Browsing by Author "Pankuweit, Sabine (7003360984)"

Cardiac tamponade is a medical emergency caused by the progressive accumulation of pericardial fluid (effusion), blood, pus or air in the pericardium, compressing the heart chambers and leading to haemodynamic compromise, circulatory shock, cardiac arrest and death. Pericardial diseases of any aetiology as well as complications of interventional and surgical procedures or chest trauma can cause cardiac tamponade. Tamponade can be precipitated in patients with pericardial effusion by dehydration or exposure to certain medications, particularly vasodilators or intravenous diuretics. Key clinical findings in patients with cardiac tamponade are hypotension, increased jugular venous pressure and distant heart sounds (Beck triad). Dyspnoea can progress to orthopnoea (with no rales on lung auscultation) accompanied by weakness, fatigue, tachycardia and oliguria. In tamponade caused by acute pericarditis, the patient can experience fever and typical chest pain increasing on inspiration and radiating to the trapezius ridge. Generally, cardiac tamponade is a clinical diagnosis that can be confirmed using various imaging modalities, principally echocardiography. Cardiac tamponade is preferably resolved by echocardiography-guided pericardiocentesis. In patients who have recently undergone cardiac surgery and in those with neoplastic infiltration, effusive–constrictive pericarditis, or loculated effusions, fluoroscopic guidance can increase the feasibility and safety of the procedure. Surgical management is indicated in patients with aortic dissection, chest trauma, bleeding or purulent infection that cannot be controlled percutaneously. After pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be considered to prevent recurrence and effusive–constrictive pericarditis. © 2023, Springer Nature Limited.

In this position statement of the ESC Working Group on Myocardial and Pericardial Diseases an expert consensus group reviews the current knowledge on clinical presentation, diagnosis and treatment of myocarditis, and proposes new diagnostic criteria for clinically suspected myocarditis and its distinct biopsy-proven pathogenetic forms. The aims are to bridge the gap between clinical and tissue-based diagnosis, to improve management and provide a common reference point for future registries and multicentre randomised controlled trials of aetiology-driven treatment in inflammatory heart muscle disease. © 2013 The Author.

Cardiac amyloidosis is a serious and progressive infiltrative disease that is caused by the deposition of amyloid fibrils at the cardiac level. It can be due to rare genetic variants in the hereditary forms or as a consequence of acquired conditions. Thanks to advances in imaging techniques and the possibility of achieving a non-invasive diagnosis, we now know that cardiac amyloidosis is a more frequent disease than traditionally considered. In this position paper the Working Group on Myocardial and Pericardial Disease proposes an invasive and non-invasive definition of cardiac amyloidosis, addresses clinical scenarios and situations to suspect the condition and proposes a diagnostic algorithm to aid diagnosis. Furthermore, we also review how to monitor and treat cardiac amyloidosis, in an attempt to bridge the gap between the latest advances in the field and clinical practice. © European Society of Cardiology 2021

Cardiac amyloidosis is a serious and progressive infiltrative disease that is caused by the deposition of amyloid fibrils at the cardiac level. It can be due to rare genetic variants in the hereditary forms or as a consequence of acquired conditions. Thanks to advances in imaging techniques and the possibility of achieving a non-invasive diagnosis, we now know that cardiac amyloidosis is a more frequent disease than traditionally considered. In this position paper the Working Group on Myocardial and Pericardial Disease proposes an invasive and non-invasive definition of cardiac amyloidosis, addresses clinical scenarios and situations to suspect the condition and proposes a diagnostic algorithm to aid diagnosis. Furthermore, we also review how to monitor and treat cardiac amyloidosis, in an attempt to bridge the gap between the latest advances in the field and clinical practice. © The Author(s), 2021.

Advances in molecular genetics present new opportunities and challenges for cardiologists who manage patients and families with cardiomyopathies. The aims of this position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases are to review the general issues related to genetic counselling, family screening and genetic testing in families with a cardiomyopathy, and to provide key messages and suggestions for clinicians involved in their management. © 2010 The Author.

Background: The most frequent pericardial emergency is cardiac tamponade, but complications of an acute coronary syndrome and aortic dissection may also involve the pericardium. Acute pericarditis can also represent a medical emergency due to chest pain of upsetting intensity. Decompensations in chronic advanced constriction and in the clinical course of purulent pericarditis necessitate critical care as well. Diagnosis and Management: The diagnosis of cardiac tamponade is based on clinical presentation and physical findings, confirmed by echocardiography and cardiac catheterization. Tamponade is an absolute indication for urgent drainage, either by pericardiocentesis or surgical pericardiotomy. The approach for pericardiocentesis can be subxiphoid or intercostal using echocardiographic or fluoroscopic guidance. Urgent drainage, combined with intravenous antibiotics, is also mandatory in suspected purulent pericarditis. If confirmed, it should be combined with intrapericardial rinsing (best by a surgical drainage). Pericardiocentesis is contraindicated in cardiac tamponade complicating aortic dissection. This condition should immediately lead to cardiac surgery. Although pericardiectomy is the only treatment for permanent constriction, this procedure is contraindicated when extensive myocardial fibrosis and/or atrophy are demonstrated. Case Study: Iatrogenic tamponade may occur during percutaneous mitral valvuloplasty, implantation of pacemakers, electrophysiology and radiofrequency ablation procedures, right ventricular endomyocardial biopsy, percutaneous coronary interventions, and rarely during Swan-Ganz catheterization. The authors report on a 79-year-old who suffered coronary perforation and cardiac tamponade during elective stent implantation. Tamponade was successfully treated with pericardiocentesis and implantation of a membrane-covered graft stent. Subsequent recurrent pericarditis/postpericardial injury syndrome with moderate pericardial effusion was initially treated with aspirin and then with aspirin and colchicine. At 6 months, the patient is in stable remission even after withdrawal of colchicine. Conclusion: Natural history of pericardial diseases can be complicated with pericardial emergencies requiring prompt diagnosis, intensive care with hemodynamic monitoring, and early aggressive management. Medical supportive measures, drainage of pericardial effusion, surgical pericardiotomy, and pericardiectomy should be applied when needed with no delay. This procedural approach also applies to iatrogenic interventions leading to tamponade. © Urban & Vogel 2006.

Interventional procedures for pericardial diseases include pericardiocentesis, drainage of pericardial effusion, intrapericardial therapy, and percutaneous balloon pericardiotomy or percutaneous pericardiostomy. Echocardiographic and fluoroscopic guidance have greatly increased safety and feasibility. Several devices for pericardiocentesis have been tested (PerDucer, PeriAttacher, visual puncture systems, Grasper, Scissors, and Reverse slitter), mainly to facilitate access to the pericardium in the absence of effusion for epicardial ablations or left atrial appendage ligation. In selected patients with pericardial effusions that cannot be managed medically or with prolonged drainage, various medications can be applied intrapericardially to prevent further recurrences or induce sclerosis of the pericardial space. © 2017 Elsevier Inc.

Pericardial cytokine patterns in various diseases are not well established. We have analyzed pericardial proinflammatory (interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha) and immunoregulatory cytokines (transforming growth factor (TGF)-beta1 and interferon (IFN)-gamma) in patients with pericarditis, myocarditis, and ischemic heart disease. Pericardial fluid was obtained in 30 subsequent patients undergoing pericardiocentesis (Group 1: 60 % males, 52.4 ± 14.2 years) and in 21 patients during aortocoronary bypass surgery (Group 2: 42.9 % males, age 67.2 ± 7.4 years). After clinical, laboratory, echocardiography examination, fiberoptic pericardioscopy (Storz-AF1101Bl, Germany) and pericardial/epicardial biopsy Group 1 was subdivided to 40 % neoplastic, 36.6 % autoreactive, 10 % iatrogenic, and 13.3 % viral pericarditis. Samples were promptly aliquoted, frozen, and stored at -70 C. The cytokines were estimated using quantikine enzyme amplified-sensitivity immuno-assays (R&D Systems, USA) and the results compared between neoplastic, viral, iatrogenic, and autoreactive pericarditis and surgical groups. IL-6 was significantly increased in PE versus serum in all forms of pericarditis (except in autoreactive) and increased in comparison with pericardial fluid of surgical patients. TNF-alpha was increased only in PE of patients with viral pericarditis in comparison with Group 2. TGF-beta1 was strikingly lower in the PE than in the serum of all pericarditis patients. However, TGF-beta1 levels in PE were significantly higher in Group 1 than in Group 2, except in viral pericarditis. IFN-gamma levels did not significantly differ between PE and serum or in comparison with Group 2. The cytokine pattern "high TNF-alpha/low TGF-beta1" was found in viral pericarditis and low IL-6 in autoreactive PE. Different etiologies of pericardial inflammation did not influence the IFN-gamma levels. IL-6 pericardial to serum ratio was significantly higher in autoreactive PE than in viral and neoplastic forms. However, TNF-alpha and IFN-gamma pericardial to serum ratios were significantly higher in viral than in autoreactive and neoplastic PE. © 2012 Springer Science+Business Media, LLC.

Despite a myriad of causes, pericardial diseases present in few clinical syndromes. Acute pericarditis should be differentiated from aortic dissection, myocardial infarction, pneumonia/pleuritis, pulmonary embolism, pneumothorax, costochondritis, gastroesophageal reflux/neoplasm, and herpes zoster. High-risk features indicating hospitalization are: fever >38 °C, subacute onset, large effusion/tamponade, failure of non-steroidal anti-inflammatory drugs (NSAIDs), previous immunosuppression, trauma, anticoagulation, neoplasm, and myopericarditis. Treatment comprises 10-14-days NSAID plus 3 months colchicine (2 × 0.5 mg; 1 × 0.5 mg in patients <70 kg). Corticosteroids are avoided, except for autoimmunity, as they facilitate the recurrences. Echo-guided pericardiocentesis (±fluoroscopy) is indicated for tamponade and effusions >2 cm. Smaller effusions are drained if neoplastic, purulent or tuberculous etiology is suspected. In recurrent pericarditis, repeated testing for autoimmune and thyroid disease is appropriate. Pericardioscopy and pericardial/epicardial biopsy may clarify the etiology. Familial clustering was recently associated with tumor necrosis factor receptor-associated periodic syndrome (TNFRSF1A gene mutation). Treatment includes 10-14 days NSAIDs with colchicine 0.5 mg bid for up to 6 months. In non-responders, low-dose steroids, intrapericardial steroids, azathioprine, and cyclophosphamide can be tried. Successful management with interleukin-1 receptor antagonist (anakinra) was recently reported. Pericardiectomy remains the last option in >2 years severely symptomatic patients. In constriction, expansion of the heart is impaired by the rigid, chronically inflamed/thickened pericardium (no thickening ∼20 %). Chest radiography, echocardiography, computerized tomography, magnetic resonance imaging, hemodynamics, and endomyocardial biopsy indicate the diagnosis. Pericardiectomy is the only treatment for permanent constriction. Predictors of poor survival are prior radiation, renal dysfunction, high pulmonary artery pressures, poor left ventricular function, hyponatremia, age, and simultaneous HIV and tuberculous infection. © 2012 Springer Science+Business Media, LLC.

The etiology of pericardial effusions remains unresolved in many cases because not the full spectrum of diagnostic methods including cytology, histology, immunohistology and PCR on cardiotropic agents, which are currently available, used in many institutions. After comprehensive clinical workup and use of imaging methods, such as echocardiography and cardiac MRI, pericardiocentesis and epicardial and pericardial biopsy were carried out under pericardioscopical control of the biopsy site. Biopsies and fluid were evaluated by cytological, histological, immunological and molecular (PCR) methods in 259 patients of our tertiary referral center following an identical clinical pathway, diagnostic and therapeutic algorithm in all cases. A standard clinical pathway and the same diagnostic and therapeutic algorithms were used in all cases. When all methods are applied to patients with pericardial effusions, "idiopathic" pericardial effusion is no longer a relevant diagnosis. Autoreactive and lymphocytic pericardial effusions are the leading diagnosis in 35 % of patients in the prospective Marburg registry, followed by malignant effusions in 28 % of cases. Viral genome was assessed in fluid and epi- as well as pericardial biopsies in 12 %, followed by post-traumatic/iatrogenic effusions in 15 % and purulent/bacterial effusions in only 2 %. Pericardioscopy permits the macroscopic inspection of the pulsating heart and its disease-associated macroscopic alterations. It also permits safe and targeted biopsy for further investigations of the tissue. Therapy, tailored to the individual etiology, can be selected such as intrapericardial instillation in autoreactive effusions with triamcinolone and with cisplatin or thiotepa in neoplastic effusions. With this approach the recurrence of pericardial effusion can be avoided effectively. A comprehensive approach to the diagnosis of pericardial effusions in conjunction with pericardioscopy for targeted tissue sampling is the prerequisite for an etiologically based intrapericardial and systemic treatment, which improves outcome and prognosis. © 2013 Springer Science+Business Media New York.