Mid-ventricular Takotsubo Research Articles

A rare form of midventricular Tako Tsubo cardiomyopathy

We report a case of a rare form of midventricular Tako Tsubo cardiomyopathy characterized by left ventricular angiography and cardiac MRI.

Atypical Takotsubo syndrome during anagrelide therapy

Anagrelide is a phosphodiesterase III inhibitor utilized in the treatment of essential thrombocythemia. Anagrelide can be responsible for positive inotropic and chonotropic activity of the cardiovascular system. Moreover, it can induce vasospam directly on the epicardial coronary arteries. In the literature, it is well reported that this inhibitor can determine serious cardiovascular side effects, including congestive heart failure, arrhythmia and acute coronary syndrome. We describe the case of a 75-year-old woman who developed a mid-ventricular Takotsubo syndrome while on anagrelide therapy. Takotsubo cardiomyopathy, also known as left ventricular ballooning syndrome, is characterized by a reversible ventricular contractile dysfunction with akinesis and expansion of apical segments and hyperkinesis of the basal segments. Recently, atypical cases with akinesia and dilation of mid-ventricular segment and hypercontraction of the apical segments, also called mid-ventricular and inverted Takotsubo syndrome, have been described. Even though the pathogenesis of Takotsubo syndrome is poorly understood, several mechanisms have been proposed, including catecholamine-induced myocardial stunning, and ischemia-mediated stunning due to multivessel epicardial or microvascular spasm. We think that in our case, the adverse response of anagrelide therapy was determined, by accumulated dosage of the drug, through an intensive inotropic stimulation and a sympathetic hyperactivation in a vulnerable myocardium. To our knowledge, this is one of the first reports of an association between anagrelide therapy and Takotsubo cardiomyopathy.

Iatrogenic epinephrine-induced reverse Takotsubo cardiomyopathy: direct evidence supporting the role of catecholamines in the pathophysiology of the “broken heart syndrome”

Sirs Stress-induced transient cardiomyopathy (also known as Takotsubo cardiomyopathy) has been recognized as a disease entity since 1991 and accounts for 1% of acute coronary syndromes (ACS) that present with elevated cardiac biomarkers [1, 2]. About 80% of Takotsubo cardiomyopathy occurs in postmenopausal women [3]. The diagnosis depends on four criteria: (1) ST-segment changes or Twave inversions on the electrocardiogram, (2) transient wall motion abnormalities that are often inconsistent with coronary anatomy, (3) absence of obstructive coronary artery disease or evidence of acute plaque rupture, and (4) absence of significant head trauma, intracranial hemorrhage, pheochromocytoma, or other causes of myocardial dysfunction [3, 4]. The cardiomyopathy can be classified into a left ventricular (LV) apical ballooning variant (classic Takotsubo cardiomyopathy—most common), an inverted or reverse Takotsubo variant (basal akinesis with hyperdynamic apex), or a midventricular Takotsubo variant. The condition is often associated with catastrophic life events and severe psychological or physical stress. Due to this association with psychological stress, the cardiomyopathy is often referred to as the ‘‘Broken Heart Syndrome’’. Although the pathophysiology of stress-induced cardiomyopathy is not fully understood, it is thought that intense psychological or physical stress results in a catecholamine surge that adversely affects myocardial contractility, where postmenopausal women appear to be at a higher risk for developing the disease. The evidence for this was obtained from observational and case-control studies that have found an association between elevated catecholamine levels and disease onset [1, 4, 9]. In this paper, we present a case of iatrogenic epinephrine-induced reverse Takotsubo cardiomyopathy in a young 24-year-old female with no previous history of cardiac disease. While this case is unfortunate, it provides a unique opportunity to observe the triggering of stress-induced transient cardiomyopathy and provides evidence to support the role of epinephrine in the pathogenesis of this disease.