All data suggest unstable angina, but the angiogram is normal. Ken Grauer on stress testing.

A 50-something woman who has a gastric ulcer was experiencing epigastric pain for which she decided to come to the ED.  Then, approxiately one hour prior to arrival, she experienced some chest discomfort which was sharp, central, 10/10, with SOB, diaphoresis, dizziness, and nausea.  Since that time it has been intermittent.   She called 911 and still had pain when the medics arrived, but it resolved with sublingual NTG x 2.   On arrival she was chest pain free, but still had the epigastric pain.

Prehospital vitals:

We could not find the prehospital EKG.

Here is the first ED ECG, recorded while asymptomatic:

There is what appears to be ischemic ST depression in II, III, aVF, and V5, V6.  There is no other good explanation for it.

She did have a previous ECG available:

This confirms that the ST depression is new.  The precordial T-waves were more robust on the previous than they are on the present ECG.

The first high sensitivity troponin I returned at ＜ 4 ng/L (below the LoD, which all but rules out acute MI)

During her ED stay, one hour later, she had recurrent chest pain and another ECG was recorded.

Strangely, the ST depression is GONE during pain and it was present while she was asymptomatic.

I was worried about the ST depression on the first ECG, and then even more worried when I saw that it was dynamic.

The 2nd high sens trop returned at ＜ 4 ng/L, still below the LoD.  Thus, there is no acute MI.

But I know that unstable angina still exists, and I can read an EKG, so I insisted that the patient be admitted.

It turns out that she did indeed have a prehospital ECG recorded also (we could not find it at the time -- this is a common problem, as the EHR systems do not immediately sync, but we can usually find the paper printout).

Here it is:

Similar to the old ECG.

Echo

Normal

Stress Echo:

The patient exercised for 4:37 minutes on the Bruce protocol and achieved a peak heart rate of 144 bpm representing 87% of age predicted maximum heart rate and an estimated work load of 6.4 METs. Test was terminated because of fatigue, nausea and chest pain.

 

Abnormal stress echocardiogram with a moderate degree of certainty.

 

1. No echocardiographic evidence of ischemia at the cardiac workload achieved.

2. Left ventricular function normal at rest, with mild improvement with stress on most views. There was anterior wall hypokinesis with stress and in the 2 chamber view the LV EF appears to worsen with stress.

She was noted to have dynamic EKG changes with ST depressions in lateral leads that later resolved.  She underwent a stress test yesterday during which she exercised for 4.6 minutes achieving 6.4 METS and 87% of age-predicted maximal heart rate.  Her blood pressure increased from 130 mmHg systolic to 221 mmHg systolic.  Her EF was noted to be normal at rest with mild improvement with stress on most views.  There was an anterior wall hypokinesis noted with stress and it seemed the EF may have worsened in some views.  The patient did experience angina with stress.

 

She has multiple risk factors for coronary artery disease including hypertension, dyslipidemia, obesity, family history and tobacco use.  Differential diagnosis for presentation includes coronary artery disease, hypertensive heart disease, gastroesophageal reflux disease or esophageal spasm.  Given her elevated risk of coronary artery disease, it would be reasonable to rule out obstructive disease with a coronary angiogram.

Angiogram:

Normal!!

Based on these results, presentation is most likely attributed to hypertensive urgency and cardiomyopathic response to stress, given marked hypertension on presentation and hypertensive response to stress associated with symptoms of dyspnea and chest pain. It is reassuring there is no obstructive coronary artery disease. Primary prevention is of the utmost importance. 

 

BP was intermittently elevated to 214/91 in the hospital 

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MY Comment by KEN GRAUER, MD (7/2/2022):

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Excellent step-by-step discussion by Dr. Smith of this 50-something year old woman — who presented to the ED for epigastric pain and new-onset chest discomfort.

• I’ve reproduced the initial ECG in today’s case in Figure-1. For clarity — I’ve highlighted the abnormal ST segment flattening and slight-but-real J-point ST depression in the lateral chest leads (parallel BLUE lines — and RED arrows in Figure-1). Similar-looking (albeit more subtle) ST-T wave changes are seen in the inferior leads.
• As per Dr. Smith — these ECG findings have to be interpreted as ischemic until proven otherwise because i) There is no indication of LVH that might alter ST-T wave appearance (ie, if LV “strain” was present); ii) The heart rate is slow (ie, tachycardia may sometimes produce some ST depression); and, iii) This patient’s chest pain had already resolved at the time ECG #1 was obtained — so there was no plausible reason other than ischemia for these ST-T wave changes.
• As per Dr. Smith — the fact that this patient’s prior ECG did not show these ST-T wave changes confirmed the assumption of ischemia on her initial ECG (given her recent chest pain) — until proven otherwise.
• Change (ie, resolution) of the ECG abnormalities seen on ECG #1 during an episode of chest pain while in the ED — solidified the presumption of “dynamic” ST changes during chest pain (until proven otherwise).

Figure-1: I’ve labeled the abnormal ST-T wave findings in the lateral chest leads of the initial ECG in today's case. Of note — the patient's chest pain had already resolved at the time this ECG was recorded (See text).

For me — the most interesting part of today’s case — was the finding of a completely normal cardiac catheterization. MY Thoughts regarding these results were the following:

• The literature suggests more than 50 potential causes of ST-T wave abnormalities. Cardiac entities make up only a minority of these causes. Entities such as tachycardia, electrolyte disorders, hyperventilation, excess sympathetic or parasympathetic tone, emotions, temperature extremes (cold or heat, including the drinking of very cold or hot beverages), fear, pain, and “sick” patient (among others) — have all been associated with ST-T wave abnormalities on ECG.
• 
  
• Evaluation of the patient in today's case progressed appropriately. Since this patient presented to an ED with a complaint of new chest discomfort (especially in view of the above described ECG abnormalities) — 1st priority needed to be given to ruling out an acute event. Once this was done — further evaluation was in order, especially in view of the medical history of this woman in her 50s (ie, with cardiac risk factors of hypertension, hyperlipidemia, obesity, positive family history and tobacco use).
• 
  
• The patient underwent Exercise Stress Testing (EST). She was only able to exercise for 4:37 minutes on the standard Bruce Protocol. Although she attained a maximum exercise heart rate of 144/minute ( = 87% her predicted “max” for age, which indicates a satisfactory exercise effort) — the test was terminated because of fatigue, nausea and chest pain! Regardless of whether or not her EST resulted in exercise-induced ST segment changes — this is an abnormal and very concerning result! The inability of an adult in their 50s to complete at least 6 minutes on the standard Bruce Protocol — with termination of the test at least in part because of chest pain — is consistent with an “early-positive" test. This result clearly increases the post-test likelihood for coronary disease — which means additional evaluation is indicated until significant coronary disease can or cannot be ruled out.
• 
  
• NOTE #1: Assessment of exercise-induced ST segment changes will be difficult in this patient — because her initial ECG in the ED (ie, as shown in Figure-1) is not normal. The validity of assessing the ST segment response to exercise is far less specific when the pre-test ECG already shows lateral lead ST depression as seen here (ie, that in essence, already “looks” like a positive EST with horizontal ST depression).
• Confirmation of an early-positive EST — was attained by the Stress Echo finding of anterior wall hypokinesis with exercise. Cardiac catheterization was clearly indicated as the next step in evaluation.
• 
  
• NOTE #2: As per Dr. Smith — the normal cardiac cath was reassuring in ruling out obstructive coronary disease as the cause of this patient's symptoms. This narrowed down the differential diagnosis.
• 
  
• NOTE #3: This patient’s formal cardiac Echo was reported as “normal”. I would want to see specific indices of her Echo report — since this patient fits the profile for diastolic dysfunction (ie, an overweight, middle-aged or older woman with longstanding hypertension).
• A diagnosis of diastolic dysfunction could explain this patient's normal EF (Ejection Fraction) at rest — despite symptoms of fatigue and chest pain at a relatively low level of exercise. It is also consistent with her hypertensive response to exercise (ie, BP increasing from 130 mm Hg systolic — to 221 mm Hg systolic with exercise).
• In my experience of assessing Echo reports over years in primary care — mention of "diastolic dysfunction" is often not indicated on the final Echo report. Even when direct mention of "reduced compliance" parameters is not made on the Echo report — a likely diagnosis of diastolic dysfunction can be made when a patient with the "right" clinical profile manifests: i) Some degree of concentric hypertrophy without LV chamber dilatation; ii) Left atrial enlargement; and, iii) An estimated normal EF at rest.

Final Thought: Rather than "unstable angina" — I thought of this case as illustrative of appropriate evaluation for this patient who had non-coronary chest pain, probably with diastolic dysfunction. As per Dr. Smith — risk factor modification, with special attention to BP control will be KEY to her longterm outcome.