A 60 something-year-old man with a history of ESRD, LVH and prior CABG presented after an episode of hypotension during his hemodialysis, run followed by a syncopal episode which caused his run to be terminated early. His other symptoms on presentation were general lethargy and mild shortness of breath. No chest pain. His vitals were initially normal.
This is his presenting EKG (T= 26min):
What do you think?
Presenting EKG (T= 26min):
Compared to the baseline EKG which looks fairly typical of normal LVH, this presenting EKG has what we call “pseudonormalization” of the ST segments in V2 and V3 – the ST elevation that was once present at baseline is now “normalizing”, to the point where there is virtually no elevation in V3. Hence, the term “pseudonormalization”, because it is not really normal – LVH should have repolarization changes seen in the baseline EKG. Thus, there is relative ST depression. It is analogous to a normal EKG having ST depression in V2 and V3, which would be abnormal and concerning for posterior MI in the right clinical context. But because of LVH, this is masked in this patient. There is also ST depression in the inferior leads – this was present on the old EKG, but there is also NEW ST depression in aVL.
Closer look at V2 and V3 side by side:
Furthermore, in both V2 and V3, the ST segment has flattened, resulting in more concavity of the ST-T complex. Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring – see this study). But in this case, the concavity is actually more concerning because now we are worried about posterior MI. Given the inverted voltage from the posterior myocardium that we see on a normal EKG, deepening concavity would be analogous to elevating convexity in the posterior myocardium.
Same image above with V3 inverted and flipped on its axis to better visualize the posterior ST segment:
|This is inverted: it is as if you were looking from the posterior wall.
The baseline is on the left, and now it looks as if the ST segment is rising, with less downsloping.
The patient’s initial troponin I was 2.0 ng/mL (99% reference level = 0.030 ng/mL. With his ESRD, he does have an elevated baseline troponin at ~0.40 ng/mL. His ED cardiac ultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF. His prior EF from an ECHO 6 months prior indicated 35% LVEF.
What would you do in this scenario?
I think a good start would be a posterior EKG and a high quality contrast echocardiogram read by an expert. Unfortunately, neither were done in this case.
This was the patient’s second EKG in the ED, 3 hours after the first (T= 217min):
|Deeper and more downsloping ST in V5 and V6
There is also pseudonormalization of the previously inverted T-wave in aVL
The patient’s symptoms were attributed to probable hypovolemia secondary to poor oral intake and to a UTI, but given his troponin elevation he was admitted on a heparin drip and serial troponins due to his high risk history.
His inpatient clinicians did not think that an urgent angiogram was warranted given that he was chest pain free, his EKG appeared nondiagnostic, and serial troponins were not elevating beyond 2 ug/L.
Later on during the night of his admission he had a short episode of chest pain that resolved with sublingual nitroglycerin.
Around midnight, the patient became more hypotensive with systolic BP in the 60s, and was complaining of feeling nauseous and “sick to his stomach”.
He had another EKG recorded at this time (T = 487 min):
|More subtle flattening of ST segment in V2 and V3.
Around 4AM, the patient had worsening dyspnea and hypoxia with continued hypotension.
He became confused and had another EKG done (T = 899 min):
|Even more pseudonormalization. V2 hardly has any ST elevation now.
Overall voltage is decreased as well.
Just as importantly, the pseudonormalized T-wave in aVL is now larger, with deeper reciprocal T-wave inversion in inferior leads
Shortly after this EKG, his HR dropped into the 40’s and he subsequently had a PEA arrest requiring 1 round of chest compressions, followed by ROSC. He was taken to the cath lab at that time (T = 1024 min).
He was found to have a 100% occlusion of the proximal anastomotic portion of a prior SVG from the aorta to the OM1 which in turn had a vein graft to the distal RCA. There was initially TIMI 0 flow . The lesion was intervened on with balloon angioplasty and had subsequent TIMI 3 flow. It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior.
His troponin I peaked at 97 ng/mL (very large MI!).
His follow up ECHO the next day revealed an EF of 24% and a posterior wall motion abnormality. Fortunately, he was extubated several days later in the ICU with intact baseline mental status and was discharged shortly thereafter to subacute rehab.
Acute myocardial infarction in patients with dialysis
Patients on dialysis have a well studied history of underdiagnosis and undertreatment for acute myocardial infarction. This is paradoxical given the absurdly high 2 year mortality rate of 70% after a MI in dialysis patients.
This study from Herzog et al (from our own Hennepin County Medical Center) included patients from a national registry and compared 3049 patients on dialysis admitted and eventually found to have acute MI compared with 534,395 patients not on dialysis admitted with an eventual diagnosis of acute MI. Of these groups, only 22% of dialysis patients had an admission diagnosis consistent with acute MI while 43.8% of nondialysis patients had the correct admission diagnosis of acute MI. Dialysis patients had double the rate of cardiac arrest (11% vs 5%), were less likely to receive reperfusion therapy when eligible (47% vs. 75%), and had an increased odds ratio of death compared to nondialysis patients 1.5 (95% CI 1.3-1.7).
Why is this? One reason for underdiagnosis might be that only 44% of these dialysis patients presented with chest pain while over 68% of those not on dialysis had chest pain on presentation. Another reason may be that the EKG is more difficult to interpret in patients with dialysis due to baseline abnormalities, including LVH. In this study of dialysis patients with severe CAD, 77% had an abnormal resting EKG and the most common abnormality was LVH.
Herzog et al. comment on this latter study: “There is a lower index of clinical suspicion and a higher level of inaccuracy for initial diagnosis of acute coronary syndromes in dialysis patients with AMI because twice as many patients were incorrectly diagnosed on admission. Further diagnostic confusion may have resulted from the greater prevalence of hypertension and likely attendant hypertensive heart disease and uninterpretable ST depression in the dialysis cohort.”
What can we learn?
1. Occlusion Myocardial Infarction (OMI) often does not present with diagnostic ST elevation, or even any STE, especially in dialysis patients.
2. Pseudonormalization of ST segments, and also of T-waves, may be a useful sign to help detect OMI in the setting of LVH.
3. Patients on dialysis often do not have chest pain in the setting of acute MI. Have a high index of suspicion for MI in these patients and advocate for them.
3. Think about, and use, emergent contrast echocardiography more liberally.