Giant Inverted T waves in an Elderly Patient

This is another contribution from Victoria Stephen.  Victoria is a third year EM Registrar from at the University of the Witwatersrand in Johannesburg, South Africa, and a great asset to FOAMed.  Follow her on Twitter: @EMcardiac.

Here is her previous contribution: Pulseless ventricular tachycardia – why did the AED not advise a shock?  

Case

A 91 year old presented to the ED of a small hospital with a history of sudden onset syncope. A family member thought she was having a seizure. She reported no chest pain or dyspnoea when conscious. The patient had a history of hypertension which was poorly controlled.

She appeared alert and well-oriented. Her initial BP was 184/90, HR 41 BPM. An ECG was recorded in the ED:

There is second degree heart block with a HR of 41 BPM. The QRS complex is 144ms indicating an infranodal escape. There is an RBBB configuration with a LAFB, indicating it may be originate from the left posterior hemi-fascicle. The QTc is significantly prolonged at 535 ms. There are deep wide bizarre looking T waves seen in virtually all the leads, but most notably in the precordial leads.

She had a CT of the Brain which showed no intracranial bleed. Her renal function was normal and the electrolytes including calcium and magnesium were normal. Two troponin I were increased at 140 ng/L (0.14 ng/mL) and 70 ng/L (0.070 ng/mL) on consecutive days, (negative is less than 40 ng/L for this assay). 

Two days later she was referred to a regional hospital where she was admitted to the CCU with the following ECG:

Complete Heart block still present, HR 33 BPM, QTc prolonged, 503ms. T waves are now upright in leads I and AVL.

An informal bedside echo done by a cardiologist showed a normal ejection fraction with no regional wall motion abnormalities. In view of the positive troponins and the T wave inversions she was taken to the cath lab for angiography, as well as for a pacemaker. No obstructive coronary artery disease was present. She subsequently developed runs of VT while in the lab which were too transient to determine the specific type of VT. A transvenous pacing wire was inserted for temporary pacing and the decision was made to bring her back for a permanent pacemaker.

Here is the ECG post venous pacemaker:

Notice the T-wave inversion is present in spite of the ventricular pacing, which should result in discordant T-waves (opposite the QRS).  Concordant T-waves of this dimension indicate ischemia that cannot be hidden by pacing.

And here is the ECG post permanent pacemaker, recorded 7 days after the first ECG:

This is a single chamber pacemaker. HR 62 BPM. The T waves are upright in in the inferior leads and biphasic in the precordial leads.

Commentary

This patient suffered a Stokes-Adams attack, which is a sudden loss of consciousness due to a high grade atrioventricular block. Seizure like activity is commonly seen in this form of syncope. Two very different arrhythmogenic mechanisms have been shown to induce the abrupt loss of cardiac output causing the syncope. At the onset of complete heart block, asystole can occur for a brief period before a new pacemaker has kicked in. Either 1) the AV node may act as the new pacemaker, leading to a junctional or narrow escape on the ECG,  or 2) infranodal tissue will take over the pacemaker role.

The second arrhythmia which can abruptly occur during complete heart block (CHB) is Torsade de Pointes (TdP).  TdP is an example of a triggered dysrhythmia. Triggered dysrhythmias are heart rate dependent and are either triggered by a fast or slow heart rate. TdP is triggered by slow heart rates. (This is why overdrive pacing to a higher rate works in terminating TdP) In some patients, at the onset of complete heart block, there is an abrupt decrease in heart rate as well as prolongation of the QTc. The resulting pause plus a well-timed PVC then triggers the onset of TdP. Both asystole and TdP following CHB are often brief, allowing the patient to regain consciousness.

The giant inverted T waves are not common in CHB, but are commonly seen in CHB complicated by Stokes-Adams attacks. Their presence is not fully understood but has been associated with TdP and stress cardiomyopathy occurring after the onset of Complete Heart Block. Stress cardiomyopathy is a spectrum disorder characterized by transient left ventricular systolic dysfunction clinically, ST elevation or T wave inversions on the ECG, and regional wall motion abnormalities on echo which are induced by a catecholamine surge. Takotsubo cardiomyopathy is a specific form of stress cardiomyopathy. This paper demonstrates takotsubo cardiomyopathy developing in patients with complete heart block, preceding TdP:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644362/ (Open access)

Stress cardiomyopathy has been seen frequently in a myriad of different critical illnesses, particularly in subarachnoid haemorrhage, which often is associated with giant inverted T waves on the ECG:

http://circ.ahajournals.org/content/118/4/397.full#F1 (Open access)

Troponins can be elevated in stress cardiomyopathy and demonstrate a rising and falling pattern like an acute myocardial infarction. It is very difficult to differentiate SCM from MI; it often produces a PseudoSTEMI pattern that is very difficult, and sometimes impossible, to distinguish based on the ECG, though there are some guidelines.   Even echo can be misleading: the takotsubo apical ballooning can also be seen in acute STEMI.

If there is ST elevation, and the differential diagnosis is acute coronary occlusion vs. SCM, an angiogram is usually required.  

However, in this setting of Stokes Adams attack with CHB and bizarre T-wave inversion, emergent angiogram is not necessary.

Here is another blog case of Stokes Adams attack, this one with alternating left and right BBB.

Summary:

Complete Heat Block accompanied by giant inverted T waves is associated with Stokes-Adams attacks.

A prolonged QTc with CHB is at risk of torsades. Treat any associated electrolyte abnormalities that may be present.

Torsade de Pointes is triggered by bradycardia, a prolonged QTc and an abrupt change in heart rate, which creates a pause.

Inverted T waves are often seen in stress cardiomyopathy syndromes. Stress cardiomyopathy is a diagnosis of exclusion after formal echocardiography with or without angiography. 

Other references:

Mechanisms of syncope and Stokes-Adams attacks: 

http://www.bmj.com/rapid-response/2011/10/28/mechanisms-syncope-and-stokes-adams-attacks-bradyarrhythmia-asystole-and-t  (open access)

Giant T wave inversion: 

http://heart.bmj.com/content/28/6/768.full.pdf  (open access)

Cardiac and non-cardiac causes of T-wave inversion in the precordial leads:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325305/ (open access)