Iyengar Yoga Increases Cardiac Parasympathetic Nervous Modulation Among Healthy Yoga Practitioners

Relaxation techniques are established in managing of cardiac patients during rehabilitation aiming to reduce future adverse cardiac events. It has been hypothesized that relaxation-training programs may significantly improve cardiac autonomic nervous tone. However, this has not been proven for all available relaxation techniques. We tested this assumption by investigating cardiac vagal modulation during yoga.We examined 11 healthy yoga practitioners (7 women and 4 men, mean age: 43 ± 11; range: 26–58 years). Each individual was subjected to training units of 90 min once a week over five successive weeks. During two sessions, they practiced a yoga program developed for cardiac patients by B.K.S. Iyengar. On three sessions, they practiced a placebo program of relaxation. On each training day they underwent ambulatory 24 h Holter monitoring. The group of yoga practitioners was compared to a matched group of healthy individuals not practicing any relaxation techniques. Parameters of heart rate variability (HRV) were determined hourly by a blinded observer. Mean RR interval (interval between two R-waves of the ECG) was significantly higher during the time of yoga intervention compared to placebo and to control (P < 0.001 for both). The increase in HRV parameters was significantly higher during yoga exercise than during placebo and control especially for the parameters associated with vagal tone, i.e. mean standard deviation of NN (Normal Beat to Normal Beat of the ECG) intervals for all 5-min intervals (SDNNi, P < 0.001 for both) and root mean square successive difference (rMSSD, P < 0.01 for both). In conclusion, relaxation by yoga training is associated with a significant increase of cardiac vagal modulation. Since this method is easy to apply with no side effects, it could be a suitable intervention in cardiac rehabilitation programs

Termination of Ventricular Tachycardia with Antitachycardia Pacing after Ineffective Shock Therapy in an ICD Recipient with Hypertrophic Cardiomyopathy

Implantable Cardioverter Defibrillator (ICD) implantation is the only established therapy for primary or secondary prevention of sudden cardiac death in patients with Hypertrophic Cardiomyopathy (HCM). Ineffectiveness of shock therapy for the termination of potentially fatal ventricular arrhythmias in ICD recipients is rare in the presence of appropriate arrhythmia detection by the device. We report the case of a 48-year-old woman with HCM and a single chamber ICD, who received five inefficient high-energy (35 Joules) shocks for the termination of an appropriately detected episode of Ventricular Tachycardia (VT). The episode was safely terminated with a subsequent application of Antitachycardia Pacing (ATP) by the device. At the following ICD control, an acceptable defibrillation threshold was detected

Comparison of dual antiplatelet therapy versus oral anticoagulation following transcatheter aortic valve replacement: A retrospective single-center registry analysis

Background: The choice of optimal antithrombotic regimen after transcatheter aortic valve replace-ment (TAVR) remains a matter of debate. The objective of this study was to compare both efficacy and safety outcomes based on the type of antithrombotic therapy prescribed after TAVR Methods: This is a retrospective analysis of 514 consecutive patients treated with either dual antiplate¬let therapy (DAPT) (n = 315; 61.3%) or oral anticoagulation (OAC) plus clopidogrel (n = 199; 38.7%) for a minimum of 3 months after TAVR followed by antiplatelet monotherapy or OAC only, respectively. Patients had pre-defined clinical and echocardiographic follow-ups at 30 days, 6 and 12 months. The key efficacy endpoint was a composite of all-cause death, myocardial infarction, stroke and valve throm¬bosis at 1 year. The key safety endpoint was the occurrence of life-threatening/major bleeding at 1 year. Results: Baseline characteristics did not differ between both groups, except for a higher incidence of atrial fibrillation in the OAC group. No significant differences in both efficacy and safety endpoints were observed at 30 days and 6 months. At 1 year, the key efficacy endpoint occurred in 21.5% of the DAPT group compared to 19.7% of the OAC group (p = 0.61). The key safety endpoint occurred in 25.1% and 27.8%, respectively (p = 0.53). However, after 1 year valve thrombosis was reported in 8 (2.5%) patients in the DAPT group but not in the OAC group (p = 0.02). Conclusions: OAC after TAVR seems to reduce the risk of clinical valve thrombosis without a statisti-cally significant increase in bleeding complications

Statin effect on thrombin inhibitor effectiveness during percutaneous coronary intervention: a post-hoc analysis from the ISAR-REACT 3 trial

Objective: To determine whether statin therapy influences the efficacy of thrombin inhibitor bivalirudin or unfractionated heparin (UFH) during PCI. Setting and patients: The post-hoc analysis of the ISAR-REACT 3 Trial included 4,570 patients: 3,106 patients were on statin therapy and 1,464 patients were not on statin therapy at the time of PCI procedure. Main outcome measures: The primary outcome of this analysis was the 30-day composite of death, myocardial infarction, target vessel revascularization (TVR) or major bleeding. Results: The primary outcome occurred in 7.9% patients (n=246) in the statin group versus 9.8% (n=143) in the non-statin group (P=0.036). There was an interaction in univariate (P=0.028) and multivariable (P=0.026) analysis between pre-PCI statin therapy and the type of antithrombotic therapy regarding myocardial infarction. In the statin group, bivalirudin significantly reduced the incidence of major bleeding (2.6 vs. 4.3%, P=0.013) with no significant difference in the incidence of myocardial infarction (4.9 vs. 5.2%; P=0.73) compared with UFH. In the non-statin group, bivalirudin was inferior to UFH regarding the incidence of myocardial infarction (7.1 vs. 4.1%, P=0.013), yet major bleeding remained lower among bivalirudin-treated patients (4.0 vs. 5.2%, P=0.25). Conclusion: This post-hoc analysis suggests the existence of an interaction between statin therapy before PCI and antithrombotic therapy during PCI. Patients receiving bivalirudin therapy at the time of PCI showed less periprocedural myocardial infarction when on pre-PCI statin therapy which has to be investigated in further studie