NstemiI21.4

Author:Dr. med. S. Leah Schröder-Bergmann

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Last updated on: 29.10.2020

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Synonym(s)

(e) Non- ST- elevation myocardial infarction; Non- transmural infarction

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DefinitionThis section has been translated automatically.

A NSTEMI (Non- ST- elevation myocardial infarction) is the occurrence of an acute myocardial infarction in which the persistent ST- elevation is missing. The increase of troponin and CK- MB is present, as is necrosis of the myocardium.

Note: In this article only those things which are important for the NSTEMI are mentioned. For more detailed information on myocardial infarction, please consult the article on acute myocardial infarction.

ClassificationThis section has been translated automatically.

NSTEMI belongs to the group of acute coronary syndromesalong with STEMI and unstable angina pectoris.

Occurrence/EpidemiologyThis section has been translated automatically.

The NSTEMI occurs more frequently than the STEMI (15 % - 20 % vs 5 % - 10 %) (Roffi 2015) The annual frequency is 3 per 1,000 inhabitants (Pinger 2019).

PathophysiologyThis section has been translated automatically.

In NSTEMI there is partial necrosis of the respective affected myocardium with embolization by a thrombus in case of plaque rupture or subtotal vascular stenosis (Hamm 2014).

Clinical featuresThis section has been translated automatically.

For detailed symptoms see myocardial infarction

According to the MONICA study (Keil 2005), the typical infarction symptoms only occur in about 40% of all infarctions. These typical symptoms are:

  • Intense and persistent angina pectoris pain, which can hardly be influenced by rest or nitro administration (in contrast to stable angina pectoris)
  • the retrosternal pain may radiate in
  • the neck / nape of the neck
  • Lower jaw
  • Teeth
  • Shoulder area
  • both (!) arms (with focus on the ulnar sides of the forearms), which can radiate into the ulnar fingertips
  • Pain below the xyphoid in the epigastrium (rarely also below the navel)
  • typically the region of the trapezius muscle remains painless (pain in this area is typical of pericarditis) (Kasper 2015)
  • Cardiac arrhythmias in the form of ventricular tachycardia, ventricular fibrillation, AV blockages occur in approx. 95% of cases
  • often drop in blood pressure with cerebral dysfunction
  • Symptoms of left heart failure with shortness of breath occur in about 33
  • in right ventricular infarction:
  • lack of congestion in the lungs
  • Neck vein stasis
  • often bradycardia (Herold 2020)
  • Weld eruption
  • cold extremities
  • Increase of body temperature up to 38 degrees C (Kasper 2015)

Approximately 5% of patients experience reproducible chest pain triggered by local pressure (Pinger 2019).

DiagnosticsThis section has been translated automatically.

Inspection and palpation: Typically, patients hold the clenched fist in the middle of the sternum (Levine's sign) when describing pain, the hand is placed flat on the sternum or both hands, fingertips facing each other, are placed on the sternum from the side to indicate belt-shaped tightness.

The sensitivity to cardiac pain is about 80%, the specificity is about 49% (Edmondstone 1995)

ECG: The NSTEMI lacks the ST segment elevation typical of the STEMI. It may be present:

  • in 20 % - 25 % reductions of the ST segment, which can persist for several days (Kasper 2015)
  • transient ST- elevations
  • T- waves can be normal or negative (Stierle 2017)

A NSTEMI mainly affects the area of the left chamber. From the ECG with derivations typical for an infarct, the exact area of the occlusion can practically not be localized, because the coronaries are variable and the type of supply is not known (Herold 2020). The following classification is a guide to the location of the infarct:

  • RIVA proximal:
    • large infarct in the area of the anterior wall
    • V1 to V6, aVL, I as direct infarction signs
    • (II), III, aVF as indirect infarction signs
  • RIVA after departure of the diagonal branches:
    • anteroseptic infarction
    • V1 to V4, aVL, I as direct infarction signs
    • (II), III, aVF as indirect infarction signs
  • diagonal branch:
    • Lateral Infarction
    • V5 to V7, aVL, I as direct infarction signs
    • no indirect infarction signs
  • posterolateral branch:
    • Posterolateral Infarction
    • V5 to V6, aVF, II, III as direct infarction signs
    • V1 to V3, aVL, I as indirect infarction signs
  • RCX:
    • apoplectic fit posterior to the posterior wall
    • V7 to V9, aVF, III as direct infarction signs
    • V 1 to V2 as indirect infarction signs
  • RCA:
    • inferior posterior wall infarction / right ventricular infarction
    • V1 , V 3r to V6r, aVF, II, III as direct infarction signs
    • V1 to V3 as indirect infarct signs

LaboratoryThis section has been translated automatically.

Troponin T:

  • at NSTEMI ≥ 0.01 to ≤ 1.0
  • CK- MB- Increase (Stierle 2017)

The probability of a NSTEMI can be determined with the help of highly sensitive troponin assays by so-called 1- h- or 3- h- exclusion logarithms (0- h / 1 h or 3 h) as "rule in" or "rule out". The negative predictive value lies between 98 % - 100 %, the positive predictive value between 75 % and 80 % (Mehilli 2016).

Differential diagnosisThis section has been translated automatically.

Unstable angina pectoris (differentiation by highly sensitive troponin assays possible, see "Laboratory"). Further differential diagnoses: see "myocardial infarction" and "acute coronary syndrome".

TherapyThis section has been translated automatically.

Patients with a clear NSTEMI should be immediately admitted to coronary angiography according to ACC / AHA (2016). The further therapeutic procedure should be decided depending on the findings of the coronary angiography (Pinger 2019). Thrombolysis is not performed in patients with a NSTEMI (Stierle 2017).

For detailed information on the therapy see Acute myocardial infarction.

Progression/forecastThis section has been translated automatically.

The 30-day mortality in NSTEMI is 10.4 %, the 6-month lethality 18.7 % (Stierle 2017).

After a NSTEMI with a low risk of cardiac arrhythmia (criteria: hemodynamically stable, no severe arrhythmias, left ventricular ejection fraction > 40 %, successful reperfusion) the patient should be monitored for 24 h. All other patients require monitoring for > 24 h (Roffi 2015).

Bed rest is recommended for 12 - 24 h or until the CK value drops significantly. In the case of a very small NSTEMI, discharge from inpatient treatment is possible after 72 h at the earliest, provided early rehabilitation is organised (Stierle 2017).

The integration into everyday or professional life can be carried out gradually. The patient should be encouraged to participate in an outpatient heart group (Herold 2020).

Initially, the prognosis of a NSTEMI in the acute stage is better than that of STEMI, since there is a smaller extent of myocardial damage in NSTEMI. In the further course, however, the prognosis is equal to that of a STEMI (Hamm 2014).
In patients with Z. n. NSTEMI, angina pectoris recurs in up to 20% of patients (Stierle 2017).

AftercareThis section has been translated automatically.

An improvement of the prognosis is possible through the following general measures:

  • observance of nicotine withdrawal
  • mediterranean diet
  • aerobic physical exercise ≥ 3x a week for 30 - 45 min
  • optimal adjustment of any arterial hypertension that may be present
  • optimal adjustment of any diabetes mellitus that may be present
  • regular flu vaccination 1 x per year (Herold 2020)

An improvement of the prognosis can be achieved by the following medicinal or therapeutic measures:

  • Beta blockers without intrinsic activity (these lead to a decrease in cardiac output. Prolonged use leads to a decrease in heart rate, cardiac output and plasma inactivity. This reduces the risk of a reinfarction and heart failure. There is also a decrease in rhythmically induced deaths). Dosage recommendation: Initially only 1/10 of the target dose should be administered. Increase the target dose very slowly and under constant clinical control of symptoms, weight, auscultation findings. Increase the dose every 14 days. Usually the adjustment takes several months.
    • Bisoprolol 1 x 23, 75 mg / d, target dose 2 x 100 mg / d
    • Carvedilol 3 x 3.125 mg / d, target dose 2 x 25 mg / d (Herold 2020 / Braun 2018 / Rietbrock 1991 / )
    • Platelet aggregation inhibitor
  • DAPT: after a NSTEMI a dual antiplatelet therapy (DAPT) should be given for 1 year. Recommended dosage:
    • Acetylsalicylic acid: ASS 75 mg - 100 mg /d lifelong (Herold 2020)
    • plus clopidogrel: initially 300 - 600 mg, then 75 mg / d for 1 year
    • or
    • Ticagrelor: initially 180 mg, then 2 x 90 mg / d (contraindications: anamnestic intracranial bleeding, current bleeding)
    • or
    • Prasugrel: initial 60 mg, then 10 mg / d (contraindications: anamnestic intracranial bleeding, ischemic insult, transient ischemic attack, recent bleeding; prasugrel is not used in patients ≥ 75 years or with a body weight ≤ 60 kg)
  • Oral anticoagulation in addition to DAPT: In the event of atrial fibrillation, a left ventricular thrombus or the necessity of inserting a heart valve, oral anticoagulation should also be administered (see thrombosis prophylaxis) (Herold 2020)
  • Cholesterol reducer / statins. Dosage recommendation:
    • Pravastatin: 40 - 80 mg / d (Pinger 2019): The target value of LDL cholesterol should be < 70 mg / dl If this cannot be achieved, additional
    • Ezetimib or PCSK9 inhibitors. Dosage recommendation: Ezetimib 10 mg / d; PCSK9 inhibitor e.g. Evolocumab 10 mg / d (Herold 2020 / Schwabe 2016)
  • ACE inhibitor: After a NSTEMI, the heart undergoes a structural change and adaptation process, the so-called "remodeling". These changes can lead to hypertrophy, expansion of the myocardial scar and dilatation of the left ventricle, which considerably worsens the further prognosis. With ACE inhibitors it is possible to stop this process and thus reduce overall mortality, as several studies (such as SAVE, TRACE, AIRE etc.) have shown (Herold 2020). Recommended dosage:
    • Captopril: 6.25 mg initial, 2 h later 12.5 mg, 12 h later 25 mg, then 2 x 50 mg / d or:
    • Ramipril 2 x 2.5 mg, followed by 2 x 5 mg / d orally (Pinger 2019). If the patient experiences intolerances such as coughing or if there are contraindications, it is possible to switch to:
    • Sartane (AT1- Blocker). Dosage recommendation: Valsartan: 20 mg in 4 steps to 2 x 160 mg as maintenance dose (Herold 2020)
  • Aldosterone receptor antagonist: If, despite treatment with beta-blockers and ACE inhibitors (or AT1 blockers), the patient's heart failure persists or the left ventricular ejection fraction (LV-EF) is reduced by < 35%, the use of an aldosterone receptor antagonist is recommended. Recommended dosage:
    • Spironolactone: starting dose: 1 x 25 mg, target dose 2 x 25 mg - 50 mg (Herold 2020 / Aktories 2017).

Cardiac re-chronization therapy: Cardiac re-chronization therapy should be performed at:

  • - a left femoral block QRS complex > 120 ms - 150 ms
  • - of a LV- EF ≤ 35
  • - progressive heart failure (NYHA > II) despite optimal drug therapy (Herold 2020)

Implantable defibrillator (ICD): If after optimal drug treatment > 40 days symptomatic heart failure NYHA II - III or a reduced left ventricular ejection fraction ≤ 35%, there is an indication for an ICD (Herold 2020).

LiteratureThis section has been translated automatically.

  1. Aktories K et al (2017) General and special pharmacology and toxicology. Elsevier 378
  2. Braun J et al (2018) Clinical Guide to Internal Medicine. Elsevier Urban and Fischer Publishers S 73 - 74
  3. Edmondstone W M (1995) Cardiac chest pain: does body language help the diagnosis? The BMJ 311: 1660
  4. Hamm C et al (2014) Checklist ECG. Thieme Verlag Chapter 17.2.3.
  5. Herold G et al. (2020) Internal Medicine. Herold Verlag S 250 - 259
  6. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1593 - 1598, 1599 - 1608
  7. Kasper D L et al (2015) Harrison's Internal Medicine. Georg Thieme Publishing House 1938 - 1952, 1954 - 1967
  8. Keil U et al (2005) The WHO MONICA global project: results and outlook. Public health 67: 38 - 45
  9. Mehilli J et al (2016) Commenting on the 2015 European Society of Cardiology (ESC) guidelines for the management of acute coronary syndrome without ST elevation (NSTE-ACS). Cardiology 10: 351 - 358
  10. Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German publisher for physicians S 87 - 165
  11. Rietbrock N et al (1991) Clinical Pharmacology: A Guide for Practice. Steinkopff Publishing House Darmstadt S 73
  12. Roffi M et al (2015) Guidelines Acute Coronary Syndrome without ST elevation. ESC Pocket Guidelines. Björn- Bruckmeier Publisher
  13. Schwabe U et al (2016) Arzneiverordnungs-Report 2016: Current data, costs, trends and comments. Springer publishing house S 55
  14. Stierle U et al (2014) Clinical Guide to Cardiology. Elsevier Urban and Fischer S 128 - 151

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Last updated on: 29.10.2020