Background/Objectives: Patients with chronic kidney disease (CKD) are associated with a significantly elevated cardiovascular risk. The incidence and prevalence of mediated cardiac disorders and major adverse cardiac events (MACEs), such as heart failure, arrhythmias, acute coronary syndrome (ACS) based on coronary artery disease (CAD), stroke, venous thromboembolism, and peripheral artery disease, are significantly higher in CKD patients as compared with the general population. Methods: This narrative review summarizes the current clinical understanding, the pathophysiological mechanisms, and the clinical consequences in the context of cardiovascular risk and disease in CKD. Results: The impact of CKD on mediated cardiovascular disorders and elevated MACE prevalence is complex and multifactorial. The underlying mechanisms involve various traditional cardiovascular risk factors, such as arterial hypertension, smoking, dyslipidemia, and diabetes. Furthermore, CKD-specific molecular and pathophysiological factors, such as chronic inflammation and associated oxidative stress and endothelial cell dysfunction, pro-coagulatory status, uremic toxins and uremic lipids, progressive vascular calcification, and alterations in the regulation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic activation cause an increased cardiovascular risk. Conclusions: Understanding the complex disease mechanisms between CKD and elevated cardiovascular risk might contribute to optimizing individual patients’ risk stratification and result in individualized diagnostic and treatment strategies via appropriate clinical biomarker application and individualized anti-inflammatory approaches.

Introduction: We analyzed data of 27 professional basketball players to prove cardiac remodeling referring echocardiographic parameters, cardiopulmonary exercise testing (CPET), and 12-lead electrocardiogram (ECG) analyses. The aim of our study was to present different characteristics in the athletes, on the one hand signs of a high vagal tone in the 12-lead ECG as criteria of early repolarization (ER), furthermore echocardiographic remodeling parameters and finally the performance in CPET. Therefore, we divided the cohort into a group with signs of ER pattern in the 12-lead ECG and without these criteria and presented the differences in detail.Materials and Methods: This was a single-center, retrospective study performed in 27 professional basketball players (age: 26.5 ± 7.5 years, male: 27, height: 197.2 ± 12 cm, weight: 100 ± 17 kg, BMI: 25.7 ± 3.4 kg/m²). All participants underwent a sports medicine checkup, ECG analysis, transthoracic echocardiographic examination, and a CPET on a cycle ergometer between 2015 and 2019 during their pre-season preparation time. All individuals were healthy people without cardiological advance anamnesis. After assessment, two groups were built based on electrocardiographic criteria of ER pattern and a group without these criteria and compared against each other for parameters of echocardiographic assessment, CPET, and 12-lead ECG analysis. Data were analyzed with Minitab statistic program (Minitab Inc., State College, PA, United States) and Graph Pad Prism 8.2.1 (279; Graph Pad Software, San Diego, CA, United States) using ANOVA testing with post-hoc testing and unpaired t-testing (p ≤ 0.05).Retrospectively additional information was collected referring to the management of training sessions, recovery time, and nutrition by interviewing the athletic training staff in order to understand the principles for individual athlete’s training management and physiological and cardiopulmonary interactions.Results: Comparing professional basketball players with ER pattern to those with no ER pattern, significant differences were found for CPET, echocardiographic, and ECG analysis (p < 0.05). Absolute and relativized peak oxygen uptake (VO_{2 peak}; ER 4120 ± 750 ml/min (39 ± 5.4 ml/kg/min) vs. non-ER 3556 ± 393 ml/min (37.2 ± 5.3 ml/kg/min), p = 0.018) and maximum workload during CPET (ER 310 ± 51.5 Watt (2.94 ± 0.35 W/kg) vs. non-ER 271 ± 32 Watt (2.85 ± 0.49 W/kg), p = 0.026) was higher in athletes with an ER pattern. Furthermore, ER pattern athletes showed a higher enddiastolic left ventricular diameter (LVedd; ER 58.3 ± 7.9 mm vs. non-ER 53.6 ± 3.6 mm, p = 0.048) and a significantly enlarged left atrial (LA) endsystolic diameter (ER 23.33 ± 2.71 mm vs. non-ER 20.47 ± 2.29 mm, p = 0.006) as well as a significantly enlarged right atrial (RA) endsystolic diameter (ER 23.42 ± 2.15 mm vs. non-ER 20.93 ± 3.28 mm, p = 0.033). Significant differences between the two compared groups could be revealed for left ventricular mass Index (LVMI gr/m²; LVMI ER 113 gr/m² ± 17.5 vs. LVMI non-ER 91.3 gr/m² ± 15.1, p = 0.002), but no significant differences for the relative wall thickness were found (RWT; RWT ER 0.49 ± 0.11 vs. RWT non-ER 0.38 ± 0.06, p = 0.614).Conclusion: Professional basketball players with criteria of ER pattern showed different results in CPET and cardiac remodeling as athletes with no ER pattern. These findings should encourage the athletic training staff to emphasize the quality of an individual training schedule for each athlete based on the cardiopulmonary pre-season sport medicine checkup. Nevertheless, echocardiographic findings, ER pattern, and performance in CPET have to be interpreted referring the sport-specific and athlete’s ethnical background.

Physical activity and exercise have many beneficial effects on general and type 1 diabetes (T1D) specific health and are recommended for individuals with T1D. Despite these health benefits, many people with T1D still avoid exercise since glycemic management during physical activity poses substantial glycemic and psychological challenges – which hold particularly true for unannounced exercise when using an AID system. Automated insulin delivery (AID) systems have demonstrated their efficacy in improving overall glycemia and in managing announced exercise in numerous studies. They are proven to increase time in range (70-180 mg/dL) and can especially counteract nocturnal hypoglycemia, even when evening exercise was performed. AID-systems consist of a pump administering insulin as well as a CGM sensor (plus transmitter), both communicating with a control algorithm integrated into a device (insulin pump, mobile phone/smart watch). Nevertheless, without manual pre-exercise adaptions, these systems still face a significant challenge around physical activity. Automatically adapting to the rapidly changing insulin requirements during unannounced exercise and physical activity is still the Achilles' heel of current AID systems. There is an urgent need for improving current AID-systems to safely and automatically maintain glucose management without causing derailments – so that going forward, exercise announcements will not be necessary in the future. Therefore, this narrative literature review aimed to discuss technological strategies to how current AID-systems can be improved in the future and become more proficient in overcoming the hurdle of unannounced exercise. For this purpose, the current state-of-the-art therapy recommendations for AID and exercise as well as novel research approaches are presented along with potential future solutions - in order to rectify their deficiencies in the endeavor to achieve fully automated AID-systems even around unannounced exercise.

In 1992, Brugada syndrome (BS) was first described; an often unrecognized cardiac conduction disorder mainly associated with unexplained sudden cardiac arrest and consecutive syncope. Nevertheless, the pathomechanism of BS and sudden cardiac death remains mainly explained. Mutations in the cardiac sodium channels, which cause a reduction or functional loss of these channels, are associated with characteristic electrocardiographic (ECG) abnormalities and malignant arrhythmia. The majority of affected people are previously healthy and unaware of their genetic predisposition for BS and might experience ventricular tachyarrhythmias and cardiac arrest potentially triggered by several factors (e.g., alcohol, sodium channel blockers, psychotropic drugs, and fever). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was firstly identified in Wuhan in early December 2019 and rapidly spread worldwide as coronavirus disease (COVID-19). COVID-19 is typically characterized by a severe inflammatory response, activation of the immune system, and high febrile illness. Due to this condition, symptomatic COVID-19 infection or vaccination might serve as inciting factor for unmasking the Brugada pattern and represents a risk factor for developing proarrhythmic complications. The aim of this narrative review was to detail the association between virus-related issues such as fever, electrolyte disturbance, and inflammatory stress of COVID-19 infection with transient Brugada-like symptoms and ECG-pattern and its susceptibility to proarrhythmogenic episodes.

Nine Ski mountaineering (Ski-Mo), ten Nordic-Cross Country (NCC) and twelve world elite biathlon (Bia) athletes were evaluated for cardiopulmonary exercise test (CPET) performance as the primary aim of our descriptive preliminary report. A multicenter retrospective analysis of CPET data was performed in 31 elite winter sports athletes, which were obtained in 2021 during the annual medical examination. The matched data of the elite winter sports athletes (14 women, 17 male athletes, age: 18–32 years) were compared for different CPET parameters, and athlete’s physique data and sport-specific training schedules. All athletes showed, as estimated in elite winter sport athletes, excellent performance data in the CPET analyses. Significant differences were revealed for VE _VT2 (respiratory minute volume at the second ventilatory threshold (VT2)), highest maximum respiratory minute volume (VE_maximum), the indexed ventilatory oxygen uptake (VO₂) at VT2 (VO₂/kg _VT2), the oxygen pulse at VT2, and the maximum oxygen pulse level between the three professional winter sports disciplines. This report provides new evidence that in different world elite winter sport professionals, significant differences in CPET parameters can be demonstrated, against the background of athlete’s physique as well as training control and frequency.

Autoimmune pancreatic β-cell loss and destruction play a key role in the pathogenesis and development of type 1 diabetes, with a prospective increased risk for developing micro- and macrovascular complications. In this regard, orally administrated verapamil, a calcium channel antagonist, usually intended for use as an anti-arrhythmic drug, has previously shown potential beneficial effects on β-cell preservation in new-onset type 1 diabetes. Furthermore, observational data suggest a reduced risk of type 2 diabetes development. The underlying pathophysiological mechanisms are not well investigated and remain widely inconclusive. The aim of this narrative review was to detail the role of verapamil in promoting endogenous β-cell function, potentially eligible for early treatment in type 1 diabetes, and to summarize existing evidence on its effect on glycemia in individuals with type 2 diabetes.