February CCU: When is it Just Demand Ischemia?

Manasi Shah PGY 3

CCU Case Presentation

 

Demand Ischemia: How Do You Know?

 

Case Presentation:

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.

Inpatient Management:

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.

Discussion:

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) [2]. 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 [3]. 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 [4]. 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 [5].

 

References:

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

Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Eur Heart J 2007; 28:2525.

Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation 2012; 126:2020.

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

 

3 Comments on "February CCU: When is it Just Demand Ischemia?"

  • Nice case and well described management that was effective. I would argue that despite troponin elevation – neither the history (chest pain and dyspnea for 1 week – but without mention of acute exacerbation … ) nor the ECG (diffuse ST depression with ST elevation in aVR,V1) suggest acute coronary occlusion – which is the principal indication for PCI. Given something obvious that “you can fix” (ie, marked worsening of his anemia) with potential downside of anticoagulation (cirrhosis) – correction of the underlying precipitating cause of his problem seemed the best way to go. But such decisions as you skillfully describe are indeed a “balancing act”.

    I respectfully submit my ECG Video-3 as another illustration of demand ischemia in a patient who presented with chest pain and an SVT. Initial ECG showed alarming diffuse ST depression with ST elevation in aVR,V1 – which resulted in post-conversion cath that failed to show acute coronary occlusion. Here is the link that should take you directly to the 12-lead in question – GO TO -http://youtu.be/5E3_MKuvr9c?t=8m40s (or you can fast forward to 8 minutes, 40 seconds in the video).

    Thanks again for presenting your case!

  • Very good. We tend to forget that in the heart, 100% of the oxygen carried in the blood is extracted in the first pass through the coronaries. The only way to increase oxygenation delivery is by increasing blood supply to the heart in demand situations by vasodilation. The mechanism here is a “double tap”; the patient can’t vasodilate to increase delivery and what blood that does get through has a reduced O2 carrying capacity. By treating the “devil you know- the anemia”, you correct the deficit as quickly if not more quickly than catheterization, and avoid the “devil you don’t know”, the unfortunate fact that this patient ended up with lesions not amenable to intervention. You also optimize the patient for the rigors of the procedure.

  • Why give ASA if you know the patient is having demand ischemia? If you could get a chance to do the case over again, would you have given ASA (ASA is an anti-thrombotic as well)?

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