Open Heart最新文献

Background: Drug-eluting stents (DESs) have become the gold standard of coronary angioplasty since their inception in 2002. Biodegradable polymer DESs (BP-DESs) have been postulated to be superior to durable polymer DESs (DP-DESs) due to their more biocompatible polymer. To date, no study has shown the superiority of one type of polymer compared with the other. We aimed to compare outcomes between a broad range of second-generation DP-DES and BP-DES in an all-comer population.

Methods: We analysed data from 2824 patients who underwent percutaneous coronary intervention (PCI) with BP-DES or DP-DES in the Cardio-FR database. Of these, 2079 (1286 DP-DES and 793 BP-DES) met the inclusion and exclusion criteria and completed a 2-year follow-up: The primary outcome was the device-oriented composite endpoint (DOCE) of cardiac death, non-fatal target vessel myocardial infarction and target lesion revascularisation.

Results: Mean age was 67 years, with 75% male. Despite the DP-DES group exhibiting significantly higher rates of risk factors, such as arterial hypertension (63.1% vs 57.5%, p=0.010), a greater average number of stents implanted per patient (1.72±0.92 vs 1.63±0.84, p=0.040), more acute coronary syndrome (ACS) (55.1% vs 50.2%, p=0.031) and a higher rate of post-dilatation (42.2% vs 35.2%, p<0.001), the rate of acute stent thrombosis (ST) was significantly lower than in the BP-DES group (HR 0.240, 95% CI 0.075 to 0.766; p=0.016). This difference remained significant even after adjusting for covariates using a Cox proportional hazards model and performing a win ratio analysis (4.09, 95% CI 1.28 to 13.09; p=0.018). Despite this increased rate of acute ST, there was no difference in DOCE (12.1% vs 14.5%, OR 1.218, 95% CI 0.926 to 1.600; p=0.158) between the two groups up to 2 years.

Conclusion: Clinical follow-up up to 2 years shows similar outcomes between BP-DES and DP-DES. The rate of acute ST is higher in patients with BP-DES.

Objectives: Peak exercise systolic blood pressure (SBP) is associated with future cardiovascular disease (CVD) and mortality. We aimed to evaluate the predictive value of different SBP patterns at the end of exercise with these outcomes.

Methods: We studied 6329 adults (45% women) referred for exercise testing, with test duration of 6-14 min, maximal effort and valid SBP measurements at the end of exercise. The two last SBPs were indexed to work rate (mmHg/Watt), defining responses as: drop (negative change), plateau (no change), slow (lower tertile of increase), intermediate (middle tertile) and steep (upper tertile). Data were cross-linked with nationwide disease and mortality registries. Associations with all-cause mortality and incident CVD were analysed using Cox proportional hazards regression (hazard ratio (HR), 95% confidence interval), using slow SBP increase as reference, adjusted for sex, age, body mass index, baseline CVD (mortality analysis only), beta-blockers and exercise capacity (peak Watt).

Results: The prevalence of SBP responses at the end of exercise were drop (1.1%), plateau (15.0%), slow (30.4%), intermediate (25.2%) and steep increase (28.3%). Follow-up was 8.8±3.4 years. Compared with a slow increase, the adjusted all-cause mortality risks were not statistically different for a drop (HR 1.16 (0.50-2.65)), plateau (HR 1.19 (0.85-1.66)), intermediate (HR 1.24 (0.93-1.66)) or steep SBP increase (HR 1.16 (0.89-1.52)). CVD risk was increased in those with a SBP drop (HR 3.10 (1.85-5.19), but not significantly for plateau (HR 1.17 (0.92-1.48)), intermediate or steep SBP increases (HRs 0.99-1.00).

Conclusion: Subjects with a slow SBP increase at the end of exercise tended to have the lowest mortality risk, although no SBP response pattern predicted all-cause mortality independently. CVD risk was strongly increased in patients with a drop in SBP and tended to be increased (non-significantly) also in patients with a plateau in SBP at the end of exercise, in comparison with increasing SBP.

Background: In congenital aortic stenosis (CAS), commissurotomy is an option in patients not suitable to receive a valve prosthesis. However, there is often a need for future additional interventions on the aortic valve. The fate of the aortic valve is, however, essentially unknown. This study reports the need for reinterventions after surgical commissurotomy, based on a national register.

Materials and methods: The national register on congenital heart diseases (CHDs) was searched for patients with CAS, simple or associated with other CHD and an index commissurotomy with later data from follow-up.

Results: 300 patients with CAS and an index commissurotomy (mean age at the operation 7.4±7.8 years, 72.4% males) were identified. After an observation time of 27.4±10.0 years, 54.7% of the patients had a reintervention that occurred 14.2±10.1 years after the index operation. The cumulative incidence of reintervention was approximately 25% 10 years after and 60% 30 years after the index intervention. The prevalence of left ventricular hypertrophy (LVH) was higher among those that needed reintervention (41.3 vs 26.8%, p=0.023). Furthermore, eight patients died with a cumulative incidence of 7% 30 years after the index intervention, where most were (7/8) without reintervention (p=0.025). There were no additional important differences between patients with and without reintervention. The prevalence of left ventricular dysfunction and New York Heart Association class >1 was low.

Conclusion: Most (54.7%) patients with a commissurotomy, more than half of them within 30 years and eventually all will need a reintervention. This is important information to patients, especially for women in childbearing age. The higher prevalence of LVH in the group with reintervention needs attention during follow-up. Furthermore, those without reintervention, for unknown reasons, had a higher mortality. Our data strengthen the arguments for close outpatient follow-up among patients with a previous commissurotomy.

Background: Sex differences have not been fully explored for certain risk factors or by age or age-related factors, such as menopause. We addressed this issue in a large population cohort.

Methods: UK Biobank participants with ≥1 risk factor measured at baseline were included. We assessed sex differences, by age and menopausal status, in prevalence, treatment and control of cardiometabolic risk factors.

Results: 501 389 adults (54.4% women, mean age 56.6 (SD 8.1) years) were included. Mean risk factor levels that were lower in women than men include systolic blood pressure (women-to-men difference: -5.6 mm Hg), diastolic blood pressure (-3.4 mm Hg), body mass index (-0.75 kg/m²), waist circumference (-12.2 cm), triglycerides (0.34 mmol/L), glycated haemoglobin (-0.52 mmol/mol) and glucose (-0.08 mmol/L), while high-density lipoprotein cholesterol (+0.31 mmol/L) and C reactive protein (+0.08 mg/L) were higher among women. Total cholesterol and low-density lipoprotein cholesterol (LDL-C) were lower in women than men at younger ages (-0.23 and -0.30 mmol/L, respectively, at <50 years), and higher at older ages (+0.74 and +0.41 mmol/L, at ≥60 years). Total cholesterol and LDL-C were lower in premenopausal women (-0.29 and -0.34 mmol/L, respectively) and higher in postmenopausal women (+0.61 and +0.31 mmol/L), compared with similarly aged men. Prevalence was lower among women than men for current smoking (-3.6%), hypertension (-13.9%), obesity (-1.9%) and diabetes (-2.0%), and sex differences were smaller at older ages and in postmenopausal women. Dyslipidaemia prevalence was lower in women aged <50 years (-8.8%) and premenopausal women (-11.0%), and higher in women aged ≥60 years (+5.4%) and postmenopausal women (+4.6%). Treatment and control of dyslipidaemia were lower in women than men (-12.5% and -12.6%, respectively).

Conclusions: Effective public health policy is required to address suboptimal risk factor prevalence, treatment and control in both sexes. Targeted interventions may be warranted to address dyslipidaemia among women at older ages.

Background: Understanding pandemic-related reductions and subsequent recovery of cardiovascular testing in Asia is important for guiding regional public health efforts.

Objectives: This study sought to evaluate the recovery of cardiovascular testing in Asia 1 year into the COVID-19 pandemic.

Methods: In this subanalysis of a worldwide survey on the impact of COVID-19 on cardiovascular diagnostic care in April 2020 and April 2021, recovery of testing volume in Asia was compared among subregions, World Bank income groups and imaging modalities.

Results: Of 669 sites worldwide, 164 sites were in 33 Asian countries. Cardiovascular testing volumes in Asia decreased by 53% from March 2019 to April 2020, then recovered 96% of this decrease by April 2021, compared with 98% recovery in the rest of the world. Eastern Asia and Western and Central Asia reported recovery rates of 123% and 110%, compared with 50% and 80% recovery in Southern and South-eastern Asia. Testing volumes among high-income and upper-middle-income Asian countries recovered to 117% and 121% but remained depressed at 49% and 14% recovery in lower-middle and low-income countries, respectively. Stress ECG, stress echo and stress positron emission tomography studies experienced median reductions of 48%, 35% and 57% in testing volume between March 2019 and April 2021, while volumes of coronary artery calcium, coronary CT angiography and cardiac MR remained stable during this period.

Conclusions: The recovery of cardiovascular testing in Asia 1 year into the COVID-19 pandemic lagged in the Southern and South-eastern subregions, as well as in lower-income countries. Recovery favoured advanced cardiac imaging modalities over standard stress testing modalities.

Background: Pre-procedural and post-procedural plasma B-type natriuretic peptide (BNP) levels can predict rhythm outcomes after catheter ablation for atrial fibrillation (AF). However, the significance of long-term events remains unclear. Therefore, this study aimed to investigate the significance of integrating pre-ablation and post-ablation BNP levels on major adverse cardiovascular events (MACE) and arrhythmic recurrence in patients with persistent AF undergoing catheter ablation.

Methods: We analysed 392 patients who underwent first catheter ablation. Patients were stratified into four subgroups based on pre-ablation plasma BNP level and its relative change after ablation (ΔBNP) using their respective median values (pre-ablation BNP: 148.0 pg/mL, ΔBNP: -52.6%): Low-Low (pre-ablation<148.0 pg/mL, ΔBNP<-52.6%), Low-High (pre-ablation<148.0 pg/mL, ΔBNP≥-52.6%), High-Low (pre-ablation≥148.0 pg/mL, ΔBNP<-52.6%) and High-High (pre-ablation≥148.0 pg/mL, ΔBNP≥-52.6%). The primary endpoint was MACE, which included all-cause death, heart failure hospitalisation and other cardiovascular hospitalisations. The secondary endpoint involved arrhythmic recurrence.

Results: Of the 392 patients, 101 were classified as Low-Low, 91 as Low-High, 97 as High-Low and 103 as High-High. During a median follow-up of 5.3 (IQR: 3.2-7.2) years, 63 patients (16%) experienced MACE. Heart failure hospitalisation accounted for the majority of events (63%). The High-High subgroup showed significantly higher MACE rates than others (cumulative incidence (95% CI): 26.3% (16.2% to 35.2%), p<0.001). Low-High and High-High subgroups demonstrated a higher arrhythmic recurrence (p<0.001). After multivariate adjustment, the High-Low and High-High subgroups demonstrated progressively higher risks of MACE incidence compared with the Low-Low and Low-High subgroups. Both Low-High and High-High subgroups showed an elevated arrhythmic recurrence risk (both p<0.001).

Conclusions: Integrating pre-ablation and post-ablation BNP levels can be useful for identifying patients with persistent AF at high risk of MACE and arrhythmic recurrence during long-term follow-up.

Background: Iron deficiency (ID) is a highly prevalent comorbidity in patients with chronic and acute heart failure and is associated with worse clinical outcomes. We aimed to evaluate the prevalence and clinical characteristics of ID and its association with in-hospital congestion and postdischarge outcomes.

Methods: FiER deficit in Insuficienta Cardiaca in Romania was a prospective, multicentric study, enrolling 163 patients hospitalised for worsening chronic heart failure (WCHF) irrespective of left ventricular ejection fraction. ID was evaluated at discharge and defined as ferritin<100 ng/mL or ferritin 100-299 ng/mL with transferrin saturation<20%. Patients were classified based on ID status. In-hospital changes of clinical signs of congestion and natriuretic peptides (NT-proBNP) were reported and correlated with ID status. Additionally, survival analysis at 30 and 90 days was performed and compared between patients with ID+ and ID-.

Results: The prevalence of ID was 54.6% (N=89) among 163 eligible patients. Patients with ID+ had more clinical signs of congestion and advanced New York Heart Association functional class at discharge (classes III and IV 58.4% vs 31.1%; p 0.002). NT-proBNP values at admission were higher in ID+ (9288 pg/dL vs 4414 pg/dL, p<0.001), with lower NT-proBNP decrease during hospitalisation (-45.7% vs -63.3%, p 0.003). Additionally, there was no difference in ID prevalence between discharge and 30 days after (54.6% vs 51.3%, p 0.782). Postdischarge all-cause mortality did not differ between ID+ and ID- at 30 days (5.6%% vs 2.7%, p 0.361), but at 90 days, it was higher in ID+ group (30.9% ID+ vs 9.6% ID-, p 0.005).

Conclusions: Patients hospitalised for WCHF and ID had more residual congestion, higher absolute values and significantly lower in-hospital change of NT-proBNP. A significant difference in survival between the two ID groups emerged within 90 days of hospital discharge.

Background: Unlike other suggested therapies, myosin inhibitors have been shown to change the course of hypertrophic cardiomyopathy by altering the contractile mechanics of cardiomyocytes. This meta-analysis sought to determine the efficacy of mavacamten and aficamten in hypertrophic cardiomyopathy.

Methods: The online databases were searched from inception to July 2024, including the Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, ClinicalTrials.gov. The meta-analytical data were pooled using risk ratios (RRs) with 95% CI, standard mean difference (SMD) and SE.

Results: A total of 6 randomised controlled trials with 826 hypertrophic cardiomyopathy patients (mean age±SD up to 59.8±14.2 years in intervention vs 60.9±10.5 years in placebo) were included in our study. Of these, 443 received a cardiac myosin inhibitor and 383 received a placebo. The resting left ventricular outflow tract (LVOT) gradient between the two groups was considerably improved by cardiac myosin inhibitors (MD -57.27; 95% CI -63.05 to -51.49). Significant differences were also observed in the post-Valsalva LVOT gradient between the two groups (MD -55.86; 95% CI -65.55 to -46.18). Significantly decreased left ventricle ejection fraction (LVEF) was also seen (MD -4.74; 95% CI -7.22 to -2.26). The New York Health Association (NYHA) class improvement between the two groups also changed significantly (RR 2.21; 95% CI 1.75 to 2.80). Cardiac myosin inhibitors also caused significant improvement in the Kansas City Cardiomyopathy Questionnaire in a Clinical Summary Score between the two groups (MD 7.71; 95% CI 5.37 to 10.05) and significant reduction in the N-terminal pro-B-type natriuretic peptide (SMD -13.27; 95% CI -17.51 to -9.03) and the cardiac troponin I (SMD -11.90; 95% CI -15.07 to -8.72).

Conclusion: According to our meta-analysis, cardiac myosin inhibitors significantly improve the resting and post-Valsalva LVOT gradient, reduce the LVEF and improve the NYHA class and cardiac biomarkers when compared with the placebo.

Prospero registration number: CRD52024586161.

Background: Earlier studies showed that measured changes in plasma B-type natriuretic peptide (BNP) levels are inconsistent after sacubitril/valsartan administration. The reason remains unknown but may reflect the fact that BNP immunoreactivity measured with commercial BNP assays (BNPcom) includes both mature BNP and proBNP, and neprilysin degrades only mature BNP. In addition, the responsiveness to sacubitril/valsartan varies among patients with heart failure. We investigated the mechanism underlying the inconsistency of BNP measurements after sacubitril/valsartan.

Methods: We measured plasma mature BNP, proBNP and total BNP (mature BNP+proBNP) levels with our immunochemiluminescent assay as well as NT-proBNP, A-type natriuretic peptide (ANP) and BNPcom with conventional assays in 54 patients with heart failure, before (baseline) and after 2, 4, 8 and 12 weeks of sacubitril/valsartan administration. Responders were defined as having NT-proBNP levels at <70% of baseline after 12 weeks.

Results: Among all patients, total BNP and BNPcom did not change with sacubitril/valsartan treatment, whereas NT-proBNP and proBNP decreased, mature BNP modestly increased and ANP greatly increased. Responders (n=31) exhibited smaller %changes in all natriuretic peptide levels than non-responders (n=23; all p<0.01). Receiver operating characteristic curves analysis to assess the ability of the %change in each natriuretic peptide at 4 weeks to detect responders showed that the area under the curve was about 0.80 for each peptide. There were good correlations between plasma natriuretic peptides levels at baseline and throughout the sacubitril/valsartan administration.

Conclusion: These results suggest that the magnitude and direction of change in each BNP form depends on its substrate specificity for neprilysin, that differences in plasma levels of each BNP form between responders and non-responders appear early and persist and that BNPcom levels at 4 weeks can be applicable to prediction of the responders. Notably, our findings show that the idea that BNPcom cannot be used as a marker of heart failure after sacubitril/valsartan should be reconsidered.

Background: Individual cardiometabolic diseases (CMDs) increase atrial fibrillation (AF) risk; however, whether multiple CMDs exert a cumulative effect on AF risk remains unclear. Our objective was to examine the link between coexisting CMDs and AF, as well as their cumulative impact.

Methods: This UK Biobank-based prospective cohort study included data from participants with information related to CMDs and AF. The assessment of CMDs and AF was based on participants' self-reported medical histories and electronic health records. Cox proportional hazard regression models were employed to analyse the link between the number of CMDs and AF and to determine the cumulative effect of multiple CMDs. Further, we performed stratified analyses and adjusted for confounding factors.

Results: The study included 308 916 participants. The risk of AF was substantially associated with varying numbers of CMDs after multivariable adjustment in comparison to the reference group (all p<0.001). In the fully adjusted model, participants with 1, 2 and ≥3 CMDs exhibited elevated risks of 54% (HR: 1.54, 95% CI 1.48 to 1.59), 104% (HR: 2.04, 95% CI 1.94 to 2.15) and 212% (HR: 3.12, 95% CI 2.87 to 3.38), respectively. A significant cumulative dose-response relationship was noted between the number of CMDs and AF risk (HR: 1.45, 95% CI 1.42 to 1.48, p<0.001). A consistent dose-dependent cumulative relationship was observed in both stratified and sensitivity analyses.

Conclusions: Multiple CMDs increased AF risk and exhibited a significant cumulative effect based on the number of CMDs.