Background and methods Recent guidelines have included glycated haemoglobin (HbA1c) ≥48 mmol/L as a diagnostic criterion for diabetes mellitus (DM) in addition to plasma glucose (PG) concentrations, mainly based on the relationship between hyperglycemia and microvascular disease [1]. However, increased HbA1c may stem not only from hyperglycemia, and the risk association between HbA1c and long-term survival in patients with stable coronary heart disease and HbA1c ≥48 mmol/L but no previous DM according to PG is uncertain. We explored the relationship between HbA1c and survival among patients with and without DM who were evaluated for stable angina in the period 2000–2004. Endpoints were obtained from the Norwegian Cause of Death Registry. Results In total, 4164 patients were evaluated by cardiac cathetherization, of whom 576 patients (13.8%) had DM (median HbA1c 55 mmol/L) according to self-report and/or baseline PG concentrations. Of the remaining 3588 patients 1026 had HbA1c ≥48 mmol/L; however, HbA1c did not correlate with the HOMA2 insulin resistance index or fasting PG in these patients. During median (25–75 percentile) follow-up time of 14.0 (12.1–15.4) years a total of 1328 patients (31.9%) died, of whom 582 from cardiovascular causes. In patients with DM according to PG, HbA1c trended towards positive associations with all-cause and CVD mortality when adjusted for age and gender (HRs (95% CIs) 1.13 (0.99–1.28) and 1.16 (0.98–1.39) per 1SD, respectively). However, HbA1c was not associated with survival in either the group of patients without DM and HbA1c <48 mmol/L (median HbA1c 38 mmol/L) (HRs (95% CIs) 0.99 (0.92–1.06) and 0.96 (0.86–1.08) for all-cause and CVD mortality, respectively) or patients without DM but having HbA1c ≥48 mmol/L (median HbA1c 53 mmol/L) (HRs (95% CIs) 0.99 (0.88–1.12) and 1.04 (0.88–1.22)). Conclusion In patients evaluated for stable angina pectoris about two decades ago, almost a third of patients with no history of DM according to PG still had HbA1c concentrations indicating DM according to current guidelines. Including these patients in the DM category yielded similar percentages of patients with DM as observed in recent populations with stable coronary disease [2]. However, as opposed to what we observed in patients with DM, HbA1c did not show any association with very long-term survival among patients without DM. Our findings therefore question the use of HbA1c in the diagnosis of DM, especially in terms of risk assessment for longevity among patients with chronic coronary syndrome. Funding Acknowledgement Type of funding sources: None.
Background Trimethylamine N-oxide (TMAO) is an amine oxide generated by gut microbial metabolism. Emerging evidence suggests pro-atherosclerotic and pro-inflammatory properties of TMAO; however, the clinical utility of circulating TMAO in risk stratification is uncertain. Purpose We prospectively assessed relationships of plasma TMAO with long-term risk of all-cause, cardiovascular (CV) and non-CV mortality in community-dwelling adults and patients with coronary heart disease. Methods By Cox modelling, risk-associations were examined in the Hordaland Health Study (HUSK; 6393 community-based adults) and the Western Norway Coronary Angiography Cohort (WECAC; 4132 patients with suspected chronic coronary syndrome). Results Median follow-up time was 11.0 and 10.3 years in HUSK and WECAC, respectively. Following adjustments for established CV risk factors in HUSK, the HRs (95% CIs) comparing the 4th vs. 1st TMAO-quartile were 1.11 (0.88–1.40), 0.97 (0.65–1.46) and 1.17 (0.88–1.54) for all-cause, CV and non-CV mortality, respectively. Corresponding risk estimates in WECAC were 1.07 (0.86–1.32), 1.16 (0.83–1.62) and 1.02 (0.77–1.34). Similar results were observed in patients with angiographically significant coronary artery disease and patients with reduced left ventricular ejection fraction. Conclusion Plasma TMAO was not predictive of long-term all-cause, CV or non-CV mortality in patients with or without established coronary heart disease. This large-scale study does not support a role of TMAO for patient risk stratification in primary or secondary prevention. Funding Acknowledgement Type of funding sources: None.
Funding Acknowledgements Type of funding sources: None. Background/Aim Increased plasma trimetyllysine (TML), a methylated amino acid, has recently been linked to higher risk of acute myocardial infarction (AMI). TML is also a precursor of trimethylamine-N oxide (TMAO), which has been linked to increased cardiovascular risk, including that of atrial fibrillation (AF). We investigated the association between TML and new-onset AF in two large Norwegian cohorts. Methods The primary cohort consisted of 6396 participants in the community-based Hordaland Health Study (HUSK). The validation cohort consited of 2027 patients who underwent coronary angiography due to suspected stable angina pectoris in the Western Norway Coronary Angiography Cohort (WECAC). Information on new-onset AF was obtained by linking patient data to Norwegian public health registries. Risk associations were explored by Cox regression. Results During median (25th-75th percentile) follow-up of 10.9 (10.6-11.3) and 7.0 (6.3-8.6) years, 560 (8.8%) patients in the HUSK and 210 (10.4%) in the WECAC was diagnosed with AF. In the HUSK, the age and gender adjusted HR (95 % CI) for the 4th vs. 1st plasma TML quartiles 1.84 (1.37-2.48) p < 0.001. In multivariable models the association was only slightly attenuated. Correspondingsly, the age and gender adjusted HR (95% CI) for the 4th vs. 1st TML quartiles in the WECAC was 1.48 (0.96-2.27) p = 0.07. Testing for collinearity between TMAO and TML revealed variance inflation factors between 1.0-1.1 in HUSK and WECAC, thus ruling out collinearity. Conclusion Plasma TML was associated with new-onset AF among subjects from the general population, and the relationship was independent from established AF risk factors. A similar trend was also seen in patients with suspected stable angina pectoris, strengthening our findings, which motivate further studies to explore potential pathophysiological relationships between one-carbon metabolism and cardiac arrhythmias
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.