Complete mesocolic excision does not increase short-term complications in laparoscopic left-sided colectomies : a comparative retrospective single-center study

Background: Since the implementation of total mesorectal excision (TME) in rectal cancer surgery, oncological outcomes improved dramatically. With the technique of complete mesocolic excision (CME) with central vascular ligation (CVL), the same surgical principles were introduced to the field of colon cancer surgery. Until now, current literature fails to invariably demonstrate its oncological superiority when compared to conventional surgery, and there are some concerns on increased morbidity. The aim of this study is to compare short-term outcomes after left-sided laparoscopic CME versus conventional surgery. Methods: In this retrospective analysis, data on all laparoscopic sigmoidal resections performed during a 3-year period (October 2015 to October 2018) at our institution were collected. A comparative analysis between the CME group-for sigmoid colon cancer-and the non-CME group-for benign disease-was performed. Results: One hundred sixty-three patients met the inclusion criteria and were included for analysis. Data on 66 CME resections were compared with 97 controls. Median age and operative risk were higher in the CME group. One leak was observed in the CME group (1/66) and 3 in the non-CME group (3/97), representing no significant difference. Regarding hospital stay, postoperative complications, surgical site infections, and intra-abdominal collections, no differences were observed. There was a slightly lower reoperation (1.5% versus 6.2%, p = 0.243) and readmission rate (4.5% versus 6.2%, p = 0.740) in the CME group during the first 30 postoperative days. Operation times were significantly longer in the CME group (210 versus 184 min, p < 0.001), and a trend towards longer pathological specimens in the CME group was noted (21 vs 19 cm, p = 0.059). Conclusions: CME does not increase short-term complications in laparoscopic left-sided colectomies. Significantly longer operation times were observed in the CME group

Successes and challenges of artificial intelligence in cardiology

In the past decades there has been a substantial evolution in data management and data processing techniques. New data architectures made analysis of big data feasible, healthcare is orienting towards personalized medicine with digital health initiatives, and artificial intelligence (AI) is becoming of increasing importance. Despite being a trendy research topic, only very few applications reach the stage where they are implemented in clinical practice. This review provides an overview of current methodologies and identifies clinical and organizational challenges for AI in healthcare

Hyperactive ryanodine receptors in human heart failure and ischaemic cardiomyopathy reside outside of couplons

Aims In ventricular myocytes from humans and large mammals, the transverse and axial tubular system (TATS) network is less extensive than in rodents with consequently a greater proportion of ryanodine receptors (RyRs) not coupled to this membrane system. TATS remodelling in heart failure (HF) and after myocardial infarction (MI) increases the fraction of non-coupled RyRs. Here we investigate whether this remodelling alters the activity of coupled and non-coupled RyR sub-populations through changes in local signalling. We study myocytes from patients with end-stage HF, compared with non-failing (non-HF), and myocytes from pigs with MI and reduced left ventricular (LV) function, compared with sham intervention (SHAM).Methods and resultsSingle LV myocytes for functional studies were isolated according to standard protocols. Immunofluorescent staining visualized organization of TATS and RyRs. Ca2+ was measured by confocal imaging (fluo-4 as indicator) and using whole-cell patch-clamp (37°C). Spontaneous Ca2+ release events, Ca2+ sparks, as a readout for RyR activity were recorded during a 15 s period following conditioning stimulation at 2 Hz. Sparks were assigned to cell regions categorized as coupled or non-coupled sites according to a previously developed method. Human HF myocytes had more non-coupled sites and these had more spontaneous activity than in non-HF. Hyperactivity of these non-coupled RyRs was reduced by Ca2+/calmodulin-dependent kinase II (CaMKII) inhibition. Myocytes from MI pigs had similar changes compared with SHAM controls as seen in human HF myocytes. As well as by CaMKII inhibition, in MI, the increased activity of non-coupled sites was inhibited by mitochondrial reactive oxygen species (mito-ROS) scavenging. Under adrenergic stimulation, Ca2+ waves were more frequent and originated at non-coupled sites, generating larger Na+/Ca2+ exchange currents in MI than in SHAM. Inhibition of CaMKII or mito-ROS scavenging reduced spontaneous Ca2+ waves, and improved excitation–contraction coupling.ConclusionsIn HF and after MI, RyR microdomain re-organization enhances spontaneous Ca2+ release at non-coupled sites in a manner dependent on CaMKII activation and mito-ROS production. This specific modulation generates a substrate for arrhythmia that appears to be responsive to selective pharmacologic modulation

Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies <i>in vivo</i> triggered activity and repolarization instability

Ventricular arrhythmias are a major complication early after myocardial infarction (MI). The heterogeneous peri‐infarct zone forms a substrate for re‐entry while arrhythmia initiation is often associated with sympathetic activation. We studied the mechanisms triggering these post‐MI arrhythmias in vivo and their relation to regional myocyte remodelling. In pigs with chronic MI (6 weeks), in vivo monophasic action potentials were simultaneously recorded in the peri‐infarct and remote regions during adrenergic stimulation with isoproterenol (ISO). Sham animals served as controls. During infusion of ISO in vivo, the incidence of delayed afterdepolarizations (DADs) and beat‐to‐beat variability of repolarization (BVR) was higher in the peri‐infarct than in the remote region. Myocytes isolated from the peri‐infarct region, in comparison to myocytes from the remote region, had more DADs, associated with spontaneous Ca2+ release, and a higher incidence of spontaneous action potentials when exposed to ISO (9.99 ± 4.2 vs. 0.16 ± 0.05 APs/min, p = 0.004); these were suppressed by CaMKII inhibition. Peri‐infarct myocytes also had reduced repolarization reserve and increased BVR (26 ± 10 ms vs. 9 ± 7 ms, p 2+ handling at baseline and myocyte hypertrophy were present throughout the LV. Expression of some of the related genes was however different between the regions. In conclusion, altered myocyte adrenergic responses in the peri‐infarct, but not in the remote region, provide a source of triggered activity in vivo and of repolarization instability amplifying the substrate for re‐entry. These findings stimulate further exploration of region‐specific therapies targeting myocytes and autonomic modulation

QRS micro-fragmentation as a mortality predictor.

AIMS Fragmented QRS complex with visible notching on standard 12-lead electrocardiogram (ECG) is understood to represent depolarization abnormalities and to signify risk of cardiac events. Depolarization abnormalities with similar prognostic implications likely exist beyond visual recognition but no technology is presently suitable for quantification of such invisible ECG abnormalities. We present such a technology. METHODS AND RESULTS A signal processing method projects all ECG leads of the QRS complex into optimized three perpendicular dimensions, reconstructs the ECG back from this three-dimensional projection, and quantifies the difference (QRS 'micro'-fragmentation, QRS-μf) between the original and reconstructed signals. QRS 'micro'-fragmentation was assessed in three different populations: cardiac patients with automatic implantable cardioverter-defibrillators, cardiac patients with severe abnormalities, and general public. The predictive value of QRS-μf for mortality was investigated both univariably and in multivariable comparisons with other risk factors including visible QRS 'macro'-fragmentation, QRS-Mf. The analysis was made in a total of 7779 subjects of whom 504 have not survived the first 5 years of follow-up. In all three populations, QRS-μf was strongly predictive of survival (P < 0.001 univariably, and P < 0.001 to P = 0.024 in multivariable regression analyses). A similar strong association with outcome was found when dichotomizing QRS-μf prospectively at 3.5%. When QRS-μf was used in multivariable analyses, QRS-Mf and QRS duration lost their predictive value. CONCLUSION In three populations with different clinical characteristics, QRS-μf was a powerful mortality risk factor independent of several previously established risk indices. Electrophysiologic abnormalities that contribute to increased QRS-μf values are likely responsible for the predictive power of visible QRS-Mf. KEY QUESTION KEY FINDING TAKE-HOME MESSAGE QRS-μf is a strong predictor of worsened survival. It can be assessed in standard short-term 12-lead electrocardiograms

Non-Invasive Risk Stratification of Ventricular Arrhythmia and Sudden Cardiac Death

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Implanteerbare defibrillatoren voor de preventie van plotse dood bij niet-ischemisch hartfalen

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Voor wie zijn implanteerbare cardioverter-defibrillatoren voor primaire preventie van plotse hartdood nuttig?

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Clinical Updates in Cardiac Pacing&mdash;The Future Is Bright

The history of cardiac pacing has been defined by many innovation milestones starting in the early 1960s [...

p16(INK4a): A central player in cellular senescence and a promising aging biomarker in elderly cancer patients

The p16INK4a tumor suppressor protein functions as a cyclin-dependent kinase inhibitor, preventing phosphorylation of the retinoblastoma protein and consequently arresting the cell cycle in the G1-phase. Together with p53 and p21CIP1 it has an important function in inducing permanent cell cycle arrest, called senescence, in response to all sorts of cellular damage. Bypass of these senescence pathways has been shown to be associated with increased occurrence of multiple malignancies. In this review we focus on the role of p16INK4a in cellular senescence, its tumor suppression potential and its effect on aging. Also, the consequences of senescence in cancer therapy and its possible side-effects are considered. p16INK4a expression in peripheral blood T-lymphocytes is discussed as a promising candidate biomarker which could reflect biological age and could be used to guide individual optimal treatment in the elderly cancer population. © 2011 Elsevier Inc.status: publishe