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The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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Patient Summary

A male in his mid 40s with a 30 pack year smoking history, EVALI (e-cigarette and vaping associated lung injury), and asthma presented with dyspnea and persistent chest pain. He had been vaping for the past year. One month prior , CT chest showed bilateral patchy infiltrates and he was diagnosed with EVALI and started on a steroid taper with resolution of his CT abnormalities. A nuclear stress test at that time was negative for ischemia. On arrival, he was in sinus tachycardia, normotensive, and not on oxygen supplementation. Physical exam was negative for volume overload or heart murmurs. EKG showed new Q waves with STE in V2-V4, with associated Q waves and TWI in the lateral leads and troponin returned moderately elevated. He was emergently taken to the cath lab which showed an abrupt cutoff of flow to the LAD. He received a single DES with resolution of coronary flow. A post-cath TTE showed an LVEF of 40-45% with apical anterior and anteroseptal WMA. He was monitored in the CCU the next day and he was treated with aspirin, ticagrelor, ACEi, metoprolol succinate and high intensity statin and subsequently discharged in stable condition with cardiac rehab follow-up.

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Case Media

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Episode Schematics & Teaching

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The CardioNerds 5! – 5 major takeaways from the #CNCR case

1. The patient presented with a STEMI following a diagnosis of EVALI. What is known about the cardiovascular risks of vaping and e-cigarette use? 

• The overall cardiovascular risks of e-cigarette use remains to be elucidated 
• In preclinical studies, e-cigarettes use have been linked to increased sympathetic activity, oxidative stress, endothelial dysfunction, vascular injury, and altered platelet activity 
• One observational study has suggested that daily e-cigarette users were 1.79 times more likely to experience MI than individuals who had never used e-cigarettes. 
• Additional high-quality randomized controlled trials are needed to conclusively establish the safety and efficacy of e-cigarettes. 

2. So the data is still emerging regarding the overall cardiovascular risks of e-cigarette use. Of note, the patient had a negative stress test a month prior. Should that not translate into low likelihood of cardiovascular events? 

• Remember that stress testing for the diagnosis of obstructive coronary disease is most helpful in patients with an intermediate pretest probability for coronary artery disease. Further myocardial ischemia can occur not only secondary to obstructive epicardial disease (which may be new and acute from plaque rupture/erosion), but also from microvascular disease, vasospastic disease, and so forth. Stress testing with radionuclide myocardial perfusion imaging (e.g., SPECT, PET) is a well-established method for assessing coronary disease, but it is not an anatomic assessment. With nuclear stress tests, the causes of a false-negative result could include submaximal exercise (if doing exercise stress), collateral or overlapping epicardial circulation, suboptimal images (including artifact and poorly timed stress images), inaccurate interpretation, and balanced ischemia.  

• Nonetheless, sensitivity for obstructive CAD in SPECT approaches 85-90% with specificity around 70-75%. As SPECT imaging is not an anatomic assessment, a recent negative nuclear stress test does not necessarily mean very low risk for future major adverse cardiovascular events. Even with a normal nuclear stress test, there is a 0.65% – 1.78% annual event rate of death or non-fatal MI.  

3. Can non-obstructive and potentially “vulnerable” plaque be detected before an event? 

• Remember ECG, echocardiographic and radionuclide stress testing are different modalities to assess for obstructive CAD after inducing ischemia via exercise or medications. These modalities typically assess for flow-limiting lesions (e.g., typically greater than 50%). However, acute coronary syndrome can occur subsequently from lesions that were not initially obstructive.  
• In the PROSPECT study looking at patients who presented with ACS and underwent PCI to the culprit lesion and were followed afterward for ~ 3 years for adverse events, recurrent major adverse plaque rupture events were noted equally at the culprit lesion and at non-culprit lesions. Non-culprit lesions that were responsible for unanticipated events were angiographically mild on initial evaluation, had thin-cap fibroatheromas, or had large plaque burden as determined by gray-scale and radiofrequency intravascular ultrasound. 
• This is where coronary CTA has an increasingly larger role. A study looking at coronary CTA determined that plaques with positive remodeling and low attenuation features were at higher risk of ACS developing over time. Those individuals with neither of those features had high NPV in ruling out future ACS events. Typically, as a lesion increases in size, it can compromise luminal blood flow when 50% or greater narrowing of the lumen is observed (remember this is slightly different than labeling a lesion as “obstructive” to the point of potentially necessitating intervention). However, when there is an absence of luminal loss regardless of lesion size in early lesions, this is called “positive coronary artery remodeling” and there is compensatory enlargement of the epicardial vessel. Post-mortem studies have found that vessels with positive remodeling have been associated with increased lipid content, as well as features associated with unstable plaque (e.g., thin-cap fibroatheroma).  

4.  The patient had an MI at age 45! Apart from e-cigarette use, what other evaluation is warranted in a young patient with ACS or STEMI? 

• Traditional risk factors such as dyslipidemia, T2DM, HTN, and family history of premature CAD must be evaluated as plaque rupture events are still the most common cause of MI in young patients (age < 45 years). Furthermore, the differential for young individuals presenting with acute myocardial infarction should include non-atherosclerotic causes such as: anomalous coronary artery, spontaneous coronary artery dissection, coronary embolus, coronary vasculitis, coronary aneurysm (all of which have been discussed in the @cardionerds #CNCR episodes!).  
• If thrombus is present on angiography without traditional risk factors, workup should include evaluation for hypercoagulable states (e.g., Protein C and S deficiency, Factor V Leiden, APLS) or evaluating for a source of embolism (e.g., Afib, valvular lesion, LV thrombus, or even PFO [Enjoy Ep #51 – ACS & PFO]). Coronary thrombus may arise in situ from plaque rupture/erosion or as an embolus; recall that coronary emboli may be categorized as: direct, paradoxical, or iatrogenic. 
• Angiographic and multi-modal imaging findings may reveal the underlying etiology, including SCAD (Enjoy Ep #65 – SCAD), or one of the other non-atherosclerotic coronary processes listed above. If no obvious lesion is present, one should evaluate for Myocardial Infarction with non-obstructive coronaries (MINOCA) such as coronary vasospasm, and coronary microvascular dysfunction 
• Other considerations in young patients should include drug use, such as cocaine and methamphetamine use. Furthermore, oral contraceptives combined with another pro-thrombotic risk factor (e.g., tobacco use) may lead to acute myocardial infarction.  

5.  Sounds like the patient improved symptomatically after PCI placement. Going back to the basics, why do we obtain a TTE after STEMI and monitor in the CCU?  

•  Assessment of resting LV function helps us risk stratify patients, as it is one of the strongest predictors of survival. Furthermore, it will help us guide our medical therapy after STEMI. Echocardiographic evaluation can also help us characterize any suspected mechanical complications of STEMI. Beyond just survival, residual LV systolic function is one of the strongest predictors of sudden cardiac death risk after STEMI. Patients with an initially reduced LV function (e.g., <40%), who do not warrant ICD therapy before discharge, should undergo re-assessment of LV function >40 days after the index event to assess eligibility for ICD therapy. The delay to ICD therapy in this circumstance comes from the results of the DINAMIT trial in which ICD therapy 6 to 40 days after MI in patients with LVEF  ≤ 35% was not shown to reduce overall cardiac death risk.  
• The cardiac intensive care unit was initially established as a separate ward for the early detection and treatment of arrhythmias following acute myocardial infarction. Monitoring for arrhythmia in the CCU remains a cornerstone of post-STEMI management, as well as mechanical, embolic and inflammatory complications.  
• Mechanical complications after a STEMI include LV failure and cardiogenic shock, acute severe mitral regurgitation from papillary muscle rupture, ventricular septal rupture, LV free wall rupture, ventricular pseudoaneurysm, and ventricular aneurysm.  
• LV mural thrombus can cause an embolic complication, especially after a large anterior wall MI and delayed reperfusion.  
• Inflammatory complications include early and late pericarditis (i.e. Dressler’s syndrome – though this is rarely seen). 

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References

1. Buchanan, N. D. et al. Cardiovascular risk of electronic cigarettes: a review of preclinical and clinical studies. Cardiovasc. Res. 116, 40–50 (2020). 
2. Hachamovitch, R. et al. Incremental prognostic value of myocardial perfusion single photon emission computed tomography for the prediction of cardiac death: differential stratification for risk of cardiac death and myocardial infarction. Circulation 97, 535–543 (1998). 
3. Arbab-Zadeh, A. Stress testing and non-invasive coronary angiography in patients with suspected coronary artery disease: time for a new paradigm. Heart Int. 7, (2012). 
4. Falk Erling, Shah Prediman K. & Fuster Valentin. Coronary Plaque Disruption. Circulation 92, 657–671 (1995). 
5. Motoyama, S. et al. Computed tomographic angiography characteristics of atherosclerotic plaques subsequently resulting in acute coronary syndrome. J. Am. Coll. Cardiol. 54, 49–57 (2009). 
6. Stone, G. W. et al. A Prospective Natural-History Study of Coronary Atherosclerosis. N. Engl. J. Med. 364, 226–235 (2011). 
7. Gulati, R. et al. Acute Myocardial Infarction in Young Individuals. Mayo Clin. Proc. 95, 136–156 (2020). 
8. O’Gara, P. T. et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. J. Am. Coll. Cardiol. 61, e78–e140 (2013). 

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CardioNerds Case Reports: Recruitment Edition Series Production Team

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