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    2019-06-11


    Conflict of interest
    Ethics
    Acknowledgment This study was supported by TRF Grants from the Senior Research Scholar Grant, Thailand Forskolin Research Fund Grant number RTA5580004, and the Higher Education Research Promotion and National Research University Project of Thailand, Office of the Higher Education Commission, Thailand, through the Health Cluster (SHeP-GMS), Khon Kaen University.
    Introduction Takotsubo (ampulla) cardiomyopathy (TCM), a well-known cardiac syndrome, is characterized by transient apical ballooning resulting from an unknown etiology, electrocardiography (ECG) changes, and minimal myocardial enzyme release that occurs in the absence of significant organic stenosis or coronary artery spasms [1–4]. Although several reports of TCM as a complication of permanent pacemaker implantation and ventricular-paced rhythm have been described [5–10], the ECG manifestations of TCM in patients with right ventricular apical (RVA) pacing have not been detailed.
    Case report A 76-year-old woman with hypertension, diabetes mellitus, dyslipidemia, chronic pulmonary emphysema, and a 4-year history of VDD pacemaker implantation for a 2:1 atrioventricular block was referred to the Department of Respiratory Care in our hospital in November 2011 with a chief complaint of sore throat, productive cough, and general fatigue. She was diagnosed with acute Forskolin and treated with levofloxacin and fluticasone oral inhalation. After 8 days, she was referred to the Department of Cardiology in our hospital because the patient׳s symptoms persisted. On examination, her blood pressure was 108/58mmHg and the pulse rate was 66beats/min. However, her N-terminal pro-brain natriuretic peptide level was elevated to 726pg/mL (normal <125pg/mL), and other routine hematological test results were unremarkable with a normal-troponin T level (negative), a creatine phosphokinase level of 62ng/mL (normal <160ng/mL), and a creatine kinase MB level of 5ng/mL (normal <9ng/mL). Chest radiography indicated no lung congestion or cardiomegaly. A 12-lead ECG showed an atrial-sensed and ventricular-paced rhythm with significant QTc prolongation (QTc interval=670ms) and new T-wave inversions in leads I, II, III, aVF, and V2 through V6. There were especially deep T-wave inversions in the precordial leads (Fig. 1). Echocardiography showed severe left ventricular (LV) apical akinesis and hyperkinetic contractile function of the basal LV segments. Because acute coronary syndrome could not be excluded and a cardiac catheterization laboratory in our hospital is absent, the patient was urgently transferred to the Department of Cardiovascular Medicine of Saga University on the same day. Pacemaker interrogation revealed an acute increase in the RVA pacing threshold from a baseline value of 1.62V at 0.6ms to 2.125V at 0.6ms, and the right ventricular pacing lead impedance was decreased from a value of 1173 to 740Ω. The R wave amplitude was not measured. Cardiac catheterization performed on the third hospital day showed no significant coronary artery disease (provocation tests for coronary vasospasm were not performed) (Fig. 2), but left ventriculography showed mid-to-apical akinesis with basal hyperkinesis and apical ballooning (Fig. 3). Therefore, she was diagnosed with TCM and treated with conservative therapy. Follow-up echocardiography on the fifth hospital day showed almost complete resolution of the LV apical ballooning with only mild residual LV apical hypokinesis. On the 11th hospital day, she was asymptomatic and discharged. Three weeks after discharge, her ECG indicated persistence of T-wave inversions in leads I and V3 through V6, although their values had decreased, and the QTc interval had normalized (Fig. 1). Echocardiography demonstrated complete recovery of regional LV wall motion abnormalities. Two months after discharge the ECG returned to baseline (Fig. 1). The RVA pacing threshold and right ventricular lead impedance values were restored to 1.62V at 0.6ms and 1068Ω on February 7, 2012, respectively. The R wave amplitude was 8.0mV; there were no changes in the R wave amplitude around the time of TCM onset. However, arrhythmia is often observed in TCM patients, but no arrhythmias had been recorded by Holter monitoring of the implanted pacemaker.