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The trouble with STEMI

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Sonja discuss the problems with our current paradigm for diagnosing occlusive myocardial infarction by relying predominantly upon ST segment elevation. Watch Sonja present this information at: https://youtu.be/-AkP3I93e8Y

Veröffentlicht in: Gesundheit & Medizin
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The trouble with STEMI

  1. 1. The trouble with STEMI Sonja Maria Senior academic, researcher & lecturer
  2. 2. The current guideline-recommended paradigm of acute MI management (“STEMI vs. NSTEMI”) is irreversibly flawed, and has prevented meaningful progress in the science of emergent reperfusion therapy over the past 25 years Pendell Meyers, MD Scott Weingart, MD, FCCM Stephen Smith, MD
  3. 3. STEMI • ST Elevation Myocardial Infarction NSTEMI • Non ST Elevation Myocardial Infarction ACO • Acute Coronary Occlusion (ACO) or near occlusion, with insufficient collateral circulation, whose myocardium is at imminent risk of irreversible infarction without immediate reperfusion therapy OMI • Occlusion Myocardial Ischaemia and/or Infarction Firstly, lets define some (un)familiar terms
  4. 4. Another passing fad… or revolutionary? STEMI - Became a fashionable term in early 2000’s Replaced the ‘q wave’ terminology (Q-wave vs. Non-Q-wave) Ambulance service guidelines introduce STEMI infarct protocols ≈ 2010 onwards Becoming a ‘KPI focus’ for healthcare systems as society recognises the expense of treatment costs in survivors1 Push to shorten needle to balloon times within paramedicine.
  5. 5. Alas… Unfortunately the term "STEMI" restricts our minds into thinking that ACO is diagnosed reliably and/or only by "STEMI criteria" and the ST segments. In reality, the STEMI criteria and widespread current performance under the current paradigm have unacceptable accuracy, routinely missing at least 25-30% of ACO in those classified as “NSTEMI” and generating a similar false positive rate of emergent cath lab activations.
  6. 6. The biggest problems Overestimating STEMI 1 Undertreating NSTEMI 2 Not looking for STEMI equivalents 3
  7. 7. Myth 1: NSTEMI patients are probably healthier STEMI (n=17287) NSTEMI (n=28912) Prior Myocardial infarction 19.1% 29.2% Prior Heart Failure 6.6% 16.1% Prior PCI 30% 28.2% Prior CABG 10.2% 25% Prior stroke 7.4% 10.7% Peripheral artery disease 8.8% 15.6% Hypertension 73.7% 82.5% Diabetes Mellitis 25.6% 37.1% Dyslipidemia 56.7% 68.7% Current/recent smoke 19.9% 15.5% Vora, A. N., Wang, T. Y., Hellkamp, A. S., Thomas, L., Henry, T. D., Goyal, A., & Roe, M. T. (2016). Differences in Short- and Long-Term Outcomes Among Older Patients With ST-Elevation Versus Non-ST-Elevation Myocardial Infarction With Angiographically Proven Coronary Artery Disease. Circ Cardiovasc Qual Outcomes, 9(5), 513-522. doi:10.1161/circoutcomes.115.002312
  8. 8. Myth 2 – NSTEMI and STEMI are really different, so we should manage them differently Answer: By definition, STEMI and NSTEMI are only different with respect to the reflection of acute myocardial ischaemia and necrosis on the ECG. The pathogenesis may actually be the same. Bode, C., & Zirlik, A. (2007). STEMI and NSTEMI: the dangerous brothers. European heart journal, 28(12), 1403-1404. doi:10.1093/eurheartj/ehm159
  9. 9. Myth 3 – Focus on the STEMI patient Answer: NSTEMI patients appear to be undertreated with respect to reperfusion and also after discharge from hospital. The similar prognosis of NSTEMI and STEMI patients should lead to a more aggressive in- hospital and secondary prevention treatment of both groups, particularly the NSTEMI population Bode, C., & Zirlik, A. (2007). STEMI and NSTEMI: the dangerous brothers. European heart journal, 28(12), 1403-1404. doi:10.1093/eurheartj/ehm159
  10. 10. The most Important fact : STEMIs lie.. The big 5 mimickers • Pericarditis • Left Ventricular Hypertrophy • Left Bundle Branch Block • Ventricular rhythms • Benign Early Repolarisation Can you tell the difference?
  11. 11. STEMI equivalents a quick snapshot • Brugada syndrome • Wellens A and B • De Winters T wave • aVR – how can we use it?
  12. 12. Brugada Syndrome Is a genetic disorder (affect 1 in 2000 people worldwide)1 8 – 10 times more common in men (testosterone may account for the difference) Most commonly a mutation of the gene SCN5A This gene provides instructions for making a sodium channel, which normally transports positively charged sodium atoms (ions) into heart muscle cells. Plays a critical role in maintaining the heart's normal rhythm. Mutations in the SCN5A gene alter the structure or function of the channel, which reduces the flow of sodium ions into cells. A disruption in ion transport alters the way the heart beats, leading to the abnormal heart rhythm characteristic of Brugada syndrome. 1. https://ghr.nlm.nih.gov/condition/brugada-syndrome#statistics
  13. 13. Brugada Syndrome - ECG ST-segment elevation in right precordial ECG leads and associated with sudden cardiac death in young adults. The ECG manifestations are often concealed but can be unmasked by sodium channel blockers and fever. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.
  14. 14. Brugada Syndrome - ECG (typical) A) Normal electrocardiogram of the precordial leads V1-3, B) Changes in Brugada syndrome
  15. 15. 3 Forms and their changes on the ECG Type 1 has a coved type ST elevation with at least 2 mm (0.2 mV) j point elevation and a gradually descending ST segment followed by a negative Twave. Type 2 has a saddle-back pattern with a least 2 mm J-point elevation and at least 1 mm ST elevation with a positive or biphasic T-wave. Type 2 pattern can occasionally be seen in healthy subjects. Type 3 has either a coved (type 1 like) or a saddle-back (type 2 like) pattern, with less than 2 mm J-point elevation and less than 1 mm ST elevation. Type 3 pattern is not rare in healthy subjects. Postema, P. G., Wolpert, C., Amin, A. S., Probst, V., Borggrefe, M., Roden, D. M., … Wilde, A. A. (2009). Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (www.brugadadrugs.org). Heart rhythm, 6(9), 1335–1341. doi:10.1016/j.hrthm.2009.07.002
  16. 16. Wellens Syndrome • Wellens syndrome describes a pattern of ECG changes that represent a pre-infarction state of coronary artery disease. • Wellens syndrome results from a temporary obstruction of the LAD coronary artery. Usually, this is caused by the rupture of an atherosclerotic plaque leading to LAD occlusion, with subsequent clot lysis or other disruption of the occlusion before complete myocardial infarction has taken place • The exact mechanism of the ECG changes of Wellens syndrome is not known, but some theorise that coronary artery spasm and stunned myocardium cause it. Others postulate that it is caused by repetitive transmural ischaemia- reperfusion leading to myocardial oedema.
  17. 17. Wellens Syndrome - ECG Wellens syndrome is not always an acute process. It can develop over days to weeks. The ECG pattern often develops when the patient is not experiencing chest pain. When the patient does experience chest pain, the ST segment and T-wave pattern can appear to normalise into hyperacute upright T waves (so- called “pseudo-normalisation”) or even develop into ST- segment elevations.
  18. 18. Wellens – 2 types Type A • 25% of cases • Biphasic pattern • More likely to be misrecognised non-specific normal pattern Type B • 75% of cases • Deep inverted symmetric T-Waves The T waves evolve over time from a Type A to a Type B pattern
  19. 19. Wellens Syndrome – ECG (Type A) • Biphasic precordial T waves with terminal negativity, most prominent in V2-3. • Minor precordial ST elevation. • Preserved R wave progression (R wave in V3 > 3mm)
  20. 20. Wellens Syndrome – ECG (Type B) There are deep, symmetrical T wave inversions throughout the anterolateral leads (V1-6, I, aVL).
  21. 21. De Winters T wave The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST segment elevation, but instead changes to the T wave. First reported by de Winter in 2008.
  22. 22. Key features of De Winters Key diagnostic features include ST depression and peaked T waves in the precordial leads. The de Winter pattern is seen in ~2% of acute LAD occlusions and is under-recognised by clinicians. Unfamiliarity with this high-risk ECG pattern lead to under identification and under treatment Patients may be instead misidentified as NSTEMI
  23. 23. What does it look like? Anything look odd ?
  24. 24. Cont’ • Tall, prominent, symmetric T waves in the precordial leads • Upsloping ST segment depression >1mm at the J-point in the precordial leads • Absence of ST elevation in the precordial leads • ST segment elevation (0.5mm- 1mm) in aVR • “Normal” STEMI morphology may precede or follow the deWinter pattern
  25. 25. Example - 20 minutes before ED arrival
  26. 26. Example – Arriving at ED
  27. 27. aVR – the forgotten lead The lead aVR is a very important lead in localisation of Coronary Artery Disease. Also can be used for identification of arrhythmias (PSVT), acute pericarditis, tricyclic overdoses, tension pneumothorax, dextrocardia, pulmonary embolism and malposition/technical errors on taking an ECG,
  28. 28. aVR (the widow maker sign)
  29. 29. What are we doing about it? National study on all undergraduate teaching of cardiology and STEMIs – what are the learning objectives? Use the study result to inform curriculum changes Consult with other academics Inform Stakeholders (Ambulance Services, Council of Deans, NHMRC guidelines) Continue our Research and stay on top of changes.
  30. 30. Questions? smaria@csu.edu.au

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