Case 1.
Chief complaint: A 60-something African American male with 5 days of increasing SOB with dyspnea on exertion.
This male in his 60's has a PMH of CAD with MI and CABG, HTN with LVH, hyperlipidemia, and mild HF with only moderately reduced ejection fraction (and some diastolic dysfunction as well).
He presents with 5 days of worsening shortness of breath with orthopnea as well as chest pain. His BP is 191/90. He also has a history of venous thromboembolism and has not been taking his anticoagulants. He was also off of his BP meds (lisinopril, amlodipine and carvedilol).
Here is his ED ECG (ECG #1):
Bedside ultrasound:
The lung ultrasound (not shown) had B-lines, all but diagnostic of pulmonary edema.
There is severe LVH. There appears to my eye to be less than optimal systolic function and also less than optimal LV diastolic function.
Here is the short axis view:
Same interpretation as above.
Here is the chest X-ray:
Clinical Course:
--The D dimer was barely elevated at 327 ng/mL (upper limit of normal: 230 ng/mL).
--The initial troponin I was 0.083 ng/mL (99% = 0.030); this patient does not have baseline elevated troponin (does not have chronic myocardial injury, which is not uncommon in patients with heart failure), so this was a new troponin elevation.
That is to say, there appears to be acute myocardial injury.
--The Creatinine was 1.5 mg/dL, with a GFR of 69 ml/min (low).
--The NTproBNP was 1564 pg/mL (slightly elevated -- normal for patients with GFR less than 60 is 1800 pg/mL).
The emergency physicians correctly interpreted the ECG repolarization abnormalities as being entirely due to LVH combined with some injury due to acute heart failure exacerbation and hypertension, and understood that the newly elevated troponin (with rise and fall) was due to demand ischemia (type 2 MI) due to hypertension and acute heart failure.
They administered furosemide.
Learning point:
1. ST Elevation with Convexity in the presence of LVH does not necessarily mean STEMI
2. The ST/S ratio in STEMI would be significantly higher.
See discussion at this post:
Clinical course continued:
They gave furosemide and obtained a CT pulmonary angiogram which ruled out pulmonary embolism. He was not given any BP management.
Comment on management:
1. With B-lines and this chest x-ray and only a minimally elevated D Dimer, CTPA is unnecessary. The diagnosis is clearly acute decompensated heart failure.
2. This patient should get some immediate treatment to lower blood pressure (afterload reduction). IV nitroglycerine is best, but requires ICU monitoring. For a patient who is only moderately ill and does not require an intensive monitoring, a good choice, especially for African Americans with renal dysfunction, is afterload reduction with IV hydralazine (see references below). Often, in a patient who has not been taking his/her antihypertensive, I simply give those medications immediately in the ED. As this usually includes either an ACE inhibitor or an angiotensin receptor blocker, this is often sufficient.
Vasodilator Therapy of ADHF
http://circ.ahajournals.org/content/123/21/2414
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808524/
Clinical Course continued:
Subsequent troponins were 0.078, 0.076, 0.064
A formal echo showed:
2.5 weeks later, after recovering from acute decompensated heart failure, his ECG continued to show high voltage and convexity, although he was recovered from the acute heart failure.
Case 2:
A middle-aged patient with a history of severe persistent asthma, heart failure with preserved ejection fraction (HFpEF), and pulmonary hypertension presented presented very short of breath. Here was her first ECG (ECG #3):
A previous formal echo showed:
She improved with therapy for asthma in the ED and had this ECG recorded 5 hours later (ECG #5):
There was no myocardial infarction. All troponins were negative. She improved with therapy for asthma and was discharged from the ED.
Learning Points:
1. Patients with LVH who are in acute respiratory distress, especially with elevated BP and/or acute decompensated heart failure, frequently have convex ST elevation. This does not imply STEMI.
2. The ST/S ratio in STEMI with LVH is not established. The article by Armstrong et al. which is discussed in the referenced blog post above did not have appropriate methodology and their ratio of 0.25 is far too high. There certainly should be a ratio higher than 0.10 and probably higher than 0.15. (Armstrong EJ, Kulkarni AR, Bhave PD, et al. Electrocardiographic Criteria for ST-Elevation Myocardial Infarction in Patients With Left Ventricular Hypertrophy. Am J Cardiol. 2012;110(7):977-983. doi:10.1016/j.amjcard.2012.05.
Chief complaint: A 60-something African American male with 5 days of increasing SOB with dyspnea on exertion.
This male in his 60's has a PMH of CAD with MI and CABG, HTN with LVH, hyperlipidemia, and mild HF with only moderately reduced ejection fraction (and some diastolic dysfunction as well).
He presents with 5 days of worsening shortness of breath with orthopnea as well as chest pain. His BP is 191/90. He also has a history of venous thromboembolism and has not been taking his anticoagulants. He was also off of his BP meds (lisinopril, amlodipine and carvedilol).
Here is his ED ECG (ECG #1):
 |
| There is 2-3 mm of ST Elevation in V2. There is an upwardly convex ST segment in V2 and V3. The computer read ****STEMI****Of note, the S-wave in V2 is almost 50 mm. This is severe LVH. Thus, the ST/S ratio is no more than 0.06 (6%) Note there is also a very prominent negative P-wave in V1, diagnostic of left atrial enlargement and supportive of severe LVH. |
Here is his previous ECG (ECG #2):
 |
| Here all ST segments are concave upward. There is slightly less ST elevation. There is no convexity. Thus, the convexity is new. I cannot explain the marked difference in voltage from ECG #1. They both used 1 millivolt per 10 mm in both limb leads and precordial leads |
The lung ultrasound (not shown) had B-lines, all but diagnostic of pulmonary edema.
Bedside ultrasound parasternal long axis view is shown below.
There is severe LVH. There appears to my eye to be less than optimal systolic function and also less than optimal LV diastolic function.
Here is the short axis view:
Same interpretation as above.
Here is the chest X-ray:
 |
| There is obvious pulmonary edema. |
Clinical Course:
--The D dimer was barely elevated at 327 ng/mL (upper limit of normal: 230 ng/mL).
--The initial troponin I was 0.083 ng/mL (99% = 0.030); this patient does not have baseline elevated troponin (does not have chronic myocardial injury, which is not uncommon in patients with heart failure), so this was a new troponin elevation.
That is to say, there appears to be acute myocardial injury.
--The Creatinine was 1.5 mg/dL, with a GFR of 69 ml/min (low).
--The NTproBNP was 1564 pg/mL (slightly elevated -- normal for patients with GFR less than 60 is 1800 pg/mL).
The emergency physicians correctly interpreted the ECG repolarization abnormalities as being entirely due to LVH combined with some injury due to acute heart failure exacerbation and hypertension, and understood that the newly elevated troponin (with rise and fall) was due to demand ischemia (type 2 MI) due to hypertension and acute heart failure.
They administered furosemide.
Learning point:
1. ST Elevation with Convexity in the presence of LVH does not necessarily mean STEMI
2. The ST/S ratio in STEMI would be significantly higher.
See discussion at this post:
LVH with anterior ST Elevation. When is it anterior STEMI?
Clinical course continued:
They gave furosemide and obtained a CT pulmonary angiogram which ruled out pulmonary embolism. He was not given any BP management.
Comment on management:
1. With B-lines and this chest x-ray and only a minimally elevated D Dimer, CTPA is unnecessary. The diagnosis is clearly acute decompensated heart failure.
2. This patient should get some immediate treatment to lower blood pressure (afterload reduction). IV nitroglycerine is best, but requires ICU monitoring. For a patient who is only moderately ill and does not require an intensive monitoring, a good choice, especially for African Americans with renal dysfunction, is afterload reduction with IV hydralazine (see references below). Often, in a patient who has not been taking his/her antihypertensive, I simply give those medications immediately in the ED. As this usually includes either an ACE inhibitor or an angiotensin receptor blocker, this is often sufficient.
Vasodilator Therapy of ADHF
http://circ.ahajournals.org/content/123/21/2414
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808524/
Clinical Course continued:
Subsequent troponins were 0.078, 0.076, 0.064
A formal echo showed:
Decreased left ventricular systolic performance - mild.
The estimated left ventricular ejection fraction is 45-50%.
Regional wall motion abnormality-anterior and septum.
Regional wall motion abnormality-inferior.
Left atrial enlargement, moderate.
Diastolic septum measurement = 1.25 cm (LVH)
Based on Doppler indices, the LV filling pressure is markedly elevated.
The patient improved simply by re-starting his hypertension medications, lowering his BP, and with one dose of furosemide.
Case 2:
A middle-aged patient with a history of severe persistent asthma, heart failure with preserved ejection fraction (HFpEF), and pulmonary hypertension presented presented very short of breath. Here was her first ECG (ECG #3):
 |
| The computer read this as ****STEMI**** Note the marked ST elevation and the convex ST segments. |
This is her previous ECG from earlier in the year (ECG #4):
 |
| Much less ST elevation and less convexity |
A previous formal echo showed:
Hyperdynamic systolic performance.
The estimated left ventricular ejection fraction is 80 %.
There is no left ventricular wall motion abnormality identified.
Left ventricular hypertrophy concentric severe
She improved with therapy for asthma in the ED and had this ECG recorded 5 hours later (ECG #5):
 |
| Improved ST Segments and convexity has resolved. |
There was no myocardial infarction. All troponins were negative. She improved with therapy for asthma and was discharged from the ED.
Learning Points:
1. Patients with LVH who are in acute respiratory distress, especially with elevated BP and/or acute decompensated heart failure, frequently have convex ST elevation. This does not imply STEMI.
2. The ST/S ratio in STEMI with LVH is not established. The article by Armstrong et al. which is discussed in the referenced blog post above did not have appropriate methodology and their ratio of 0.25 is far too high. There certainly should be a ratio higher than 0.10 and probably higher than 0.15. (Armstrong EJ, Kulkarni AR, Bhave PD, et al. Electrocardiographic Criteria for ST-Elevation Myocardial Infarction in Patients With Left Ventricular Hypertrophy. Am J Cardiol. 2012;110(7):977-983. doi:10.1016/j.amjcard.2012.05.
Excellent post that highlights the importance of clinical correlation. As per the title of this blog post — LVH (especially when marked) may be associated with ST segment coving. So although we can’t rule out the possibility of acute coronary syndrome solely from the 1st ECG — the overall picture of this 1st ECG is of marked LVH in a patient presenting with shortness of breath (not chest pain) over 5 days, and a clinical presentation of heart failure. Similarly, in the 2nd case — the clinical presentation is pulmonary. The initial tracing here is again one that defies ruling out an acute event solely on that tracing — but the principal ECG finding (poorly localized ST coving in many leads with some inferior ST depression) in light of the pulmonary presentation (without chest pain) is a clinical picture that strongly suggests treating her asthma as first priority with close follow-up to ensure that no significant cardiac event follows. I am NOT surprised that these eye-catching ECGs in both of these insightful cases did not evolve into an acute cardiac event.
ReplyDeleteI LOVE the term, “ST coving”. It is a picture description that evokes a reproducible ST-T wave pattern on ECG — which Dr. Smith wonderfully illustrates is not specific for acute stemi. While this pattern may reflect acute ischemia, it can also be due to LVH, cardiomyopathy, LV aneurysm, drug/electrolyte effect, or other chronic change. So I often use the term, “ST coving” in the Descriptive Analysis part of my interpretation — and then integrate clinical correlation to formulate my Clinical Impression of what a given ECG is or is not likely to really be showing.
Dr. Smith,
ReplyDeleteThanks for the great post. A non-ECG related question for my learning concerning case #1: would it be wrong not to have ordered a D-dimer (and also not to have done a CTPA) on this patient? My thinking is either or both: 1) we already have a clear diagnosis of heart failure by all clinical, ECG, and radiographic data, and 2) the patient will need to go back on their anticoagulation anyway, so the diagnosis of recurrent PE and/or DVT would perhaps not change management in this stable patient?
Pendell,
DeleteNo. In fact, it is right not to order d dimer and CTPA. This patient has a clear diagnosis without thinking of PE.
Good question!
Steve