1.
Impact of empagliflozin on right ventricular parameters and function among patients with type 2 diabetes.
Sarak, B, Verma, S, David Mazer, C, Teoh, H, Quan, A, Gilbert, RE, Goodman, SG, Bami, K, Coelho-Filho, OR, Ahooja, V, et al
Cardiovascular diabetology. 2021;(1):200
Abstract
BACKGROUND Sodium-glucose cotransporter 2 (SGLT2) inhibition reduces cardiovascular events in type 2 diabetes (T2DM) and is associated with a reduction in left ventricular (LV) mass index. However, the impact on right ventricular (RV) remodeling is unknown. Accordingly, the objective of this study was to assess the impact of SGLT2 inhibition on RV parameters and function in T2DM and coronary artery disease (CAD). METHODS In EMPA-HEART CardioLink-6, 97 patients with T2DM and CAD were randomly assigned to empagliflozin 10 mg (n = 49) once daily or placebo (n = 48). Cardiac magnetic resonance imaging was performed at baseline and after 6 months. RV mass index (RVMi), RV end-diastolic and end-systolic volume index (RVEDVi, RVESVi) and RV ejection fraction (RVEF) were assessed in blinded fashion. RESULTS At baseline, mean RVMi (± SD) (11.8 ± 2.4 g/m2), RVEF (53.5 ± 4.8%), RVEDVi (64.3 ± 13.2 mL/m2) and RVESVi (29.9 ± 6.9 mL/m2) were within normal limits and were similar between the empagliflozin and placebo groups. Over 6 months, there were no significant differences in RVMi (- 0.11 g/m2, [95% CI - 0.81 to 0.60], p = 0.76), RVEF (0.54%, [95% CI - 1.4 to 2.4], p = 0.58), RVEDVi (- 1.2 mL/m2, [95% CI - 4.1 to 1.7], p = 0.41) and RVESVi (- 0.81 mL/m2, [95% CI - 2.5 to 0.90], p = 0.35) in the empaglifozin group as compared with the placebo group. In both groups, there was no significant correlation between RVMi and LVMi changes from baseline to 6 months. CONCLUSIONS In this post-hoc analysis, SGLT2 inhibition with empagliflozin had no impact on RVMi and RV volumes in patients with T2DM and CAD. The potentially differential effect of empagliflozin on the LV and RV warrants further investigation. CLINICAL TRIAL REGISTRATION URL: https://www.clinicaltrials.gov/ct2/show/NCT02998970?cond=NCT02998970&draw=2&rank=1 . Unique identifier: NCT02998970.
2.
Effects of quinidine on the action potential duration restitution property in the right ventricular outflow tract in patients with brugada syndrome.
Ashino, S, Watanabe, I, Kofune, M, Nagashima, K, Ohkubo, K, Okumura, Y, Mano, H, Nakai, T, Kunimoto, S, Kasamaki, Y, et al
Circulation journal : official journal of the Japanese Circulation Society. 2011;(9):2080-6
Abstract
BACKGROUND On a cellular level, Brugada syndrome has been attributed to a deep phase 1 notch and subsequent shallow and prolonged repolarization in the right ventricular outflow tract (RVOT). A sodium channel mutation that leads to early inactivation of the late sodium current has been identified in some patients. Thus, drugs that inhibit the transient outward current (I(to)) responsible for the phase 1 notch and/or enhance the late sodium current might suppress arrhythmic events in patients with Brugada syndrome. The effects of quinidine gluconate, a potent inhibitor of I(to), on RVOT action potential duration (APD) restitution kinetics in patients with Brugada syndrome were evaluated. METHODS AND RESULTS Programmed ventricular stimulation was performed in 9 Brugada syndrome patients by delivering up to 3 extrastimuli from the right ventricular apex and RVOT. RVOT monophasic action potentials (MAPs) were recorded before and after intravenous administration of quinidine (n=6) or ibutilide (n=3). All patients had inducible ventricular fibrillation (VF) before drug administration. Both quinidine and ibutilide increased steady-state and minimum RVOT MAP duration during programmed stimulation. Quinidine decreased the maximum slope of the RVOT APD restitution curve and VF could not be induced after administration of quinidine in 5 of the 6 patients. CONCLUSIONS Quinidine appears to suppress the induction of VF by increasing RVOT MAP duration and decreasing the maximum slope of the restitution curve.
3.
Ischemic preconditioning protects right ventricular function in coronary artery bypass grafting patients experiencing angina within 48-72 hours.
Wu, ZK, Pehkonen, E, Laurikka, J, Kaukinen, L, Honkonen, EL, Kaukinen, S, Tarkka, MR
The Journal of cardiovascular surgery. 2002;(3):319-26
Abstract
BACKGROUND To test whether ischemic preconditioning (IP) is able to protect the myocardium in recently unstable CABG patients. EXPERIMENTAL DESIGN prospective, randomised, controlled clinical study. SETTING University Hospital. PATIENTS Forty CABG patients with recent unstable angina were randomised into an IP group (n=20) and a control group (n=20). Subgroup was divided based on the time of the most recent ischemia onset before the operation. INTERVENTION The IP group was preconditioned with 2 cycles of 2-min ischemia followed by 3-min reperfusion before cross clamping. MEASURES Hemodynamic data were monitored till the 1st POD. Biochemical markers were measured till the 2nd POD. RESULTS There were no differences in cardiac index (Cl) and right ventricular ejection fraction (RVEF) in patients experiencing angina within 48 hours prior to operation. The percentage changes in CI and RVEF at 1 hour after declamping were significantly better in the IP group in patients experienced angina within 48-72 hours (106% vs 88% of baseline, p=0.027 and 103% vs 81% of baseline, p=0.023). No difference in postoperative cardiac troponin I (CTnI) and CK-MB was found between the IP and controls in either subgroup. CONCLUSIONS IP has a beneficial effect on global and right ventricular hemodynamic functional recovery in unstable CABG patients experiencing angina within 48-72 hours prior to the operation. However, IP has no additional protective effects in unstable CABG patients who experience angina within 48 hours.
4.
Unwashed shed blood infusion causes deterioration in right ventricular function after coronary artery surgery.
Kitano, T, Hattori, S, Miyakawa, H, Yoshitake, S, Iwasaka, H, Noguchi, T
Anaesthesia and intensive care. 2000;(6):642-5
Abstract
We investigated right ventricular function after infusion of unwashed shed blood collected from mediastinal and chest tube drainage. Changes in thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, which are stable metabolites of thromboxane A2 (TXA2) and prostacyclin respectively, were also investigated. The amount of infused shed blood was 484 +/- 76 ml (mean +/- SD). Right ventricular ejection fraction decreased rapidly after the infusion and did not return to its original level until 120 minutes later (P < 0.05). Mean pulmonary artery pressure rose after infusion of the shed blood (P < 0.05). The TXB2 level in the unwashed shed blood was about 20,000 times higher than the preoperative plasma level. The plasma TXB2 level at 30 minutes after the infusion was significantly elevated (P < 0.05), and at 120 minutes it had returned to the original level. Unwashed shed blood may contain vasoactive substances that induce the release of TXA2 and increase right ventricular afterload.