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Transcatheter alcohol septal ablation (ASA) treatment of symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM) is based on the existence and degree of intraventricular obstruction. Patients with significant gradient and symptoms who do not respond to optimal medical therapy are eligible to gradient reduction through a surgical (septal myectomy) or a transcatheter (alcohol septal ablation) septal reduction. The latter encompasses occlusion of a septal branch perfusing the hypertrophied septum, which is involved in the generation of obstruction, by injecting ethanol into the supplying septal branch(es). ASA has been established as a highly effective and safe method and has outnumbered the surgical gold standard. Although the technique is straightforward, patient selection and some technical details may influence the efficacy and safety of the procedure. The technique is based on echocardiographic contrast guidance, which allows accurate target septal branch selection and optimisation of the result. Published long-term results from high-volume centres have confirmed the effectiveness of ASA and have shown excellent survival, which is comparable to that in the general population. Choice and performance of the surgical or interventional treatment should be implemented in highly specialised centres in terms of a heart-team approach, taking notice of anatomic characteristics as well as comorbidities. Involvement of all cases in international registries may reveal the individual merits and indications for the surgical and interventional treatment in HOCM.

Despite recent advances in the management of heart failure with reduced ejection fraction (HFrEF), the burden of acute heart failure (AHF) remains significant with a high morbidity and mortality that has not been improved by any treatment modality. A meta-analysis summarized the study results on the effects of tolvaptan on AHF, which failed to demonstrate an improvement in short-term and long-term mortality, length of hospital stay and reduced frequency of worsening heart failure (WHF). Similar trial results were also reported in other AHF studies, such as the ASCEND-HF and the RELAX-AHF-2 trials. In view of these inconclusive studies it is evident that improving the prognosis of AHF patients remains an unmet medical need. Further efforts should focus on organ damage protection, individualized treatment, patient benefits and standardized management programs, including immediate identification and management of cardiogenic shock and establishment of HF networks for close monitoring of AHF patients.

To date there is no validated evidence for standardized treatment of patients with Takotsubo syndrome (TTS). Medication therapy after final TTS diagnosis remains unclear. Previous data on patient outcome is ambivalent. Aim of this study was to evaluate medication therapy in TTS and to analyze patient outcome.Within an observational retrospective cohort study we analyzed our medical records and included 72 patients with TTS that underwent cardiovascular magnetic resonance imaging (CMR) after a median of 2 days interquartile range (IQR 1-3.5). We investigated medication therapy at discharge. Medication implementation and major adverse clinical events (MACE) were prospectively evaluated after a median follow-up of 24 months (IQR 6-43). Left ventricular function, myocardial oedema and late gadolinium enhancement were analyzed in a CMR follow-up if available.Antithrombotic therapy was recommended in 69 (96%) patients including different combinations. Antiplatelet monotherapy was prescribed in 28 (39%) patients. Dual antiplatelet therapy was recommended in 29 (40%) patients. Length of therapy duration varied from one to twelve months. Only in one case oral anticoagulation was prescribed due to apical ballooning with a left ventricular ejection fraction30%. In all other cases oral anticoagulation was recommended due to other indications. ß-adrenoceptor antagonists and ACE inhibitors were recommended in 63 (88%), mineralocorticoid receptor antagonists were prescribed in 31 (43%) patients. After a median of 2 months (IQR 1.3-2.9) left ventricular function significantly recovered (49.1% ± 10.1 vs. 64.1% ± 5.7, P 0.001) and myocardial oedema significantly decreased (13.5 ± 11.3 vs. 0.6% ± 2.4, P = 0.001) in the CMR follow-up. The 30-day mortality was 1%. MACE rate after 24 months was 12%.Although therapy guidelines for TTS currently do not exist, we found that the majority of patients were treated with antithrombotic and heart failure therapy for up to twelve months. Left ventricular function and myocardial oedema recovered rapidly within the first two months. Outcome analysis showed a low bleeding rate and a high short-term survival. Therefore, TTS patients might benefit from antithrombotic and heart failure therapy at least for the first two months.