scholarly journals Elevated plasma cystathionine is associated with increased risk of mortality among patients with suspected or established coronary heart disease

2019 ◽  
Vol 109 (6) ◽  
pp. 1546-1554 ◽  
Author(s):  
Indu Dhar ◽  
Vegard Lysne ◽  
Gard F T Svingen ◽  
Per M Ueland ◽  
Jesse F Gregory ◽  
...  
Author(s):  
Espen Ø Bjørnestad ◽  
Indu Dhar ◽  
Gard F T Svingen ◽  
Eva R Pedersen ◽  
Mads M Svenningsson ◽  
...  

Abstract Aims Trimethyllysine (TML) is involved in carnitine synthesis, serves as a precursor of trimethylamine N-oxide (TMAO) and is associated with cardiovascular events in patients with established coronary heart disease (CHD). We prospectively examined circulating TML as a predictor of all-cause and cardiovascular mortality in community-dwelling adults and patients with CHD. Methods and Results By Cox regression modelling, risk associations were examined in 6393 subjects in the community-based Hordaland Health Study (HUSK). A replication study was conducted among 4117 patients with suspected stable angina pectoris in the Western Norway Coronary Angiography Cohort (WECAC). During a mean follow-up of 10.5 years in the HUSK-cohort, 884 (13.8%) subjects died, of whom 287 from cardiovascular causes. After multivariable adjustments for traditional cardiovascular risk factors, the hazard ratio (HR) (95% CI) for all-cause mortality comparing the 4th vs. 1st TML-quartile was 1.66 (1.31-2.10, p < 0.001). Particularly strong associations were observed for cardiovascular mortality (HR [95% CI] 2.04 [1.32-3.15, p = 0.001]). Corresponding risk-estimates in the WECAC (mean follow-up of 9.8 years) were 1.35 [1.10-1.66, p = 0.004] for all-cause and 1.45 [1.06-1.98, p = 0.02] for cardiovascular mortality. Significant correlations between plasma TML and TMAO were observed in both cohorts (rs≥0.42, p < 0.001); however, additional adjustments for TMAO did not materially influence the risk associations, and no effect modification by TMAO was found. Conclusion Elevated TML-levels were associated with increased risk of all-cause and cardiovascular mortality both in subjects with and without established CHD.


2010 ◽  
Vol 72 (7) ◽  
pp. 664-671 ◽  
Author(s):  
Lana L. Watkins ◽  
James A. Blumenthal ◽  
Michael A. Babyak ◽  
Jonathan R. T. Davidson ◽  
Charles B. McCants ◽  
...  

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii493-iii493
Author(s):  
Stephen Zewinger ◽  
Marcus Kleber ◽  
Hubert Scharnagl ◽  
Danilo Fliser ◽  
Winfried März ◽  
...  

Author(s):  
Paddy Ssentongo ◽  
Anna E. Ssentongo ◽  
Emily S. Heilbrunn ◽  
Djibril M Ba ◽  
Vernon M. Chinchilli

Background Exploring the association of coronavirus-2019 disease (COVID-19) mortality with chronic pre-existing conditions may promote the importance of targeting these populations during this pandemic to optimize survival. The objective of this systematic review and meta-analysis is to explore the association of pre-existing conditions with COVID-19 mortality. Methods We searched MEDLINE, OVID databases, SCOPUS, and medrxiv.org for the period December 1, 2019, to May 1, 2020. The outcome of interest was the risk of COVID-19 mortality in patients with and without pre-existing conditions. Comorbidities explored were cardiovascular diseases (coronary artery disease, hypertension, cardiac arrhythmias, and congestive heart failure), chronic obstructive pulmonary disease, type 2 diabetes, cancer, chronic kidney disease, chronic liver disease, and stroke. Two independent reviewers extracted data and assessed the risk of bias. All analyses were performed using random-effects models and heterogeneity was quantified. Results Ten chronic conditions from 19 studies were included in the meta-analysis (n = 61,455 patients with COVID-19; mean age, 61 years; 57% male). Overall the between-study study heterogeneity was medium and studies had low publication bias and high quality. Coronary heart disease, hypertension, congestive heart failure, and cancer significantly increased the risk of mortality from COVID-19. The risk of mortality from COVID-19 in patients with coronary heart disease was 2.4 times as high as those without coronary heart disease (RR= 2.40, 95%CI=1.71-3.37, n=5) and twice as high in patients with hypertension as high as that compared to those without hypertension (RR=1.89, 95%CI= 1.58-2.27, n=9). Patients with cancer also were at twice the risk of mortality from COVID-19 compared to those without cancer (RR=1.93 95%CI 1.15-3.24, n=4), and those with congestive heart failure were at 2.5 times the risk of mortality compared to those without congestive heart failure (RR=2.66, 95%CI 1.58-4.48, n=3). Conclusions COVID-19 patients with all any cardiovascular disease, coronary heart disease, hypertension, congestive heart failure, and cancer have an increased risk of mortality. Tailored infection prevention and treatment strategies targeting this high-risk population are warranted to optimize survival.


2021 ◽  
pp. jech-2020-214358
Author(s):  
Pekka Martikainen ◽  
Kaarina Korhonen ◽  
Aline Jelenkovic ◽  
Hannu Lahtinen ◽  
Aki Havulinna ◽  
...  

BackgroundGenetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events.MethodsThe data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers.ResultsAllowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education.ConclusionsPRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.


2017 ◽  
Vol 3 ◽  
pp. 233372141769667 ◽  
Author(s):  
Minjee Lee ◽  
M. Mahmud Khan ◽  
Brad Wright

Objective: We investigated the association between childhood socioeconomic status (SES) and coronary heart disease (CHD) in older Americans. Method: We used Health and Retirement Study data from 1992 to 2012 to examine a nationally representative sample of Americans aged ≥50 years ( N = 30,623). We modeled CHD as a function of childhood and adult SES using maternal and paternal educational level as a proxy for childhood SES. Results: Respondents reporting low childhood SES were significantly more likely to have CHD than respondents reporting high childhood SES. Respondents reporting both low childhood and adult SES were 2.34 times more likely to have CHD than respondents reporting both high childhood and adult SES. People with low childhood SES and high adult SES were 1.60 times more likely than people with high childhood SES and high adult SES to report CHD in the fully adjusted model. High childhood SES and low adult SES increased the likelihood of CHD by 13%, compared with high SES both as a child and adult. Conclusion: Childhood SES is significantly associated with increased risk of CHD in later life among older adult Americans.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Elena M. Yubero-Serrano ◽  
Juan F. Alcalá-Diaz ◽  
Francisco M. Gutierrez-Mariscal ◽  
Antonio P. Arenas-de Larriva ◽  
Patricia J. Peña-Orihuela ◽  
...  

Abstract Background Peripheral artery disease (PAD) is recognized as a significant predictor of mortality and adverse cardiovascular outcomes in patients with coronary heart disease (CHD). In fact, coexisting PAD and CHD is strongly associated with a greater coronary event recurrence compared with either one of them alone. High-density lipoprotein (HDL)-mediated cholesterol efflux capacity (CEC) is found to be inversely associated with an increased risk of incident CHD. However, this association is not established in patients with PAD in the context of secondary prevention. In this sense, our main aim was to evaluate the association between CEC and PAD in patients with CHD and whether the concurrent presence of PAD and T2DM influences this association. Methods CHD patients (n = 1002) from the CORDIOPREV study were classified according to the presence or absence of PAD (ankle-brachial index, ABI ≤ 0.9 and ABI > 0.9 and < 1.4, respectively) and T2DM status. CEC was quantified by incubation of cholesterol-loaded THP-1 cells with the participants' apoB-depleted plasma was performed. Results The presence of PAD determined low CEC in non-T2DM and newly-diagnosed T2DM patients. Coexisting PAD and newly-diagnosed T2DM provided and additive effect providing an impaired CEC compared to non-T2DM patients with PAD. In established T2DM patients, the presence of PAD did not determine differences in CEC, compared to those without PAD, which may be restored by glucose-lowering treatment. Conclusions Our findings suggest an inverse relationship between CEC and PAD in CHD patients. These results support the importance of identifying underlying mechanisms of PAD, in the context of secondary prevention, that provide potential therapeutic targets, that is the case of CEC, and establishing strategies to prevent or reduce the high risk of cardiovascular events of these patients. Trial registrationhttps://clinicaltrials.gov/ct2/show/NCT00924937. Unique Identifier: NCT00924937


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