10/22/16 Lay of the land Update on Acute Coronary Syndrome: § Case studies with an emphasis on discussions Five Things Hospitalists Must Know § Focus on five key take-home points § Grounded in evidence, not acronyms Dhruv S. Kazi, MD, MSc, MS Assistant Professor Department of Medicine (Cardiology), Department of Epidemiology and Biostatistics, Center for Vulnerable Populations, and Center for Health Care Value University of California San Francisco Division of Cardiology Zuckerberg San Francisco General Hospital Email: kazi@ucsf.edu Twitter: @kardiologykazi Conflicts of Interest: None Definition of ACS Why do we worry about ST elevations? § Spectrum of clinical conditions that produce acute § We used to define MIs by Q waves: but those are fickle myocardial ischemia and/or infarction, usually due to an (early/transient, transient) abrupt reduction in coronary blood flow. § EKG criteria: ST elevations of ≥ 1mm in 2 contiguous leads or ≥ 2 mm in V2-V3. Asymptomatic coronary dz à Stable angina à Unstable angina à NSTEMI à STEMI § ST elevation is a powerful predictor of occlusion or high- grade stenosis of epicardial coronary artery, determines management (early reperfusion), and is a marker of a higher in-hospital mortality 1
10/22/16 Presenting EKG: Case 1: A 62 year old woman with diabetes and hypertension presents with nausea, vomiting, 4/10 substernal discomfort, and 6/10 abdominal pain. In the ED, she is noted to be afebrile with a heart rate in the 90s, BP 155/95. MOC question Audience Response 62yo woman with DM, HTN presenting with substernal discomfort, nausea, vomiting, and abdominal pain, with LBBB on initial EKG. What do you do next? a. Don’t know if the LBBB is new, contact primary care doc for an old EKG b. LBBB makes the initial EKG uninterpretable, repeat EKGs every 10 minutes c. Request a stat echocardiogram for wall motion abnormalities d. Send off stat cardiac troponins, drill deeper into the history and clinical presentation e. LBBB is a STEMI-equivalent, activate the cath lab 2
10/22/16 Anatomy of the conducting system So why fret over LBBB? § Right bundle is a discrete structure that is subendocardial § 7% of patients who present with an acute MI have a for the proximal and distal thirds of its course (Cue: LBBB on the presenting EKG fragile) § Almost half these patients did not have concomitant CP § Abnormal depolarization leads to abnormal § Left bundle is a fan-like structure that quickly divides into repolarization, so ST-T changes not interpretable. the anterior and posterior fascicles (Cue: relatively resilient) § Produces delays in diagnosis and initiation of evidence- based therapies, and therefore adversely affects outcomes. 3
10/22/16 Caveat emptor: MOC question § Patients with old LBBB can occlude a coronary, we just What do you do next? wouldn’t see it on the EKG a. Don’t know if the LBBB is new, call around for an old EKG § Patients can have a new LBBB from causes other than b. LBBB makes the initial EKG uninterpretable, repeat EKGs ischemia every 10 minutes § LBBB is not a STEMI equivalent – it simply makes a c. Request a stat echocardiogram for wall motion abnormalities STEMI more challenging to diagnose. d. Send off stat cardiac troponins, drill deeper into the history and clinical presentation e. LBBB is a STEMI-equivalent, activate the cath lab MOC question Take-Home Point #1 What do you do next? The primary challenge with LBBB in the setting of acute chest pain is that it may mask an ongoing MI. a. Don’t know if the LBBB is new, call around for an old EKG b. LBBB makes the initial EKG uninterpretable, repeat EKGs every 10 minutes In the setting of LBBB, the diagnosis of ACS comes c. Request a stat echocardiogram for wall motion abnormalities down to a good clinical story. But even when ACS is d. Send off stat cardiac troponins, drill deeper into the history established, cannot distinguish between an NSTEMI and and clinical presentation a STEMI à hence the cath lab. e. LBBB is a STEMI-equivalent, activate the cath lab 4
10/22/16 Case 2: § 68 yo man with obesity, hypertension, and diabetes, 30 pack-year smoking history was driving home from work when he had a head-on collision with a truck operated by a drunk teenager. In the ED, he was in pain but hemodynamically stable, and noted to have multiple, displaced fractures of the pelvis and both lower extremities. On hospital day 4, he notes shortness of breath and new 7/10 substernal chest pain. He is tachycardic 120s, normotensive, sating 94% on 2L nc. EKG showed sinus tachycardia and non-specific ST-T changes. MOC question Audience Response What would you NOT do next? a. Obtain serial EKGs b. Send off cardiac troponins c. Request an echocardiogram d. Obtain a CT chest with contrast e. Activate the cath lab 5
10/22/16 Suspicion for ACS but initial EKG non- Right-sided infarct Posterior infarct specific: § Infarct of the RIGHT ventricle § infarct the LEFT ventricle § Look carefully for ST elevations: § Complicates inferior MI or § Complicates inferior MI or isolated event isolated event – Serial EKGs every 5-10 minutes § Obtain a right-sided EKG § Obtain a posterior EKG – right-sided or posterior leads § Look for ST elevations in V4R § Look for ST elevations in V7-9 § Echo may help § Echo may help Bottom line: Suspicion for ACS, evaluation must include Right-sided + Posterior EKGs. Cath lab? Detectable Tropoinin = Death of Myocytes Ischemia-mediated myocardial injury : § § Patients presenting with a NSTEMI may still benefit from – Decreased supply due to coronary disease: Plaque rupture , an early invasive therapy if there are high-risk features: coronary vasospasm, dissection, vasculitis, embolic disease, cocaine/meth use – Ongoing pain despite antiplatelet + anticoagulation – Decreased supply due to non-coronary conditions: shock, hypoxia, pulmonary embolism – Electrical or hemodynamic instability – Increased demand: tachycardia or severe hypertension, – Heart failure cocaine/meth use § Direct myocardial injury : – Myocarditis, chest trauma, toxic meds, electrical shock, CO Note that contemporary data suggest patients with exposure, heart failure, malignancy NSTEMI and those presenting with a STEMI have similar one-year mortality. § Myocardial injury from other systemic conditions : – Sepsis, stress-cardiomyopathy, infiltrative diseases, stroke, sub- arachnoid hemorrhage, acute respiratory failure. 6
10/22/16 MOC question MOC question What would you NOT do next? What would you NOT do next? a. Obtain serial EKGs a. Obtain serial EKGs b. Send off cardiac troponins b. Send off cardiac troponins c. Request an echocardiogram c. Request an echocardiogram d. Obtain a CT chest with contrast d. Obtain a CT chest with contrast e. “Activate” the cath lab e. “Activate” the cath lab Take-home point #2 Take-home point #3 Ask yourself: Would this person benefit from early § Even if it’s “just a NSTE-ACS”, many patients benefit from reperfusion? an early-invasive approach § ST elevations? – Evidence of ongoing injury (e.g., unrelenting pain) § LBBB? à Think it through – Electrical or hemodynamic instability § Neither? – Heart failure – Obtain serial EKGs – Obtain right-sided and posterior-EKGs – Are there high-risk features? – Consider alternative explanations for an elevated troponin level 7
10/22/16 Case 3: MOC question 63 yo man with diabetes and ongoing 1pack per day cigarette use Would our patient with an NSTEMI benefit from a second presents with chest pain that woke him up from his sleep at 6am. antiplatelet agent, even though he did not undergo PCI? In the emergency room, he is hemodynamically stable and chest pain free. Presenting EKG shows 2mm ST depressions in II, III, aVF, with no ST elevations in right-sided or posterior leads. a. No, patients who present with an NSTEMI but do not undergo Troponin I is 0.2 ng/dL (reference value < 0.04). A diagnosis of a PCI were not included in trials of dual antiplatelet therapy, NSTEMI is made. and bleeding risk exceeds any potential benefit b. Yes, I would start clopidogrel for six months because it is the Aspirin, statin, heparin, and metoprolol are initiated. The next day, only agent studied in this context coronary angiography reveals a 60% lesion of the mid-RCA and c. Yes, I would pick prasugrel for nine months because it is a 50% lesion of the left anterior descending. LV systolic function is more potent antiplatelet agent that is not affected by normal on the transthoracic echocardiogram. A decision is made to CYP2C19 polymorphisms “medically manage” the coronary disease with aspirin, statin, an ACE-inhibitor, and a betablocker. d. Yes, I would pick ticagrelor and use it for at least one year. Does a patient who presents with an NSTEMI Audience Response but does not undergo PCI still benefit from dual antiplatelet therapy? § Yes, this has been VERY WELL studied in randomized trials and observational data § One year of DAPT after medically managed NSTEMI § Remains an enormous evidence-practice gap in ACS management. 8
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