Pump Problems
Case Presentation:
A 59 year old male with PMH of coronary artery disease (CAD) s/p 3 vessel coronary artery bypass graft (CABG) >10 years ago, hypertension (HTN), diabetes (DM), and hyperlipidemia (HLD) who presents with progressive chest pain. While at first the episodes only occurred with heavy exertion, he started feeling the chest pain at rest this morning, which prompted his visit to the Emergency Department. He just received nitroglycerin and his chest pain has resolved. EF 50%.
Vitals: BP 160/89, HR 73, RR 16, saturating 100% on room air
Labs: High sensitivity troponin 5, BNP 130. Lactate WNL. All other labs WNL.
EKG: Normal sinus rhythm with rates in the 70s. Incomplete right bundle branch block. Normal intervals. No ST elevations / depressions or T wave inversions (all unchanged from previous).
Ask Yourself:
Questions:
Would you admit this patient to the hospital?
If this patient is admitted to the hospital, what medications would you order for him?
Is there any additional workup you would want to order before this patient is discharged home
What are the indications for emergent catheterization?
Stages of Coronary Artery Disease Leading to Acute Coronary Syndrome (ACS)
Stable Coronary Artery Disease: Pictured you can see how the artery on the left has atherosclerosis; however, the plaque is stable. As such, there is no cardiac injury or structural changes appreciated on echocardiogram or on the EKG.
Unstable Angina: Here you can see that the plaque has ruptured, which activates both the coagulation cascade and the platelets. While this is an emergency, there is still blood flow through the artery. As such, the patient may have a normal troponin and echocardiogram, while the EKG may only show nonspecific T wave inversions or look normal. In this scenario, the story is what clues you into the ACS.
Non-ST segment elevation myocardial infarction (aka NSTEMI): Unlike with unstable angina, there is a significant degree of ischemia occurring due to the thrombus forming. Since the artery is not fully blocked, the full myocardium is not damaged (as seen by the only partially affected myocardium that is shaded) - consider removing since NSTEMIs can cause transmural damage if big enough; NSTEMI mostly implies there is ischemia and injury to the myocardium. On the EKG, ST segment depressions or T wave inversions may be seen.
ST segment elevation myocardial infarction (STEMI): The most feared complication in which there is complete occlusion of the coronary artery. Since there is complete occlusion, no blood can get through. This causes full necrosis of the affected myocardium and ST elevations seen on EKG.
How to Classify What is Occurring:
Type 1 Myocardial Infarction: This is Acute Coronary Syndrome with plaque rupture. As seen in Figure 3, this refers to Unstable Angina, NSTEMI, and STEMI.
Troponin: Can be elevated or normal, depending on the timing of presentation
The EKG: May be normal, show non-specific T wave inversions (i.e. inverted T waves that do not follow a specific perfusion pattern), ST depressions, or ST elevations
Echo: Can be normal or show new wall motion abnormalities
The story: Very concerning for ACS. The patient suddenly has crushing chest pain that may radiate to the jaw or down the left arm. The pain may be relieved after 10-15 minutes of rest or nitroglycerin.
Note: Women, diabetics, and the elderly can present atypically, so it is important to use clinical data plus the story to determine whether or not ACS is present.
Figure 3 represents a cardiac catheterization with coronary angiogram, which helps us determine the extent of the coronary artery disease. In this procedure, access is usually obtained via the radial or femoral artery (seen 3A), pictured to the left). Dye is then injected into the coronary arteries (3B). This allows us to visualize the anatomy of the coronary arteries and intervene via stent placement if the occlusion is significant.
Type 2 Myocardial Infarction: Unlike Type 1, Type 2 occurs due to stable coronary artery disease plus a stressor (i.e. tachycardia, hypotension, anemia, infection, etc). Colloquially speaking, this is known as Demand Ischemia, where the demand on the heart outweighs the supply. There is NO PLAQUE RUPTURE. Just stable plaque that is prevent adequate perfusion of the heart.
Troponin: Will be elevated due to supply vs demand mismatch. The sicker the patient, the worse the mismatch, and the higher the troponin. Patients can also have elevated troponin when they have increased stress on their bodies when they have multi-vessel disease
The EKG: May show non-specific T wave inversions
Echo: Can be hyperdynamic or show poor filling. However, you should NOT see new wall motion abnormalities. You can see normal ejection fractions or even new heart failure if the the patient has multivessel disease or is in severe shock..
The story: Does NOT sound like ACS.
ACS Medications:
During ACS, whether it’s a STEMI or NSTEMI, there is plaque rupture, which activates both Primary and Secondary Hemostasis. Primary Hemostasis is focused on platelet activation, while Secondary Hemostasis utilizes the clotting cascade to create thrombin and fibrinogen to stabilize clot (Figure 3).
The medications that we give during ACS are meant to prevent further inflammatory response and propagating clot formation.
Patients with ACS must be started on:
Aspirin A COX inhibitor that prevents prostaglandin release and platelet activation.
Heparin Drip This is the preferred anticoagulant. Heparin specifically works on antithrombin III to prevent activation of Factors II and X.
High Intensity Statin Helps to stabilize the lipid core in the acute phase, as well as preventing future plaque build up.
P2Y12 receptor antagonists Important for directly preventing platelet activation.
Note: Some institutions will wait until after coronary angiograms to start a P2Y12 inhibitor in case the patient will instead require a coronary artery bypass graft (CABG) in order to no delay surgery
Additional medications include:
5. Nitrates (sublingual or IV nitroglycerin drips) help reduce preload and afterload by concerting to nitric oxide and causing venous and arterial vasodilation. Contraindicated in right ventricular infarcts.
6. Morphine for pain control (to be used VERY sparingly! )
7. Beta blockers to help reduce contractility, decrease cardiac work, and improve mortality
Figure 4 shows an acute plaque rupture with subsequent activation of Primary and Secondary Hemostasis in which the body tries to form clot in response to the increased inflammation. Also shown is how the ACS medications prevent further clot formation
When patients have ACS, we use high intensity statins with the goal of lowering their LDL-C to <70 mg/dL. If the LDL-C is not at goal and the patient is already on a high intensity statin, we may need to add a PCSK9 inhibitor or ezetimibe
2025 ACS Updates
Oxygen: Per the 2025 ACS Guidelines, there is only benefit for supplemental O2 if the patient is saturating <90%. If the patient’s O2 is > 90%, giving supplemental O2 has not shown to be beneficial and may even be harmful increased vasoconstriction and oxidative stress.
P2Y12 Inhibitors: When thinking about P2Y12 inhibitors, there are three main medications: ticagrelor, prasugrel, and clopidogrel. When patients present with ACS, the guidelines recommend ticagrelor or prasugrel as they had decreased major adverse cardiac events (MACE) and stent thrombosis as compared with clopidogrel.
The figure above from the updated 2025 ACS Guidelines shows which P2Y12 Inhibitor is preferred when patients come in with ACS, CABG, have not had any invasive intervention, or were initially treated with fibrinolytic therapy.
The above figure, from CORE IM 5 Pearls on Dual Anti-platelet Therapy helps to show the difference between the 3 main P2Y12 Inhibitors.
When thinking about length of anti-platelet therapy, the guidelines have changed in regards to patients who are at higher bleeding risk. Generally speaking, the guidelines prefer 12 of months DAPT therapy when patients present with ACS. If they are very high bleeding risks, PPI should be used. Additionally, they can potentially continue DAPT therapy for 1 month post-PCI and continue ticagrelor monotherapy after 1 month. See the chart below for more details.
Lipid Therapy: Patients with ACS must automatically be put on a high intensity statin with plan to recheck lipids in 4-8 weeks post statin initiation. The goal LDL is < 70 mg/dL. If the patient was already on a high intensity statin and LDL was < 70 mg/dL, an additional agent should be started such as Ezetimibe.
The figure above, taken from the 2025 ACS Guidelines, helps to detail what to detail lipid management post-MI.
NSTEMI vs Demand Ischemia:
If patients do not have plaque rupture (i.e. STEMI vs NSTEMI) but have an elevated high sensitivity troponin, this may be due to demand ischemia. In these cases, the patients may have underlying coronary artery disease (CAD) with increased demand. Sometimes this can be due to critical illness, prolonged tachycardia, or cardiac injury (i.e. post compressions or shock). In these situations, there is no role for the aspirin, heparin drip, high intensity statin, or P2Y12 inhibitors as there is no plaque rupture. Depending on how high the troponin trended, some physicians may recommend catheterization to determine the extent of the CAD once the patient is more stable.
There are multiple other causes of elevated troponin that are not due to acute plaque rupture, such as:
Pulmonary Embolism
Pericarditis
Myocarditis
Lung pathologies (i.e. pneumonia, pneumothorax)
Vasospasm
MI with non-obstructive coronary arteries (MINOCA)
Therefore, we need to think broadly. We can get a chest XR, EKG, and basic labs to help rule out other pathologies. If you are still concerned, use the HEART or TIMI score to help determine the patient’s risk factors of having an acute cardiac event. If these scores are moderately high, consider getting further imaging, like an echo or stress test.
If these scores are extremely high, consider consulting cardiology in the event that the patient needs to go to the cath lab.
When to bring patients with NSTEMIs to cath lab:
Patients who present with an acute plaque rupture with ST elevations require emergent revascularization, as the ST elevations signal signification thrombus formation and occlusion. After all, time is heart.
However, when patients have acute plaque rupture without ST elevations, this is what we classify as an NSTEMI. The lack of ST elevations means the myocardium is still getting perfused. We must stabilize the plaque with aspirin and heparin (as well as the lipid core with the high intensity statin); however, not all of these patients require emergent revascularization.
When patients present with NSTEMIs, we calculate their GRACE or TIMI scores, i.e. to help guide how quickly these patients need revascularization. The higher these scores are, the higher risk the patients are and the faster they should be revascularized.
To the right, you can see the GRACE Score (left) and the TIMI Score (right) from MD Calc.
Any patient who is clinically unstable with refractory angina, continuous arrhythmias, or hemodynamic instability, are considered unstable. These patients are considered high risk and should be brought to the cath lab ASAP.
When patients are not in the high risk category (i.e. lower GRACE and TIMI scores and are not considered unstable), they do not need emergent catheterization. These intermediate / low-risk patients can even have a delayed revascularization within 48-72 hours. Multiple randomized trials have not shown a difference in rates of death or MI between revascularizing this group of patients early (<24 hours) or delayed (48-72 hours)
This flow chart from the 2021 ACC/AHA/SCAI Coronary Artery Revascularization Guidelines helps to demonstrate how time to cath for patients with NSTEMI is determined based on the patient’s risk stratification.
Patients who present to the hospital with stable CAD are not having acute plaque rupture and fall into Type 2 MI. They may have chest pain and elevated troponin due to demand ischemia; however, their CAD is stable. When these patients present with stable ischemic heart disease (SIHD), i.e. not with acute plaque rupture, they can be candidates for both PCI and CABG. Ultimately, there needs to be a multidisciplinary discussion between the patient’s heart team to determine the best option for the patient.
The figure to the right from the 2021 ACC/AHA/SCAI Coronary Artery Revascularization Guidelines shows how we determine if patients with stable ischemic heart disease (SIHD) should get percutaneous coronary intervention (PCI) vs coronary artery bypass graft (CABG).
What are some of the indications for emergent catheterization?
When there is high concern for ACS (with STEMI vs NSTEMI): In these cases, it is important to start the aspirin, heparin, and a high intensity statin immediately to help stabilize the clot. In the case of STEMIs, there is a 90 minute door to balloon time
New Ventricular Arrhythmias (i.e. VT, polymorphic VT, VF)--see Figure 4
Hemodynamic instability with new cardiogenic shock or worsening heart failure The Shock Trial showed that early revascularization in patients with cardiogenic shock due to ACS actually helped reduce mortality
Persistent chest pain despite medical therapy The name of the game is no chest pain. Many times, the nitro will work; however, if patients have persistent or recurrent pain despite multiple doses of nitroglycerin and there is high concern for a cardiac cause, the patients may need to go to the cath lab or to the ICU for a nitroglycerin drip.
Polymorphic VT due to prolonged QTc – In this case, a premature ventricular complex (PVC) occurs during the prolonged QTc (seen by the red arrow). When this happens, the patient goes into polymorphic VT. This is also known as the R on T phenomenon and why there is so much emphasis placed on ensuring the QTc does not get too prolonged.
Polymorphic VT– If this is NOT due to prolonged QTc, this patient MUST BE TAKEN TO THE CATH LAB because this is due to ischemia until proven otherwise.
Back to the Case:
1. Would you admit this patient to the hospital?
When you calculate this patient’s TIMI and HEART scores, he is high risk for having a cardiac event. Although his troponin and EKG look normal, his story is very concerning for unstable angina. Given his risk factors and his story, this patient should definitely be admitted for further evaluation.
2. If this patient is admitted to the hospital, what medications would you order for him?
The patient’s chest pain at rest is very concerning for unstable angina. As such, he should be started on aspirin 324mg, a heparin drip, and a high intensity statin. No need to start a P2Y12 inhibitor until the angiogram shows a need for PCI. In order to help him with his pain, you can also give him morphine and nitroglycerin. A beta blocker should be started within 24 hours after the ACS event.
3. Is there any additional workup you would want to order before this patient is discharged home?
This patient should probably get a coronary angiogram before he leaves the hospital. If his TIMI and HEART score weren’t as high, he might be able to avoid invasive imaging and instead undergo a stress test, so long as he was no longer having any chest pain.
4. What are the indications for emergent catheterization?
As stated previously, concern for ACS (STEMI, NSTEMI, or unstable angina), new ventricular arrhythmias, hemodynamic instability with cardiogenic shock / worsening heart failure, and persistent chest pain despite therapy.
Further Learning:
Resident Responsibilities
Listen to the story, as this is a crucial part of determining whether or not the patient has ACS.
If you’re worried about ACS, whether it’s a STEMI or NSTEMI, patients MUST be started on Aspirin, Heparin, high intensity statin, +/- P2Y12 inhibitors.
Don’t forget the Statin!! It’s not just for preventing future atherosclerosis. Rather, it helps to stabilize the lipid core in the acute setting!
If a patient gets a stent placed, remember to start dual antiplatelet therapy!!
If a patient goes for catheterization, remember to get a post procedure EKG!
Attending Pearls:
The name of the game is no chest pain! If patients are having any sort of refractory chest pain, whether it’s after multiple doses of nitroglycerin or even after a stent was placed, you must take this seriously. Continue to get troponins or EKGs if indicated.
Be careful when giving morphine as this will take away all chest pain– however, the patient may still have underlying ischemia. That said, only use morphine after the cath lab has been activated. The last thing you want is to mask the patient’s chest pain!
If patients have HIT and cannot be put on heparin or lovenox, Bivalirudin can be used instead.
In the US, we tend to put patients on heparin drips if we are concerned for NSTEMI, while in Europe they usually use lovenox injections. While these two agents are similar in the immediate setting, lovenox requires additional loading in the cath lab if given >8 hours prior in order to be therapeutically anticoagulated. As such, many interventionalists prefer heparin.
Further Reading:
The SHOCK Trial showed that quick catheterization help improve cardiac outcomes and decrease mortality
PLATO, TRITON TIMI, ISAR REACT 5
2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines
AHA/ACC recommendations for lipid lowering agents in patients with ACS:
How’d we do?
The following individuals contributed to this topic: Rebecca Garber, MD, Stephanie Vamenta, MD
Chapter Resources
Lawton, Jennifer S., et al. “2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.” Journal of the American College of Cardiology, vol. 79, no. 2, 2022, pp. e21–129, https://doi.org/10.1016/j.jacc.2021.09.006.
Bhatt DL, Lopes RD, Harrington RA. Diagnosis and Treatment of Acute Coronary Syndromes: A Review. JAMA. 2022;327(7):662–675. doi:10.1001/jama.2022.0358
Gwon, H. C., Hahn, J. Y., Park, K. W., Song, Y. B., Chae, I. H., Lim, D. S., … & Kim, H. S. (2012). Six-month versus 12-month dual antiplatelet therapy after implantation of drug-eluting stents: the Efficacy of Xience/Promus Versus Cypher to Reduce Late Loss After Stenting (EXCELLENT) randomized, multicenter study. Circulation, 125(3), 505-513.
Crea, Filippo, and Peter Libby. “Acute Coronary Syndromes: The Way Forward From Mechanisms to Precision Treatment.” Circulation (New York, N.Y.), vol. 136, no. 12, 2017, pp. 1155–66, https://doi.org/10.1161/CIRCULATIONAHA.117.029870.