T for Three - Case 2 - The T Wave Tease

This is the second case in the T for Three trilogy.

Thanks to Cecil Johnny for this case. 


The patient is a 24 year old Sri Lankan man with a 4 day history of increasing dyspnoea, with exercise tolerance limited to 200 metres. He has not had a cough or chest pain or fever.  Four weeks ago he had a self-limited influenzal type illness.

He has been hypertensive since 20 years of age, and is currently taking a angiotensin-converting-enzyme inhibitor (enalapril) and a calcium channel blocker (lercanidipine).

There is no family history of heart disease or sudden death.

There are no risk factors for venous thromboembolism.

On examination: 

  • The patient was very obese, with a body mass index of 41.
  • Vital signs: He was afebrile, heart rate was 96 beats per minute, blood pressure was 160⁄80 mm Hg, respiratory rate was 14 breaths per minute and the SaO2 was 100% on room air.
  • His jugular venous pulse was nor visible, auscultation of the heart and lungs was normal, abdominal examination was normal (but limited by his obesity), and there was slight pedal oedema.

Initial Investigations

The following investigations were done:

Figure 1 - ECG

This main findings in this ECG are:

  • Sinus rhythm with a heart rate of 85 beats per minute and a normal frontal QRS axis. The PR⁄QRS intervals are within normal limits and the computer calculated QTc is at the upper limit of normal.
  • QRS changes: a small q wave is seen in Lead III, the transition zone is in Lead V3, and slight notching of the QRS complex is seen in Lead aVL and in Leads V2to V4.
  • QRS amplitude:
    • The sum of the R wave in Lead I (R = 20 mm) and the S wave in Lead III (S= 11 mm) in the frontal leads is 31 mm. These values meet the Sokolow and Lyon criteria for left ventricular hypertrophy (LVH). The voltages in Lead aVR (S = 15 mm) and in Lead aVL (R = 15 mm) also meet these criteria.
    • The sum of the S wave in Lead V1 (S =  20 mm) and the R wave Lead V6 (R = 14 mm) is 34 mm which is just below the value for LVH in precordial leads.
  • Widespread ST-T changes:
    • Horizontal ST elevation (1-2 mm) with upright T waves is seen in Leads III, aVR, V1 and V2.
    • Horizontal ST depression (1-2 mm) and T inversion is seen in Leads I, II, aVL, V4 to V6. The inverted T waves have a narrow base and an amplitude of 5-8 mm. The amplitude of the inverted T waves is less than the 10 mm or greater that defines giant T wave inversion.
    • A biphasic T wave in Lead V3
    • All the leads with T wave inversion have a preceding positive (R) wave, and the leads with upright T waves (Leads III, V1 and V2) have a large S wave. These are (probably) "secondary"T wave changes as the T waves are opposite in direction to the main QRS deflection.

Figure 2. Chest Xray (A): Antero-posterior view. (B) Lateral view. There is borderline cardiomegaly and possible left ventricular enlargement.

And blood tests:

Figure 3 Bloods - abnormal results in red

The relevant findings were a troponin I concentration of 1226 ng/L (N ≤ 26 ng/L) and a raised white cell count of 17.94 x 109/L (N 4.5-13.5 x 109/L). The d-dimer and the B-Type natriuretic peptide (BNP) concentrations were normal.

Emergency Department Diagnosis

The ECG findings are a combination of left ventricular hypertrophy and repolarization changes involving the ST-T segment. Although the patient is hypertensive the ST-T changes are not typical of the ST-T changes that usually accompanies LVH (See examples below). An alternative cause of the changes is cardiomyopathy.

The patient did not have chest pain before he came to hospital, but the troponin I concentration was elevated. This could be due to myocarditis, although some of the ST-T changes are possible STEMI equivalents:

  • there is 1 mm of ST elevation in Lead aVR and the T waves are inverted in the lateral leads, raising the possibility of left main stem coronary artery (LMCA) disease. The ST elevation in Lead aVR (1mm) is less than the ST elevation in Lead V1 (2mm), which is opposite to the pattern seen in LMCA disease (where ↑ ST- aVR > ↑ ST- V1)
  • there is a biphasic T wave in Lead V3, with T wave inversion in Leads V4 to V6. In the absence of chest pain this could be Wellens' syndrome due to a critical stenosis of the left anterior descending artery.

The history of a viral illness four weeks and a elevated troponin suggests a viral myocarditis.

The main diagnoses in the ED were:

  • Viral myocarditis
  • Possible cardiomyopathy
  • 'Rule out' coronary artery disease


Inpatient Management

The patient was admitted under the Cardiology Unit and had the following investigations:

  • Transthoracic echocardiogram: Normal left ventricular size and systolic function with increased wall thickness. Right ventricle not well seen but appeared to be normal in size and function. Non dilated atria
  • CT coronary angiogram: this showed normal coronary arteries, with left ventricular morphology suggesting apical hypertrophic cardiomyopathy
  • Cardiac MRI (Figure 4): Normal left ventricle size and systolic function. Moderate infero-septal and severe apical hypertrophy. Diffuse delayed myocardial enhancement in the entire apex, the basal mid-lateral segments and the mid-septum. Cardiac MRI features are consistent with apical hypertrophic cardiomyopathy. No evidence of acute myocarditis.
  • The results of viral serology tests was normal apart from equivocal mycoplasma serology

Figure 4 - Cardiac MRI showing hypertrophic cardiomyopathy (*) confined to the apex of the heart

Final Diagnosis

  • Apical hypertrophic cardiomyopathy
  • Hypertension
  • Morbid obesity



1. Typical ECG Changes in LVH

The following 3 ECGs showing typical changes of LVH are included for comparison with the case above

Example 1 (Figure 5):

Figure 5 - Example 1

Example 1 is the ECG of a 70 year old man with hypertension and palpitations.

  • The rhythm is sinus and the axis is normal. The transition zone is between Lead V4 and V5. The rhythm strip shows a ventricular premature beat (VPB) with a (complete) compensatory pause (the R-R interval [of 47mm] that includes the VPB is double the R-R interval [of 23-24mm ] between consecutive sinus beats).
  • The sum of the voltages in Lead V2 and Lead V6 is 47 mm (criteria for LVH include S in V2 + R in V6 > 43 mm). T wave inversion is seen in Leads I and aVL. TheT waves are upright in the praecordial leads and flattened in Leads V5 and V6. 
  • An inverted U wave (*) is seen in Lead V6; this is due to the LVH.

Comment on Example 1: LVH diagnosed on the presence of a single set of voltage criteria. There are no ST-T changes of LVH "strain"

Example 2 (Figure 6)

Figure 6 - Example 2

Example 2 is the pre-operative ECG of a 79 year old woman with hypertension and atrial fibrillation.

  • Coarse atrial fibrillation waves are seen in Lead V1. The axis is normal.
  • Multiple voltage criteria for LVH are present:
    • R in I + S in III = 36 mm (LVH criteria ≥ 25 mm)
    • S in aVR = 14 mm (LVH criteria ≥ 14 mm)
    • R in aVL = 17 mm (LVH criteria ≥ 11mm)
    • S in V1 + R in V6 = 52 mm (LVH criteria ≥ 35 mm).
  • The ST-T changes in Leads I, II, aVL and V6 are slight ST depression and asymmetric T wave inversion, with the downslope longer than the upstroke. This pattern in an ECG with LVH is called a strain pattern, although a similar appearance can be seen in persons on digoxin
  • Other ST wave changes are slight ST elevation in Leads III, V1 and V2, and horizontal depression in Leads V4 and V5.

Comment on Example 2: LVH with ST-T changes that could be a "LVH strain" pattern or digoxin effect or both


Example 3 (Figure 7):

Figure 7 - Example 3

Example 3 is the ECG of a 66 year old man with a history of hypertension. 

  • Sinus rhythm is present, and the axis is normal. The transition zone is in Lead V4.
  • The voltage criteria for LVH are:
    • S in V1 + R in V6 = 56 mm (LVH criteria ≥ 35 mm)
    • S in V2 + R in V6 = 54 mm (LVH criteria ≥ 43 mm)
    • ST-T changes of "strain" are seen in Leads I, II and V6. 
  • Horizontal ST depression is seen in Lead V5. There is slight ST elevation in Leads V1 to V3, and the T wave has a slightly broad base. These changes could be due to cardiac ischaemia. 
  • U waves (*) are present: they are upright in Leads V2 and V3, and inverted in Leads V5 and V6. 

Comment on Example 3: LVH with a strain pattern.

A comparison of the ECG changes in V4 to V6 in C_0009 and the three examples of LVH is shown in Figure 8.

Figure 8 - Comparison of the changes in Leads V4 to V6 in a case of apical hypertrophic cardiomyopathy and in three examples of left ventricular hypertrophy


2. Apical Hypertrophic Cardiomyopathy

A morphological classification of cardiomyopathy is shown in Figure 9.

Figure 9. Drawings of the normal heart (A) and the heart in various phenotypes of hypertrophic cardiomyopathy (HCM). The diagnostic criteria of HCM is that the maximal end-diastolic LV wall thickness is greater than or equal to 15 mm.

(B):  Asymmetric (septal)  HCM with left ventricular outflow tract (LVOT) obstruction

(C):  Asymmetric (septal)  HCM withoutleft ventricular outflow tract (LVOT) obstruction

(D):  Apical HCM

(E):  Symmetric (concentric) HCM

(F):  Mid-ventricular HCM

(G):  Mass-like HCM

(H):  Non-contiguous HCM

Source: Chun at al. Hypertrophic cardiomyopathy: assessment with MR imaging and multi-detector CT. Radiographics. 2010; 30:1309-1328


Apical hypertrophic cardiomyopathy was first described in 1976. The described ECG changesinclude some or all of the following: giant negative T waves, ST depression and negative U waves in Leads II, III, aVF, V4-V6, and a prolonged QTc. Other changes are very tall R waves in the praecordial leads, and (less commonly) marked ST elevation that can mimic coronary artery disease. The long term prognosis is relatively benign, although the outcome is somewhat worse in females than males.


3. Obesity and Cardiomyopathy

Obesity is an independent risk factor for the development of heart failure, but the mechanism(s) are multifactorial. Obesity increases central and total blood volumes along with decreased systemic arterial resistance resulting in high cardiac output state that may be associated with worsening diastolic function independent of other co-morbid conditions. 

Patients with obesity also have higher overall oxygen requirements. There is no evidence of a direct effect of obesity on systolic function causing a dilated cardiomyopathy.

Obese persons with HCM have significantly larger left ventricular mass, left ventricular mass index, and higher subsequent rates of symptom development.

  1. Khan MF, Movahed MR. Obesity cardiomyopathy and systolic function: obesity is not independently associated with dilated cardiomyopathy. Heart Fail Rev. 2013;18:207-217. doi: 10.1007/s10741-012-9320-4.
  2. Olivotto I, Maron BJ, Benedetta Tomberli B et al. Obesity and its association to phenotype and clinical course in hypertrophic cardiomyopathy. J Am Coll Cardiol 2013;62:449–457