Aké sú kritériá diagnózy akútneho infarktu myokardu?
Najprv si odpoveď povedz nahlas alebo v duchu – až potom ju odkry.
🫀 Interná medicína · 13
| akútny infarkt myokardu | infarctus myocardii acutus |
| akútny koronárny syndróm | |
| nestabilná angína pektoris | angina pectoris instabilis |
| elevácia úseku ST | |
| srdcový troponín | |
| primárna perkutánna koronárna intervencia | |
| fibrinolýza | fibrinolysis |
| duálna antiagregačná liečba |
AMI is defined as cardiomyocyte necrosis in the clinical setting of acute myocardial ischaemia.
The diagnosis of myocardial infarction (MI) is associated with cTn release and is made based on the fourth universal definition of MI.
Acute coronary syndromes (ACS) encompass a spectrum of conditions
range from unstable angina to non–ST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI)
This includes MI due to atherothrombotic events (Type 1 MI)
Atheromatous plaque sometimes becomes unstable or inflamed, causing it to erode or rupture, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus.
Platelet activation involves a conformational change in membrane glycoprotein (GP) IIb/IIIa receptors, allowing cross-linking (and thus aggregation) of platelets.
Type 2: Ischemia due to increased oxygen demand (eg, hypertension) or decreased supply (eg, coronary artery spasm or embolism, arrhythmia, hypotension)
Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially reversible ischemia adjacent to infarcted tissue. MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria.
UA is defined as myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis.
It is characterized by specific clinical findings of prolonged (>20 min) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of MI.
Often, the first symptom of infarction is deep, substernal, visceral pain, described as aching or pressure, often radiating to the back, jaw, left arm, right arm, shoulders, or all of these areas.
The pain is similar to stable angina but is usually more severe and long-lasting; more often accompanied by dyspnea, diaphoresis, nausea, and/or vomiting; and relieved little or only temporarily by rest or nitroglycerin.
Females, older adults, and patients with diabetes are more likely to have atypical symptoms
Older patients may report dyspnea more than ischemic-type chest pain
a fourth heart sound (S4) is almost universally present. A soft systolic blowing apical murmur (reflecting papillary muscle dysfunction causing mitral regurgitation) may occur.
In right ventricular (RV) infarction, signs include elevated RV filling pressure, distended jugular veins (often with Kussmaul sign), clear lung fields, and hypotension.
The resting 12-lead ECG is the first-line diagnostic tool in the assessment of patients with suspected ACS. It is recommended that an ECG is obtained immediately upon FMC and interpreted by a qualified emergency medical technician or physician within 10 min.
New ST elevation at the J-point in at least two contiguous leads: • ≥2.5 mm in men <40 years, ≥2 mm in men ≥40 years, or ≥1.5 mm in women regardless of age in leads V2–V3 • and/or ≥1 mm in the other leads (in the absence of left ventricular [LV] hypertrophy or left bundle branch block [LBBB]).
ECG changes such as ST-segment depression, T-wave inversion, or both may be present.
ECG changes such as ST-segment depression, ST-segment elevation, or T-wave inversion may occur during unstable angina, but they are transient. Troponin may be detectable with high-sensitivity troponin tests (hs-cTn), but, by definition, is < 99th percentile of the upper reference limit (URL)
An abnormal cTn level, using an appropriate cutoff, is the primary distinguishing factor between unstable angina and myocardial infarction. Highly sensitive cTn assays are preferred
High-sensitivity troponin measurements and rapid ‘rule-in’ and ‘rule-out’ algorithms should be used in patients with suspected NSTE-ACS.
For STEMI and very high-risk NSTE-ACS, an immediate invasive strategy is recommended. For patients with NSTE-ACS an inpatient invasive strategy is recommended; in NSTE-ACS patients with high-risk characteristics, an early invasive strategy (<24 h) should be considered.
While routine immediate angiography and PCI (if indicated) are clearly associated with clinical benefit in patients presenting within 12 h of symptom onset
If timely (within 120 min from time of diagnosis) PPCI cannot be performed in patients with STEMI, fibrinolytic therapy is indicated within 12 h of symptom onset in patients without contraindications.
Transfer to a PCI-capable centre is recommended in all patients immediately after fibrinolysis.
these very high-risk criteria include haemodynamic instability or CS, recurrent or refractory chest pain despite medical treatment, life-threatening arrhythmias, mechanical complications of MI, HF clearly related to ACS
(confirmed NSTEMI as per the hs-cTn-based ESC algorithm, NSTE-ACS with GRACE score >140, dynamic ST-segment or T wave changes, or transient ST-segment elevation) should be considered for early invasive angiography (i.e. within 24 h)
An invasive strategy during hospital admission is recommended in NSTE-ACS patients with high-risk criteria or with a high index of suspicion for UA.
A selective invasive approach after appropriate ischaemia testing or detection of obstructive CAD by CCTA is recommended in patients without very high- or high-risk features and a low index of suspicion for NSTE-ACS.
Antithrombotic therapy is indicated in all ACS patients, regardless of the management strategy. This consists of both antiplatelet and anticoagulant therapy.
LD of 150–300 mg orally or 75–250 mg i.v. if oral ingestion is not possible, followed by oral MD of 75–100 mg o.d.
By default, DAPT consisting of a potent P2Y12 receptor inhibitor in addition to aspirin is recommended for a minimum of 12 months after an ACS event
exceptions include patients for whom surgery is urgently needed, patients in whom OAC is indicated, and patients in whom the risk of bleeding is too high for other reasons.
Oxygen is recommended in patients with hypoxaemia (SaO2 <90%).
Routine oxygen is not recommended in patients without hypoxaemia (SaO2 >90%)
Sublingual nitrate may be helpful to relieve ischaemic symptoms.
Nitrates should not be given to patients with hypotension, marked bradycardia or tachycardia, RV infarction, known severe aortic stenosis, or phosphodiesterase 5 inhibitor use within the previous 24–48 h.
Electrical dysfunction (eg, conduction defects, arrhythmias, sudden cardiac death)
Myocardial dysfunction (eg, heart failure, interventricular septum or free wall rupture, ventricular aneurysm, pseudoaneurysm, mural thrombus formation, cardiogenic shock)
Valvular dysfunction (typically mitral regurgitation)
Ischemia involving the papillary muscle may lead to mitral valve regurgitation.
Other complications of ACS include recurrent ischemia, left ventricular thrombus, and pericarditis. Pericarditis can occur during or immediately after MI or more than one week later (post-MI syndrome, or Dressler syndrome).
Aké sú kritériá diagnózy akútneho infarktu myokardu?
Najprv si odpoveď povedz nahlas alebo v duchu – až potom ju odkry.
Vymenujte znaky veľmi vysokého rizika pri NSTE-AKS, ktoré podľa ESC 2023 vyžadujú okamžitú invazívnu stratégiu.
Najprv si odpoveď povedz nahlas alebo v duchu – až potom ju odkry.
Vymenujte hlavné skupiny komplikácií akútneho infarktu myokardu s príkladmi.
Najprv si odpoveď povedz nahlas alebo v duchu – až potom ju odkry.