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Takotsubo syndrome masking apical hypertrophic cardiomyopathy

Session Poster Session 4

Speaker Sofiya Lypovetska

Event : Heart Failure 2019

  • Topic : arrhythmias and device therapy
  • Sub-topic : Hypertrophic Cardiomyopathy
  • Session type : Poster Session

Authors : S Lypovetska (Ternopil,UA), M Shved (Ternopil,UA), V Gurskyi (Ternopil,UA)

S Lypovetska1 , M Shved1 , V Gurskyi1 , 1Ternopil State Medical University - Ternopil - Ukraine ,


Apical akinesis and dilation without occlusive coronary artery disease presented  by acute and usually reversible heart failure  are  typical signs of  Takotsubo syndrome. Since other diseases can be masked under certain clinical presentation.
Case report.  A 63 years old white woman presented with acute chest pain, palpitation  and shortness of  breath, induced by unexpected emotional stress.  Her medical history included hypertension (BP 140-160/90 mm Hg) with irregular usage of antihypertensive drugs, extirpation of uterus for fibro-myoma 10 years ago. She had no known coronary artery disease. Her heart rate 105 beats/min; BP 110/85 mmHg; oxygen saturation 96% on room air. Physical examination revealed tachycardia and mild pitting edema in the lower extremities. An electrocardiogram (ECG) showed sinus tachycardia with ST elevation 5 mm in V2-V6, pathological Q wave and ST elevation 2 mm  in II, III, avF. Laboratory results included an elevated troponin T level of 886.3 pg/mL (normal <14 pg/mL),  creatine phosphokinase MB – 31,6 Un/l (normal < 25,0 Un/l), NT-proBNP  2234 pg/ml (normal < 300 pg/mL).  A transthoracic echocardiogram (TTE) showed a  left ventricle ejection fraction - 45 %  with hyperdynamic basal function but with a dilated, akinetic apex and lateral wall.  Results of coronary angiography were normal. Left ventriculography revealed apical ballooning dilatation with akinesis.
The diagnosis of Takotsubo syndrome was defined based on results of  apical motion abnormalities of LV, preceded by a emotional stressful trigger, absence of culprit atherosclerotic coronary artery disease, new ECG abnormalities, positive troponin test and significantly elevated NT –pro BNP.
On the 12th hospital day, TTE showed no change in the apical ballooning and akinesis. The level of troponin T was decreased in dynamics: 58,0 – 22,5 -12,7 pg/mL. The ECG  revealed positive dynamics: decreasing of ST elevation in anterolateral leads to 1,5 mm, absence of pathological Q wave and ST elevation  in II, III, avF.  The patient was discharged from the hospital on metaprolol and ramipril therapy.
The patient returned 3 weeks later for repeat TTE. The apical wall-motion abnormalities had resolved, and  the LVEF had returned to normal 59 %. Newly apparent hypertrophy of the LV myocardium at the apex was onsistent with apical variant HCM. A contrast agent was administered, and no apical pouches, thrombi were found.  The maximal LV wall thickness was 17 mm at end-diastole. The ECG  showed repolarization changes and giant (>10 mm), inverted T waves in the anterolateral leads (particularly in leads V4 and V5). The patient was counseled in regard to the diagnosis of apical HCM. At her 2-month follow-up examination, she was asymptomatic. Apical HCM was masked  by Takotsubo cardiomyopathy with apical ballooning. The apical HCM was not apparent until the apical myocardium had fully recovered and patient underwent repeat TTE.

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