ST Elevation
Diagnosis: Myocardial Infarction, ST Elevation
Reference: https://www.cvphysiology.com/CAD/CAD012
Explanation
[The anterior leads are technically V3 and V4; however, it is common for the septum and/or lateral wall to be involved during anterior MIs, as the LAD supplies septal branches to the interventricular septum and diagonal branches to the lateral wall.]
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The septum is represented on the ECG by leads V1 and V2, whereas the lateral wall is represented by leads V5, V6, lead I and lead aVL. To make things more complicated, sometimes the LAD “wraps around” the cardiac apex, which is a common anatomic variant. This results in part of the inferior wall being supplied by the LAD, as well.
More basics of anterior MIs.
If the thrombus is in the proximal LAD, the septum and lateral walls will often also be involved, in addition to the anterior segments, resulting in ST segment elevation in leads V1 through V6 and perhaps lead I and aVL, as well.
When the thrombus is in the mid LAD (after the septal branch), the diagonal branch(es) may or may not be involved. If this is the case, then the ST segment elevation will be in V3 to V6 — and not the septal leads.
Because the anatomical opposite of the precordial leads would be posterior leads, which we do not commonly check in this setting, there are no “reciprocal changes” during anterior or septal MIs. Now, “high lateral” MIs with ST segment elevation in the limb leads I and aVL can show reciprocal ST segment depression in leads II, III and aVF.
Here is some more terminology. When there is not only anterior ST segment elevation (V3 and V4), but also septal (V1 and V2) and lateral (V5, V6, lead I and lead aVL), an “extensive anterior” MI is said to be present.
Recall, as well, that a STEMI is a STEMI is a STEMI. Treatment for all of them is the same, regardless of what pattern it takes — that is quick coronary revascularization.
Lastly, the official definition of STEMI according to the American College of Cardiology/American Heart Association guidelines for STEMI is “new ST segment elevation at the J point in at least two contiguous leads of ≥ 2 mm (0.2 mV) in men or ≥ 1.5 mm (0.15 mV) in women in leads V2-V3 and/or of ≥ 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.” This means 1 mm in any two contiguous leads except leads V2 or V3, where the elevation must be 2 mm in men or 1.5 mm in women.
Below are the anterior MI ECG patterns that you may encounter.
Anterior MI Pattern – Tombstoning
This is named for obvious reasons. The J point is elevated and, along with the T wave, and it looks like a tombstone. In an anterior MI that shows “tombstoning,” there is frequently 4 to 6 millimeter of ST segment elevation. Do not confuse the ST segment elevation with the T wave. Look specifically where the ST segment is — waaaaay up from the baseline. Recall that the J point is where we need to measure the elevation from baseline, and the baseline is always the TP segment (between the T wave and the P wave).
Below is another example of tombstoning with a slightly different shape. There is septal involvement (lead V2) and a bit laterally, as well (lead V5 and V6). The more examples you see, the better.
The anteroseptal STEMI ECG example below is good enough to call a tombstone in lead V3. There is no lateral involvement here.
Anterior MI Pattern – Typical ST Segment Elevation
Although not quite a tombstone, there is still significant ST segment elevation here. The ST segment elevation barely reaches 5 mm in V3, and there is a bit of ST segment elevation laterally in lead V5 and V6. Thus, this example is an anterior STEMI with a little lateral involvement — no tombstones here. The ST segment in V3 is a good example of ST segment elevation that is “concave upward;” this is unlike the previous examples, where it is “concave downward” — also called “coving” of the ST segment.
The next example below is trying to tombstone — and maybe did in lead V4. There is definite elevation of the J point in V2 to V6, at least, and minimal elevation in V1 and V6. This is a good example to quickly point out something else. Say all the precordial leads (V1-V6) looked like the minimal ST segment/J point elevation in lead V1 and V6 below — not technically 1 mm, but looks abnormal, right? If that were the case, a non-STEMI or unstable angina may be present, as the changes are indeed from myocardial ischemia, but not officially a STEMI — meaning a big time difference in regards to treatment. Read the Unstable Angina/Non-STEMI Topic Review.
Anterior MI Example – Isolated J Point Elevation
Sure, all of these anterior MIs technically have J point elevation, and we already know that the actual definition of a STEMI from the ACC/AHA is based on the J point. However, as you can see, sometimes it is quite obvious that an anterior STEMI is present, and sometimes it is not. Below is an example where there is J point elevation, but it does not quite tombstone and does not really have eye-catching ST segment elevation.
This pattern is less common during an acute MI. But again, a STEMI is a STEMI is a STEMI, and you don’t want to miss any. There are only a few times that I recall isolated J point elevation that looks more like early repolarization but really occurred during acute chest pain from an anterior STEMI. It is important to compare to an old ECG if available. If the ST segment and J point were previously normal, then an anterior STEMI should be suspected — even if only the J point is elevated in the correct clinical setting such as acute chest pain. Here are some examples of what isolated J point elevation looks like.
If you looked quickly, you may miss this one. Again, it’s not dramatic, but the J point in lead V3 is up almost 3 mm from the baseline, and maybe 2mm in lead V4. Everything else looks fine. There is no septal or lateral involvement here, which is a bit unusual. This patient had an acute mid-LAD thrombus after the septal branches and after the first major diagonal branch.
This example below actually does not meet criteria for an anterior MI based on the J point in V3 or V4, but it does in the septal leads V1 and V2. Note that even though there is barely ST segment elevation in the high lateral leads (I and aVL), there is some good reciprocal depression in the inferior leads.
Type #2: Inferior ST Segment Elevation MI
Fortunately, recognizing the inferior STEMI is a bit more straightforward. This MI involves ST segment elevation in the inferior leads II, III and aVF and only requires 1 mm in 2 contiguous leads. There is usually reciprocal depression in leads I and aVL, which helps to distinguish this from pericarditis. There is not a lot of variation in how an inferior MI looks in regards to shape or ST segments; however, some are more dramatic than others based on the amplitude of ST segment elevation. Also, during an inferior MI, the ST segment elevation is usually concave upwards.
Below are some examples to see what they look like.
Inferior STEMI Example #1
Inferior STEMI Example #2
Inferior STEMI Example #3
Inferior STEMI Example #4
Type #3: Posterior ST Segment Elevation MI
This one is tricky when isolated, but it is very important not to miss. We treat it just like any other ST segment elevation MI, which is of course time sensitive.
The posterior wall is supplied by the posterior descending artery. The PDA branches from the right coronary artery in 80% of people (those who are right coronary dominant); therefore, occlusion of RCA can result in both an inferior STEMI and a posterior MI as well. Sometimes, it is obvious on the ECG when a posterior MI accompanies an inferior STEMI, but it can also occur all by itself.
The ECG criteria to diagnose a posterior MI — treated like a STEMI, even though no real ST segment elevation is apparent — include:
- ST segment depression (not elevation) in V1 to V4. Think of things backwards. These are the septal and anterior ECG leads. The MI is posterior (opposite to these leads anatomically), so there is ST depression instead of elevation. Turn the ECG upside down, and it would look like a STEMI.
- The ratio of the R wave to the S wave in leads V1 or V2 is greater than 1. This represents an upside-down Q wave (similar in reason to the ST depression instead of elevation).
- ST segment elevation in the posterior leads of a posterior ECG (leads V7-V9). A posterior ECG is done by simply adding three extra precordial leads wrapping around the left chest wall toward the back.
Below are some examples including isolated posterior MIs, inferior STEMIs with posterior involvement and a posterior ECG.
Here is a patient with an isolated posterior MI. There is no inferior involvement here. It would have been nice to see more ST depression in V2, but there is some. Note the R/S ratio in V1 is quite high.
Now, here is the same patient with a posterior ECG tracing. Leads V7 to V9 were added. Leads V1 and V2 were moved a bit just to confuse us. There is not quite 1 mm ST segment elevation in these posterior leads, but you can see at least some slight elevation.
Below are two examples of ECG tracings with both inferior STEMI and posterior involvement. Remember, the more you look at the better!
Inferior-Posterior STEMI Example #1
Inferior-Posterior STEMI Example #2
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https://www.heart.org/idc/groups/heart-public/%40wcm/%40mwa/documents/downloadable/ucm_467056.pdf
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All patients with ACS should receive aspirin therapy indefinitely. Regardless if medically managed or revascularized with PCI or surgery, patients should receive low dose 81 mg daily as it appears to be equally efficacious as higher doses but with lower bleeding complications. In addition to aspirin, all patients with ACS should receive a P2Y12 antagonist for 1 year regardless if treated with a bare metal stent or a drug eluting stent or without PCI. There are three options for patients who undergo PCI for ACS: clopidogrel, prasugrel, or ticagrelor. There are two options for patients who are medically managed without PCI: clopidogrel or ticagrelor. There is no consensus to the optimal P2Y12 antagonist in ACS at present.
The benefits of 1 year of dual antiplatelet therapy was established from the CURE trial, where dual antiplatelet therapy (clopidogrel and aspirin) resulted in a 20% reduction (NNT = 48) in cardiovascular death, myocardial infarction, or cerebrovascular accident compared with aspirin alone in 12,562 patients with ACS. This benefit was noted in patients who were managed both conservatively and invasively with PCI. Now that clopidogrel is generic, the low cost makes it an attractive option in ACS.
Prasugrel is a P2Y12 antagonist that is more efficiently metabolized to its active metabolite with greater potency and more rapid onset of action than clopidogrel. In 13,608 patients with ACS in the TRITON TIMI 38 trial, there were lower composite of death, myocardial infarction, and stroke in patients randomized to prasugrel compared to clopidogrel (9.9% vs 12.1%, NNT45, p < 0.001). However, there was significantly more major bleeding with prasugrel (2.4% vs 1.8%, NNH167, p = 0.03). Furthermore, patients over 75 years of age, body weight less than 60 pounds, and a history of stroke or transient ischemic attack had worse outcomes with prasugrel and there is a black box warning to avoid prasugrel in these patients. Despite the warning, up to 18% of patients in real word practice receive received prasugrel with these contraindications. In addition, there is little benefit to prasugrel in patients medically managed for ACS without PCI. In the TRILOGY ACS (Targeted Platelet Inhibition to Clarify the Optimal Strategy to Medically Manage Acute Coronary Syndromes) trial, prasugrel failed to reduce cardiac event rates compared to clopidogrel in patients with ACS undergoing medical therapy.
Ticagrelor is a direct acting P2Y12 antagonist that does not require metabolic activation. In 18,624 patients with ACS in the PLATO trial, ticagrelor reduced the composite of death, myocardial infarction, and stroke compared to clopidogrel (9.8% vs 11.7%, NNT53, p = 0.003). This benefit was noted in patients undergoing PCI and those medically managed without PCI. Using the same bleeding definition used in TRITON TIMI 38 (non-CABG TIMI major bleeding), there was again more major bleeding with tiacagrelor compared to clopidogrel (2.8% vs 2.2%, NNH167, p = 0.03). Interestingly, patients randomized in the United States and Canada did not derive a benefit with ticagrelor and trended toward harm. While this finding may be due to chance, interactions with the higher aspirin dose may also explain this finding. Therefore, in the United States ticagrelor is approved for use only with the lower aspirin dose (81 mg) with a warning against the use with the higher aspirin dose.
How is one to choose between these three P2Y12 antagonist agents: clopidogrel, prasugrel, and ticagrelor? All three agents have a similar recommendation in the ACCF/AHA guidelines (Class I,LOE B). However, these medications have very different costs, efficacy, and safety considerations. While both ticagrelor and prasugrel were shown to be superior to clopidogrel in large randomized trials, the benefits of these medications over clopidogrel seem to be most pronounced in patients with abnormalities in clopidogrel metabolism. Clopidogrel is a prodrug that requires two-step metabolism into an active metabolite. Patients with abnormalities in the CYP2C19 allele have impaired metabolism, higher on-treatment platelet reactivity, and worse outcomes with clopidogrel. Up to 30% of the US population has abnormalities in this CYP2C19 allele, and clopidogrel carries a warning of reduced efficacy in these patients. In the genetic subgroup analysis of the TRITON TIMI 38 trial, prasugrel and clopidogrel had similar outcomes in patients with normal CYP2C19 alleles. In contrast, the benefit of prasugrel was much greater in patients with abnormal CYP2C19 alleles (NNT16) compared to overall trial (NNT50). A similar trend was noted for ticagrelor in the genetic subgroup analysis of the PLATO trial. Taken together, these trials suggest that the benefits of prasugrel and ticagrelor are most pronounced in patients with abnormal CYP2C19 alleles with clopidogrel. However, for the remaining 65% to 75% of the ACS population, clopidogrel may be as effective, safer, easier to use, and more cost effective. Whether a tailored strategy based on genotype or platelet function testing is safe and effective with improved value is unknown and randomized trials are warranted.
Oral β-blockers are recommended within 24 hours of presentation for patients with STEMI (Class I, LOE B) and NSTE-ACS (Class I, LOE A) and should be continued at discharge. β-Blockers decrease heart rate, contractility, blood pressure, and myocardial oxygen consumption. While early β-blockers do not reduce short-term mortality in patients with ACS, they decrease ischemia, reinfarction, and ventricular arrhythmia. Furthermore, β-blockers improve long-term survival in patients with MI complicated by heart failure and ventricular arrhythmia. The long-term duration of routine β-blocker therapy after myocardial infarction without heart failure or hypertension has not been prospectively addressed, but guidelines recommend a 3-year treatment course then reassess the clinical need for the medication. Meta-analysis from the reperfusion era suggests β-blockers can reduce MI (RR 0.72 [95% CI, 0.62-0.83], NNT = 209) and angina (RR 0.80 [95% CI, 0.65-0.98], NNT = 26) at the expense of increased heart failure (RR 1.1 [95% CI, 1.05-1.16], NNH = 79) and increased cardiogenic shock (RR 1.29 [95% CI, 1.18-1.41], NNH = 90)with no significant impact on mortality. While oral β-blockers are an important part of ACS management, IV β-blockers should usually be avoided as they increase the risk for shock (Class III, LOE B). In addition, oral β-blockers are contraindicated in patients with signs of acute heart failure, evidence of low-output state, increased risk for cardiogenic shock, second- or third-degree heart block, and active asthma. When β-blockers are contraindicated due to asthma exacerbation, then nondihyophyidine calcium channel blockers could be considered as long there are no contraindications (Class I, LOE B).
Angiotensin Converting Enzyme (ACE) inhibitors have been shown to lower mortality in patients with recent myocardial infarction and reduced left ventricular ejection fractions (LVEF) less than 40% (Class I, LOE A). Furthermore, ACE inhibitors should be strongly considered in patients with diabetes mellitus and stable chronic kidney disease (Class I, LOE A). In patients who are intolerant to ACE inhibitors, angiotensin receptor blockers (ARBs) should be considered. While meta-analyses suggest a small (0.48% absolute, NNT = 208) reduction in 30-day mortality with ACE inhibitors in ACS, the clinical significance of this finding is unclear and ACE inhibitor should be used with caution without the above indications given the risk for renal dysfunction and hypotension.
Aldosterone antagonists (eg, eplerenone, spironolactone) are recommended for patients with AMI and LVEF less than or equal to 40% (Class I, LOE B). In the EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival) study, demonstrated significantly reduced rates of death from cardiovascular causes or hospitalization for cardiovascular events (relative risk, 0.87; 95% CI, 0.79-0.95; P = 0.002, NNT = 30) in patients with eplerenone initiated within days of admission.
High-intensity statin therapy should be given to all patients with ACS without contraindications (Class I, LOE A). Statins should be started at moderate to high doses as soon as possible on admission and continued indefinitely. The benefits of statin therapy are well known in the primary prevention for high-risk patients and in secondary prevention for patients with CAD. There may also be an early acute benefit in patients with NSTE-ACS. Several studies have demonstrated reduced rates of periprocedural MI with high-dose statin loading before PCI; therefore, a statin is recommended before PCI when possible (Class IIa, LOE A for statin naive).
The choice of stent, P2Y12 antagonist, duration of dual antiplatelet therapy, and anticoagulant is important for patients that require anticoagulation after ACS. This includes patients with atrial fibrillation, venous thromboembolism, mechanical heart valves, and left ventricular thrombus. When anticoagulation is warranted, warfarin is the most common anticoagulant agent and clopidogrel and aspirin the most common antiplatelet agents used. Very little data support the safety of the novel anticoagulants and P2Y12 inhibitors in this setting. In addition, patients with a history of gastrointestinal bleeding who require anticoagulation and antiplatelet therapy should also receive proton pump inhibitors (PPIs) (Class I, LOE C). A PPI can also be considered in patients without history of gastrointestinal bleeding when anticoagulation and antiplatelet therapy are warranted (Class IIa, LOE C). While there were early concerns over potential interactions with certain PPIs and clopidogrel metabolism, more recent registry and randomized trials suggest reductions in bleeding complications without increased cardiac events with the combination of PPIs and clopidogrel.
Triple therapy (aspirin, clopidogrel, and warfarin) after PCI is associated with two- to fivefold greater risk of major bleeding compared to dual antiplatelet therapy. Recent studies suggest that aspirin can often be omitted when anticoagulation is warranted after PCI. In the 573 patient randomized WOEST trial, omission of aspirin decreased major bleeding complications (44.4% vs 19.4%, NNH [by adding aspirin] 4, p < 0.0001) without any increase in ischemic events. Similar findings were noted in a meta-analysis of 1263 patients from six randomized trials as well as a larger real world registry of 12,165 patients undergoing PCI requiring anticoagulation.
Left ventricular (LV) mural thrombus is found in 3% to 15% of anterior MIs treated with percutaneous coronary revascularization. Pooled studies have noted a fivefold increased risk for systemic embolism with LV thrombus after anterior MI, and anticoagulation therapy decreases this embolic risk. Thus, anticoagulation is recommended for patients with acute MI and asymptomatic LV mural thrombus (Class IIa, LOE C). Anticoagulation after anterior MI without mural thrombus formation is controversial. Currently, the guidelines suggest that anticoagulation therapy may be considered for patients with STEMI and anterior apical akinesis or dyskinesis (IIb, LOE C). However, in a recent retrospective analysis of 460 undergoing PCI for anterior MI without LV thrombus, anticoagulation was actually associated with an increased incidence of stroke (3.1% vs 0.3%, p = 0.02), major bleeding (8.5% vs 1.8%, p < 0.0001), mortality (5.4% vs 1.5%, p = 0.04), length of stay, and readmissions. Furthermore, after propensity matching, anticoagulation was still associated with a fourfold greater incidence of net adverse cardiac events. These findings certainly question the routine use of triple therapy in this population without LV thrombus. Until larger randomized trials are conducted, if anticoagulation is used in this setting, clinicians should probably omit aspirin, add proton pump inhibitors, target lower INR ranges, shorten the anticoagulation course (3 months), and use radial access when possible.
All patients with ACS should be referred to a comprehensive cardiovascular rehabilitation program (Class I, LOE B). These programs provide patient education, regular exercise, monitor risk factors, and address lifestyle modification. The pneuomococcal vaccine is recommended for patients 65 years and older and high-risk patients with cardiovascular disease (Class I, LOE B). In addition, annual influenza vaccination is recommended for all patients with ACS (Class I, LOE C), and based on randomized controlled trial data has been shown to reduce MACE (NNT = 17) and hospitalization for ACS (NNT = 31). NSAIDs have been associated with increased cardiovascular risk and should largely be avoided in patients with ACS (Class III, LOE B). For patients with chronic musculoskeletal pain, acetaminophen, nonacetylated salicylates, tramadol, or low dose narcotics should be used as required (Class I, LOE C). If NSAIDs are required when these therapies are insufficient, then the nonselective naproxen is preferred over other NSAIDS (Class IIa, LOE C).
PRACTICE POINT
Late Hospital ACS Care and Hospital Discharge
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All patients with ACS should be discharged with dual antiplatelet therapy.
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Options for P2Y12 antagonists include clopidogrel, prasugrel, and ticagrelor after PCI.
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Options for P2Y12 antagonists include clopidogrel and ticagrelor with medical management without PCI.
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All patients with ACS should receive high-intensity statin therapy.
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All patients with MI should receive oral β-blocker therapy for at least 3 years after myocardial infarction and indefinitely for patients with congestive heart failure and/or hypertension.
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All patients with reduced LVEF ≤ 40% should receive an ACEI or ARB and aldosterone antagonist unless contraindications.
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When anticoagulation is warranted in patients with PCI for ACS, warfarin is preferred and aspirin can usually be omitted.
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All patients should be counseled about smoking cessation, diet, and exercise.
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All patients should be referred to cardiac rehabilitation programs at discharge.
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Dual antiplatelet therapy
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High-intensity statin
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Referral to cardiac rehabilitation
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Smoking cessation education
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β-Blocker if myocardial infarction and no contraindications
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ACE inhibitor (or ARB) if diabetic, chronic renal failure, or LVEF≤40% and no contraindications
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Aldosterone inhibitor if LVEF≤40% and no contraindications
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- Reperfusion by thrombolytic treatment or mechanical means can restore oxygen levels and return the metabolic processes to aerobic metabolism. A secondary consequence of reperfusion is reperfusion injury in which the highly reduced state of injured cells meets increased oxygen concentration and produces reactive oxygen radicals. Most notable of these is the hydroxyl radical (OHo), which attacks tissue components such as lipids and protein sulfhydryl groups.