About this trial
The underlying mechanisms of microvascular dysfunction in Takotsubo cardiomyopathy remain incompletely understood. As CD34+ cells are essential to coronary microvascular homeostasis we will investigate the potential association between CD34+ cell count and changes in left ventricular function in patients with Takotsubo cardiomyopathy at baseline and 6-month follow-up.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
Minimum age 18 years
Established TTS per InterTak registry criteria
Signed consent form
Disqualifiers
Patients under the age of 18 years
Ischemic heart disease with at least one complete total occlusion
Other concurrent cardiomyopathies
Active infectious myocarditis
Trial population
Adult patients, predominantly females, with cardiovascular risk factors.
Trial design
Cohort
Prospective
Treatments tested in this trial
Not listed
Trial groups
Trial outcomes
Primary outcomes
Recovery of left ventricular systolic function assessed by change in left ventricular ejection fraction (LVEF)
Change in LVEF (%), measured by transthoracic echocardiography using Biplane Simpson's method.
Secondary outcomes
Improvement in myocardial contractility and deformation assesed by change in left ventricular global longitudinal strain (LV GLS)
Change in LV GLS (%), measured by transthoracic echocardiography using speckle-tracking method.
Reduction in left ventricular filling pressure assessed by change in early mitral inflow velocity (E-wave) and the average of the septal and lateral early diastolic mitral annular velocities ratio (E/e' average)
Change in E/e' average, calculated from transthoracic echocardiography by dividing the peak early mitral inflow velocity (E-wave) by the average of the septal and lateral early diastolic mitral annular velocities (e') obtained via tissue doppler imaging.
Recovery of impaired myocardial relaxation assessed by change in peak early mitral inflow velocity and peak atrial contraction wave velocity ratio (E/A ratio)
Change in E/A ratio, calculated from transthoracic echocardiography by dividing the peak early mitral inflow velocity (E-wave) by the peak atrial contraction velocity (A-wave), both measured via pulsed-wave Doppler in the apical four-chamber view.
Reduction in pulmonary artery systolic pressure assessed by change in tricuspid regurgitation maximum gradient (TR max gradient)
Change in TR max gradient (mmHg), measured using transthoracic echocardiography by applying continuous wave (CW) doppler to the TR jet to determine the peak velocity, then applying the modified Bernoulli equation.
Sponsors and contacts
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