Manasi Shah PGY 3
CCU Case Presentation
Demand Ischemia: How Do You Know?
51M with history of DM II, ETOH cirrhosis presents with generalized weakness, constant pressure-like sub sternal chest pain worse with exertion associated with dyspnea on exertion for 1 week, associated w/ palpitations. Pt. denies fever, cough, hemoptysis, bloody vomitus, abdominal pain, hematuria, bloody stools, anticoagulation use, prior adverse cardiac events, recent travel. Pt had stable VS at triage, had positive guaiac and benign heart, lungs, and abdominal exams.
Initial ED Management:
He had a stat EKG done in ED which showed ST depressions in II, V4-V6 and STE in avR and V1. Labs were immediately sent, and patient was given an ASA, morphine, and Nexium in ED. When labs came back, pt had a troponin of 4.73 with normal renal function, and an H&H of 6.4/19 (also decreased from baseline). He was immediately transfused 1u pRBC and EKG was repeated, showing no changes from prior. Pt was transferred to Weiler shortly thereafter for cardiac catheterization.
While at Weiler, patient was not taken to cardiac catheterization immediately, but instead was medically managed with blood products. He received 2 more units pRBC. His troponins continued to trend downward, his symptoms improved significantly, and his EKG normalized the following morning. Pt then had an elective cardiac catheterization on his 3rd hospital day which showed 80% 3 vessel disease, however patient was not a candidate for CABG nor anticoagulation. He was discharged with aspirin and statin and cardiology follow up.
This case poses a very interesting question: when do you jump straight to anticoagulation and immediate cardiac catheterization versus conservative medical management as was done in this case? The patient presented with a classic chest pain story accompanied by STE in avR and V1 with reciprocal ST depressions and high troponins right from the start. Many physicians would argue that this patient is having an acute STEMI and needs to be sent for catheterization immediately while others would opt for medical management and treatment of anemia prior to more invasive intervention. Who is correct?
It is important to start of the discussion by defining what an MI is. In 2012, ACC/AHA/WHF all agreed that the definition of MI as a clinical event consequent to the death of cardiac myocytes (myocardial necrosis) that is caused by ischemia (as opposed to other etiologies such as myocarditis or trauma) . This death can be detected by detection of rise/fall of cardiac biomarkers with at least one value above the 99th percentile upper reference limit and with at least one of the following: Symptoms of ischemia, development of pathological Q waves on EKG, new or presumed new significant ST-T changes or new LBBB, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality . In this case, the patient met multiple criteria listed above and should have been considered for catheterization immediately, but was not. What about this case was different that caused it to be treated as demand ischemia? This concept of demand ischemia refers to a discordance between myocardial oxygen demand and supply. Anemia exacerbates this imbalance by causing a decrease in oxygen carrying capacity. This patient had a history of mild anemia, but his H&H this time were significantly lower than his baseline, and whenever he exerted himself, he would have classic chest pain. Also taking into account that this patient is cirrhotic and therefore a bleeding risk, it is a safer bet to give him blood products and trend his troponins than it is to anti-coagulate him.
Both short- and long-term survival are impaired among patients with troponin elevation in many different clinical settings, including congestive heart failure, sepsis, and pulmonary disease. The reasons for this increase in mortality are currently poorly understood but may be related to myocardial necrosis with myocyte loss or underlying quiescent coronary artery disease. However, another possibility is that increased troponin merely reflects a more fulminant disease process. Given this substantially increased risk for adverse outcomes, patients with troponin elevation in general require appropriate diagnostic evaluation and therapy aimed at the underlying disorder . At this time, there are no randomized controlled trials that assess the efficacy of interventions that reduce the risk for adverse events among patients with troponin elevations in the absence of an acute coronary syndrome. General recommendations include giving aspirin, but with-holding anti-thrombotics and anti-platelet agents .
Guest TM, Ramanathan AV, Tuteur PG, Schechtman KB, Ladenson JH, Jaffe AS. Myocardial injury in critically ill patients. A frequently unrecognized complication. JAMA. 1995; 273:1945-9. PubMed
Jeremias, Allen. “Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels When Acute Coronary Syndromes Are Excluded.” Annals of Internal Medicine 142.9 (2005): 786. Web.
Impact of Blood Transfusions in Patients Presenting With Anemia and Suspected Acute Coronary Syndrome Ish Singla – Maliha Zahid – Chester B.Good – Alanna Macioce – Ali F.Sonel – The American Journal of Cardiology – 2007