Background: Subclinical myocardial injury (SCMI) is associated with an increased risk of poor cardiovascular disease (CVD) outcomes. Understanding the underlying risk factors for SCMI is crucial for the prevention and management of CVD. We hypothesized that atherogenic dyslipidemia, a combination of high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C), is associated with an increased risk of SCMI. Methods: This analysis from the third National Health and Nutrition Examination Survey (NHANES-III) included 7093 participants (age 59.3 ± 13.4 years, 52.8% women, and 49.4% White) free of CVD. Atherogenic dyslipidemia was defined as TG ≥ 150 mg/dL and HDL-C < 40 mg/dL in men or <50 mg/dL in women. A validated electrocardiographic-based cardiac infarction injury score (CIIS) ≥ 10 was considered positive for SCMI. Multivariable logistic regression analysis was used to examine the association of different combinations of TG and HDL-C groups, including atherogenic dyslipidemia with SCMI. Results: About 22.5% (n = 1594) of participants had atherogenic dyslipidemia, and 26.3% (n = 1862) had SCMI. Compared to participants with normal TG and normal HDL-C, those with atherogenic dyslipidemia had a higher prevalence of SCMI (31.2% vs. 23.9%, p-value < 0.001). In a multivariable logistic regression model, atherogenic dyslipidemia was associated with the highest odds of SCMI followed by high TG/normal HDL-C, then low HDL-C/normal TG [OR (95% CI): 131 (1.14, 1.52), 1.13 (0.97, 1.33), and 1.01 (0.86, 1.20), respectively). Conclusions: Atherogenic dyslipidemia is associated with a higher risk of SCMI, which highlights the role of nontraditional risk factors in the development of subclinical CVD.

Background: The impact of oral anticoagulants (OACs) on cognitive impairment and dementia in patients with atrial fibrillation (AF) is not well characterized. This systematic review aims to address this knowledge gap. Methods: SCOPUS and PubMed searches were conducted to identify articles in the English language investigating the association between the use of OACs and cognitive impairment and dementia. We excluded non-original research studies and studies that did not report data on cognitive impairment or included patients who underwent open heart surgery or had psychiatric illnesses or cancer. Results: Out of 22 studies (n = 606,404 patients), 13 studies (n = 597,744 patients) reported a reduction in cognitive impairment/dementia in those undergoing thromboprophylaxis. Using direct oral anticoagulants (DOACs) was associated with a lower incidence of cognitive impairment in 10 studies (n = 284,636 patients). One study found that patients undergoing dual therapy (n = 6794 patients) had a greater incidence of cognitive impairment compared to those undergoing monotherapy (n = 9994 patients). Three studies (n = 61,991 patients) showed that AF patients on DOACs had a lower likelihood of dementia diagnosis than those on vitamin K antagonists (VKAs). Dementia incidence was lower when VKAs were under good control. Conclusions: The use of oral anticoagulants has the potential to prevent cognitive impairment and dementia in patients with AF. Since most of the published research on this subject is observational in nature, more randomized controlled trials are needed to fully understand the effect of anticoagulants on cognitive function.

Background: Both atrial cardiopathy and impaired renal function are independently associated with increased mortality, but their interrelationship and combined impact remain uncertain. Methods: We analyzed 6573 participants from NHANES-III (mean age 57 years; 50.5% women; 74.6% White) with available electrocardiograms (ECGs). Estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI equation. Atrial cardiopathy was defined by any of the following ECG markers: abnormal P-wave axis (75°), deep terminal negativity in lead V1 (>100 µV), or prolonged P-wave duration in lead II (>120 ms). Participants with eGFR <15 mL/min/1.73 m² or major ECG abnormalities were excluded. Logistic regression assessed the association between impaired renal function (eGFR < 45 vs. ≥45 mL/min/1.73 m²) and atrial cardiopathy. Cox models evaluated independent and joint associations of impaired renal function and atrial cardiopathy with all-cause mortality. Results: About 47.9% (n = 3151) had atrial cardiopathy at baseline, of whom 161 (4.7%) had impaired renal function. Impaired renal function was associated with higher odds of atrial cardiopathy (OR 1.44; 95% CI 1.16–1.78). Over a median follow-up of 18.1 years, 3076 deaths occurred. Compared with participants without either condition, those with both had the highest mortality risk (HR 1.68; 95% CI 1.46–1.94), exceeding risks from atrial cardiopathy alone (HR 1.10; 95% CI 1.02–1.18) or impaired renal function alone (HR 1.42; 95% CI 1.18–1.70; p = 0.011 for interaction). Conclusions: Impaired renal function is associated with a greater prevalence of atrial cardiopathy. Their coexistence exerts a synergistic effect, substantially amplifying mortality risk beyond either condition alone.

Background: The combined impact of impaired kidney function and subclinical myocardial injury (SCMI) on cardiovascular (CV) mortality has not been well studied. We aimed to evaluate their individual and joint associations with cardiovascular mortality. Methods: We analyzed data from 6057 participants (mean age 57.0 ± 13.0 years) in the U.S. Third National Health and Nutrition Examination Survey. Estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI equation. Electrocardiographic SCMI was defined as a cardiac infarction/injury score ≥ 10. CV mortality was determined from the National Death Index. Multivariable logistic regression assessed baseline cross-sectional associations between eGFR and SCMI. Cox proportional hazards models were used to examine the individual and combined associations of eGFR and SCMI with CV mortality. Results: At baseline, 1297 participants (21.4%) had SCMI. In multivariable logistic regression analysis, eGFR < 45 mL/min/1.73 m² (vs. ≥45) was not associated with SCMI (OR [95% CI]: 1.10 [0.84–1.45]). Over a median follow-up of 18.4 years, 690 CV deaths occurred. In separate Cox models, both SCMI (vs. no SCMI) and eGFR < 45 (vs. ≥45) were associated with increased CV mortality risk (HR [95% CI]: 1.36 [1.16–1.60] and 1.56 [1.24–1.99], respectively). Compared with participants with eGFR ≥ 45 and no SCMI, those with both eGFR < 45 and SCMI had the highest CV mortality risk (HR [95% CI]: 2.36 [1.65–3.36]), followed by eGFR < 45 alone (1.47 [1.09–1.96]) and SCMI alone (1.33 [1.11–1.58]). Conclusions: Both reduced eGFR and SCMI were independently associated with CV mortality. Their coexistence showed the highest risk, but without statistical significance compared with each alone, possibly reflecting limited power and distinct mechanisms.

Background: The empirical dietary inflammatory potential (EDIP) score is designed to assess the inflammatory potential of a diet based on the pro- and anti-inflammatory properties of its various components. This study examined the association of EDIP with all-cause mortality in a large, community-based, multiracial sample of the United States population. Study Design: A prospective cohort study. Methods: This analysis included 13155 participants (44.6±18.4 years, 54.21% women, and 40.33% White) without prior history of cardiovascular disease (CVD) from the Third National Health and Nutrition Examination (NHANES III) Survey. A 24-hour dietary recall information was used to calculate EDIP. The National Death Index was employed to identify the date and cause of death. Cox proportional hazard analysis was utilized to evaluate the association between the tertiles of EDIP and all-cause mortality over a median follow-up of 26.6 years. Results: In a model adjusted for demographics and CVD risk factors, a higher EDIP tertile, compared with the lowest tertile, was associated with an increased risk of all-cause mortality (hazard ratio [HR]=1.10; 95% CI: 1.02, 1.19). A standard-deviation increase in EDIP (0.27 units) was related to a 4% increased risk of mortality (HR=1.04; 95% CI: 1.01, 1.08). This association was stronger in older participants compared to younger ones (HR=1.09; 95% CI: 0.98, 1.21 vs. HR=0.89; 95% CI: 0.80, 1.01), respectively, interaction P=0.030)]. Conclusion: Pro-inflammatory diet is associated with an increased risk of mortality, especially in the older population. Dietary changes that reduce inflammation may have the potential to reduce the risk of poor outcomes.

Background: Subclinical myocardial injury (SCMI) is associated with an increased risk of poor cardiovascular disease (CVD) outcomes. Understanding the underlying risk factors for SCMI is crucial for the prevention and management of CVD. We hypothesized that atherogenic dyslipidemia, a combination of high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C), is associated with an increased risk of SCMI. Methods: This analysis from the third National Health and Nutrition Examination Survey (NHANES-III) included 7,093 participants (age 59.3±13.4 years, 52.8% women, and 49.4% White) free of CVD. Atherogenic dyslipidemia was defined as TG ≥150 mg/dL and HDL-C <40 mg/dL in men or <50 mg/dL in women. A validated electrocardiographic-based cardiac infarction injury score (CIIS) ≥10 was considered positive for SCMI. Multivariable logistic regression analysis was used to examine the association of different combinations of TG and HDL-C groups, including atherogenic dyslipidemia with SCMI. Results: About 22.5% (n=1,594) of participants had atherogenic dyslipidemia, and 26.3% (n=1862) had SCMI. Compared to participants with normal TG and normal HDL-C, those with atherogenic dyslipidemia had a higher prevalence of SCMI (31.2% vs. 23.9%, p-value <0.001). In a multivariable logistic regression model, atherogenic dyslipidemia was associated with the highest odds of SCMI followed by high TG/normal HDL-C, then low HDL-C/normal TG [OR (95% CI): 131 (1.14,1.52), 1.13 (0.97,1.33), and 1.01(0.86,1.20), respectively). Conclusions: Atherogenic dyslipidemia is associated with a higher risk of SCMI, which highlights the role of nontraditional risk factors in the development of subclinical CVD.