Rare but real: Takotsubo syndrome following mitral valve surgery.

BACKGROUND: Takotsubo syndrome has been widely recognized as a stress cardiomyopathy and only recently has been also reported following cardiac surgery. AIMS: We present a case of takotsubo syndrome two days following a mitral valve replacement with a mechanical prosthesis. MATERIALS AND METHODS: A 64-year-old female patient underwent mitral valve replacement with a mechanical prosthesis. Two days later she presented clinical symptoms and diagnostic evidence supporting the diagnosis of takotsubo syndrome. RESULTS: Patient underwent full left ventricle function recovery and was discharged home on 10th postoperative days. DISCUSSION: The peculiar aspect of this case consist of the early postoperative transthoracic echocardiography, which showed, clearly, an optimal left ventricle function the day before sudden onset of the symptoms, thus allowing for a clear differential diagnosis with other potential causes of postoperative left ventricle failure. CONCLUSION: This case confirms that takotsubo syndrome has to be carefully considered in differential diagnosis in case of acute left ventricle dysfunction following cardiac surgery.

Are the leukocyte telomere length attrition and telomerase activity alteration potential predictor biomarkers for sporadic TAA in aged individuals?

A large variability in occurrence, complications, and age/gender manifestations characterizes individual susceptibility of sporadic thoracic aortic aneurysms (TAA), even in subjects with the same risk factor profiles. The reasons are poorly understood. On the other hand, TAA pathophysiology mechanisms remain unclear than those involved in abdominal aorta aneurysms. However, recent evidence is suggesting a crucial role of biological ageing in inter-individual risk variation of cardiovascular diseases, including sporadic TAA. Biological age rather than chronological age is a better predictor of vascular risk. Relevant assumptions support this concept. In confirming this evidence and our preliminary data, the mean of blood leukocyte telomere length, through use of terminal restriction fragment assay and in blood samples from sporadic TAA patients and controls, was examined. Telomerase activity was also analyzed in two groups. In addition, we verified the weight of genetic inflammatory variants and the major TAA risk factors in telomere/telomerase impairment. Aorta histopathological abnormalities and systemic inflammatory mediators were ultimately correlated with telomere/telomerase impairment. Data obtained demonstrated shorter telomeres and a reduced telomerase activity in TAA patients significantly associated with a genetic inflammatory risk profile, age, gender, smoking, hypertension, a histopathological phenotype, and higher levels of systemic inflammatory mediators than controls. In conclusion, telomere and telomerase activity's detection might be used as predictor biomarkers of sporadic TAA. Their impairment also suggests a strong role of vascular ageing in sporadic TAA, evocated by both environmental and genetic inflammatory factors.