Tako-tsubo syndrome: a form of spontaneous aborted myocardial infarction?
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Biomedical subjects
Publications and source records attributed to Borja Ibanez.
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Our recent understanding of acute coronary syndrome as an atherothrombotic process has led to research efforts in the development of markers of thrombosis and fibrinolysis for risk prediction in cardiovascular heart disease. Although American Heart Association/American College of Cardiology guidelines recommend fibrinogen as a category I risk factor and also suggest factor VII, plasminogen activator inhibitor-1, tissue-type plasminogen activator, and von Willebrand factor as other potentially clinically useful markers, these tests have not come into routine clinical use. Their development as predictors of risk may be hampered by inconsistent laboratory methodology, which causes difficulty in comparing result interpretation with published trial studies. This article presents the history of development for these tests, proper laboratory handling, the best trial data that present evidence of their accuracy, and current guidelines for clinical use.
Current treatments for myocardial infarction have significantly reduced the acute mortality of ischemic cardiomyopathy. This reduction has resulted in the survival of a large cohort of patients left with a significant 'myocyte deficit'. Once this deficit leads to heart failure there is no available therapy to improve long-term cardiac function. Recent developments in stem cell biology have focused on the possibility of regenerating contractile myocardial tissue. Most of these approaches have entailed the transplantation of exogenous cardiac-regenerating cells. Recently, we and others have reported that the adult mammalian myocardium, including that in humans, contains a small pool of cardiac stem and progenitor cells (CSCs) that can replenish the cardiomyocyte population and, in some cases, the coronary microcirculation. The human CSCs (hCSCs) are involved in maintaining myocardial cell homeostasis throughout life and participate in remodeling in cardiac pathology. They can be isolated, propagated and cloned. The progeny of a single cell clone differentiates in vitro and in vivo into myocytes, smooth muscle and endothelial cells. Surprisingly, in response to different forms of stress, hCSCs acquire a senescent, dysfunctional phenotype. Strikingly, these nonfunctional CSCs constitute around 50% of the total CSC pool in older individuals-those most likely to be candidates for hCSC-based myocardial regeneration. Therefore, the challenge to develop clinically effective therapies of myocardial regeneration is twofold: to produce the activation of the hCSCs in situ in order to obviate the need for cell transplantation, and to elucidate the mechanisms responsible for hCSC senescence in order to prevent or reverse its development.
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A 67 year-old asymptomatic patient was referred to our echo-lab because of hypertension. Transthoracic 2D-echocardiogram showed a non-prolapsing ovoid mass attached to the left side of the interatrial septum. Transesophageal echocardiography evidenced an ovoid cavitated mass with internal areas of calcification. Color Doppler revealed flow inside the cavities. At surgery, a multicavitated mass was observed attached to interatrial septum. Macroscopically revealed cavities filled with blood, as well as partially calcified areas. Microscopically there were collections of "lipidic" cells embedded in the myxoid matrix, typical of cardiac myxoma. Cardiac hydatid cysts usually have a rounded shape. Most myxomas are solid masses without a cystic architecture or cavitations. Calcification is usually identified at a microscopic level. The combination of a polycystic appearance of the mass and macroscopic areas of calcification is more frequently observed in hydatid cysts than in cardiac myxomas. This appearance of the mass leads us to consider a cardiac echinococcal cyst as the first diagnostic possibility. This peculiar structure of cardiac myxoma, to the best of our knowledge, has never been documented. Transthoracic echocardiography and particularly transesophageal imaging, enable us to delineate this kind of tumors. Surgical resection is the appropriate treatment for these tumors, even in asymptomatic patients.
We present the case of a 70-year-old man admitted in congestive heart failure. The patient was diagnosed 22 years ago of hypertrophic cardiomyopathy (HC). ECG showed a very peculiar and pathological form of left bundle branch block (LBBB). 2D-echocardiogram revealed a dilated left ventricle (LV) and ejection fraction of 25%. LV remodeling represents an important component of the pathophysiology of HC and, paradoxically, some patients develop LV wall thinning, systolic dysfunction, and congestive heart failure (in the absence of coronary artery disease). This evolution is designated as "end-stage" or "burned-out"phase. We present this rare LBBB and his pathological evolution along the time as unique manifestation of this "burned-out" phase. The mechanism of this wall thinning remains unclear but changes in ECG may alert us about it.