The serine protease plasmin is distributed throughout the human body in the form of the zymogen plasminogen. The plasminogen activation system is mostly recognized for its fibrinolytic activity but is also upregulated in chronic inflammatory diseases, including atherosclerosis and arthritis. Plasmin can bind to a variety of cells, including monocytes, through low-affinity binding sites and triggers aggregation of neutrophils, platelet degranulation and arachidonate release from endothelial cells. In monocytes, plasmin elicits full-scale proinflammatory activation, including lipid mediator release, chemotaxis and cytokine expression, as well as induction of other proinflammatory genes. The effects of plasmin are specific, require the active catalytic center and can be antagonized by lysine analogues, implying binding of the plasmin molecule to the cell membrane through its lysine binding sites. In view of the upregulation of the fibrinolytic genes in chronic inflammatory diseases, cell activation by plasmin is likely to play a major pathophysiological role, a view that is further supported by data from transgenic mice.

Novel aspects and new roles for the serine protease plasmin.

Aim
The aim of the article is to review the etiology, pathology and epidemiology of a disease entity named Tako-Tsubo syndrome, receiving this name according to the picture obtained during ventriculography resembling a Japanese octopus trap. The Tako-Tsubo syndrome is a diagnosis encountered in patients with acute coronary syndrome and, therefore, is important to consider.

Tako-Tsubo syndrome: dying of a broken heart?

Introduction: Takotsubo cardiomyopathy (TTC) remains a life-threatening disease with the risk of decompensated heart failure and arrhythmias. Valid markers for the prediction of outcome are unavailable. The novel biomarkers fetuin-A, matrix metalloproteinases-2 (MMP-2), myeloperoxidase (MPO), Syndecan-1 and CD40-L show promising results for risk stratification of cardiovascular patients. Nevertheless, clinical implementation has not been investigated in TTC patients. Methods: To investigate this issue, we evaluated clinical complications in 51 patients hospitalized for TTC and measured the serum levels of fetuin-A, MPO, MMP-2, Syndecan-1 and CD40-L within 24 h after admission. Results: Serum levels of Fetuin-A correlated inversely with the risk of cardiac decompensation and all cause complications within the acute phase of TTC. Fetuin-A levels over 190.1 µg/mL (AUC: 0.738, sensitivity 87.5%, specificity: 52.6%) indicate an acute phase of TTC without cardiac decompensation. Despite lower fetuin-A levels in patients with all cause complications, the combined endpoint remained slightly unmet (p = 0.058, AUC: 0.655). Patients with fetuin-A levels over 213.3 µg/mL are at risk of experiencing hemodynamic relevant rhythm disorders (AUC: 0.794; sensitivity: 75.0%, specificity: 79.1%). Other biomarkers failed to reveal a prognostic impact. Pro-BNP and hs troponin levels at admission did not predict adverse cardiac events. Conclusion: Fetuin-A is a promising marker in our study and could be of benefit for the prediction of short-term adverse cardiac events in TTC patients. Therefore, fetuin-A might be of value to evaluate an individual’s risk for complications within the acute phase of TTC and to individually choose the time of intensive care and hospitalization.

The Value of Fetuin-A as a Predictor to Identify Takotsubo Patients at Risk of Cardiovascular Events.

Remote ischemic postconditioning for patients with takotsubo syndrome

A surge in catecholamine levels has been postulated as a potential mechanism causing cardiomyopathy, particularly Takotsubo Syndrome (TTS). Consequently, repeated exposure to β1/β2 agonists could contribute to the development of TTS in patients with asthma during periods of intense exacerbation.Even when no guidelines have been proposed for the identification and management of asthmatic patients who might develop TTS, recurrent asthma exacerbation requiring prolonged use of β1/β2 agonists have the potential of triggering life-threatening arrhythmias and increasing hospital deaths.We conducted a PubMed search for published case reports, experimental studies, animal studies, and review articles examining TTS documentation among patients with asthma. We encountered 45 articles, of which 21 were case reports that were reviewed separately for age, sex, diagnosis, recurrence, electrocardiogram findings, echo results, and mortality.Based on our review, it appears as if the use of high doses of β-agonists may predispose patients with asthma to cardiac events that might be preventable if physicians are aware of this association and become more judicious in their use of β-agonists. A standardized identification and treatment protocol would certainly be most helpful.

Assessing the Role of High-Dose β-Agonists Use in Triggering Takotsubo Syndrome During Asthma Exacerbation.

The prognosis of patients presenting with Tako-Tsubo cardiomyopathy (TTC) is generally considered to be favorable. However, in the acute phase of the disorder complications are not infrequent and, therefore, continuous monitoring and consistent therapy in an intensive care unit is essential. Typical complications in patients with TTC are cardiogenic shock, obstruction of the left ventricular outflow tract (LVOT), occasionally accompanied by acute mitral regurgitation, arrhythmias, predominantly torsade de pointes tachycardias due to QT prolongation, left ventricular (LV) thrombus formation with or without consecutive thromboembolic events, and LV rupture. After confirmation of TTC by coronary angiography, repeat echocardiography should be performed. A standardized therapy for patients with TTC has so far not been established. Recommendations for the acute phase include the administration of anxiolytic agents for patients who present with preceding emotional stress, consistent therapy of physical stressors (such as pain or asthma) and avoidance of catecholamine therapy. Shock due to LVOT obstruction is treated by administration of volume and β-blockers. With respect to the occurrence of torsade de pointes tachycardias, drugs which might cause QT prolongation should not be given. The notable incidence of LV thrombus formation justifies therapeutic anticoagulation. Systematic studies and treatment recommendations for the prophylaxis of recurrent TTC do not exist. The recently reported association between TTC and malignant disorders should prompt tumor screening and subsequent preventive medical checkups in patients affected by TTC.

[Patient care in the acute phase of stress induced cardiomyopathy (Tako-Tsubo cardiomyopathy)--and thereafter?].

Umsetzung der ILCOR-Leitlinien zur therapeutischen Hypothermie nach Reanimation auf deutschen Intensivstationen

Im Folgenden wird uber eine 64-jahrige Patientin mit den klinischen Zeichen eines akuten Koronarsyndroms ohne Nachweis einer koronaren Herzkrankheit berichtet. In der Ventrikulographie stellte sich eine ballonartige Akinesie der apikalen Segmente des linken Ventrikels dar, die sich im Verlauf vollstandig zuruckbildete. Dieses Syndrom wurde aufgrund der Ahnlichkeit zu einer Tintenfischfalle als Tako-Tsubo-Kardiomyopathie erstmalig in Japan beschrieben. Diese Form der Kardiomyopathie ist typischerweise durch eine transiente Akinesie der linken Ventrikelspitze bei normalen epikardialen Kranzgefasen charakterisiert. Es betrifft haufig altere Frauen in der Postmenopause, die sich in den meisten Fallen mit typischer Angina pectoris, ST-Strecken-Hebungen in den prakordialen Ableitungen und geringer Erhohung der kardialen Markerenzyme prasentieren. Haufig lasst sich eine vorausgegangene Episode mit starker emotioneller Belastung anamnestizieren. Die Mortalitat scheint gering zu sein, ebenso wie die Wahrscheinlichkeit eines wiederholten Auftretens. Die Atiologie und die pathophysiologischen Zusammenhange dieser transienten Kardiomyopathie sind bislang nicht aufgeklart.

Transiente linksventrikuläre apikale Ballonierung, Differentialdiagnose des akuten Koronarsyndroms : Broken heart of a priest

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[Patient care in the acute phase of stress induced cardiomyopathy (Tako-Tsubo cardiomyopathy)--and thereafter?].

Umsetzung der ILCOR-Leitlinien zur therapeutischen Hypothermie nach Reanimation auf deutschen Intensivstationen

Transiente linksventrikuläre apikale Ballonierung, Differentialdiagnose des akuten Koronarsyndroms : Broken heart of a priest