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Aim: To investigate the impact of hypoglycaemia, hyperglycaemia and glycaemic variability on arrhythmia susceptibility in people with type 1 diabetes. Materials and Methods: Thirty adults with type 1 diabetes were included in a 12‐month observational exploratory study. Daytime and night‐time incident rate ratios (IRRs) of arrhythmias were determined for hypoglycaemia (interstitial glucose [IG] <3.9 mmol/L), hyperglycaemia (IG >10.0 mmol/L) and glycaemic variability (standard deviation and coefficient of variation). Results: Hypoglycaemia was not associated with an increased risk of arrhythmias compared with euglycaemia and hyperglycaemia combined (IG ≥ 3.9 mmol/L). However, during daytime, a trend of increased risk of arrhythmias was observed when comparing time spent in hypoglycaemia with euglycaemia (IRR 1.08 [95% CI: 0.99‐1.18] per 5 minutes). Furthermore, during daytime, both the occurrence and time spent in hyperglycaemia were associated with an increased risk of arrhythmias compared with euglycaemia (IRR 2.03 [95% CI: 1.21‐3.40] and IRR 1.07 [95% CI: 1.02‐1.13] per 5 minutes, respectively). Night‐time hypoglycaemia and hyperglycaemia were not associated with the risk of arrhythmias. Increased glycaemic variability was not associated with an increased risk of arrhythmias during daytime, whereas a reduced risk was observed during night‐time. Conclusions: Acute hypoglycaemia and hyperglycaemia during daytime may increase the risk of arrhythmias in individuals with type 1 diabetes. However, no such associations were found during night‐time, indicating diurnal differences in arrhythmia susceptibility. [ABSTRACT FROM AUTHOR]

Aims: To investigate changes in cardiac repolarisation during exercise‐related hypoglycaemia compared to hypoglycaemia induced at rest in people with type 1 diabetes. Material and methods: In a randomised crossover study, 15 men with type 1 diabetes underwent two separate hyperinsulinaemic euglycaemic‐hypoglycaemic clamp experiments during Holter‐ECG monitoring. One experiment included a bout of moderate‐intensity cycling exercise (60 min) along with declining plasma glucose (PG; Clamp‐exercise). In the other experiment, hypoglycaemia was induced with the participants at rest (Clamp‐rest). We studied QTc interval, T‐peak to T‐end (Tpe) interval and hormonal responses during three steady‐state phases: (i) baseline (PG 4.0–8.0 mmol/L); (ii) hypoglycaemic phase (PG <3.0 mmol/L); and (iii) recovery phase (PG 4.0–8.0 mmol/L). Results: Both QTc interval and Tpe interval increased significantly from baseline during the hypoglycaemic phase but with no significant difference between test days. These changes were accompanied by an increase in plasma adrenaline and a decrease in plasma potassium on both days. During the recovery phase, ΔQTc interval was longer during Clamp‐rest compared to Clamp‐exercise, whereas ΔTpe interval remained similar on the two test days. Conclusions: We found that both exercise‐related hypoglycaemia and hypoglycaemia induced at rest can cause QTc‐interval prolongation and Tpe‐interval prolongation in people with type 1 diabetes. Thus, both scenarios may increase susceptibility to ventricular arrhythmias. [ABSTRACT FROM AUTHOR]

Aim: To investigate changes in cardiac repolarization abnormalities (heart rate‐corrected QT [QTc] [primary endpoint], T‐wave abnormalities) and heart‐rate variability measures in people with type 1 diabetes during insulin‐induced hypoglycaemia followed by recovery hyperglycaemia versus euglycaemia. Methods: In a randomized crossover study, 24 individuals with type 1 diabetes underwent two experimental clamps with three steady‐state phases during electrocardiographic monitoring: (1) a 45‐minute euglycaemic phase (5‐8 mmol/L), (2) a 60‐minute insulin‐induced hypoglycaemic phase (2.5 mmol/L), and (3) 60‐minute recovery in either hyperglycaemia (20 mmol/L) or euglycaemia (5‐8 mmol/L). Results: All measured markers of arrhythmic risk indicated increased risk during hypoglycaemia. These findings were accompanied by a decrease in vagal tone during both hyperglycaemia and euglycaemia clamps. Compared with baseline, the QTc interval increased during hypoglycaemia, and 63% of the participants exhibited a peak QTc of more than 500 ms. The prolonged QTc interval was sustained during both recovery phases with no difference between recovery hyperglycaemia versus euglycaemia. During recovery, no change from baseline was observed in heart‐rate variability measures. Conclusions: In people with type 1 diabetes, insulin‐induced hypoglycaemia prolongs cardiac repolarization, which is sustained during a 60‐minute recovery period independently of recovery to hyperglycaemia or euglycaemia. Thus, vulnerability to serious cardiac arrhythmias and sudden cardiac death may extend beyond a hypoglycaemic event, regardless of hyperglycaemic or euglycaemic recovery. [ABSTRACT FROM AUTHOR]

Aim: To investigate echocardiographic changes during acute hypoglycaemia followed by recovery to hyperglycaemia or euglycaemia in patients with type 1 diabetes. Materials and Methods: In a randomized crossover study, 24 patients with type 1 diabetes took part in two experimental study days, consisting of a hyperinsulinaemic‐euglycaemic phase (5.0‐8.0 mmol/L) for 45 minutes followed by a hyperinsulinemic‐hypoglycaemic phase (2.5 mmol/L) for 60 minutes, and a recovery phase in either hyperglycaemia (20 mmol/L) or euglycaemia (5.0‐8.0 mmol/L) for 60 minutes. Cardiac function was evaluated with echocardiography during each phase. Results: Acute hypoglycaemia increased all markers of left ventricular (LV) systolic function, including LV ejection fraction (LVEF), global longitudinal strain (GLS), GLS rate and peak systolic velocity of mitral annular longitudinal movement (s'; P < 0.001 for all). During the recovery phases, all markers of LV systolic function were increased during hyperglycaemia (P < 0.01 for all), and LVEF and GLS remained increased during euglycaemia (P = 0.0116 and P = 0.0092, respectively). The increment in LVEF during the recovery phase was greater during hyperglycaemia than euglycaemia (P = 0.0046). Conclusions: Hypoglycaemia, recent hypoglycaemia, and overcorrection of hypoglycaemia to rebound hyperglycaemia increased LV systolic function in type 1 diabetes and may imply consideration of plasma glucose when evaluating LV function in patients with type 1 diabetes. An increase in LV systolic function may cause increased strain on the heart and partly explain the link between hypoglycaemia, high glycaemic variability and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background and objective: Tuberculosis disease (TB) and tuberculosis infection (TBI) have been associated with increased risk of cardiovascular disease which may be connected to infection-related haemostatic changes. It is unknown if treatment of Mycobacterium tuberculosis influences haemostasis. Here, we assessed if TB or TBI treatment affects thrombelastography (TEG)-assessed haemostasis. Methods: Individuals with TB or TBI were included from a TB outpatient clinic in Copenhagen, Denmark. Patients treated with antithrombotic medication or systemic immunosuppressants were excluded. TEG analysis was performed before and after TB/TBI treatment using the TEG®6s analyser to provide data on the reaction time of clot initiation (R) (min), the speed of clot formation (K) (min) and clot build-up (Angle) (°), maximum clot strength (MA) (mm), and clot breakdown/fibrinolysis (LY30) (%). Differences in TEG were assessed using paired t tests. Results: We included eleven individuals with TB with median [interquartile range] [IQR] age 52 (Liu et al. in Medicine (United States) 95, 2016) years and mean (standard deviation) (SD) body mass index (BMI) 24.7 (6.3) kg/m2 as well as 15 individuals with TBI with median [IQR] age 49 (Wells et al. in Am J Respir Crit Care Med 204:583, 2021) years and BMI 26.0 (3.2) kg/m2. Treatment reduced MA for both TB (64.0 (6.3) vs. 57.9 (5.2) mm, p = 0.016) and TBI (61.3 (4.1) vs. 58.6 (5.0) mm, p = 0.023) whereas R, K, Angle and LY30 were unaffected. Conclusion: TEG analysis showed that treatments of TB and TBI were associated with reduced MA which may indicate the existence of cardiovascular benefits from therapy. Trial registration: Registered at ClinicalTrials.gov 05 April 2021 with registration number NCT04830462. [ABSTRACT FROM AUTHOR]

Insulin treatment in patients with type 1 diabetes (T1D) causes rapid and large fluctuations in plasma glucose (PG) concentrations, and patients with T1D and poor glycemic control have an increased risk of cardiovascular disease including heart failure. We evaluated echocardiographic changes in cardiac function during experimental hypoglycemia and rebound hyperglycemia in patients with T1D. Patients with T1D (age 52.8±11.4 years, HbA1c 7.5±0.8% [57.6±8.9 mmol/mol], BMI 25.7±3.1 kg/m2) underwent two clamp days in random order. Both clamp days included three steady-state phases: 1) a 45-min hyperinsulinemic euglycemic phase (PG=6 mmol/L); 2) a 60-min hyperinsulinemic hypoglycemic phase (PG=2.5 mmol/L), and 3) a 60-min recovery phase in either hyperglycemia or euglycaemia (Clamp A: PG: 20 mmol/L; Clamp B: PG: 6 mmol/L). Cardiac function was evaluated with echocardiography at each phase by a blinded observer. Acute hypoglycemia increased left ventricular ejection fraction (LVEF) (absolute change, Clamp A: 6.5% [5.0;8.1], P=0.0001; Clamp B: 6.2% [4.6;7.9], P<0.0001) and global longitudinal strain (GLS) (absolute change, Clamp A: -3.1% (-4.5;-1.6), P<0.001; Clamp B: -3.5% (-4.6;-2.3), P<0.0001) from baseline. In Clamp A during hyperglycemia, LVEF and GLS were increased compared to baseline euglycemia (5.0% [3.2;6.8] (P<0.0001) and 2.1% [-3.7;-0.6] (P<0.01), respectively). An increase in LVEF was also observed in the recovery phase in Clamp B despite normalization of PG for 60 min (2.1% [0.5;3.8], P<0.05). In the recovery phase, LVEF was greater during hyperglycemia in Clamp A (2.9% [1.0;4.7], P<0.01) compared to euglycaemia in Clamp B. In conclusion, our findings suggest that acute fluctuations in PG affect echocardiographic-derived measures of systolic function in patients with T1D. Disclosure: C. R. Andreasen: None. F. K. Knop: Advisory Panel; Self; MSD Corporation, Novo Nordisk A/S, Sanofi, Consultant; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Novo Nordisk A/S, Pharmacosmos, Zealand Pharma A/S, Research Support; Self; Novo Nordisk A/S, Zealand Pharma A/S, Speaker's Bureau; Self; AstraZeneca, Bayer AG, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, MSD Corporation, Novo Nordisk A/S. T. Vilsbøll: Consultant; Self; Amgen Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Bristol-Myers Squibb Company, Gilead Sciences, Inc., Lilly Diabetes, Merck Sharp & Dohme Corp., Mundipharma International, Novo Nordisk, Sanofi, Sun Pharmaceutical Industries Ltd. A. Andersen: None. P. G. Hagelqvist: None. K. U. Abelin: None. J. V. Lauritsen: None. P. G. Jørgensen: Speaker's Bureau; Self; AstraZeneca. S. Engberg: None. J. J. Holst: Consultant; Self; Novo Nordisk, Other Relationship; Self; Antag Therapeutics, Bainan Biotech, MSD Corporation, Novo Nordisk, Other Relationship; Spouse/Partner; Antag Therapeutics, Bainan Biotech, Synklino ApS. U. Pedersen-bjergaard: Advisory Panel; Self; Novo Nordisk A/S, Sanofi-Aventis, Consultant; Self; Abbott, Speaker's Bureau; Self; Novo Nordisk A/S. Funding: Novo Nordisk Foundation (NNF17SA0031406) [ABSTRACT FROM AUTHOR]