Pharmacodynamic Effect of Clopidogrel in Patients Undergoing Transcatheter Aortic Valve Implantation

The aim of this study was to analyze periprocedural and mid-term effect of clopidogrel on platelet function using the VerifyNow P2Y12 point-of-care assay in patients undergoing TAVI. Platelet reactivity was measured at the beginning of the procedure after 300 mg clopidogrel bolus administration and during the follow-up (at 1 month after the procedure) in 52 patients undergoing TAVI using the Medtronic CoreValve prosthesis (Medtronic CoreValve). A cutoff value of 240 PRU was used to identify nonresponders to clopidogrel treatment with high residual platelet reactivity (HRPR). Baseline HRPR was identified in 80% of patients and in 72% of patients during 6-month follow-up. There was no significant difference in the pharmacodynamic effects of clopidogrel on platelet reactivity from baseline to 6-months follow-up (297±57 vs. 275±62; P=0.058). Ischemic event occurred only in 3 patients (5.8%) from the study group. In conclusion, majority of patients undergoing TAVI had high residual platelet reactivity after pretreatment with 300 mg of clopidogrel and during the 6-month follow-up at dual antiplatelet treatment. The noneffectiveness of clopidogrel in the TAVI population raises the question of the routine use of dual antiplatelet treatment in this setting

Ventricular Dyssynchrony and Pacing-induced Cardiomyopathy in Patients with Pacemakers, the Utility of Ultra-high-frequency ECG and Other Dyssynchrony Assessment Tools

The majority of patients tolerate right ventricular pacing well; however, some patients manifest signs of heart failure after pacemaker implantation and develop pacing-induced cardiomyopathy. This is a consequence of non-physiological ventricular activation bypassing the conduction system. Ventricular dyssynchrony was identified as one of the main factors responsible for pacing-induced cardiomyopathy development. Currently, methods that would allow rapid and reliable ventricular dyssynchrony assessment, ideally during the implant procedure, are lacking. Paced QRS duration is an imperfect marker of dyssynchrony, and methods based on body surface mapping, electrocardiographic imaging or echocardiography are laborious and time-consuming, and can be difficult to use during the implantation procedure. However, the ventricular activation sequence can be readily displayed from the chest leads using an ultra-high-frequency ECG. It can be performed during the implantation procedure to visualise ventricular depolarisation and resultant ventricular dyssynchrony during pacing. This information can assist the electrophysiologist in selecting a pacing location that avoids dyssynchronous ventricular activation

A randomized comparison of HBP versus RVP: Effect on left ventricular function and biomarkers of collagen metabolism

Background: Right ventricular pacing (RVP) can result in pacing-induced cardiomyopathy (PICM). It is unknown whether specific biomarkers reflect differences between His bundle pacing (HBP) and RVP and predict a decrease in left ventricular function during RVP. Aims: To compare the effect of HBP and RVP on the LV ejection fraction (LVEF) and to study how they affect serum markers of collagen metabolism. Methods: Ninety-two high-risk PICM patients were randomized to HBP or RVP. Their clinical characteristics, echocardiography, and serum levels of TGF-β1, MMP-9, ST2-IL, TIMP-1, and Gal-3 were studied before and six months after pacemaker implantation. Results: Fifty-three patients were randomized to HBP and 39 patients to RVP. HBP failed in 10 patients, which crossed over to the RVP group. Patients with RVP had significantly lower LVEF compared to HBP after six months of pacing (−5% and −4% in as-treated and intention-to-treat analysis, respectively). Levels of TGF-β1 after 6 months were lower in HBP than RVP (mean difference −6 ng/ml; P = 0.009) and preimplant Gal-3 and ST2-IL levels were higher in RVP patients with a decline in the LVEF ≥ 5% compared to those with a decline of < 5% (mean difference 3 ng/ml and 8 ng/ml; P = 0.02 for both). Conclusion: In high-risk PICM patients, HBP was superior to RVP in providing more physiological ventricular function, as reflected by higher LVEF and lower levels of TGF-β1. Among RVP patients, LVEF declined more in those with higher baseline Gal-3 and ST2-IL levels than those with lower levels

Invasive Hemodynamic Assessment of Cardiac Output State after MitraClip Therapy in Nonanaesthetized Patients with Functional Mitral Regurgitation

Background. Surgical correction of mitral regurgitation (MR) can lead to postoperative low cardiac output state. We aimed to assess the acute hemodynamic changes after percutaneous MitraClip therapy (a unique model without influence of factors linked to surgical procedure) in patients with functional MR without the influence of general anaesthesia. Methods. We studied invasive hemodynamic parameters in 23 patients before procedure (conscious, nonsedated patients), during procedure (intubated patients), and the first day after MitraClip implantation (conscious, extubated patients). Results. Mitral valve clipping significantly increased cardiac index (CI) (from 2.0 ± 0.5 to 3.3 ± 0.6 L/min/m2; p<0.01). Conversely, there was significant reduction in the mean pulmonary capillary wedge pressure (PCWP) (from 18.6 ± 5.7 to 10.5 ± 3.8 mmHg; p<0.01), mean pulmonary artery pressure (from 29.8 ± 10.9 to 25.2 ± 10.3 mmHg; p=0.03), and pulmonary vascular resistance index (from 531 ± 359 to 365 ± 193 dyn·s·cm−5/m2; p=0.03). Conclusions. The functional MR therapy with percutaneous MitraClip device results in significant increase in CI (+66%) and concomitant decrease in PCWP (−42%). None of our patients developed low cardiac output state. Our results support the idea that significant part of low cardiac output state after cardiac surgery is due to surgery related factors rather than due to increase in afterload after MR elimination