HV interval in calcific aortic stenosis. Relation to left ventricular function and effect of valve replacement

Intracardiac electrography and 24 hour ambulatory electrocardiographic monitoring were carried out in 20 patients with calcific aortic stenosis (mean pressure gradient 86 mm Hg) to investigate (a) the role of bradycardia and tachycardia in the pathogenesis of syncope in aortic stenosis, (b) the relation between haemodynamic data and electrophysiological abnormalities, and (c) whether valve replacement corrects electrophysiological abnormalities. Intracardiac electrograms showed impaired sinus node function in five patients and a prolonged HV interval (greater than or equal to 50 ms) in 11 but there was no difference in the findings of 13 patients with syncope and seven without. Ambulatory monitoring showed short pauses in three patients and brief episodes of tachycardia in four, but there was no difference in the findings of patients with and without syncope. The HV interval correlated inversely with the left ventricular ejection fraction, whereas no correlation was found between the HV interval and the pressure gradient. Nine patients were re-evaluated 15 months after aortic valve replacement. No change was found in sinus node function, but the HV interval had increased by 7.8 ms. It is concluded that in calcific aortic stenosis neither bradycardia nor tachycardia is shown to be a frequent cause of syncope, a prolonged HV interval is a frequent finding and further prolongation occurs after valve replacement, and contractility and conductivity appear to deteriorate in parallel.     

The Intentional Differences: A Qualitative Study of the Views and Experiences of Non-peer Mental Health Providers on Working Together with Peer Support Colleagues in Mental Health

Community Mental Health Journal - The study reports the results of a qualitative study on the views and experiences of non-peer mental health providers on working together with peer colleagues in...     

Cold urticaria – What we know and what we do not know

Cold urticaria (ColdU) is a common form of chronic inducible urticaria characterized by the development of wheals, angioedema or both in response to cold exposure. Recent research and guideline updates have advanced our understanding and management of ColdU. Today, its pathophysiology is thought to involve the cold-induced formation of autoallergens and IgE to these autoallergens, which provoke a release of proinflammatory mediators from skin mast cells. The classification of ColdU includes typical and atypical subtypes. We know that cold-induced wheals usually develop on rewarming and resolve within an hour and that anaphylaxis can occur. The diagnosis relies on the patient's history and cold stimulation testing. Additional diagnostic work-up, including a search for underlying infections, should only be done if indicated by the patient's history. The management of ColdU includes cold avoidance, the regular use of nonsedating antihistamines and the off-label use of omalizumab. However, many questions regarding ColdU remain unanswered. Here, we review what is known about ColdU, and we present important unanswered questions on the epidemiology, underlying pathomechanisms, clinical heterogeneity and treatment outcomes. Our aim is to guide future efforts that will close these knowledge gaps and advance the management of ColdU.     

Characteristics of culprit lesion in patients with non-ST-elevation myocardial infarction and improvement of diagnostic utility using dual energy cardiac CT

Aims

The aim of the study was to identify the characteristics of the culprit lesions compared to non-culprit lesions in patients with non-ST-elevation-myocardial infarction using dual energy computed tomography (DECT).

Methods and results

In 29 patients, we identified 29 culprit lesions and 227 non-culprit lesions.

Quantitative values such as the effective atomic number (effective-Z) and Hounsfield Units (HU) values were measured. Furthermore, all the lesions were characterised using characteristics such as composition (non-calcified, predominantly-non-calcified, predominantly-calcified, or calcified), presence of spotty calcification, remodelling index, and napkin ring sign.

The mean effective-Z and HU values were significantly lower in culprit lesions than in non-culprit lesions (8.99?±?1.21 vs 9.79?±?1.52; p?=?0.0066 and 87.41?±?84.97 vs. 154.45?±?176.13; p?=?0.0447). The culprit lesions had a higher frequency of non-calcified plaques and predominantly non-calcified plaques, and were with a greater presence of napkin ring signs in comparison with non-culprit lesions. There were no differences in the presence of spotty calcification or remodelling index.

By adding effective-Z to plaque characteristics such as non-calcified, positive remodelling, spotty calcification, and napkin rings we observed a significant increased sensitivity of detecting culprit lesions (65.5% vs.44.8%), but no significant changes in area under curve (AUC).

Conclusion

The use of DECT adds new information of the plaque composition expressed by the effective-Z, which differs significantly in culprit lesions in comparison with non-culprit lesions. The use of the effective-Z improves the diagnostic sensitivity in detection of culprit lesions.

     

Histopathologische Differenzialdiagnostik bei gelenkimplantatallergischen Fragestellungen

Total joint replacement has greatly increased over the last decades and so have endoprothesis-associated pathologies. European studies have shown a 10-year durability varying from 88 % to 95?%. By means of histopathology different pathogenetic synovial-like interface membrane (SLIM) patterns that lead to reduction of implant durability can be discerned, such as periprosthetic particles, bacterial infections and arthrofibrosis. Subsequently, SLIM types have been determined in a revised consensus classification including particle-induced type (type I) so-called non-septic loosening, infection type (type II) so-called septic loosening, combination type (type III) of bacterial and particle-induced types, indifferent type with mechanical and functional disorders (type IV), osseus pathologies (type V), arthrofibrotic type (type VI, endoprosthesis-associated arthrofibrosis) and allergic/immunological/toxic reactions to prosthesis material (type VII). Particles are characterized histopathologically according to the Krenn particle algorithm. In cases of severe lymphocyte/macrophage infiltration, necrosis, abrasion particle detection and granuloma formation, a toxic or allergic reaction to implant material should be considered. As a direct abrasion particle-induced toxicity cannot be differentiated from a particle-induced allergic type VII reaction to implant material, the histopathological diagnosis of toxic reaction to implant material or allergic reaction to implant material should be made with caution and only in association with immunological, allergic and clinical data. It is recommended that tissue samples should be arthroscopically taken from different regions: close to the prosthesis, distant from the prosthesis and from bone tissue. The pathologist should be given information concerning clinical, allergological and microbiological data.