Inferior ST Elevation. BP 250/140.

This 50-something patient with no previous CAD complained of havinng had chest pressure the day prior, but stated she was asymptomatic at the time of the ECG.  Her blood pressure was 250/140.  She was well appearing.  She admitted to long standing untreated hypertension.

Sinus rhythm.  Very high voltage in the precordium, meeting criteria for LVH, though without the repolarization abnormalities typically associated. There is ST elevation in inferior leads that is diagnostic of focal injury.  The T-wave is inverted in these leads; this is a strong sign of recent reperfusion of the infarct-related artery.  The T-waves in V2 and V3 are suggestive of anterior injury or reperfusion of the posterior wall.

Because the ST segment is elevated and T-wave inverted, it appears as if there was very recent reperfusion.  The first sign of reperfusion is inversion of the T-wave, after which the ST segment resolves.  So I imagined that she had had a recent unrecorded upright T-wave, which then reperfused, resulting in inverted ("reperfusion") T-waves, and that the next ECG would show resolution of the ST segment as long as the artery stayed open.

Could this all be due to the blood pressure?  I did not think so.  When high demand, such as hypertension, results in ischemia, it is generally subendocardial, with ST depression.

I activated the cath lab.  The interventionalist suspected that this might not be ACS because of absence of pain and the severely elevated BP, but willingly came to do the procedure.

We recorded this bedside ultrasound:

This shows good systolic function and very thick LV walls, and no apparent wall motion abnormality.

A parasternal short axix was also recorded:

This again shows very thick walls, severe concentric hypertrophy and very small chamber size and, again, no WMA.


While waiting for the cath team (nighttime), we administered (in addition to antiplatelet and antithrombotic therapy) 15 mg IV metoprolol, titrated IV nitroglycerine up to 200 mcg/min (along with giving 6 sublingual NTG tablets), and gave 10 mg IV hydralazine, after which the BP improved to 190/100, and  we recorded this repeat ECG 30 minutes after the first:

The ST elevation has resolved, as predicted.

The patient went to the cath lab.  Unexpectedly, there was minimal coronary disease and no culprit.

Troponin I peaked at 1.70 ng/mL.  Subsequent formal ultrasound showed concentric hypertrophy (septum 1.3 cm in diastole), no wall motion abnormality, and EF of 60-65%.

Outcome summary:

Apparently this was a focal type 2 MI with ST elevation due to severe hypertension, but it could also be due to thrombi from a minor atherosclerotic plaque that then lysed, and the culprit lesion is never found.  Coronary spasm (Prinzmetal's angina) is also possible.

Type 1 MI is MI due to plaque rupture (ACS) and Type 2 MI is due to demand ischemia, often in the presence of stable CAD.  Type 2 MI with ST elevation is comparatively rare, but does exist.  The expert on this is Dr. Yader Sandoval  (from HCMC's cardiology fellowship), who has just submitted a review of ST elevation in type 2 MI, suggests that we do not call this "STEMI," but reserve that term for Type 1 MI (due to acute coronary syndrome).  In our study of type 2 MI, only 4 of 99 (4%) had ST Elevation.  Type 2 MI with ST elevation is usually due to very high demand in the setting of very tight (fixed, non-ACS) coronary stenosis.  That was not the situation here.  There was chronically high BP, but there were no fixed lesions on the angiogram.   Here is another example of type 2 MI with ST elevation due to demand ischemia from atrial fibrillation with a Rapid Ventricular Response.

Whether there is ACS or not, when there is ischemia, supportive care to normalize vital signs is essential.  It is particularly common for MI patients to need blood pressure control.

Was this Type 1 STEMI or Type 2 MI with ST elevation?  We don't know for certain.