Characteristic evolutionary changes that occur over 2 to 3 days include resolution of the ST-segment elevation and subsequent development of diffuse and often deep T-wave inversion that involves most leads. New pathological Q waves may occasionally be observed and, furthermore, it has been possible to observe a prolongation of the corrected QT interval 2. Although there are rare exceptions, the proposed Echocardiographic Mayo Clinic Criteria for the clinical diagnosis of ABS underline a transient apical regional wall motion abnormalities, usually extending beyond a single epicardial vascular distribution. Most, if not all of the patients, appear to have a mild increase of cardiac biomarkers. Typically, no obstructive coronary artery disease has been found. Although the pathogenesis still remains unclear, a common element appears to be an exaggerated sympathetic activation. The mechanism underlying the association between sympathetic stimulation and myocardial stunning in unknown. One possibility is ischemia resulting from epicardial coronary arterial spasm. An alternative mechanism is microvascular spasm. A third possible mechanism is direct myocyte injury 3. Activation of cardiac adrenoreceptors is experimentally proven to induce left ventricular (apical) dysfunction. In fact, there is evidence that apical myocardium has enhanced responsiveness to symphatetic stimulation 4, potentially making the apex more vulnerable to sudden surges in circulating catecholamine levels. Aim of the present study was to describe a case series of 6 ABS observed in the last 6 years in a tertiary care referral center with high volume cardiac cath lab in Mercogliano, Southern Italy.
During the last 6 years (2001–2006), among 1674 consecutive patients (pts) referred to our coronary care units for ACS, 6 patients (age 57 ├é┬▒ 6 years; all women) presenting at admission with acute onset of cardiovascular event have been retrospectively selected. All fulfilledthe following 4 predetermined criteria to define Tako-Tsubo cardiomyopathy 2: 1) transientleft ventricularwall motion abnormalities resulting in ballooning at contrast ventricolographic or echocardiographic evaluation; 2) normal coronary artery on coronary angiography (performed 5 ├é┬▒ 9 hours from the hospitalization); 3) new electrocardiographic ischemic-like abnormalities (either ST-segment elevation or T-wave inversion) and 4) emotional or physical trigger event.
All patients underwent, at admission, two-dimensional transthoracic echocardiography, 12 lead electrocardiogram, serial measurements of cardiac isoenzymes including creatine kinase, creatine kinase MB fraction, and troponin. Transthoracic echocardiography has again been repeated at discharge. All patients have been followed-up for a median period of 40 months.
All patients underwent comprehensive transthoracic echocardiography examination at rest, upon discharge and at a median period of 40 months follow-up. End-systolic, end-diastolic volumes, ejection fraction and wall motion score index (each segment scored from 1 = normal/hyperkinetic, to 4 = dyskinetic, in a 16 segment model of the left ventricle) were calculated following the recommendations of the American Society of Echocardiography 5. The left ventricular volumes and ejection fraction were measured by modified biplane Simpson''s method and adjusted for body surface area. The systolic pulmonary artery pressure has been derived from maximal velocity of tricuspid Doppler tracing adding the value of the right atrial pressure. The right atrial pressure was estimated on the basis of inspiratory collapse index of the inferior vena cava. Diastolic function was determined from the pattern of mitral and pulmonary venous flow velocity by pulsed Doppler echocardiography, complemented by mitral annular velocity by tissue Doppler imaging, when needed 5. Diastolic dysfunction was staged as being absent" (grade 0), "mild" (grade 1, impaired relaxation), "moderate" (grade 2, pseudo-normalized filling pattern), and "severe" (grade 3, restrictive filling pattern). All echocardiographic examinations were performed using commercially available instruments with a cardiac probe (2.5–3.5 MHz): Acuson Sequoia (Mountain View, Ca), Esaote Mylab (Genoa, Italy).
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- Wittstein IS, Thiemann DR, Lima JAC, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion C: Neurohumoral features of Myocardial Stunning due to Sudden Emotional Stress. N Engl J Med 2005, 352(6):539-48.
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