P. Thein

The utility of personal activity trackers (Fitbit Charge 2) on exercise capacity in patients post acute coronary syndrome [UP-STEP ACS Trial]: a randomised controlled trial protocol

BackgroundThe benefits of physical activity and cardiovascular rehabilitation on the reduction of cardiovascular risk are well documented. Despite this, significant barriers and challenges remain in optimizing patient risk factors post acute coronary syndromes (ACS) and ensuring patient compliance. Consumer wearable personal activity trackers represent a cost effective and readily available technology that may aid in this endeavour.MethodsUP-STEP ACS is a prospective single-blinded, two-arm, parallel, randomized control trial with an aim to enrol 200 patients all undertaking cardiac rehabilitation. It will assess the affect that personal activity monitors have on change in exercise capacity in patients post acute coronary syndromes primarily measured by a six-minute walk test (6MWT). Secondary end points will be the improvement in other cardiovascular risk factors, namely; blood lipid and glucose levels, weight, waist circumference, along with mood, quality of life and cardiac rehabilitation adherence. Patients will be randomized to either receive a personal activity tracker or standard post hospital care during their index event. After the 8- week intervention period, patients will return for a clinical review and repeat of baseline assessments including the 6MWT.DiscussionThe utility and impact on exercise capacity of personal activity trackers in patient’s post-acute coronary syndrome has not been assessed. This study aims to add to the scientific evidence emerging regarding the clinical utility and validity of these devices in different patient population groups. If proven to be of benefit, these devices represent a cost effective, easily accessible technology that could aid in the reduction of cardiovascular events.Trial registrationThe trial has been registered with the Australian New Zealand Clinical Trials Registry (ANZCTR). The registration number is ACTRN12617000312347 (28/02/2017).

Preoperative Use of Oral Beta-Adrenergic Blocking Agents and the Incidence of New-Onset Atrial Fibrillation After Cardiac Surgery. A Systematic Review and Meta-Analysis

BACKGROUND Current epidemiological data suggests that postoperative atrial fibrillation or atrial flutter (POAF) causes significant morbidity and mortality after cardiac surgery. The literature for prophylactic management of POAF is limited, resulting in the lack of clear guidelines on management recommendations. AIM To examine the efficacy of prophylactic rate control agents in reducing the incidence of new-onset POAF in patients undergoing elective cardiac surgery. METHODS Cochrane Central Register of Controlled Trials (CENTRAL), Embase, and Medline were systematically searched for blinded randomised controlled studies (RCT) evaluating adults with no history of atrial fibrillation randomised to a pharmacological agent (either beta blocker, calcium channel blocker or digoxin), compared to placebo. Utilising Cochrane guidance, three reviewers screened, extracted and the quality of the evidence was assessed. We used a random effects meta-analysis to compare a rate-control agent with placebo. RESULTS Five RCTs (688 subjects, mean age 61±8.9, 69% male) were included. Beta blocker administration prior to elective cardiac surgery significantly reduced the incidence of POAF (OR 0.43, 95%Cl [0.30-0.61], I2=0%) without significant impact on ischaemic stroke (OR 0.49, 95%Cl [0.10-2.44], I2=0%), non-fatal myocardial infarction (OR 0.76, 95%Cl [0.08-7.44], I2=0%), overall mortality (OR 0.83, 95%Cl [0.19-3.66], I2=0%), or length of stay (mean -0.96days 95%Cl [-1.49 to -0.42], I2=0%). An increased rate of bradycardic episodes was observed (OR 3.53, 95%Cl [1.22-10.23], I2=0%). CONCLUSIONS This review suggests that selective administration of prophylactic oral beta blockers prior to elective cardiac surgery is safe and may reduce the incidence of POAF.

The role of antiplatelet drug resistance in subclinical leaflet thrombosis following transcatheter aortic valve replacement

We read with interest the article by Xiong et al. which described an association between gene polymorphisms and antiplatelet drug resistance in the development of leaflet thrombosis (LT) following transcatheter aortic valve replacement (TAVR) [1]. The authors found a strong correlation between a CYP2C19 gene polymorphism and the development of hypo-attenuated leaflet thickening (HALT). Aside from antiplatelet drug resistance, certain clinical risk factors have been linked to the development of HALT. Chronic kidney disease, diabetes, previous cerebrovascular events (CVE) and pro-inflammatory conditions such as active malignancy have been found to be associated with venous thromboembolism and HALT due to the pro-thrombotic nature of these conditions [2–4]. Likewise, prolonged blood stasis and reduction in trans-prosthetic flow such as in congestive cardiac failure has been shown to predispose to HALT [5, 6]. Prosthesis factors also play a role in the development of HALT. Valve crimping and aggressive ballooning have been showed to cause micro-filamentous TAVR leaflet injury and expose collagen fibers which are thrombogenic [4, 7]. Furthermore, the type of TAVR device and larger prostheses have been shown to increase the risk of HALT, whilst smaller prostheses are considered a protective factor [3, 8]. To appreciate the results presented by the authors in a better context, we hope the authors could provide the prevalence of these clinical (diabetes, hypertension, congestive cardiac failure and prior cerebrovascular event) and prosthesis (valve type, prostheses size and post-dilatation rate) risk factors for both HALT and non-HALT cohorts which have been associated with the development of LT in other studies. There are growing concerns regarding the potential clinical sequelae of HALT [9]. Pooled evidence suggests a strong correlation between bioprosthetic LT and CVE [10]. Although the results were primarily driven by transient ischaemic attacks (TIA), the rate of stroke reached borderline statistical significance. Could the authors could provide the readers the clinical outcomes in the HALT and non-HALT cohorts, especially mortality and CVE (TIA and stroke)? We commend the authors for a well-designed trial and for providing further insight into the pathophysiology of HALT. We believe future prospective trials are warranted to determine the mechanism and clinical sequelae of HALT.