Initial approach to acute chest pain presentations and the use of conventional and high-sensitivity troponins
V. General procedural management after coronary angiography: PCI, CABG, or medical therapy only
VI. Discharge medications in NSTEMI
Appendix 1. Complex angiographic disease- Moderate disease progression
Appendix 2. Women and ACS, elderly patients and ACS, CKD
Appendix 3. Bleeding, transfusion, patients on chronic warfarin or NOAC, gastrointestinal bleed
Appendix 4. Antiplatelet and anticoagulant therapy
Appendix 5. Difference between plaque rupture and plaque erosion
Appendix 6. Spontaneous coronary artery dissection
Appendix 7. Harmful effects of NSAIDs and cyclooxygenase-2 inhibitors in CAD
I. Definition, types of myocardial infarction, and pitfalls
A rise in troponin, per se, is diagnostic of myocardial necrosis or injury but is not sufficient to define myocardial infarction (MI), which is myocardial necrosis secondary to myocardial ischemia. Additional clinical, ECG, or echocardiographic evidence of ischemia is needed to define MI (Figure 1.1).
In fact, MI is defined as a troponin elevation above the 99th percentile of the reference limit (~0.03 ng/ml, depending on the assay) with a rise and/or fall pattern, along with any one of the following four features: (i) angina; (ii) new or dynamic ST-T abnormalities not explained by LVH or LBBB, or new Q waves; (iii) new wall motion abnormality on imaging; (iv) intracoronary thrombus on angiography.1,2
Isolated myocardial necrosis is common in critically ill patients and manifests as a troponin rise, sometimes with a rise and fall pattern, but no clinical or ECG features of MI. This troponin rise is not called MI but is called “non-MI troponin elevation” or “non-ischemic myocardial injury”.
A rise or fall in troponin is necessary to define MI. A mild, chronically elevated but stable troponin may be seen in chronic heart failure, severe left ventricular hypertrophy, or advanced kidney disease. While having a prognostic value, this stable troponin rise is not diagnostic of MI. A fluctuating troponin pattern may be seen in myocarditis. Different cutoffs have been used to define a relevant troponin change, but, in general, a troponin that rises above the 99th percentile with a rise or fall of > 20% is characteristic of MI (50-80% cutoff is more applicable to low troponin levels <0.1 ng/ml).3
A .Type 1 MI (spontaneous MI) = True acute coronary syndrome (ACS)
Type 1 or spontaneous MI is usually due to plaque rupture or erosion that promotes platelet aggregation, thrombus formation and microembolization of platelet aggregates.
NSTEMI is a type 1 MI without persistent ST-segment elevation. STEMI is a type 1 MI with persistent (> 20 min), ischemic ST-segment elevation.1,4 For practical purposes, ischemic symptoms with ongoing ST-segment elevation of any duration are considered STEMI and treated as such. The diagnosis may be retrospectively changed to NSTEMI if ST elevation quickly resolves without reperfusion therapy, in < 20 minutes.
Figure 1.1 Diagnosis and types of myocardial infarction.
In NSTEMI, the thrombus is most often a platelet-rich non-occlusive thrombus. This contrasts with STEMI, which is due to an occlusive thrombus rich in platelets and fibrin. Also, NSTEMI usually has greater collateral flow to the infarct zone than STEMI.
As a result of the diffuse inflammation and alteration of platelet aggregability, multiple plaque ruptures are seen in ~30–80% of MIs, although only one is usually considered the culprit.5 This shows the importance of medical therapy to “cool down” the diffuse process, and explains the high risk of MI recurrence within the following year even if the culprit plaque is stented.5
Occasionally, a ruptured plaque or, more commonly, an eroded plaque may lead to microembolization of platelets and thrombi and impaired coronary flow without any residual, angiographically significant lesion or thrombus.
B. Type 2 MI (secondary MI) with or without underlying CAD
In this case, ischemia is related to severely increased O2 demands (demand/supply mismatch). The patient may have underlying CAD, but the coronary plaques are stable without acute rupture or thrombosis. Conversely, the patient may not have any underlying CAD, in which case troponin I usually remains < 1 ng/ml and the ECG and echo are unlikely to show ischemia.6-8 About half of patients with type 2 MI have underlying CAD.
Cardiac mechanisms of type 2 MI include: severe hypertension, acute HF, arrhythmias, aortic stenosis/hypertrophic cardiomyopathy. Non-cardiac mechanisms of type 2 MI include: gastrointestinal bleed, severe anemia, sepsis, hypoxemia.
Type 1 MI and type 2 MI are differentiated by the clinical context. Type 1 MI (STEMI and NSTEMI) is generally the primary reason for a patient's presentation to the hospital with no evidence of acute noncardiac illness. Conversely, type 2 MI occurs in the setting of acute noncardiac illness. At times, a type 1 MI diagnosis is assumed, but the diagnosis is reconsidered
