[CASE] An elderly woman with stress-induced chest pain
67-year-old woman was referred from GP office to internal medicine ward because of the chest pain lasting for several hours. Onset of this blunt, persistent pain was preceeded by huge emotional stress. This ECG was registered.
There is accelerated sinus rhythm around 95/min, normal axis and low QRS voltage in limb leads, ST elevation in I (discrete), II, III, aVF with PR depression and rather convex than concave (except V2) ST elevation in V2-V6 with a slightly inverted T-wave in leads V4-V6. There is also ST depression in aVR with elevated PR segment. QTc is normal (~ 430ms).
Does it ring any bell? Or maybe too many bells?
Troponin levels were elevated (25 times the normal upper limit) and echo showed extensive akinesia of left ventricle mid and apical segments with hyperkinetic basal segments. LV ejection fraction was estimated around 28%. There was no pericardial fluid. Patient was immediately transported by air ambulance to our hospital and had coronary angiogram made which showed normal coronaries. NT-proBNP was 60 times the upper limit and CRP level was not significantly increased.
At this time diagnosis of takotsubo cardiomyopathy was made and dual antiplatelet therapy was discontinued. Beta-blocker p.o. and amiodarone i.v. was introduced because of short runs of ventricular tachycardia and later ACEI was added.
This is echo examination taken a few days later showing persistent apical segments motion abnormalities and improving LVEF around 40%.
Takotsubo cardiomyopathy (TTC, also called "broken heart" syndrome, apical ballooning syndrome or stress cardiomyopathy) is acute reversible cardiomyopathy, caused by catecholamine surge, found most often in postmenopausal women shortly after exposure to mental or physical stress, resembling an acute coronary syndrome (ACS) in its clinical presentation, frequently without presence of traditional risk factors for CVD.
Typical ECG findings are ST elevation, inverted T-waves (centered on V2-V5, II and aVR leads) and quite often QTc prolongation which are indistinguishable from anterior MI presentation and may follow typical evolution pattern seen in ACS. Temporal Q-waves and J-waves were also reported. Additionally, lack of ST depression (except in aVR) and prominent ST elevation in V1 is normally seen in TTC which may make you want to consider MI if these features are not present.
Zorzi et al. presented that PR segment depression and maximum ST elevation ≤ 2mm are independent predictors of TTC and their co-existence allowed exclusion of anterior MI with 100% specifity; there was no association between PR-segment depression and pericardial inflammation/effusion on CMR although they may coexist. PR segment depression can be explained by the effect of catecholamine storm on atrial repolarisation and mild ST elevation could be either effect of potential cancellation from opposite LV walls or a decrease in the concentration of catecholamine-sensitive repolarising ion-channels due to lack of oestrogens in post-menopausal women. Madias reported very high prevalence of low QRS voltage and/or transient attenuation of QRS amplitude in repeat ECGs in patients with TTC (possibly due to transient myocardial oedema observed in CMR).
Echo typically shows apical balooning (motion abnormalities extent beyond the distribution of one coronary artery territory) and is essential part of differential diagnosis. Troponins are markedly elevated with peak values usually lower than in ACS and natriuretic peptides are substantially increased. Ventriculography might be helpful though it is not routinely done. Nevertheless you should remember it is a diagnosis of exclusion and always requires coronary angiography to rule out ACS.
Typical ECG findings are ST elevation, inverted T-waves (centered on V2-V5, II and aVR leads) and quite often QTc prolongation which are indistinguishable from anterior MI presentation and may follow typical evolution pattern seen in ACS. Temporal Q-waves and J-waves were also reported. Additionally, lack of ST depression (except in aVR) and prominent ST elevation in V1 is normally seen in TTC which may make you want to consider MI if these features are not present.
Zorzi et al. presented that PR segment depression and maximum ST elevation ≤ 2mm are independent predictors of TTC and their co-existence allowed exclusion of anterior MI with 100% specifity; there was no association between PR-segment depression and pericardial inflammation/effusion on CMR although they may coexist. PR segment depression can be explained by the effect of catecholamine storm on atrial repolarisation and mild ST elevation could be either effect of potential cancellation from opposite LV walls or a decrease in the concentration of catecholamine-sensitive repolarising ion-channels due to lack of oestrogens in post-menopausal women. Madias reported very high prevalence of low QRS voltage and/or transient attenuation of QRS amplitude in repeat ECGs in patients with TTC (possibly due to transient myocardial oedema observed in CMR).
Echo typically shows apical balooning (motion abnormalities extent beyond the distribution of one coronary artery territory) and is essential part of differential diagnosis. Troponins are markedly elevated with peak values usually lower than in ACS and natriuretic peptides are substantially increased. Ventriculography might be helpful though it is not routinely done. Nevertheless you should remember it is a diagnosis of exclusion and always requires coronary angiography to rule out ACS.
More on TTC:
2. Zorzi, A., Baritussio, A., ElMaghawry, M., Siciliano, M., Migliore, F., Perazzolo Marra, M., … Corrado, D. (2016). Differential diagnosis at admission between Takotsubo cardiomyopathy and acute apical-anterior myocardial infarction in postmenopausal women. European Heart Journal: Acute Cardiovascular Care, 5(4), 298–307. https://doi.org/10.1177/2048872615585515
3. Madias, J. E. (2014). Transient attenuation of the amplitude of the QRS complexes in the diagnosis of Takotsubo syndrome. European Heart Journal: Acute Cardiovascular Care, 3(1), 28–36. https://doi.org/10.1177/2048872613504311
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