scholarly journals Association of Longitudinal Change in High-Sensitivity Troponin with All-Cause Mortality in Coronary Artery Disease: The Heart and Soul Study

Cardiology ◽  
2020 ◽  
Vol 145 (2) ◽  
pp. 63-70
Author(s):  
Yaanik B. Desai ◽  
Rakesh K. Mishra ◽  
Qizhi Fang ◽  
Mary A. Whooley ◽  
Nelson B. Schiller

Background: Serial increases in high-sensitivity cardiac troponin (hs-cTnT) have been associated with death in community-dwelling adults, but the association remains uninvestigated in those with coronary artery disease (CAD). Methods: We measured hs-cTnT at baseline and after 5 years in 635 ambulatory Heart and Soul Study patients with CAD. We also performed echocardiography at rest and after treadmill exercise at baseline and after 5 years. Participants were subsequently followed for the outcome of death. We used a multivariable-adjusted Cox proportional hazards model to evaluate the association between 5-year change in hs-cTnT and subsequent all-cause mortality. Results: Of the 635 subjects, there were 386 participants (61%) who had an increase in hs-cTnT levels between baseline and year 5 measurements (median increase 5.6 pg/mL, IQR 3.2–9.9 pg/mL). There were 182 deaths after a mean 4.2-year follow-up after the year 5 visit. After adjusting for clinical variables, a >50% increase in hs-cTnT between baseline and year 5 was associated with a nearly 2-fold increased risk of death from any cause (hazard ratio 1.7, 95% confidence interval 1.1–2.7). When addition of year 5 hs-cTnT was compared to a model including clinical variables and baseline hs-cTnT, there was a modest but statistically significant increase in C-statistic from 0.82 to 0.83 (p = 0.04). Conclusion: In ambulatory patients with CAD, serial increases in hs-cTnT over time are associated with an increased risk of death.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H W Zhang ◽  
Y X Cao ◽  
J L Jin ◽  
Y L Guo ◽  
Y Gao ◽  
...  

Abstract Background It has been reported that coronary artery disease (CAD) is characterized by inflammation and non-obstructive CAD (NOCAD) increases the risk of cardiovascular events (CVEs) compared with ones with normal or near-normal coronary arteries (NNCA), even is similar to obstructive CAD (OCAD). We hypothesized that elevated high-sensitivity C-reactive protein (hs-CRP) may be linked to CVEs in those patients with NOCAD. Purpose To investigate the predictive role of hs-CRP in patients with NOCAD. Methods Of 7,746 consecutive patients with angina-like chest pain admissions, 4,662 eligible patients were enrolled who received coronary artery angiography (CAG) and followed up for the CVEs comprising all-cause mortality, myocardial infarction, stroke and late revascularization. According to the results of CAG, the patients were classified as NNCA group (<20% stenosis, n=698, 15.0%), NOCAD group (20–49% stenosis, n=639, 14.3%), and OCAD group (≥50% stenosis, n=3325, 70.7%). They were further subdivided into 3 groups according to baseline hs-CRP levels (<1, 1–3 and >3 mg/L). Proportional hazards models were used to assess the risk of CVEs in all patients enrolled. Results A total of 338 patients (7.3%) experienced CVEs during an average of 13403 person-years follow-up. Patients with NOCAD and OCAD had higher rates of CVEs compared to those with NNCA (p<0.05, respectively). In Cox's models after adjustment of confounders, the risk of CVEs elevated with the increasing degrees of CAD with hazard ratio of 2.01 [95% confidence interval (95% CI): 1.07–3.79, p=0.03] for patients with NOCAD and 2.81 (95% CI: 1.60–4.93, p<0.001) for patients with OCAD compared with the NNCA group. Moreover, elevated hs-CRP levels were associated with the severity of coronary lesions and an elevated increased risk of CVEs in patients with NOCAD and OCAD compared those with NNCA (p<0.05, respectively). Conclusions Patients with NOCAD had indeed worse outcomes and hs-CRP levels were positively in relation to the CVEs in those with NOCAD, which may help to the risk assessment in ones with NOCAD. Acknowledgement/Funding This study was partly supported by Capital Health Development Fund (201614035) and CAMS Innovation Fund for Medical Sciences (2016-I2M-1-011) awarded


2017 ◽  
Vol 37 (11) ◽  
pp. 2213-2219 ◽  
Author(s):  
Xuechen Chen ◽  
Yuan Zhang ◽  
Qian Chen ◽  
Qing Li ◽  
Yanping Li ◽  
...  

Objective— The present study was designed to evaluate the association of circulating fetuin-A with cardiovascular disease (CVD) and all-cause mortality. Approach and Results— We measured plasma fetuin-A in 1620 patients using an enzyme-linked immunosorbent assay kit. The patients were members of the Guangdong coronary artery disease cohort and were recruited between October 2008 and December 2011. Cox regression models were used to estimate the association between plasma fetuin-A and the risk of mortality. A total of 206 deaths were recorded during a median follow-up of 5.9 years, 146 of whom died from CVD. The hazard ratios for the second and third tertiles of the fetuin-A levels (using the first tertile as a reference) were 0.65 (95% confidence interval, 0.44–0.96) and 0.51 (95% confidence interval, 0.33–0.78) for CVD mortality ( P =0.005) and 0.65 (95% confidence interval, 0.47–0.91) and 0.48 (95% confidence interval, 0.33–0.70) for all-cause mortality ( P <0.001), respectively. Conclusions— Lower plasma fetuin-A levels were associated with an increased risk of all-cause and CVD mortality in patients with coronary artery disease independently of traditional CVD risk factors.


Circulation ◽  
2021 ◽  
Vol 144 (13) ◽  
pp. 1024-1038 ◽  
Author(s):  
Harmony R. Reynolds ◽  
Leslee J. Shaw ◽  
James K. Min ◽  
Courtney B. Page ◽  
Daniel S. Berman ◽  
...  

Background: The ISCHEMIA trial (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches) postulated that patients with stable coronary artery disease (CAD) and moderate or severe ischemia would benefit from revascularization. We investigated the relationship between severity of CAD and ischemia and trial outcomes, overall and by management strategy. Methods: In total, 5179 patients with moderate or severe ischemia were randomized to an initial invasive or conservative management strategy. Blinded, core laboratory–interpreted coronary computed tomographic angiography was used to assess anatomic eligibility for randomization. Extent and severity of CAD were classified with the modified Duke Prognostic Index (n=2475, 48%). Ischemia severity was interpreted by independent core laboratories (nuclear, echocardiography, magnetic resonance imaging, exercise tolerance testing, n=5105, 99%). We compared 4-year event rates across subgroups defined by severity of ischemia and CAD. The primary end point for this analysis was all-cause mortality. Secondary end points were myocardial infarction (MI), cardiovascular death or MI, and the trial primary end point (cardiovascular death, MI, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest). Results: Relative to mild/no ischemia, neither moderate ischemia nor severe ischemia was associated with increased mortality (moderate ischemia hazard ratio [HR], 0.89 [95% CI, 0.61–1.30]; severe ischemia HR, 0.83 [95% CI, 0.57–1.21]; P =0.33). Nonfatal MI rates increased with worsening ischemia severity (HR for moderate ischemia, 1.20 [95% CI, 0.86–1.69] versus mild/no ischemia; HR for severe ischemia, 1.37 [95% CI, 0.98–1.91]; P =0.04 for trend, P =NS after adjustment for CAD). Increasing CAD severity was associated with death (HR, 2.72 [95% CI, 1.06–6.98]) and MI (HR, 3.78 [95% CI, 1.63–8.78]) for the most versus least severe CAD subgroup. Ischemia severity did not identify a subgroup with treatment benefit on mortality, MI, the trial primary end point, or cardiovascular death or MI. In the most severe CAD subgroup (n=659), the 4-year rate of cardiovascular death or MI was lower in the invasive strategy group (difference, 6.3% [95% CI, 0.2%–12.4%]), but 4-year all-cause mortality was similar. Conclusions: Ischemia severity was not associated with increased risk after adjustment for CAD severity. More severe CAD was associated with increased risk. Invasive management did not lower all-cause mortality at 4 years in any ischemia or CAD subgroup. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT01471522.


Author(s):  
Mouaz H Al-Mallah ◽  
Kamal Kassem ◽  
Owais Khawaja ◽  
Thomas Song ◽  
Chad Poopat ◽  
...  

Background: Myocardial bridging (MB) is frequently seen on coronary CT angiography (CCTA). However, there has been conflicting data on the prognostic value of MB. The aim of this analysis is to determine the prognostic value of MB in patients without obstructive coronary artery disease (CAD) (<50 diameter stenosis). Methods: We included patients with no known prior coronary artery disease (CAD) who underwent CCTA for various clincial reasons. Patients with obstructive CAD on CCTA were excluded. The study cohort was followed for all cause mortality or myocardial infarction (MI) (median follow-up 1.7 years). Group comparisons were made between patients with patients with or without MB. Results: A total of 715 patients were included in this analysis of which 68 patients had MB (10%). 73% of the bridges were in the mid LAD and 22% had bridging in the distal LAD. 48% of the study cohort had normal coronaries, while 52% had evidence of non obstructive CAD. There were no differences in the baseline characteristics, symptomatic status or prevalence of non obstructive CAD between the two groups (all p>0.5). After a median follow-up duration of 1.7 years, 23 patients died and 10 patients experienced myocardial infarction. There were no statistically significant differences in the rate of death/MI between the two groups (figure). Using multivariable Cox regression, the presence of MB was not associated with increased risk for death/MI (Adjusted HR 0.4, 95% confidence interval 0.1 -2.8, p=0.34) Conclusions: In patients with non-obstructive CAD, MB is not associated with increased risk for all cause death or MI.


2021 ◽  
Vol 12 ◽  
Author(s):  
He-Ping Lei ◽  
Min Qin ◽  
Li-Yun Cai ◽  
Hong Wu ◽  
Lan Tang ◽  
...  

It is widely accepted that genetic polymorphisms impact atorvastatin (ATV) metabolism, clinical efficacy, and adverse events. The objectives of this study were to identify novel genetic variants influencing ATV metabolism and outcomes in Chinese patients with coronary artery disease (CAD). A total of 1079 CAD patients were enrolled and followed for 5 years. DNA from the blood and human liver tissue samples were genotyped using either Global Screening Array-24 v1.0 BeadChip or HumanOmniZhongHua-8 BeadChip. Concentrations of ATV and its metabolites in plasma and liver samples were determined using a verified ultra-performance liquid chromatography mass spectrometry (UPLC-MS/MS) method. The patients carrying A allele for the rs4148323 polymorphism (UGT1A1) showed an increase in 2-hydroxy ATV/ATV ratio (p = 1.69E−07, false discovery rate [FDR] = 8.66E−03) relative to the value in individuals without the variant allele. The result was further validated by an independent cohort comprising an additional 222 CAD patients (p = 1.08E−07). Moreover, the rs4148323 A allele was associated with an increased risk of death (hazard ratio [HR] 1.774; 95% confidence interval [CI], 1.031–3.052; p = 0.0198). In conclusion, our results suggested that the UGT1A1 rs4148323 A allele was associated with increased 2-hydroxy ATV formation and was a significant death risk factor in Chinese patients with CAD.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kunming Bao ◽  
Haozhang Huang ◽  
Guoyong Huang ◽  
Junjie Wang ◽  
Ying Liao ◽  
...  

Abstract Background The platelet-to-hemoglobin ratio (PHR) has emerged as a prognostic biomarker in coronary artery disease (CAD) patients after PCI but not clear in CAD complicated with congestive heart failure (CHF). Hence, we aimed to assess the association between PHR and long-term all-cause mortality among CAD patients with CHF. Methods Based on the registry at Guangdong Provincial People’s Hospital in China, we analyzed data of 2599 hospitalized patients who underwent coronary angiography (CAG) and were diagnosed with CAD complicated by CHF from January 2007 to December 2018. Low PHR was defined as ˂ 1.69 (group 1) and high PHR as ≥ 1.69 (group 2). Prognosis analysis was performed using Kaplan–Meier method. To assess the association between PHR and long-term all-cause mortality, a Cox-regression model was fitted. Results During a median follow-up of 5.2 (3.1–7.8) years, a total of 985 (37.9%) patients died. On the Kaplan–Meier analysis, patients in high PHR group had a worse prognosis than those in low PHR group (log-rank, p = 0.0011). After adjustment for confounders, high PHR was correlated with an increased risk of long-term all-cause mortality in CAD patients complicated with CHF. (adjusted hazard ratio [aHR], 1.31; 95% confidence interval [CI], 1.13–1.52, p < 0.0001). Conclusion Elevated PHR is correlated with an increased risk of long-term all-cause mortality in CAD patients with CHF. These results indicate that PHR may be a useful prognostic biomarker for this population. Meanwhile, it is necessary to take effective preventive measures to regulate both hemoglobin levels and platelet counts in this population.


2019 ◽  
Vol 20 (21) ◽  
pp. 5508 ◽  
Author(s):  
Cecilia Vecoli ◽  
Andrea Borghini ◽  
Silvia Pulignani ◽  
Antonella Mercuri ◽  
Stefano Turchi ◽  
...  

Aging is one of the main risk factors for cardiovascular disease, resulting in a progressive organ and cell decline. This study evaluated a possible joint impact of two emerging hallmarks of aging, leucocyte telomere length (LTL) and common mitochondrial DNA deletion (mtDNA4977), on major adverse cardiovascular events (MACEs) and all-cause mortality in patients with coronary artery disease (CAD). We studied 770 patients (673 males, 64.8 ± 8.3 years) with known or suspected stable CAD. LTL and mtDNA4977 deletion were assessed in peripheral blood using qRT-PCR. During a median follow-up of 5.4 ± 1.2 years, MACEs were 140 while 86 deaths were recorded. After adjustments for confounding risk factors, short LTLs and high mtDNA4977 deletion levels acted independently as predictors of MACEs (HR: 2.2, 95% CI: 1.2–3.9, p = 0.01 and HR: 1.7, 95% CI: 1.1–2.9, p = 0.04; respectively) and all-cause mortality events (HR: 2.1, 95% CI: 1.1–4.6, p = 0.04 and HR: 2.3, 95% CI: 1.1–4.9, p = 0.02; respectively). Patients with both short LTLs and high mtDNA4977 deletion levels had an increased risk for MACEs (HR: 4.3; 95% CI: 1.9–9.6; p = 0.0006) and all-cause mortality (HR: 6.0; 95% CI: 2.0–18.4; p = 0.001). The addition of mtDNA4977 deletion to a clinical reference model was associated with a significant net reclassification improvement (NRI = 0.18, p = 0.01). Short LTL and high mtDNA4977 deletion showed independent and joint predictive value on adverse cardiovascular outcomes and all-cause mortality in patients with CAD. These findings strongly support the importance of evaluating biomarkers of physiological/biological age, which can predict disease risk and mortality more accurately than chronological age.


2019 ◽  
Vol 26 (12) ◽  
pp. 1273-1284 ◽  
Author(s):  
George CM Siontis ◽  
Mattia Branca ◽  
Patrick Serruys ◽  
Sigmund Silber ◽  
Lorenz Räber ◽  
...  

Aims To investigate the clinical relevance of contemporary cut-offs of left ventricular ejection fraction (LVEF) including an intermediate phenotype with mid-range reduced ejection fraction among patients with coronary artery disease undergoing percutaneous coronary intervention. Methods and results Patient-level data were summarized from five randomized clinical trials in which 6198 patients underwent clinically indicated percutaneous coronary intervention in different clinical settings. We assessed all-cause mortality as primary endpoint at five-year follow-up. According to the proposed LVEF cut-offs, 3816 patients were included in the preserved LVEF group (LVEF ≥ 50%), 1793 in the mid-range reduced LVEF group (LVEF 40–49%) and 589 patients in the reduced LVEF group (LVEF < 40%). Patients in the reduced LVEF group were at increased risk for the primary outcome of all-cause mortality compared with both, preserved and mid-range LVEF throughout five years of follow-up (adjusted hazard ratio 2.39 (95% confidence interval 1.75–3.28, p < 0.001) and 1.68 (95% confidence interval 1.34–2.10, p < 0.001), respectively). The risk of cardiac death and the composite endpoint of cardiac death, myocardial infarction, or stroke were higher for patients in the reduced LVEF group compared with the preserved and mid-range reduced LVEF groups, but also for the mid-range LVEF compared with preserved LVEF group (adjusted p < 0.05 for all comparisons) throughout five years. Irrespective of clinical presentation at baseline (stable coronary artery disease or acute coronary syndrome), patients with reduced or mid-range LVEF were at increased risk of all-cause mortality and cardiac death up to five years compared with the other group (adjusted p < 0.05 for all comparisons). Conclusion Patients with reduced LVEF <40% or mid-range LVEF 40–49% in the context of coronary artery disease undergoing clinically indicated percutaneous coronary intervention are at increased risk of all-cause mortality, cardiac death and the composite of cardiac death, stroke and myocardial infarction throughout five years of follow-up. The recently proposed LVEF cut-offs contribute to the differentiation and risk stratification of patients with ischaemic heart disease.


2011 ◽  
Vol 57 (1) ◽  
pp. 33-39 ◽  
Author(s):  
WH Wilson Tang ◽  
Yuping Wu ◽  
Stephen J Nicholls ◽  
Stanley L Hazen

BACKGROUND Myeloperoxidase (MPO) concentrations predict adverse clinical outcomes in the setting of acute coronary syndromes and heart failure, but the prognostic role of MPO in stable patients with known atherosclerotic burden is unclear. METHODS We examined plasma MPO concentrations and their relationship with prevalent significant coronary artery disease (defined as &gt;50% stenosis in any coronary vessel) and incident major adverse cardiovascular events (MACEs), including death, myocardial infarction, and stroke, in a 3-year prospective follow-up study of 1895 patients undergoing elective coronary angiography. RESULTS The median plasma MPO concentration was 101 pmol/L (interquartile range 68–187 pmol/L). Patients with plasma MPO concentrations &gt;322 pmol/L (14.6% of population) had increased risk of developing future MACEs [hazard ratio (HR) 1.78, 95% CI 1.33–2.37, P &lt; 0.001], and MPO as a single variable predictor of MACE showed an area under the ROC curve of 0.67. After adjusting for traditional cardiac risk factors, creatinine clearance, B-type natriuretic peptide, and high-sensitivity C-reactive protein (hsCRP), increased MPO concentrations remained significantly associated with incident MACEs over the ensuing 3-year period (HR 1.71; 95% CI 1.27–2.30, P &lt; 0.001). In patients with increased hsCRP, MPO ≤322 pmol/L was associated with lower event rates than observed with MPO &gt;322 pmol/L. CONCLUSIONS Plasma MPO concentrations provide independent prognostic value for the prediction of long-term incident MACEs in a stable, medically managed patient population with coronary artery disease. In individuals with increased hsCRP concentrations, we observed lower risk of incident MACEs when concomitant MPO concentrations were low vs when MPO concentrations were high.


2021 ◽  
Author(s):  
Kunming Bao ◽  
Haozhang Huang ◽  
Guoyong Huang ◽  
Junjie Wang ◽  
Ying Liao ◽  
...  

Abstract Background The platelet-to-hemoglobin ratio (PHR) has emerged as a prognostic biomarker in coronary artery disease (CAD) patients after PCI but not clear in CAD complicated with congestive heart failure (CHF). Hence, we aimed to assess the association between PHR and long-term all-cause mortality among CAD patients with CHF. Methods Based on the registry at Guangdong Provincial People’s Hospital in China, we analyzed data of 2,599 hospitalized patients who underwent coronary angiography (CAG) and were diagnosed with CAD complicated by CHF from January 2007 to December 2018. Low PHR was defined as˂1.69 (group 1) and high PHR as ≥ 1.69 (group 2). Prognosis analysis was performed using Kaplan-Meier methods. To assess the association between PHR and long-term all-cause mortality, a Cox-regression model was fitted. Results During a median follow-up of 5.2 (3.1–7.8) years, a total of 985 (37.9%) patients died. On the Kaplan-Meier analysis, patients in high PHR group had a worse prognosis than low PHR group (log-rank, p = 0.0011). After adjustment for confounders, high PHR was correlated with an increased risk of long-term all-cause mortality in CAD patients complicated with CHF. (adjusted hazard ratio [aHR], 1.21; 95% confidence interval [CI], 1.03–1.41, p = 0.02). Conclusion Elevated PHR is correlated with an increased risk of long-term all-cause mortality in CAD patients with CHF. These results indicate that PHR may be a useful prognostic biomarker for this population. Meanwhile, it is necessary to take effective preventive measures to regulate both hemoglobin levels and platelet counts in this population.


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