M. Gawaz

Background: Generation of reactive oxygen species (ROS) plays a pivotal role in the progression of heart failure. Primary endogenous sources of H2O2 und O2·− are tightly regulated NADPH oxidases (NOX), modulating redox-sensitive effector proteins. While exerting distinct physiological functions in tissue homeostasis, enhanced ROS activity, as well as upregulation of NOX expression has been identified to have detrimental effects in the progression of heart failure.

Background: Transfemoral aortic valve replacement (TAVR) is a standard therapy for aortic valve stenosis in patients with intermediate to high risk for conventional surgery. In our clinic we performed TAVR in minimalistic setting by a team of two interventional cardiologists, echocardiographist and two cardiac catheterization laboratory nurses (surgical team was available on call for the case of serious complication). After new national guidelines issued by Federal Joint Committee (G-BA) went into force (August, 2015), a complete heart team must be present in the operating room during the whole TAVR procedure. We changed the setting accordingly and the team was extended by cardiac surgeon, anesthesiologist, cardiovascular perfusionist, surgical nurse and nurse anesthetist. In this study...

Anamnese und klinischer Befund: Ein 31-jähriger Patient wurde aufgrund akuter kardialer Dekompensation in die Notaufnahme eingeliefert. Bei Aufnahme zeigten sich ausgeprägte Beinödeme, eine Herzinsuffizienz NYHA III sowie auskultatorisch basale Rasselgeräusche über beiden Lungen. Untersuchungen: Echokardiographisch imponierte eine hochgradig eingeschränkte rechts- und linksventrikuläre Funktion sowie eine Hypertrabekularisierung im rechten Ventrikel, aber auch der Apex des linken Ventrikels. In der Kardio-MRT konnten diese Befunde bestätigt werden. Eine Lungenembolie wurde bei erhöhten D-Dimeren und Rechtsherzbelastungszeichen CT-morphologisch ausgeschlossen, ebenso eine koronare Herzerkrankung in der Koronarangiographie. Diagnose, Therapie und Verlauf: In Zusammenschau der Befunde wurde eine Non-Compaction-Kardiomyopathie mit konsekutiver kardialer Dekompensation diagnostiziert. Eine diuretische Therapie erzielte rasch eine Rekompensation. Eine Antikoagulation wurde eingeleitet. Bei höhergradigen ventrikulären Rhythmusstörungen als Risikomarker für einen plötzlichen Herztod erfolgte nach zunächst frustraner Anlage eines transvenös implantierbarem Kardioverter/Defibrillator (ICD) die Implantation eines subkutanen Aggregates. Anschließend konnte er in gutem Allgemeinzustand nach Hause entlassen werden. Folgerung: Bei der Non-Compaction-Kardiomyopathie handelt es sich um eine angeborene nicht-ischämische Kardiomyopathie, die durch eine Störung des Verdichtungsprozesses während der endomyokardialen Embryogenese entsteht. Klinisch zeigt sich eine Trias aus Herzinsuffizienz, thrombembolischen Ereignissen, sowie supraventrikulären und ventrikulären Rhythmusstörungen. Diagnostik der Wahl ist die Echokardiographie. Entscheidend für die Prognose ist das Ausmaß der Herzinsuffizienz, der Schweregrad von Rhythmusstörungen sowie das Auftreten thrombembolischer Ereignisse. History and admission findings: We report on a case of a 31-year-old patient who was admitted to hospital with acute cardiac failure. At physical examination we found peripheral edema and wet rales. Investigations: Cardiac ultrasound revealed severely impaired left and right ventricular function and prominent trabeculation in the right ventricle, but also in the apex of the left ventricle. This was confirmed by cardiac magnetic resonance imaging. Both pulmonary embolism and coronary heart disease were excluded by thoracic computed tomography and coronary angiography. Diagnosis, treatment and course: These findings were in line with the diagnosis of non-compaction cardiomyopathy resulting in cardiac failure. We introduced diuretic therapy which leads to weight loss and release of dyspnoea. Due to prevention of embolic events an anticoagulative therapy was started. In light of rhythmogenic vulnerability, a subcutaneous implantable cardioverter defibrillator (ICD) system was implanted. Afterwards the patient was discharged in good general health. Conclusion: Non-compaction cardiomyopathy (NCCM) is a hereditary non-ischaemic cardiac disease which occurs due to the failure of myocardial compaction during embryogenesis. Common manifestation is the triad of heart failure, rhythmogenic vulnerability and systemic embolic events. First-line imaging technique for diagnosing NCCM is cardiac ultrasound. The prognosis depends on severity of heart failure, ventricular arrhythmia and the incidence of embolic events.

Background: Severe mitral regurgitation (MR) causes remodeling of the left ventricle (LV). After surgical mitral valve repair (MVR) reverse remodeling of the LV has been observed. Aim of this study was to assess if percutaneous MVR with the MitraClip system can also induce a reverse LV remodeling. Patients and methods: We prospectively included 33 consecutive patients with symptomatic moderate-to-severe MR and high perioperative risk undergoing percutaneous MVR. Patients underwent transthoracic echocardiography (LV volumes, LV stroke volume, ejection fraction, diameter of mitral annulus) and strain analysis (global longitudinal strain (GLS), global radial strain (GRS), global circumferential strain (GCS)) by speckle-tracking echocardiography and by MRI prior to the procedure and three months after the procedure. Results: Three months after MitraClip procedure reverse LV remodeling was documented by a significant reduction of LV endsystolic (116.2±71.0 mL to 102.9±58.3 mL, pConclusions: Successful percutaneous MRV not only leads to an improvement of MR, but additionally allows a reverse LV remodeling within 3 months, which might contribute to the symptomatic and prognostic success in these patients.

Atrioventricular nodal reentrant tachycardia (AVNRT) is a frequent supraventricular tachycardia in children and young adults. Despite favourable success rates of catheter ablation, conventional fluoroscopic catheter guidance is associated with risks of low-dose ionizing radiation for the patient and the personnel. Here we describe a technique for zero-fluoroscopy catheter ablation using contact force technology. Zero-fluoroscopy catheter ablation was attempted in 12 patients with AVNRT (median age 20 years; range 11-75 years). An ablation catheter with integrated contact force sensor and a nonfluoroscopic electroanatomical mapping system was used for visualization of cardiovascular structures. Mean contact forces during mapping and ablation were restricted to an upper limit of 50 g to avoid cardiovascular injuries. Zero-fluoroscopy catheter ablation was performed successfully and uneventfully in all patients. There were no arrhythmia recurrences during a median follow-up of 6.2 months (range 2.7-12.8). Zero-fluoroscopy catheter ablation of AVNRT is possible and appears simple yet safe, when a nonfluoroscopic electroanatomical mapping system is used in combination with an ablation catheter with integrated contact force sensor. The presented technique could thus be easily employed in most electrophysiological laboratories.

Problemstellung: Die Katheterablation stellt eine kurative Therapie zur Behandlung von tachykarden Herzrhythmusstörungen im Kindes- und Jugendalter dar, ist aber durch die notwendige Durchleuchtungskontrolle in der klinischen Routine weltweit mit einer Strahlenbelastung verbunden. Patienten und Methoden: Hier beschreiben wir die erfolgreiche durchleuchtungsfreie Katheterablation bei einem 10-jährigen Jungen mit offenem WPW-Syndrom und linkslateral gelegenem Kent-Bündel. Die elektrophysiologische Untersuchung und Ablation erfolgte mit Hilfe des 3D-Mappingsystems Ensite NavX (St. Jude Medical) und des TactiCath RF-Ablationskatheters (7F, gekühlter 3,5mm Tip, Endosense). Dieser Katheter erlaubt eine kontinuierliche Messung der totalen, sowie der axialen und tangentialen Anpresskraft in Echtzeit mit einer Empfindlichkeit von weniger als 1g. Ergebnisse: Zunächst wurde über den TactiCath-Ablationskatheter und die Hautelektroden unter kontinuierlicher Anpresskraftkontrolle eine Geometrie von unterer Hohlvene, rechtem Vorhof (RA), His-Bündel und Koronarsinus erstellt. Anschließend konnten elektrophysiologische Diagnostikkatheter problemlos im Koronarsinus und im rechten Ventrikel platziert werden. Mit dem Koronarsinuskatheter als Referenz wurde eine erneute RA-Geometrie unter Anpresskraft-Kontrolle erstellt. Nach dem Nachweis eines linkslateral gelegenen Kentbündels (antegrade Refraktärzeit 250ms) und Ausschluss eines persistierenden Foramen ovale erfolgte unter transösophagealer echokardiografischer Kontrolle die transseptale Punktion. Die Fusion von Vorhof und Kammer zeigte sich am linkslateralen Mitralklappenanulus, wo das Kentbündel problemlos abladiert werden konnte. Durch die Verwendung des speziellen Ablationskatheters konnten Anpresskräfte >50g vermieden werden. Schlussfolgerung: Die durchleuchtungsfreie Katheterablation eines linksatrialen akzessorischen Leitungsbündels ist unserer Einschätzung nach auch im Kindesalter durch die Verwendung eines Katheters mit Anpresskraft-Kontrolle möglich und sicher.

Background and purpose:  Platelet collagen receptor glycoprotein VI (GPVI) contributes significantly to platelet adhesion and thrombus formation. We aimed to investigate GPVI in patients presenting with symptoms of acute cerebrovascular disease and to define GPVI as biomarker for acute stroke.Methods:  We consecutively evaluated 205 patients, who admitted the stroke unit with symptoms for stroke. Surface expression of the platelet activation markers (GPVI, CD62P, GPIb) was determined by two‐color whole blood flow cytometry.Results:  Patients with transient ischemic attack (TIA) (n = 18; 8.8%) as well as with stroke (n = 133; 64.9%) showed a significantly enhanced GPVI expression (mean fluorescence intensity ± SD) on admission compared to patients with non‐ischemic (NI) events (n = 54; 26.3%) (TIA: 20.9 ± 7.1 vs. NI: 16.2 ± 3.9; P = 0.002; stroke: 20.4 ± 5.7 vs. NI; P = 0.002). Neither CD62P nor GPIb surface expression showed a significant difference. Logistic regression analysis revealed that on admission GPVI was associated with stroke independent of conventional laboratory markers such as C‐reactive protein, blood glucose, and creatine kinase. Using a receiver operating characteristic curve on GPVI, we have determined the cut off value of 18.2 for stroke. Thus, patients with enhanced GPVI expression levels (≥18.2) had a 2.4‐fold relative risk for stroke. Patients with elevated platelet GPVI expression level had a poorer clinical outcome in cumulative event‐free survival for stroke, myocardial infarction, and cerebro‐/cardiovascular death at 3‐month follow‐up (log rank; P = 0.045).Conclusions:  These findings indicate that platelet GPVI surface expression is significantly enhanced in patients with TIA and stroke compared to patients with NI events. Determination of platelet‐specific GPVI may be useful as an early biomarker for cerebral ischemia.

Safeguarding of antiplatelet drug efficacy represents a cornerstone for the optimal treatment of patients with symptomatic coronary artery disease requiring coronary interventions. This means a challenge to modern cardiology since there has been cumulative evidence, that response to common oral antiplatelet therapy is a highly variable phenomenon underlying various mechanisms. It is known, that particular risk groups exhibit a high residual platelet aggregability (RPA) despite conventional antiplatelet therapy. Additionally, a relevant association between high RPA and recurrent ischaemic events after PCI exists. Individualization of antiplatelet therapy by dose increase or alternative application of novel P2Y12-receptor antagonists might lead to improved cardiovascular outcome in patients with poor responsiveness to conventional antiplatelet therapy. Identification of risk patients who might benefit from tailored therapy by increased net benefit without excess of major bleedings means a challenge. Clinical risk scores might help in the process of risk stratification and therapeutic decision. Subsequently, literature on risk assessment for antiplatelet drug responsiveness and different strategies will be discussed to identify patients who might benefit from personalized antiplatelet strategies.