bluuebunny/crossref_metadata_2025_split huggingface dataset:
Risk Prediction Models for Renal Function Decline After Cardiac Surgery Within Different Preoperative Glomerular Filtration Rate Strata
Authors: Wang Chunrong , Gao Yuchen , Ji Bingyang , Li Jun , Liu Jia , Yu Chunhua , Wang Yuefu 
Published: April 2024

Background
Our goal was to create a simple risk‐prediction model for renal function decline after cardiac surgery to help focus renal follow‐up efforts on patients most likely to benefit.

Methods and Results

This single‐center retrospective cohort study enrolled 24 904 patients who underwent cardiac surgery from 2012 to 2019 at Fuwai Hospital, Beijing, China. An estimated glomerular filtration rate (eGFR) reduction of ≥30% 3 months after surgery was considered evidence of renal function decline. Relative to patients with eGFR 60 to 89 mL/min per 1.73 m
2
(4.5% [531/11733]), those with eGFR ≥90 mL/min per 1.73 m
2
(10.9% [1200/11042]) had a higher risk of renal function decline, whereas those with eGFR ≤59 mL/min per 1.73 m
2
(5.8% [124/2129]) did not. Each eGFR stratum had a different strongest contributor to renal function decline: increased baseline eGFR levels for patients with eGFR ≥90 mL/min per 1.73 m
2
, transfusion of any blood type for patients with eGFR 60 to 89 mL/min per 1.73 m
2
, and no recovery of renal function at discharge for patients with eGFR ≤59 mL/min per 1.73 m
2
. Different nomograms were established for the different eGFR strata, which yielded a corrected C‐index value of 0.752 for eGFR ≥90 mL/min per 1.73 m
2
, 0.725 for eGFR 60–89 mL/min per 1.73 m
2
and 0.791 for eGFR ≤59 mL/min per 1.73 m
2
.

Conclusions
Predictors of renal function decline over the follow‐up showed marked differences across the eGFR strata. The nomograms incorporated a small number of variables that are readily available in the routine cardiac surgical setting and can be used to predict renal function decline in patients stratified by baseline eGFR.
Systolic Blood Pressure, Diastolic Blood Pressure and Pulse Pressure and the Risk of Subclinical Myocardial Injury: The HUNT Study
Authors: Young Juliet , Lyngbakken Magnus Nakrem , Hveem Kristian , Røsjø Helge , Omland Torbjørn 
Published: April 2024

Background
Subclinical myocardial injury expressed as higher cardiac troponin concentrations may represent an important intermediary between hypertension and the risk of cardiovascular disease. The study aimed to assess the relative strength of associations between systolic blood pressure (BP), diastolic BP, and pulse pressure, and subclinical myocardial injury, and how change in BP variables over time associates with subclinical myocardial injury.

Methods and Results

cTnl (cardiac troponin I) was measured in 32 968 participants of the fourth wave of the population‐based cohort HUNT4 (Trøndelag Health Study) without a history of cardiovascular disease. An additional longitudinal analysis included participants from HUNT4 with BP measurements from HUNT3 (n=18 681). Associations between BP variables and cTnI concentrations were assessed by linear and logistic regression analyses. The median cTnI concentration was 1.6 ng/L (25th–75th percentiles, 0.6–3.1 ng/L), median age was 52 years (39.1–65.6 years), and 57% were female subjects. Cross‐sectionally, only systolic BP categories ≥130 mm Hg associated with higher cTnI concentrations, compared with a reference systolic BP of <110 mm Hg. All categories of diastolic BP and pulse pressure were positively associated with higher cTnI concentrations when diastolic BP 70 to 79 mm Hg and pulse pressure <40 mm Hg were used as references, respectively. When comparing systolic BP, diastolic BP, and pulse pressure as continuous variables, cross‐sectionally, pulse pressure most strongly associated with cTnI concentrations (
P
for all comparisons <0.001), whereas longitudinally, change in diastolic BP was most strongly associated with cTnI concentrations (
P
for all comparisons <0.05).

Conclusions
Subjects with high pulse pressure and longitudinal increase in diastolic BP are at higher risk for subclinical myocardial injury.
Association of Age‐ and Body Mass Index‐Stratified High On‐Treatment Platelet Reactivity With Coronary Intervention Outcomes in East Asian Patients
Authors: Cha Jung‐Joon , Lee Seung‐Jun , Park Jae Hyoung , Hong Soon Jun , Ahn Tae Hoon , Chang Kiyuk , Park Yongwhi , Song Young Bin , Ahn Sung Gyun , Suh Jung‐Won , Lee Sang Yeub , Cho Jung Rae , Her Ae‐Young , Jeong Young‐Hoon , Kim Hyo‐Soo , Kim Moo Hyun , Shin Eun‐Seok , Kim Byeong‐Keuk , Lim Do‐Sun 
Published: April 2024

Background
Although age and body mass index (BMI) significantly affect platelet reactivity units and clinical outcomes after percutaneous coronary intervention, there are limited data on the relationship between high on‐treatment platelet reactivity (HPR) and clinical outcomes on age and BMI differences. Thus, we investigated the association of HPR with clinical outcomes according to age and BMI.

Methods and Results

The study analyzed 11 714 patients who underwent platelet function tests after percutaneous coronary intervention. The primary end point was the occurrence of major adverse cardiac and cerebrovascular events (MACCEs), whereas the secondary end point was major bleeding. HPR was defined as platelet reactivity units ≥252. Patients were categorized by age (<67 years of age or ≥67 years of age) and BMI (≤22.6 kg/m
2
or >22.6 kg/m
2
). Patients <67 years of age with HPR had increases in both MACCEs (adjusted hazard ratio [HR], 1.436 [95% CI, 1.106–1.867];
P
=0.007) and major bleeding (adjusted HR, 1.584 [95% CI, 1.095–2.290];
P
=0.015) compared with the those with non‐HPR, respectively. In patients ≥67 years of age with HPR, there were no differences in MACCEs, but there was a decrease in major bleeding (adjusted HR, 0.721 [95% CI, 0.542–0.959];
P
=0.024). Meanwhile, patients with HPR with BMI >22.6 kg/m
2
had increases in MACCEs (adjusted HR, 1.387 [95% CI, 1.140–1.688];
P
=0.001). No differences were shown in major bleeding.

Conclusions
HPR was linked to an increase in MACCEs or a decrease in major bleeding in patients after percutaneous coronary intervention, depending on age and BMI. This study is the first to observe that clinical outcomes in patients with HPR after percutaneous coronary intervention may vary based on age and BMI. Because the study is observational, the results should be viewed as hypothesis generating and emphasize the need for randomized clinical trials.
Patients With Coronary Microvascular Dysfunction Have Less Circulating α‐Klotho
Authors: Akhiyat Nadia , Ozcan Ilke , Gulati Rajiv , Prasad Abhiram , Tchkonia Tamara , Kirkland James L. , Lewis Bradley , Lerman Lilach O. , Lerman Amir 
Published: April 2024

Background
Coronary microvascular dysfunction (CMD) represents an early functional characteristic of coronary vascular aging. Klotho (α‐klotho) is a circulating protein inversely linked to physiological aging. We examined low klotho as a potential marker for vascular aging in patients with CMD and no coronary artery disease.

Methods and Results

Patients undergoing nonurgent angiogram for chest pain who had no coronary artery disease underwent invasive coronary microvascular and endothelial function testing. CMD was defined by ≤50% increase in coronary blood flow (percentage change in coronary blood flow) in response to intracoronary acetylcholine or coronary flow reserve ≤2. Fresh arterial whole blood was used to analyze circulating endothelial progenitor cells with flow cytometry. Stored arterial plasma was used for klotho analysis by ELISA. Participants with CMD (n=62) were compared with those without CMD (n=36). Those with CMD were age 55±10 years (versus 51±11 years;
P
=0.07) and 73% women (versus 81%;
P
=0.38). Traditional risk factors for coronary artery disease were similar between groups. Patients with CMD had less klotho (0.88±1.50 versus 1.75±2.38 ng/mL;
P
=0.03), and the odds of low klotho in CMD were significant in a logistic regression model after adjusting for traditional cardiovascular risk factors (odds ratio [OR], 0.80 [95% CI, 0.636–0.996];
P
=0.05). Higher klotho was associated with higher numbers of endothelial progenitor cells with vascular regenerative potential (CD34
+
and CD34
+
CD133
+
KDR
+
). Among a subgroup of patients with atherosclerotic cardiovascular disease risk <5% (n=58), CMD remained associated with lower klotho (OR, 0.80 [95% CI, 0.636–0.996];
P
=0.047).

Conclusions
Klotho may be a biomarker for CMD and may be a therapeutic target for groups of patients without significant traditional cardiovascular risk.
Longitudinal NT‐proBNP: Associations With Echocardiographic Changes and Outcomes in Heart Failure
Authors: Teramoto Kanako , Tay Wan Ting , Tromp Jasper , Ouwerkerk Wouter , Teng Tiew‐Hwa Katherine , Chandramouli Chanchal , Liew Oi Wah , Chong Jenny , Poppe Katrina K. , Lund Mayanna , Devlin Gerry , Troughton Richard W. , Doughty Robert N. , Richards Arthur Mark , Lam Carolyn S. P. 
Published: April 2024

Background
The relationship of serial NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) measurements with changes in cardiac features and outcomes in heart failure (HF) remains incompletely understood. We determined whether common clinical covariates impact these relationships.

Methods and Results

In 2 nationwide observational populations with HF, the relationship of serial NT‐proBNP measurements with serial echocardiographic parameters and outcomes was analyzed, further stratified by HF with reduced versus preserved left ventricular ejection fraction, inpatient versus outpatient enrollment, age, obesity, chronic kidney disease, atrial fibrillation, and attainment of ≥50% guideline‐recommended doses of renin‐angiotensin system inhibitors and β‐blockers. Among 1911 patients (mean±SD age, 65.1±13.4 years; 26.6% women; 62% inpatient and 38% outpatient), NT‐proBNP declined overall, with more rapid declines among inpatients, those with obesity, those with atrial fibrillation, and those attaining ≥50% guideline‐recommended doses. Each doubling of NT‐proBNP was associated with increases in left ventricular volume (by 6.1 mL), E/e′ (transmitral to mitral annular early diastolic velocity ratio) (by 1.4 points), left atrial volume (by 3.6 mL), and reduced left ventricular ejection fraction (by −2.1%). The effect sizes of these associations were lower among patients with HF with preserved ejection fraction, atrial fibrillation, or advanced age (
P
interaction
<0.001). A landmark analysis identified that an SD increase in NT‐proBNP over 6 months was associated with a 27% increase in the risk of the composite event of HF hospitalization or all‐cause death between 6 months and 2 years (adjusted hazard ratio, 1.27 [95% CI, 1.15–1.40];
P
<0.001).

Conclusions
The relationships between NT‐proBNP and structural/functional remodeling differed by age, presence of atrial fibrillation, and HF phenotypes. The association of increased NT‐proBNP with increased risk of adverse outcomes was consistent in all subgroups.
Biomarker Periodic Repolarization Dynamics Indicates Enhanced Risk for Arrhythmias and Sudden Cardiac Death in Myocardial Infarction in Pigs
Authors: Bauer Julia , Vlcek Julia , Pauly Valerie , Hesse Nora , Xia Ruibing , Mo Li , Chivukula Aparna Sharma , Villgrater Hannes , Dressler Marie , Hildebrand Bianca , Wolf Eckhard , Rizas Konstantinos D. , Bauer Axel , Kääb Stefan , Tomsits Philipp , Schüttler Dominik , Clauss Sebastian 
Published: April 2024

Background
Periodic repolarization dynamics (PRD) is an electrocardiographic biomarker that captures repolarization instability in the low frequency spectrum and is believed to estimate the sympathetic effect on the ventricular myocardium. High PRD indicates an increased risk for postischemic sudden cardiac death (SCD). However, a direct link between PRD and proarrhythmogenic autonomic remodeling has not yet been shown.

Methods and Results

We investigated autonomic remodeling in pigs with myocardial infarction (MI)–related ischemic heart failure induced by balloon occlusion of the left anterior descending artery (n=17) compared with pigs without MI (n=11). Thirty days after MI, pigs demonstrated enhanced sympathetic innervation in the infarct area, border zone, and remote left ventricle paralleled by altered expression of autonomic marker genes/proteins. PRD was enhanced 30 days after MI compared with baseline (pre‐MI versus post‐MI: 1.75±0.30 deg
2
versus 3.29±0.79 deg
2
,
P
<0.05) reflecting pronounced autonomic alterations on the level of the ventricular myocardium. Pigs with MI‐related ventricular fibrillation and SCD had significantly higher pre‐MI PRD than pigs without tachyarrhythmias, suggesting a potential role for PRD as a predictive biomarker for ischemia‐related arrhythmias (no ventricular fibrillation versus ventricular fibrillation: 1.50±0.39 deg
2
versus 3.18±0.53 deg
2
[
P
<0.05]; no SCD versus SCD: 1.67±0.32 deg
2
versus 3.91±0.63 deg
2
[
P
<0.01]).

Conclusions
We demonstrate that ischemic heart failure leads to significant proarrhythmogenic autonomic remodeling. The concomitant elevation of PRD levels in pigs with ischemic heart failure and pigs with MI‐related ventricular fibrillation/SCD suggests PRD as a biomarker for autonomic remodeling and as a potential predictive biomarker for ventricular arrhythmias/survival in the context of MI.
Development and Validation of a Nomogram of Persistent Pulmonary Hypertension in Adult Pretricuspid Shunts After Correction
Authors: Zhou Zeming , Gu Yuanrui , Tian Lili , Zheng Hong , Li Shiguo 
Published: April 2024

Background
Pretricuspid shunts have been associated with poorer survival rates in patients with Eisenmenger syndrome compared with postricuspid shunts and complex lesions. However, the risk stratification for persistent pulmonary hypertension (PH) in this population remains uncertain.

Methods and Results

We retrospectively enrolled 103 patients with pretricuspid shunts with high total pulmonary resistance >4.5 Wood units (estimated pulmonary vascular resistance ≥3 Wood units). During a mean±SD follow‐up of 20.95±24.84 months, 32 patients developed postoperative persistent PH after shunt correction. We identified 3 significant predictors of postoperative persistent PH, including mean pulmonary artery pressure after inhaled oxygen ≥40.5 mm Hg (odds ratio [OR], 7.78 [95% CI, 2.02–30.03];
P
<0.01), total pulmonary resistance after inhaled oxygen ≥6.5 Wood units (estimated pulmonary vascular resistance ≥5 Wood units; OR, 12.23 [95% CI, 2.12–70.46];
P
<0.01), and artery oxygen saturation at rest <95% (OR, 3.34 [95% CI, 1.07–10.44];
P
=0.04). We established the prediction model with the C‐statistics of 0.85 (95% CI, 0.77–0.93;
P
<0.01), and the C‐statistic was 0.83 (95% CI, 0.80–0.86) after bootstrapping 10 000 times with a good performance of the nomogram calibration curve for predicting persistent PH.

Conclusions
Our study presents a multivariable risk stratification model for persistent PH after shunt correction in adults with pretricuspid shunts. This model, based on 3 hemodynamic predictors after inhaled oxygen, may assist in identifying individuals at higher risk of persistent PH after shunt correction.
In Vivo Mapping of Myocardial Injury Outside the Infarct Zone: Tissue at an Intermediate Pathological State
Authors: Ren Kaixi , Hou Songwang , Johnson Steven E. , Lomasney Jon , Haney Chad R. , Lee Jungwha , Ge Zhi‐dong , Lee Daniel C. , Goldberger Jeffrey J. , Arora Rishi , Zhao Ming 
Published: April 2024

Background

The goal was to determine the feasibility of mapping the injured‐but‐not‐infarcted myocardium using
99m
Tc‐duramycin in the postischemic heart, with spatial information for its characterization as a pathophysiologically intermediate tissue, which is neither normal nor infarcted.

Methods and Results

Coronary occlusion was conducted in Sprague Dawley rats with preconditioning and 30‐minute ligation. In vivo single‐photon emission computed tomography was acquired after 3 hours (n=6) using
99m
Tc‐duramycin, a phosphatidylethanolamine‐specific radiopharmaceutical. The
99m
Tc‐duramycin
+
areas were compared with infarct and area‐at‐risk (n=8). Cardiomyocytes and endothelial cells were isolated for gene expression profiling. Cardiac function was measured with echocardiography (n=6) at 4 weeks. In vivo imaging with
99m
Tc‐duramycin identified the infarct (3.9±2.4% of the left ventricle and an extensive area 23.7±2.2% of the left ventricle) with diffuse signal outside the infarct, which is pathologically between normal and infarcted (apoptosis 1.8±1.6, 8.9±4.2, 13.6±3.8%; VCAM‐1 [vascular cell adhesion molecule 1] 3.2±0.8, 9.8±4.1, 15.9±4.2/mm
2
; tyrosine hydroxylase 14.9±2.8, 8.6±4.4, 5.6±2.2/mm
2
), with heterogeneous changes including scattered micronecrosis, wavy myofibrils, hydropic change, and glycogen accumulation. The
99m
Tc‐duramycin
+
tissue is quantitatively smaller than the area‐at‐risk (26.7% versus 34.4% of the left ventricle,
P
=0.008). Compared with infarct, gene expression in the
99m
Tc‐duramycin
+
–noninfarct tissue indicated a greater prosurvival ratio (BCL2/BAX [B‐cell lymphoma 2/BCL2‐associated X] 7.8 versus 5.7 [cardiomyocytes], 3.7 versus 3.2 [endothelial]), and an upregulation of ion channels in electrophysiology. There was decreased contractility at 4 weeks (regional fractional shortening −8.6%,
P
<0.05; circumferential strain −52.9%,
P
<0.05).

Conclusions
The injured‐but‐not‐infarcted tissue, being an intermediate zone between normal and infarct, is mapped in vivo using phosphatidylethanolamine‐based imaging. The intermediate zone contributes significantly to cardiac dysfunction.
European and US Guideline‐Based Statin Eligibility, Genetically Predicted Coronary Artery Disease, and the Risk of Major Coronary Events
Authors: Park Hanjin , Kim Daehoon , You Seng Chan , Jang Eunsun , Yu Hee Tae , Kim Tae‐Hoon , Kim Dong‐min , Sung Jung‐Hoon , Pak Hui‐Nam , Lee Moon‐Hyoung , Yang Pil‐Sung , Joung Boyoung 
Published: April 2024

Background
A study was designed to investigate whether the coronary artery disease polygenic risk score (CAD‐PRS) may guide lipid‐lowering treatment initiation as well as deferral in primary prevention beyond established clinical risk scores.

Methods and Results
Participants were 311 799 individuals from the UK Biobank free of atherosclerotic cardiovascular disease, diabetes, chronic kidney disease, and lipid‐lowering treatment at baseline. Participants were categorized as statin indicated, statin indication unclear, or statin not indicated as defined by the European and US guidelines on statin use. For a median of 11.9 (11.2–12.6) years, 8196 major coronary events developed. CAD‐PRS added to European‐Systematic Coronary Risk Evaluation 2 (European‐SCORE2) and US‐Pooled Cohort Equation (US‐PCE) identified 18% and 12% of statin‐indication‐unclear individuals whose risk of major coronary events were the same as or higher than the average risk of statin‐indicated individuals and 16% and 12% of statin‐indicated individuals whose major coronary event risks were the same as or lower than the average risk of statin‐indication‐unclear individuals. For major coronary and atherosclerotic cardiovascular disease events, CAD‐PRS improved C‐statistics greater among statin‐indicated or statin‐indication‐unclear than statin‐not‐indicated individuals. For atherosclerotic cardiovascular disease events, CAD‐PRS added to the European evaluation and US equation resulted in a net reclassification improvement of 13.6% (95% CI, 11.8–15.5) and 14.7% (95% CI, 13.1–16.3) among statin‐indicated, 10.8% (95% CI, 9.6–12.0) and 15.3% (95% CI, 13.2–17.5) among statin‐indication‐unclear, and 0.9% (95% CI, 0.6–1.3) and 3.6% (95% CI, 3.0–4.2) among statin‐not‐indicated individuals.

Conclusions
CAD‐PRS may guide statin initiation as well as deferral among statin‐indication‐unclear or statin‐indicated individuals as defined by the European and US guidelines. CAD‐PRS had little clinical utility among statin‐not‐indicated individuals.
Secondary Prevention in Patients With Stroke Versus Myocardial Infarction: Analysis of 2 National Cohorts
Authors: Rivier Cyprien A. , Acosta Julian N. , Leasure Audrey C. , Forman Rachel , Sharma Richa , de Havenon Adam , Spatz Erica S. , Inzucchi Silvio E. , Kernan Walter N. , Falcone Guido J. , Sheth Kevin N. 
Published: April 2024

Background
The implementation of preventive therapies among patients with stroke remains inadequately explored, especially when compared with patients with myocardial infarction (MI), despite sharing similar vascular risk profiles. We tested the hypothesis that participants with a history of stroke have a worse cardiovascular prevention profile in comparison to participants with MI.

Methods and Results

In cross‐sectional analyses within the UK Biobank and All of Us Research Program, involving 14 760 (9193 strokes, 5567 MIs) and 7315 (2948 strokes, 4367 MIs) participants, respectively, we evaluated cardiovascular prevention profiles assessing low‐density lipoprotein (<100 mg/dL), blood pressure (systolic, <140 mm Hg; and diastolic, <90 mm Hg), statin and antiplatelet use, and a cardiovascular prevention score that required meeting at least 3 of these criteria. The results revealed that, within the UK Biobank, patients with stroke had significantly lower odds of meeting all the preventive criteria compared with patients with MI: low‐density lipoprotein control (odds ratio [OR], 0.73 [95% CI, 0.68–0.78];
P
<0.001), blood pressure control (OR, 0.63 [95% CI, 0.59–0.68];
P
<0.001), statin use (OR, 0.45 [95% CI, 0.42–0.48];
P
<0.001), antiplatelet therapy use (OR, 0.30 [95% CI, 0.27–0.32];
P
<0.001), and cardiovascular prevention score (OR, 0.42 [95% CI, 0.39–0.45];
P
<0.001). Similar patterns were observed in the All of Us Research Program, with significant differences across all comparisons (
P
<0.05), and further analysis suggested that the odds of having a good cardiovascular prevention score were influenced by race and ethnicity as well as neighborhood deprivation levels (interaction
P
<0.05 in both cases).

Conclusions
In 2 independent national cohorts, patients with stroke showed poorer cardiovascular prevention profiles and lower adherence to guideline‐directed therapies compared with patients with MI. These findings underscore the need to explore the reasons behind the underuse of secondary prevention in vulnerable stroke survivors.