doi: 10.1136/heartjnl-2024-324744pmid: 40037763
Implantation of drug-eluting stents (DESs) remains central to percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS) and chronic coronary syndromes (CCS). DES platforms, polymers and drugs have evolved significantly to improve deliverability and safety, now being typically thin-strut with a compact layer of biocompatible or bioresorbable polymer, or no polymer at all. Ultra-thin-strut DESs push this concept further, and in some studies perform better than conventional DES, but may recoil in challenging settings such as chronic total occlusion PCI. Stent implantation has also progressed, with greater attention to lesion preparation and poststenting optimisation, increased use of intracoronary imaging helping to recognise and remedy issues. In parallel, antithrombotic therapy for patients undergoing PCI has advanced considerably, with reliable P2Y12 inhibition now possible with the newest agents. As well as progress in controlling other thrombotic risk factors such as hyperlipidaemia, hypertension and diabetes, these developments have contributed to reducing thrombotic risk. As well as preventing stent thrombosis, antithrombotic therapy can reduce the risk of non-PCI-related thrombotic events, not only in the coronary tree but also in the cerebral and peripheral circulation, however it increases bleeding risk. Twelve months of dual antiplatelet therapy (DAPT) after PCI for ACS (and 6 months after PCI for CCS) remains the default recommended strategy, but given reliable P2Y12 inhibition, good control of ischaemic risk factors and a minimally thrombogenic stent design and deployment, it is rational that earlier de-escalation to monotherapy, particularly with ticagrelor, is often appropriate, reserving longer-duration DAPT for those with highest ischaemic risk but where bleeding risk is not high. A body of trial evidence now supports this. As well as earlier de-escalation of DAPT, future developments in PCI might include increased use of ‘leave nothing behind’ strategies and further pharmacological options for optimisation of ischaemic risk factors.
Qin, Pei; Ho, Frederick K; Celis-Morales, Carlos A; Trost, Stewart G; Pell, Jill P
doi: 10.1136/heartjnl-2024-325004pmid: 40234043
ObjectivesDedicated studies aimed at investigating the relationship between walking pace and arrhythmia are limited. This study assessed associations between self-reported and accelerometer measured walking pace and incident cardiac arrhythmias, overall and by subtype, and explored metabolic and inflammatory markers as possible mediators.MethodsSelf-reported average walking pace was available for 420 925 UK Biobank participants, and accelerometer measured time spent walking at different paces was available for 81 956 participants. Outcomes were incident cardiac arrhythmias: all, atrial fibrillation (AF), other (including bradyarrhythmias and ventricular arrhythmias), bradyarrhythmias and ventricular arrhythmias. Cox proportional regression models were used to investigate the associations.ResultsCompared with slow walking pace, average and brisk walking pace were associated with significantly lower risks of all cardiac arrhythmias (hazard ratio (HR) 0.65, 95% confidence interval (CI) 0.62 to 0.68; HR 0.57, 95% CI 0.54 to 0.60), AF (HR 0.62, 95% CI 0.58 to 0.65; HR 0.54, 95% CI 0.50 to 0.57) and other arrhythmias (HR 0.69, 95% CI 0.64 to 0.73; HR 0.61, 95% CI 0.57 to 0.65). Overall, 36.0% of the association between walking pace and all arrhythmias was mediated via metabolic and inflammatory markers. The associations were stronger in women, in those aged <60 years, in those with a body mass index <30, in those who had hypertension and in those with ≥2 long term conditions.ConclusionsAverage and brisk self-reported walking pace and time spent walking at moderate and brisk pace were associated with a decreased risk of cardiac arrhythmias, in part mediated via metabolic and inflammatory pathways. Our findings suggest brisk walking may be a safe and effective exercise to reduce arrhythmias, especially for higher risk groups.
Sever, Peter S; Rostamian, Somayeh; Whiteley, William; Ariti, Cono; Godec, Thomas; Gupta, Ajay; Mackay, Judith; Whitehouse, Andrew; Poulter, Neil R
doi: 10.1136/heartjnl-2024-325104pmid: 40139683
AimsCardiovascular (CV) deaths were reduced by atorvastatin during a 16-year follow-up of participants in the Anglo-Scandinavian Cardiac Outcomes Trial-lipid-lowering arm. We now extend these observations over 20 years and report both non-fatal and fatal CV outcomes.MethodsA cohort of 4605 UK hypertensive participants with total cholesterol <6.5 mmol/L (2317 atorvastatin vs 2288 placebo) was followed for up to 21 years (IQR 9.1–19.3). Cox proportional hazard models assessed HRs for non-fatal and fatal CV events. At the end of the original trial (3.3 years), all participants were offered atorvastatin. Lipid profiles were obtained from all subjects 2 years later and from subgroups approximately 9 years post-trial.ResultsPatients allocated to atorvastatin had a significant reduction in non-fatal myocardial infarction (MI) and fatal coronary heart disease (CHD) events (HR (95% CI) 0.81 (0.69 to 0.94, p=0.006)), total coronary events (0.88 (0.80 to 0.98, p=0.017)) and CV deaths (0.86 (0.74 to 0.99, p=0.048)). No significant reduction in heart failure (HF), strokes, total CV events and all-cause mortality was observed.In participants assigned atorvastatin in the trial, 3-year mean low-density lipoprotein-cholesterol was strongly associated with long-term CV outcomes. The HRs per 1 mmol/L decrease were for non-fatal MI and fatal CHD (0.69 (0.57 to 0.85, p<0.001)), total coronary events (0.70 (0.61 to 0.79, p<0.001)), non-fatal and fatal HF (0.68 (0.57 to 0.81, p<0.001)), non-fatal and fatal stroke (0.74 (0.59 to 0.92, p=0.006)), total CV events and procedures (0.74 (0.66 to 0.81, p<0.001)), CV mortality (0.66 (0.55 to 0.81, p<0.001)) and all-cause mortality (0.81 (0.71 to 0.90, p<0.001)).Two years after the trial, approximately two-thirds of subjects in each arm were taking atorvastatin. At this time point and approximately 9 years post-trial, lipid profiles were similar between those formerly assigned atorvastatin or placebo.ConclusionsThese observations provide further evidence for the long-term legacy effects of statins and have implications for the early introduction of statins to prevent CV events and mortality.
Pasea, Laura; Mohamed, Mohamed; Dashtban, Ashkan; Bhuva, Anish; Mizani, Mehrdad A; Ali, Sarah; Oates, Thomas; Mamas, Mamas A; Morris, Tamsin; Gao, He; Mamza, Jil Billy; Banerjee, Amitava
doi: 10.1136/heartjnl-2024-325046pmid: 40037768
BackgroundEffective management of coexisting heart failure (HF), chronic kidney disease (CKD) and type 2 diabetes mellitus (T2D) is critical, yet evidence of adherence to guideline-recommended standards in routine care remains unclear. We aimed to assess primary care adherence to guideline-recommended standards for patients with overlapping HF, CKD and T2D in England.MethodsUsing UK Clinical Practice Research Datalink (1998–2020), we evaluated care adherence across 161 529 individuals with HF, CKD or T2D before and after developing a second of these conditions. We analysed disease investigation rates, medication use and predictors of guideline adherence.ResultsWe identified 161 529 patients with CKD followed by HF (CKD+HF, 40%), CKD+T2D (51.3%) and HF+T2D (8.6%) with a median of 3.1 years follow-up after the second diagnosis. In CKD+HF, CKD+T2D and HF+T2D groups, prescription rates of renin-angiotensin system inhibitors (71%, 64.1% and 74.4%), beta-blockers (53.1%,36.2% and 55.1%), antiplatelets (56.2%, 45.2% and 54.4%) and statins (56.7%, 68.5% and 72%) were suboptimal. Advanced age, female sex, peripheral arterial disease and cancer were associated with a lower likelihood of checking blood pressure, creatinine and glycated haemoglobin (HbA1C) after HF, CKD and T2D diagnoses, respectively. The first diagnosis of HF was associated with reduced odds of having HbA1C measured after T2D diagnosis (OR 0.79, 95% CI 0.72 to 0.86), compared with CKD as the first diagnosis.ConclusionsIn overlapping HF, CKD and T2D, guideline-recommended care is suboptimal, with inequalities by age, sex, disease on first presentation and comorbidities. Quality improvement requires linked data collection, monitoring and action across diseases.
Sanchis, Juan; Bueno, Hector; Martí Sánchez, David; Martinez-Selles, Manuel; Díez Villanueva, Pablo; Barrabes, Jose A; Marín, Francisco; Villa, Adolfo; Sanmartin Fernandez, Marcelo; Llibre, Cinta; Sionis, Alessandro; Elizaga, Jaime; Alfonso, Fernando;
Showing 1 to 8 of 8 Articles
doi: 10.1136/heartjnl-2024-325254pmid: 39922692
BackgroundClinical trials and meta-analyses indicate a reduced reinfarction risk with invasive management in older patients with non-ST-segment elevation myocardial infarction (NSTEMI). This study investigated whether similar benefits might be observed in frail patients.MethodsThe coMOrbilidades Síndrome Coronario Agudo - FRAIL (MOSCA-FRAIL) trial included 167 adults aged ≥70 years with frailty (Clinical Frailty Scale ≥4 points) and NSTEMI, who were randomised to invasive (n=84) or conservative (n=83) strategy during the index hospitalisation. The primary end point of this subanalysis was reinfarction, considering all-cause mortality as a competing event, at a 3-year median follow-up. The time to first reinfarction and all reinfarctions (first and recurrent) were considered. The substudy was not prespecified.ResultsThe total number of deaths (93, 56%) exceeded that of first reinfarctions (32, 19%). Invasive treatment did not influence the reinfarction risk when accounting for death as a competing risk (subdistribution HR=0.87, 95% CI 0.54 to 1.40, p=0.56). An initially increased mortality risk with invasive management (significant between days 131 and 175) shifted to a lower mortality risk over time. A total of 45 reinfarctions (first and recurrent) were observed. The longitudinal trajectories corroborated that the invasive strategy did not reduce the risk of reinfarction over time (p=0.72). However, mortality followed a biphasic pattern, with higher mortality in the invasive group during the first 6 months and a reduction between 9 months and 3 years (p=0.05 for the entire time-dependent trajectory). The win ratio for the invasive strategy versus the conservative strategy was 1.08 (95% CI 0.72 to 1.63, p=0.70).ConclusionsIn older adults with frailty and NSTEMI, routine invasive management did not reduce the reinfarction risk at a 3-year follow-up. The high all-cause mortality associated with frailty may limit the impact of invasive management. Due to the limited sample size and risk for type II error, these findings should be considered hypothesis-generating.Trial registration number NCT03208153.