Circulation Journal最新文献

Background: Continuous anticoagulation guided by the CHA₂DS₂-VASc score is standard for atrial fibrillation (AF) but does not reflect real-time AF occurrence. We evaluated an Apple Watch-guided event-triggered anticoagulation strategy that adjusts direct oral anticoagulant (DOAC) use according to smartwatch detection.

Methods and results: This multicenter prospective single-arm study enrolled postablation patients in sinus rhythm who were taking DOACs and had a CHA₂DS₂-VASc score ≤3. Apple Watch monitoring continued for 360 days. If no AF occurred during Days 1-30, anticoagulation was stopped on Day 31; thereafter, Apple Watch notification or electrocardiogram (ECG) evidence of AF prompted DOAC resumption through Day 360. Of 54 enrolled patients enrolled in the study, 50 comprised the analysis population (mean age 63 years; 10% female; median CHA₂DS₂-VASc score 2). Across 15,865 person-days, Apple Watch guidance reduced DOAC exposure by 94.6% compared with continuous anticoagulation. Reductions were similar for patients with CHA₂DS₂-VASc scores of 2-3 and 0-1 (95.0% and 94.0%, respectively; P=0.818). No deaths, strokes, systemic thromboembolic events, or bleeding events were observed. One device malfunction prevented ECG acquisition.

Conclusions: In this cohort, Apple Watch-guided event-triggered anticoagulation markedly reduced DOAC exposure without thromboembolic events. Given the limited sample size and low baseline thromboembolic risk, these safety findings should be interpreted cautiously. Results were similar in the prespecified analysis restricted to patients with CHA₂DS₂-VASc scores of 2-3, the group for whom postablation anticoagulation decisions are most clinically relevant.

Background: We aimed to clarify the impact of genetic testing on major adverse cardiovascular events (MACE) among patients with heterozygous familial hypercholesterolemia (HeFH) using data from the Hokuriku-plus FH Registry (UMIN000038210).

Methods and results: In all, 431 patients were enrolled in the study, with a median follow-up of 3.9 years. The primary outcome was time to first MACE, defined as cardiovascular death, non-fatal myocardial infarction, coronary revascularization, or non-fatal stroke. Using Cox proportional hazards regression models, we examined whether undergoing genetic testing was associated with a reduced risk of MACE. Among the 431 patients, sufficient data were available for 386 with HeFH, of whom 202 (52.3%) underwent genetic testing. Low-density lipoprotein cholesterol (LDL-C) levels at follow-up were significantly lower in group that underwent genetic testing than in the group that did not (median 102 vs. 130 mg/dL, respectively; P<0.001). During follow-up, 23 MACE occurred (18 in the non-testing group and 5 in the genetic testing group). Notably, undergoing genetic testing was significantly associated with a reduced risk of MACE, even after adjusting for LDL-C levels (hazard ratio 0.66; 95% confidence interval 0.20-0.92; P=0.033).

Conclusions: Genetic testing in patients with HeFH was associated with a reduced risk of MACE independent of LDL-C. Randomized controlled trials will be needed to clarify whether providing genetic testing can reduce MACE among patients with HeFH.

Background: No studies have compared aspirin to P2Y₁₂inhibitor monotherapy following short dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) in patients with diabetes.

Methods and results: We conducted a prespecified diabetes subgroup analysis of the 1-year STOPDAPT-3 trial; patients were randomized at the time of index PCI, and outcomes from 30 days to 1 year were assessed using a 30-day landmark analysis comparing 1-month DAPT followed by aspirin monotherapy (aspirin group) to 1-month prasugrel monotherapy followed by clopidogrel monotherapy (clopidogrel group). The effect of aspirin relative to clopidogrel was not significant for the coprimary cardiovascular endpoint (composite of cardiovascular death, myocardial infarction, definite stent thrombosis, or stroke) regardless of diabetes (aspirin/clopidogrel 5.3/5.6 vs. 3.9/3.7 per 100 person-years for diabetes vs. non-diabetes, respectively; hazard ratios [HRs] 0.96 [95% confidence interval {CI} 0.67-1.37] and 1.06 [95% CI 0.72-1.55], respectively; P_interaction=0.71), but there was a significant interaction between diabetes and the effect of aspirin relative to clopidogrel for the coprimary bleeding endpoint (Bleeding Academic Research Consortium 3 or 5; aspirin/clopidogrel 2.8/1.8 vs. 1.3/2.0 per 100 person-years diabetes vs. non-diabetes, respectively; HR 1.54 [95% CI 0.88-2.71] vs. 0.65 [95% CI 0.36-1.17], respectively; P_interaction=0.04).

Conclusions: From 30 days to 1 year after PCI, cardiovascular outcomes were similar between aspirin and clopidogrel regardless of diabetes. A nominal bleeding interaction was observed; given the exploratory and underpowered subgroup analyses, this finding should be interpreted cautiously.

Background: Type 2 diabetes (T2D) substantially increases coronary artery disease (CAD) risk, with residual risk unexplained by conventional factors. Immunometabolic dysregulation, particularly in monocytes, is implicated, but causal cell type-resolved evidence is limited.

Methods and results: We integrated peripheral blood mononuclear cells' bulk and single-cell transcriptomes, identifying 1,799 differentially expressed genes enriched in immune and metabolic pathways. Two-sample Mendelian randomization identified 10 genes showing genetically predicted associations with both T2D and CAD. Among these, ADM, PGD, and ATG7 showed consistent genetically predicted associations with higher CAD risk. Single-cell analyses localized these genes to monocyte subsets and revealed enhanced intercellular communication with vascular cells. The genes also showed good discriminatory performance for CAD in T2D (AUCs 0.741-0.837).

Conclusions: Multi-omics integration and genetic analyses supported a monocyte-centered immunometabolic framework involving ADM, PGD, and ATG7 that was consistent with elevated CAD risk in T2D, and generated testable hypotheses.

Background: Although the COVID-19 pandemic has impacted the management of acute coronary syndrome (ACS), the prognostic implications for ACS patients with concurrent COVID-19 undergoing percutaneous coronary intervention (PCI) remain to be determined, particularly in large nationwide cohorts. This study investigated the association between concomitant COVID-19 and clinical outcomes in patients undergoing emergent PCI for ACS.

Methods and results: This retrospective cohort study utilized data from the Japanese Percutaneous Coronary Intervention (J-PCI) nationwide registry, encompassing all patients presenting with ACS who underwent primary or emergent PCI between January 2021 and December 2023. Multivariable logistic regression models were employed to ascertain the independent association between COVID-19 positivity and in-hospital all-cause and cardiovascular mortality. The analysis included 279,662 ACS patients, of whom 1,812 (0.65%) tested positive for COVID-19. After multivariable adjustment, COVID-19 remained an independent predictor of in-hospital all-cause mortality (adjusted odds ratio [aOR] 1.46; 95% confidence interval [CI] 1.21-1.77). The association between COVID-19 and cardiovascular mortality was significant in univariable analysis but not after multivariable adjustment (aOR 1.22; 95% CI 0.98-1.52).

Conclusions: In this nationwide cohort, concomitant COVID-19 was independently associated with higher in-hospital all-cause mortality among patients with ACS undergoing PCI. These findings highlight the need for heightened surveillance and consideration of tailored therapeutic strategies in this high-risk population.

Background: Because the prognostic value of lipoprotein(a) [Lp(a)] levels in Japanese patients remains unclear, we assessed their distribution and association with long-term outcomes in ST-segment elevation myocardial infarction (STEMI).

Methods and results: In our retrospective analysis of 868 consecutive patients with STEMI, the median serum Lp(a) level was 15.75 mg/dL at admission, and the median follow-up was 736.5 days. Using restricted cubic spline analysis, we stratified patients into high (≥47.26 mg/dL) and low (<47.26 mg/dL) Lp(a) groups. The high Lp(a) group had a higher proportion of older and female patients, with lower body weight, estimated glomerular filtration rate, and stent use, and higher dyslipidemia prevalence than those in the low Lp(a) group. The 5-year cumulative incidence of the composite primary endpoint (cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, or any revascularization) was significantly higher in the high Lp(a) group, primarily because of a high rate of any revascularization. Patients with elevated Lp(a) levels demonstrated higher rates of any revascularization for both de novo and restenotic lesions than those with lower levels. After adjusting for confounders, a high Lp(a) level was identified as an independent predictor of the primary endpoint (hazard ratio:1.932; 95% confidence interval:1.255-2.974).

Conclusions: In Japanese patients with STEMI, elevated Lp(a) levels were independently associated with worse long-term outcomes.

Background: Atrial fibrillation (AF) burden and longest duration are important predictors of heart failure and embolism. However, burden-specific detection rates on 7-day Holter ECG remain unclear.

Methods and results: Among 25,817 recordings, 2,289 cases of paroxysmal AF and 571 cases of persistent AF were identified. Low-burden AF was common, and 7-day monitoring substantially improved detection, particularly for AF burden <10% (2.6-fold increase vs. 24-h). AF burden correlated with the longest duration (r=0.79).

Conclusions: 7-day Holter monitoring improved low-burden AF detection and confirmed a strong correlation between AF burden and longest duration.