Cardiology最新文献

Introduction: Despite contemporary practice guidelines, a substantial number of post-acute coronary syndrome (ACS) patients fail to achieve guideline-recommended LDL-C thresholds. Our study aimed to investigate this guideline recommendations-to-practice care gap. Specifically, we aimed to identify opportunities where additional lipid-lowering therapies are indicated and explore reasons for the non-prescription of guideline-recommended therapies.

Methods: ACS patients with LDL-C ≥1.81 mmol/L (70 mg/dL) despite maximally tolerated statin ± ezetimibe therapy (including those intolerant of ≥2 statins) were enrolled 1-12 months post-event from 27 Canadian and US sites from September 2018 to October 2020 and followed up for three visits during the 12 months post-event. We determined the proportion of patients who did not achieve Canadian/US guideline-recommended LDL-C thresholds, the number of patients who would have been eligible for additional lipid-lowering therapies, and reasons behind lack of escalation in lipid-lowering therapies when indicated. Individual patient and aggregate practice feedback, including guideline-recommended intensification suggestions, were provided to each physician.

Results: Of the 248 patients enrolled in the pilot study (median age 64 [57, 73] years, 31.5% female and STEMI 27.4%), 75.4% were on high-intensity statins on the first visit. A total of 18.5% of those who attended all 3 visits had an LDL-C measured only at the first visit which was above the threshold. After 1 year of follow-up, 51.9% of patients achieved LDL-C thresholds at either visit 2 or 3. In the context of feedback reminding physicians about guideline-directed LDL-C-modifying therapy in their individual participating patients, we observed an increase in the use of ezetimibe and PCSK9 inhibitor therapy at 3-12 months. This was associated with a significant lowering of the mean LDL-C (from 2.93 mmol/L [baseline] to 2.09 mmol/L [3-6 months] to 1.87 mmol/L [6-12 months]) and a significantly greater proportion of patients (from 0% [baseline] to 38.6% [3-6 months] to 53.4% [6-12 months]) achieving guideline-recommended LDL-C thresholds. The most prevalent reasons behind the non-intensification of LDL-C-lowering therapy with ezetimibe and/or PCSK9i were LDL-C levels being close to target, the pre-existing use of other lipid-lowering therapies, patient refusal, and cost.

Conclusion: Although most patients post-ACS were on high-intensity statin therapy, almost 50% failed to achieve guideline-recommended LDL-C thresholds by 1-year follow-up. Furthermore, additional lipid-lowering therapies in this high-risk group were underprescribed, and this might be linked to several factors including potential gaps in physician knowledge, treatment inertia, patient refusal, and cost.

Introduction: Coronary microvascular dysfunction (CMD) is common in patients with and without obstructive epicardial coronary artery disease (CAD). Risk factors for the development of CMD have not been fully elucidated, and data regarding sex-associated differences in traditional cardiovascular risk factors for obstructive CAD in patients with CMD are lacking.

Methods: In this single-center, prospective registry, we enrolled patients with nonobstructive CAD undergoing clinically indicated invasive assessment of coronary microvascular function between November 2019 and March 2023. Associations between coronary microvascular dysfunction, traditional cardiovascular risk factors, and sex were assessed using univariate and multivariate regression models.

Results: Overall, 245 patients with nonobstructive CAD were included in the analysis (62.9% female; median age 68 (interquartile range: 59, 75). Microvascular dysfunction was diagnosed in 141 patients (57.5%). The prevalence of microvascular dysfunction was similar in women and men (59.0% vs. 57.0%; p = 0.77). No association was found between traditional risk factors for coronary atherosclerosis and CMD regardless of whether CMD was structural or functional. In women, but not in men, older age and the presence of previous ischemic heart disease were associated with lower coronary flow reserve (β = -0.29; p < 0.01 and β = -0.15; p = 0.05, respectively) and lower resistive reserve ratio (β = -0.28; p < 0.01 and β = -0.17; p = 0.04, respectively).

Conclusion: For the entire population, no association was found between coronary microvascular dysfunction and traditional risk factors for coronary atherosclerosis. In women only, older age and previous ischemic heart disease were associated with coronary microvascular dysfunction. Larger studies are needed to elucidate risk factors for CMD.

Introduction: Patients with heart failure (HF) and bradycardia may be eligible for different types of cardiac implantable electronic devices (CIED), depending on the presence of atrioventricular conduction disease, age, and comorbidities. We aimed to assess the prognosis for these patients, after CIED implantation, stratified for the type of CIED device.

Methods: All patients with preexisting HF diagnosis who received a CIED with a right ventricular lead during the period 2005-2018 in Sweden were identified via the pacemaker registry. Data were crossmatched with the population registry and national disease registries. The outcome was 5-year risk of HF hospitalization and mortality.

Results: A total of 37,745 patients were included in the study. Comparing demographics for implantable cardioverter defibrillator versus pacemaker implants, median age was 66 years versus 83 years, 20% versus 41% were female, 64% versus 50% had ischemic heart disease, and 35% versus 67% had atrial fibrillation (all p < 0.001). Five-year mortality was highest in single-chamber pacemaker recipients (61% compared to average 40%, p < 0.001), but the proportion of cardiovascular mortality was highest for cardiac resynchronization therapy (CRT) recipients (68% vs. 63% p < 0.001). Adjusted mortality was higher for pacemaker patients in all age decile groups (ranging from <60 to >90 years old, all p < 0.001), HF hospitalization occurred in 28% (dual-chamber pacemaker) to 39% (CRT-P) of patients, and cause of death was HF in 15% (dual-chamber pacemaker) to 25% (CRT-D), all p < 0.001.

Conclusion: In this large real-world cohort of CIED-treated patients with prior HF, demography and mortality data indicate that clinicians chose devices according to the overall status of the patient. HF-related events occurred in all groups but were more common in CRT-treated patients.

Introduction: Atrial fibrillation (AF) is a common arrhythmia associated with aging. Many known risk factors are associated with AF, but many senior individuals do not develop AF despite having multiple risk factors. This finding suggests that other factors may be involved in AF onset. This study aimed to identify upregulated genes in the peripheral blood and left atrium of patients with AF. These genes may serve as potential biomarkers to predict AF onset risk and its complications.

Methods: Gene expression data were analyzed from blood (n = 3) and left atrial samples (n = 15) of patients with AF and sinus rhythm. We evaluated the significant genes identified using p value analysis of weighted average difference to confirm their rankings. We created figures for the genes using GeneMANIA and performed a functional analysis using Cytoscape3.10.1. Hub and bottleneck genes were identified based on degree and betweenness centrality. We used reference expression (RefEx) to confirm the organs in which the extracted genes were expressed. Heatmaps and Gene ontology term evaluation were performed to further elucidate the biological functions of the genes.

Results: We identified 12 upregulated genes (CAST, ASAH1, MAFB, VCAN, DDIT4, FTL, HEXB, PROS1, BNIP3L, PABPC1, YBX3, and S100A6) in both the blood and left atrium of patients with AF. We analyzed the gene functions using GeneMANIA and Cytoscape. The identified genes were involved in a variety of pathways, including lysosomal function and lipid and sphingolipid catabolism. Next, we investigated whether the 12 identified genes identified were systemically expressed or had high organ specificity. Finally, RefEx was used to analyze the gene expression levels in various tissues. Four genes, FTL, ASAH1, S100A6, and PABPC1, were highly expressed in the normal heart tissue. Finally, we evaluated the expression levels of the 12 genes in the blood of patients with AF using a heatmap. Our findings suggest that the 12 genes identified in this study, especially the lysosome-related genes (FTL and ASAH1), may be involved in AF pathogenesis.

Conclusion: Lysosome-related genes may be important to understand the AF pathophysiology and to develop AF-related future studies.

Introduction: Mortality from acute myocardial infarction (AMI) remains substantial. The current study is aimed at developing a novel simple risk score for AMI.

Methods: The Coronary Artery Tree description and Lesion EvaluaTion (CatLet) extended validation trial (ChiCTR2000033730) and the CatLet validation trial (ChiCTR-POC-17013536), both being registered with chictr.org, served as the derivation and validation datasets, respectively. Both datasets included 1,018 and 308 patients, respectively. They all suffered from AMI and underwent percutaneous intervention (PCI). The endpoint was 4-year all-cause death. Lasso regression analysis was used for covariate selection and coefficient estimation.

Results: Of 26 candidate predictor variables, the four strongest predictors for 4-year mortality were included in this novel risk score with an acronym of BACEF (serum alBumin, Age, serum Creatinine, and LVEF). This score was well calibrated and yielded an AUC (95% CI) statistics of 0.84 (0.80-0.87) in internal validation, 0.89 (0.83-0.95) in internal-external (temporal) validation, and 0.83 (0.77-0.89) in external validation. Notably, it outperformed the ACEF, ACEF II, GRACE scores with respect to 4-year mortality prediction.

Conclusion: A simple risk score for 4-year mortality risk stratification was developed, extensively validated, and calibrated in patients with AMI. This novel BACEF score may be a useful risk stratification tool for patients with AMI.

Introduction: Our team once proposed a correction of transitional zone index (CTZI) based on the transitional zone index (TZI) in view of achieving a more precise prediction of outflow tract ventricular arrhythmia (OTVA). The predictive accuracy of these two electrocardiogram (ECG) algorithms has not been validated and compared. The purpose of this study was to compare the predictive accuracy of TZI and CTZI in a much larger population with idiopathic OTVA.

Methods: The predictive accuracy of TZI and CTZI was compared in 695 individuals with idiopathic premature ventricular complex or ventricular tachycardia which exhibited a left bundle branch block pattern and inferior axis QRS morphology. Receiver operating characteristic curve analysis, decision curve analysis, and calibration curve were used to compare the predictive accuracy of TZI and CTZI.

Results: TZI and CTZI manifested the similar area under the curve. While a TZI of <0 predicted a left ventricular outflow tract (LVOT) origin with a high specificity of 88.2% but a low sensitivity of 67.1%, a CTZI of <0 yielded a high sensitivity of 84.3% but a low specificity of 59.5% in the overall analysis. Similar results were yielded in the sub-analysis of participants with a precordial transition occurring at lead V3. In the sub-analysis of participants with a TZI = 0, CTZI demonstrated a bit higher but not satisfactory predictive accuracy than TZI.

Conclusion: Based on the scientific spirit of self-criticism and seeking truth from facts, our team disproves the correction of TZI proposed previously.