occurred in an earlier period (pathologic Q-wave). The diagnosis of ACS is made almost certain by an ECG that is varying during the complaints: ST segment depression (>1 mm) seen in two conjugate leads and negativity of the T-waves (>1 mm) support the ischemic origin of the complaints. Deep, symmetrical negative T-wave observed in the chest leads in association with the complaints may be a sign of a critical stenosis of the anterior descending branch. Occasionally the ECG alteration shows no regression upon cessation of the complaint, this may indicate the so-called stunned myocardium; it certainly suggests severe ischemia.
In a part of the patients, chest pain is not associated with any ECG alteration; in such cases looking for extracardiac causes (e.g. gastroesophageal reflux, gastric ulcer etc.) is particularly useful. An ischemic origin cannot be excluded even in patients with a normal ECG. Alterations of ECG seen in patients with no chest pain may be due to other diseases (e.g. aspecific changes of ST segment and T waves observed in patients with stroke). Continuous multi-channel monitoring of the ST segment in patients with diagnosed or suspected ACS is a useful procedure. In specific situations, in coronary care units it may be required for several days as well.
I./4.4.1.2. STEMI (ST elevation myocardial infarction)
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ST elevation observed in patients with chest pain is a sign of transmural ischemia (e.g. Prinzmetal’s angina pectoris, myocardial infarction). Prolonged (>20 min.) typical chest pain and elevation of ST segment on the ECG equals the diagnosis of STEMI; no other diagnostic step is required for organizing the reperfusion care of the patient, i.e. if feasible (see later), the patient should be transported to an intervention center immediately; or if it is not possible within two hours, initiation of thrombolytic therapy is indicated. In contrast to patients with NSTE-ACS, where no localization of the ischemia is possible based on the ECG alterations, if an elevation of ST is present, it can basically be decided whether there is an anterior or an inferior localization.
In patients with inferior localization the possibility of a right ventricular infarction should always be taken into consideration; this can be diagnosed with the help of right ventricular leads; that means a mirrorwise placing of the conventional thoracic leads. Due to anatomical causes, complete obstruction of the circumflex branch appears as deep mirrorwise depression of ST in leads V 4 to 6 by causing ischemia of the posterior wall in a part of patients. Occasionally no ST segment elevation is yet present in the first minutes of infarction or in the first half, maximum 1 hour;only the T-waves become high and peaked.
If the patient has typical thoracic complaints, this phenomenon should certainly be thought of, and the ECG should be repeated with intervals of 10 to 15 minutes.
ST elevation in all, i.e. “non-conjugate” leads, often with a depression of the PR segment, seen in patients with perimyocarditis or typical cases of pericarditis, may mean a differential diagnostic problem. Unfortunately the clinical picture and the ECG are not always helpful in the decision between pericarditis and an acute ST elevation myocardial infarction. A “superfluously” performed negative coronary angiography is a much less harm than to miss the clearing of a coronary occlusion while waiting among diagnostic uncertainties in a patient whose infarction is in progress.
I./4.4.2. Laboratory diagnostics
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It is an essential part of the diagnostics of acute myocardial infarction. Necrosis of the myocardium can be confirmed by laboratory tests (CK/CKMB, Troponin), the „necroenzymes” help to determine the size of infarction, and in equivocal cases a hint on the time of the beginning of infarction may be obtained by measuring the otherwise aspecific LDH, when its elevation is late (or, in a better case the 1-2 isoenzyme alpha-HBDH). A triggering cause, potentially leading to infarction (i.e. severe anemia) may be detected, and the risk factors (fat and carbohydrate metabolism, inflammatory markers) can be figured out. In addition, the recognition of any accompanying disease, mainly a severe renal or hepatic disease is important for therapy and prognosis of the patient.
I./4.4.2.1.: Troponin
Troponin is currently the most widespread laboratory marker for confirming an infarction in the practice. Troponin exists in the form of three structural proteins (troponin I, T, C), which are located in the myofilaments of the myocardium and take part in the actomyosin contraction regulated by calcium ions. The amino acid sequence of troponins of the myocardium differs from that of those in the skeletal muscles, and therefore an elevation of troponin I and T levels suggests a lesion of the myocardium. According to a common statement of European and American Societies of Cardiology, a clinical picture associated with myocardial ischemia (chest pain, ST abnormity) showing an elevation of troponin levels should be called myocardial infarction. The rise of troponin levels can be detected from 3 to 4 hours after the cellular necrosis, and it can be observed for 7 to 14 days.
The specificity of troponin T or I is high; it should be taken into consideration, however, that it may be elevated not only due to an infarction, but also in relation to other cardiac and primarily non-cardiac causes (heart failure, arrhythmia, cardiotoxic medicines, renal failure, pulmonary embolism, shock, sepsis), and it is generally elevated in patients in a critical condition. Nevertheless, the extent of elevation is by orders of magnitude higher in a patient with an acute myocardial infarction. The newer highly sensitive or ultrasensitive tests serve for detecting very small amounts of troponin (either T or I) that entered the circulation. With their help, in case of certain negativity, an acute infarction can be excluded with a high safety. When high troponin levels are found with no clinical signs or symptoms of ischemia, other etiologic factors (myocarditis, aortic dissection, pulmonary embolism, heart and renal failure) should be sought.
I./4.4.2.2.: Creatine kinase (CK-MB isoenzyme)
It is less sensitive and less specific test in comparison to troponin. It turns to positive from 6 to 8 hours after the myocardial necrosis, and its value normalizes after 3 to 4 days so that its serial determination allows an assessment of a potential late extension of the myocardial necrosis. If no measurement of troponin is available, measurement of CK-MB (mass) is the best alternative.
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