Georgios A. Christou

Background/Objectives: Athletes are characterized by distinct haemodynamic adaptations of the cardiovascular system, including descending aorta haemodynamics, that could influence the diagnosis of coarctation of the aorta. This study aims to evaluate the normal range for the maximum velocity of blood flow in the descending aorta (Vmax-AoDesc) and the predictors of Vmax-AoDesc in apparently healthy athletes without coarctation of the aorta. Methods: We examined 559 asymptomatic healthy athletes with an age of at least 12 years and a tricuspid aortic valve (420 males, age: 29 ± 14 years). We performed evaluations of athletic history, measurements of brachial systolic and diastolic blood pressure, cardiac and aorta ultrasonography and cardiopulmonary exercise testing. Forty athletes were reassessed after a median follow-up of 3.0 (IQR: 2.1) years. Results: The median Vmax-AoDesc was 1.29 (IQR: 0.28) m/s, with a maximum of 2.00 m/s. The Vmax-AoDesc could be independently predicted by age (β = −0.392, p < 0.001), ratio of systole/diastole (β = 0.095, p = 0.023), brachial systolic blood pressure (β = 0.251, p < 0.001), left ventricular stroke volume (β = 0.256, p < 0.001), ascending aorta diameter (β = −0.230, p < 0.001), aortic arch diameter (β = −0.111, p = 0.044) and descending aorta diameter (β = −0.103, p = 0.017). Age accounted for the greatest variability of Vmax-AoDesc (5.8%). Vmax-AoDesc correlated positively with h/week of endurance exercise training (rho = 0.182, p < 0.001) and oxygen uptake at second ventilatory threshold (rho = 0.299, p = 0.001). Vmax-AoDesc did not change significantly during follow-up (p = 0.438). The median change in Vmax-AoDesc was −0.05 (IQR: 0.18) m/s. However, when Vmax-AoDesc was adjusted for all the above-mentioned independent predictors of Vmax-AoDesc apart from age and systolic blood pressure, there was a reduction in adjusted Vmax-AoDesc during follow-up (p = 0.007), indicating a reduction in Vmax-AoDesc with aging. Conclusions: The upper limit of the normal range for Vmax-AoDesc was 2.00 m/s in athletes without coarctation of the aorta. Young age was the most important predictor for the measurement of high Vmax-AoDesc. There was an upregulation of Vmax-AoDesc in athletes with a greater volume of endurance exercise training.

The detection of frequent premature ventricular contractions (PVCs) in an athlete represents one of the most important red flags during pre-participation screening. We report the case of a 6-year-old asymptomatic male athlete practicing basketball and sailing, who was examined for pre-participation screening. His resting electrocardiogram showed very frequent, isolated, monomorphic PVCs. The PVCs exhibited a left bundle branch block morphology with an inferior axis and R/S wave precordial transition in lead V3. The most likely origin of PVCs was considered the left ventricular outflow tract. Resting transthoracic echocardiography revealed reduced left ventricular systolic function, with an ejection fraction of 43%, indicating the possible existence of PVC-induced cardiomyopathy. We detected 43,149 isolated monomorphic PVCs (PVC burden: 40%) on 24-h ambulatory electrocardiographic monitoring. Initiation of treatment with atenolol 12.5 mg twice a day led to inadequate reduction of PVCs, with 29,452 isolated monomorphic PVCs (PVC burden: 29%) still observed on 24-h ambulatory electrocardiographic monitoring. After adding flecainide 25 mg twice daily to atenolol treatment, 24-h ambulatory electrocardiographic monitoring revealed complete resolution of ventricular arrhythmias, with no PVCs detected. Left ventricular systolic function recovered to normal. At 12 years of age, the athlete remained on combination therapy with atenolol and flecainide, continued participating in sports, and remained completely asymptomatic with normal cardiac examinations. The optimization of drug treatment was favored over catheter ablation since the athlete was a child and the probable origin of PVCs was the left ventricular outflow tract. This case report highlights that flecainide at a relatively low dose as an add-on therapy to a beta-blocker was highly effective and safe for treating high-burden PVCs originating from the ventricular outflow tract in a juvenile athlete.

Coronary heart disease (CHD) is the leading cause of morbidity and mortality worldwide despite significant improvements in diagnostic modalities. Emerging evidence suggests that erythrocytes, or red blood cells (RBCs), are one of the most important contributors to the events implicated in atherosclerosis, although the molecular mechanisms behind it are under investigation. We used NMR-based lipidomic technology to investigate the RBC lipidome in patients with CHD compared to those with normal coronary arteries (NCAs), all angiographically documented, and its correlation with coronary artery stenosis. Targeted and untargeted lipidomic analysis revealed that CHD patients presented significant lipid alterations in the RBC membrane, characterized by higher cholesterol, sphingolipids, saturated and monounsaturated fatty acids, lower phospholipids (glycerophospholipids and ether glycerolipids), and unsaturated and polyunsaturated fatty acids. These aberrations gradually distinguish the three subgroups of patients with mild, moderate, and severe coronary stenosis, potentially indicating their non-negligible involvement in the onset and progression of atherosclerosis. The comprehensive analysis of RBC-membrane-derived lipids with omics approaches could unravel specific lipid abnormalities taking place at the silent subclinical stage of atherosclerosis and could have the potential to identify patients with subtle, but still proatherogenic, abnormalities that may confer a higher risk for the development of CHD.

Background/Objectives: Obesity and overweight have become increasingly prevalent in different populations of people with type 1 diabetes (PwT1D). This study aimed to assess the effect of body weight on glycaemic indices in PwT1D. Methods: Adult PwT1D using continuous glucose monitoring (CGM) and followed up at a regional academic diabetes centre were included. Body weight, body mass index (BMI), waist circumference, glycated haemoglobin (HbA1c), and standard CGM glycaemic indices were recorded. Glycaemic indices were compared according to BMI, and correlation and linear regression analysis were performed to estimate the association between measures of adiposity and glycaemic indices. Results: A total of 73 PwT1D were included (48% normal weight, 33% overweight, and 19% obese). HbA1c was 7.2% (5.6–10), glucose management indicator (GMI) 6.9% (5.7–8.9), coefficient of variation (CV) for glucose 39.5% ± 6.4, mean glucose 148 (101–235) mg/dL, TIR (time in range, glucose 70–180 mg/dL) 66% (25–94), TBR₇₀ (time below range, 54–69 mg/dL) 4% (0–16), TBR₅₄ (250 mg/dL) 6% (0–40). Glycaemic indices and achievement (%) of optimal glycaemic targets were similar between normal weight, overweight, and obese patients. BMI was associated negatively with GMI, mean glucose, TAR₁₈₀, and TAR₂₅₀ and positively with TIR; waist circumference was negatively associated with TAR₂₅₀. Conclusions: CGM-derived glycaemic indices were similar in overweight/obese and normal weight PwT1D. Body weight and BMI were positively associated with better glycaemic control. PwT1D should receive appropriate ongoing support to achieve optimal glycaemic targets whilst maintaining a healthy body weight.

Background/Objectives: QRS fragmentation has not been linked with increased mortality in individuals without known cardiac disease. We aimed to investigate the physiological determinants of QRS fragmentation in individuals without cardiac disease. Methods: Study participants were 163 (54 athletes, 109 nonathletes) asymptomatic individuals with QRS fragmentation but without cardiac disease. QRS fragmentation was assessed in the supine position after deep inspiration or standing up and during exercise. The changes in QRS fragmentation were evaluated over a median follow-up period of 2.3 (0.8–4.9) years. Results: The most common lead with QRS fragmentation was III (63.0% in athletes, 61.5% in nonathletes), immediately followed by V1 (50.0%) and aVF (42.6%) in athletes and aVF (55.0%) in nonathletes. QRS fragmentation in V1 was more frequent in athletes compared to nonathletes (p < 0.001). Among athletes, the presence of QRS fragmentation in V1 could be independently predicted by increased RVOTproxi (right ventricular outflow tract proximal diameter indexed to body surface area) (p < 0.001). Among individuals with QRS fragmentation in V1, deep inspiration resulted in disappearance of QRS fragmentation more frequently in nonathletes compared to athletes (100% vs. 20%, p = 0.003). Deep inspiration resulted in disappearance of QRS fragmentation in aVF (p < 0.001). The presence of QRS fragmentation in II or aVF was associated with increased body mass index (BMI) (p = 0.003). Among athletes without QRS fragmentation in V1 at baseline, the appearance of QRS fragmentation in V1 at the end of follow-up was associated with greater training age (p = 0.034). Among individuals with QRS fragmentation in aVF at baseline, the disappearance of QRS fragmentation in aVF at the end of follow-up was associated with greater reduction in BMI (p = 0.008). Conclusions: The characteristic feature of QRS fragmentation in athletes was the presence of QRS fragmentation in V1, which was associated with RVOTproxi. The persistence of QRS fragmentation in V1 after deep inspiration could serve as a specific marker of exercise-training-related cardiac adaptation. The presence of QRS fragmentation in the leads of the frontal plane was influenced by BMI and respiration phase.

Hypoglycemia is common in patients with type 1 and type 2 diabetes (T1D, T2D), treated with insulin or sulfonylureas, and has multiple short- and long-term clinical implications. Whether acute or recurrent, hypoglycemia significantly affects the cardiovascular system with the potential to cause cardiovascular dysfunction. Several pathophysiological mechanisms have been proposed linking hypoglycemia to increased cardiovascular risk, including hemodynamic changes, myocardial ischemia, abnormal cardiac repolarization, cardiac arrhythmias, prothrombotic and proinflammatory effects, and induction of oxidative stress. Hypoglycemia-induced changes can promote the development of endothelial dysfunction, which is an early marker of atherosclerosis. Although data from clinical trials and real-world studies suggest an association between hypoglycemia and cardiovascular events in patients with diabetes, it remains uncertain whether this association is causal. New therapeutic agents for patients with T2D do not cause hypoglycemia and have cardioprotective benefits, whereas increasing the use of new technologies, such as continuous glucose monitoring devices and insulin pumps, has the potential to reduce hypoglycemia and its adverse cardiovascular outcomes in patients with T1D.

In recent years, our knowledge regarding the physiological role of vitamin K has expanded beyond regulation of coagulation to include many other aspects of human health. In the present review, we aimed to evaluate the existing evidence for beneficial effects of vitamin K on type 2 diabetes and components of the metabolic syndrome as risk factors for cardiovascular disease. Increased dietary intake of vitamin K has been linked to lower incidence of type 2 diabetes mellitus (T2DM), possibly through its enhancement of insulin production and sensitivity. Additionally, higher plasma levels of vitamin K1 have been associated with lower T2DM risk and decreased insulin resistance, and supplementation trials also suggest a positive influence of vitamin K on glucose regulation. Vitamin K might also beneficially affect serum lipids and lipid metabolism. However, the available data remain controversial. Additionally, different studies use different approaches to assess vitamin K status owing to the absence of a generally accepted marker, which further complicates data evaluation. In conclusion, vitamin K possibly improves glucose and lipid metabolism and could be an emerging target in the context of prevention and control of T2DM, insulin resistance, and dyslipidemia.

The structural adaptations of the “athlete's heart” include left atrial (LA) enlargement. A literature search was performed based on PubMed listings up to November 2, 2019 using “athletes AND left atrium,” “athletes AND LA,” “sports AND left atrium,” “sports AND LA,” “exercise AND left atrium,” and “exercise AND LA” as the search terms. Eligible studies included those reporting the influence of demographic, anthropometric and athletic characteristics on LA size in athletes. A total of 58 studies were included in this review article. Although LA volume has been reported to be greater in males compared to females when indexed for body surface area (BSA), there was no difference between sexes. The positive association between LA size and age in athletes may reflect the increase in body size with maturation in nonadult athletes and the training age of endurance athletic activity in adult athletes. Caucasian and black athletes have been demonstrated to exhibit similar LA enlargement. The positive association of LA size with lean body mass (LBM) possibly accounts for the relationship of LA size with BSA. LA enlargement has been reported only in endurance‐trained, but not in strength‐trained athletes. LA size appears to increase with an increase in both the volume and intensity of endurance training. LA size correlates independently with the training age of endurance athletes. The athlete's characteristics that independently determine LA size include LBM, endurance training, and training age.

Introduction: Myopathy is possibly the most clinically relevant statin-induced side effect. Case Presentation: We report a case of a 63-year-old healthy male with mixed dyslipidemia. He developed bilateral myalgia of the forearms with fluvastatin 40 mg/day, pravastatin 20 mg/day, and combination of atorvastatin 10 mg and ezetimibe 10 mg/day. The only hypolipidemic treatment that was tolerable was the combination of pitavastatin 1 mg and ezetimibe 10 mg/day. Discussion: Pitavastatin demonstrated less potential for the development of myalgia compared to the so far considered most tolerable statins (i.e., fluvastatin and pravastatin). All the tested statins were used at the lowest approved dose for clinical use. Conclusion: The combination of pitavastatin 1 mg and ezetimibe appears to be a promising treatment choice for individuals who are intolerant to statin therapy due to muscle complaints.