Written by Magnus Nossen MD, peer reviewed and edits by Smith, Meyers, Grauer
A 60 something previously healthy female smoker sought medical attention after 2-3 days of intermittent chest discomfort. The chest discomfort was described as sharp. Episodes lasting 5-30 minutes. On the day of presentation she experienced another episode of chest discomfort accompanied by vomiting and throat pain. She was concerned about possible throat infection. She contacted her primary care physician. Due to the vague nature of her symptoms and the fact that she had chest discomfort and no clinical sign of throat infection she was referred for further work up.
Upon admission she had ongoing slight chest discomfort. Vital signs unremarkable except borderline hypotension with a systolic BP about 102 mmHg. The following ECG was recorded.
First troponin I returned 3174 ng/l, at which point a repeat ECG was ordered.
|Not much difference from 1st ECG.|
- 1) Conditions causing volume overload of the RV. (E.g large ASD, partial anomalous pulmonary venous return, significant tricuspid regurgitation, carcinoid valvular disease, etc,)
- 2) Conditions causing pressure overload of the RV. (Any cause of pulmonary hypertension. E.g COPD, Idiopathic PAH, acute or chronic PE, pulmonary valve stenosis, etc)
- 3) Conditions affecting RV myocardial contractility, such as ARVD or RV infarction
MY Comment, by KEN GRAUER, MD (9/17/2023):
- I focus my comment on the initial ECG in today's case — which I've reproduced in Figure-1, and to which I've added the previous tracing found on file.
|Figure-1: Comparison between today's initial ECG — and the baseline ECG that was on file. (To improve visualization — I've digitized the original ECG using PMcardio).|
- There is ST elevation in each of the 3 inferior leads. Although the amount of ST elevation is not great in ECG #1, and there is J-point notching as commonly occurs with repolarization variants — the ST segment prior to the T waves in these inferior leads is straightened.
- Lead aVL is definitely not normal. Although the tiny QRS amplitude in this lead makes assessment difficult — the J-point in lead aVL is depressed, the ST segment in this lead is abnormally coved — and the T wave relative to QRS amplitude is hypervoluminous and markedly disproportionate. The shape of this ST-T wave in lead aVL is a reduced-size mirror-image opposite picture of the ST-T wave in lead III — which in a patient with CP, could clearly reflect reciprocal changes of a recent or ongoing acute process.
- In support of that these findings in lead aVL are not normal — the other high-lateral lead ( = lead I) is also not normal in appearance (ie, the ST segment in lead I is completely flat — in association with a smaller-than-expected T wave).
- My IMPRESSION re the Limb Leads: I thought the above noted limb lead findings in ECG #1 were non-diagnostic — but clearly of concern. In this woman in her 60s, with a 2-3 day history of intermittent CP (potentially consistent with an event occurring at any point during that time period) — I thought the above ECG findings could reflect recent inferior OMI. Additional evaluation (and ideally finding a prior tracing for comparison) would be very helpful.
- The ST-T wave appearance in leads V2-thru-V6 is not normal. Instead — ST segments in each of these 5 leads is abnormally flat. This is especially noted in anterior leads V2 and V3 — which normally display a slight amount of upward-sloping ST elevation. In the presence of the above-noted limb lead findings — this lack of slight, upward-sloping ST elevation in leads V2,V3 — especially in association with an R wave in lead V3 that abruptly becomes tall (given the tiny r wave amplitude in neighboring lead V2) — could be consistent with recent posterior infarction, especially given concern from the limb leads about recent inferior OMI.
- The initial troponin value came back markedly elevated!
- Repeat ECG (shown by Dr. Nossen above) — failed to show significant change.
- Bedside Echo was performed.
- Comparison with the "baseline" tracing ( = ECG #3 in Figure-1) — confirms that the subtle-but-real ST-T wave limb lead changes noted above in ECG #1 were new, as there was no ST elevation in the inferior leads and no ST depression in lead aVL of baseline ECG #3.
- That said — the earlier-than-expected transition and ST segment flattening in leads V3-thru-V6 was present in the baseline ECG (if anything, with slight ST depression in the earlier tracing) — so these chest lead changes that I suspected represented posterior OMI in ECG #1 were not new.
- Finally (as per Dr. Nossen) — the right-sided ECG that was done did show ST elevation that confirmed RV MI, albeit the amount of right-sided ST elevation was modest.
- Seeing the markedly dilated and poorly contractile RV on Echo — facilitated clinical ECG interpretation. Comparison of the initial ECG with the prior "baseline" tracing — confirmed acute inferior OMI, which "fit" with the cardiac cath finding of acute proximal RCA occlusion.
- I suspect the real-but-relatively-modest ECG changes seen on the ECGs in today's case may be because: i) The acute event in today's case may have begun 2 or 3 days earlier (as suggested by the history); and, ii) Right-sided ST elevation in association with acute RV MI tends to be a transient event that often resolves within 24 hours (Nagam et al — Perm J: Vol. 21, 2017).