An increase in post-COVID patients with late sequelae of acute COVID-19 infection is emerging as an ongoing challenge for physicians and healthcare professionals. Since the beginning of the pandemic, it has rapidly become evident that the acute infection is not limited to the respiratory tract but that several organs, including the cardiovascular system, can be affected. Moreover, in a significant proportion of patients (ranging from about 10 to up to 50%) with former COVID-19, cardiopulmonary symptoms such as dyspnea, palpitations, restricted physical capacity, and cardiac arrhythmias can persist weeks and months after the acute SARS-CoV-2 infection. The spectrum of COVID-19-associated arrhythmias is rather wide, most likely due to various pathomechanisms. In this article, the prevalence of cardiac arrhythmias and underlying pathologies are reviewed, including direct myocardial injury and abnormal consequences with an impact on cardiac electric instability. The hyperinflammatory reaction of the host immune system is specifically considered. Moreover, several distinct rhythm disorders occurring in post-COVID patients are discussed with regard to their clinical management.

Recent hypotheses have suggested the pathophysiological role of catecholamines in the evolution of the Takotsubo syndrome (TTS). The extent of cardiac and circulatory compromise dictates the use of some form of supportive therapy. This study was designed to investigate the clinical outcomes associated with catecholamine use in TTS patients. Our institutional database constituted a collective of 114 patients diagnosed with TTS between 2003 and 2015. The study-patients were subsequently classified into two groups based on the need for catecholamine support during hospital stay (catecholamine group n = 93; 81%, non-catecholamine group = 21; 19%). The primary end-point of our study was all-cause mortality. Patients receiving catecholamine support showed higher grades of circulatory and cardiac compromise (left ventricular ejection fraction (LVEF) 39.6% vs. 32.7%, p-value < 0.01) and the course of disease was often complicated by the occurrence of different TTS-associated complications. The in-hospital mortality (3.2% vs. 28.5%, p < 0.01), 30-day mortality (17.2% vs. 51.4%, p < 0.01) as well as long-term mortality (38.7% vs. 80.9%, p < 0.01) was significantly higher in the group of patients receiving catecholamine support. A multivariate Cox regression analysis attributed EF ≤ 35% (HR 3.6, 95% CI 1.6–8.1; p < 0.01) and use of positive inotropic agents (HR 2.2, 95% CI 1.0–4.8; p 0.04) as independent predictors of the adverse outcome. Rates of in-hospital events and short- as well as long-term mortality were significantly higher in TTS patients receiving catecholamine support as compared to the other study-patients. These results need further evaluation in pre-clinical and clinical trials to determine if external catecholamines contribute to an adverse clinical outcome already compromised by the initial insult.

Platelets are important cellular targets in cardiovascular disease. Based on insights from basic science, translational approaches and clinical studies, a distinguished anti-platelet drug treatment regimen for cardiovascular patients could be established. Furthermore, platelets are increasingly considered as cells mediating effects “beyond thrombosis”, including vascular inflammation, tissue remodeling and healing of vascular and tissue lesions. This review has its focus on the functions and interactions of platelets with potential translational and clinical relevance. The role of platelets for the development of atherosclerosis and therapeutic modalities for primary and secondary prevention of atherosclerotic disease are addressed. Furthermore, novel therapeutic options for inhibiting platelet function and the use of platelets in regenerative medicine are considered.

Background: Lupus anticoagulant (LA) owns procoagulant properties in vivo and prolongs phospholipid-dependent clotting times in vitro. The prolonged in vitro clotting time can be misinterpreted as a bleeding disorder. In some cases, it is necessary to differentiate LA-associated in vitro changes from in vivo coagulation factor deficiency. In this case, we used different laboratory testing in a patient with ischemic stroke and reduced prothrombin time (PT) to identify an in-vitro effect of LA excluding an in-vivo bleeding disorder. Methods: The activity of various coagulation factors was evaluated both with recombinant thromboplastin Innovin (Siemens Healthcare) and reagent tissue extracted thromboplastin Thromborel^® (Siemens Healthcare). Moreover, a 1:1 plasma mixing test with standard plasma was performed. In order to exclude the interaction of tromboplastin and LA thromboplastin, an independent global coagulation test, thromboelastography, was used. Diluted-Russel-Viper-Venom (dRVVT) assay was applied to detect the presence of LA detection. Results: The activity of several coagulation factors measured with recombinant thromboplastin Innovin (Siemens Healthcare) showed a reduced activity of the following coagulation factors: Factor V (20.9%), Factor VII (23.8%), Factor X (19.7%) and international normalized ratio (INR) of 2.33. Re-assessment of the factor's activity with another reagent tissue extracted thromboplastin Thromborel^® (Siemens Healthcare) showed a normalization of INR and factor's activity in comparison to thromboplastin reagent Innovin^®: Factor V (77%), Factor VII (45.4%), Factor X (64.2%), and INR of 1.28. A plasma mixing study with 1:1 standard plasma revealed reduced (<50%) normalization of INR as well as coagulation factor's activity confirming a LA-inhibitor in the patient plasma. Diagnostic LA testing was also performed with dRVVT assay showing a significantly prolonged (112.8 s) test time. Thromboelastography revealed no abnormalities. Conclusions: Different thromboplastin reagents and plasma mixing tests as well as thromboplastin independent coagulation tests may be helpful to differentiate LA and in vitro changes from in vivo factor deficiency in patients with LA.