Association between blood pressure levels and premature atrial contractions in patients with hypertension.

BACKGROUND: High blood pressure (BP) induces left atrial structural and functional remodeling that increases susceptibility to atrial arrhythmia. We hypothesized that lower systolic BP (SBP) levels are associated with a lower prevalence of premature atrial contractions (PACs) in patients with hypertension. METHODS: This analysis included 4,697 participants (mean age 62±13.1 years, 50% women, 25.6% blacks) with hypertension from the Third National Health and Nutrition Examination Survey who did not have a prior history of cardiovascular disease (CVD). Multivariable logistic regression was used to examine the cross-sectional association between SBP and prevalence of PACs ascertained from 12-lead resting electrocardiograms. Multivariable Cox proportional hazard analysis was used to examine the association between baseline PACs and CVD mortality. RESULTS: Approximately 1.6% (n=74) of participants had baseline PACs. Patients with SBP ≤140 mmHg had a lower prevalence of PACs than those with SBP ≥140 mmHg (1.1% vs. 1.9%, p-value=0.01). In a multivariable logistic regression model, each 10 mmHg decrease in SBP was associated with a 12% lower odds of PACs (OR (95%CI): 0.88 (0.77-0.99)). During 14 years of follow-up, 645 CVD deaths occurred. In a multivariable-adjusted Cox model, presence of PACs was associated with a 78% increased risk of CVD mortality (HR (95%CI): 1.78 (1.23-2.60)). CONCLUSIONS: In patients with hypertension, lower SBP levels are associated with a lower prevalence of PACs, and presence of PACs is associated with a higher risk of CVD mortality risk. These findings highlight the potential role of BP lowering in the management of cardiac arrhythmias.

Exploring the Link between Anticoagulation, Cognitive Impairment and Dementia in Atrial Fibrillation: A Systematic Review.

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.

Association between Blood Lead Levels and Silent Myocardial Infarction in the General Population.

Background: Although the link between lead exposure and patterns of cardiovascular disease (CVD) has been reported, its association with silent myocardial infarction (SMI) remains unexplored. We aimed to assess the association between blood lead levels (BLLs) and SMI risk. Methods: We included 7283 (mean age 56.1 ± 2.52 years, 52.5% women) participants free of CVD from the Third National Health and Nutrition Examination Survey. BLL was measured using graphite-furnace atomic absorption spectrophotometry. SMI was defined as ECG evidence of myocardial infarction (MI) without history of MI. The association between SMI and BLLs was examined using multivariable logistic regression. Results: SMI was detected in 120 participants with an unweighted prevalence of 1.65%. Higher BLL correlated with higher SMI prevalence across BLL tertiles. In multivariable-adjusted models, participants in the third BLL tertile had more than double the odds of SMI (OR: 3.42, 95%CI: 1.76-6.63) compared to the first tertile. Each 1 µg/dL increase in BLL was linked to a 9% increase in SMI risk. This association was consistent across age, sex, and race subgroups. Conclusions: Higher BLLs are associated with higher odds of SMI in the general population. These results underscore the significance of the ongoing efforts to mitigate lead exposure and implement screening strategies for SMI in high-risk populations.

Small dense low-density lipoprotein cholesterol and coronary artery calcification in the Multi-Ethnic Study of Atherosclerosis.

AIMS: Elevated small dense LDL cholesterol (sd-LDL-C) increases atherosclerotic cardiovascular disease (CVD) risk. Although coronary artery calcification (CAC) is widely used for predicting CVD events, few studies have examined the relationship between sd-LDL-C and CAC. METHODS AND RESULTS: This study included 4672 individuals with directly measured baseline sd-LDL-C and CAC from the Multi-Ethnic Study of Atherosclerosis [mean (standard deviation) age: 61.9 (10.4) years; 52.5% women; 47.3% with baseline CAC (mean score >0)]. We used multi-variable general linear models and restricted cubic splines with the goodness of fit testing to evaluate the association of sd-LDL-C with the presence of CAC. Odds ratios [OR (95% confidence interval)] were adjusted for demographics and cardiovascular risk factors, including estimated total LDL-C. Higher quartiles of sd-LDL-C were associated with the presence of CAC, even after accounting for total LDL-C. Compared with the lowest quartile of sd-LDL-C, participants in Quartiles 2, 3, and 4 had higher odds for the presence of baseline CAC [Quartile 2 OR: 1.24 (1.00, 1.53); Quartile 3 OR: 1.51 (1.19, 1.93); and Quartile 4 OR 1.59 (1.17, 2.16)]. Splines suggested a quadratic curvilinear relationship of continuous sd-LDL-C with CAC after adjustment for demographics and CVD risk factors (quadratic vs. first-order sd-LDL-C terms likelihood ratio test: P = 0.015), but not after accounting for total LDL-C (quadratic vs. first-order terms: P = 0.156). CONCLUSION: In a large, multi-ethnic sample without known CVD, higher sd-LDL-C was associated with the presence of CAC, above and beyond total LDL-C. Whether selective direct measurement of sd-LDL-C is indicated to refine cardiovascular risk assessment in primary prevention warrants further investigation.

Higher levels of small dense particles of LDL cholesterol, better known as the 'bad cholesterol', are associated with a greater risk for the presence of coronary artery calcium, a strong marker for heart disease, even when accounting for estimated total (small dense + large body particles) LDL cholesterol.This risk is stronger in older individuals.Peak risk seems to occur between 49 and 71 mg/dL and does not increase further at higher levels.

Racial differences in prevalence and impact of electrocardiographic subclinical myocardial injury risk factors.

BACKGROUND: We explored whether the reported racial differences in subclinical myocardial injury (SCMI) are due to variations in the prevalence or differential impact of the SCMI risk factors. METHODS: This analysis included 3074 Whites, 1337 Blacks, and 1441 Mexican Americans from the Third National Health and Nutrition Examination Survey who were free of cardiovascular disease. SCMI was defined from standard electrocardiograms as a cardiac infarction/injury score ≥ 10 points. Multivariable logistic regression analysis was used to assess the association of SCMI with its risk factors stratified by race. Multiplicative interaction between each risk factor and race was also examined. RESULTS: Overall prevalence of SCMI was 20.3%, with Mexican Americans exhibiting a lower prevalence than Whites and Blacks (16.5%, 20.4%, and 20.7%, respectively). Whites had more prevalence of dyslipidemia and smoking. Mexican Americans had more diabetes, while Blacks had more hypertension, obesity, and left ventricular hypertrophy. Significant risk factors for SCMI were older age, lower income (<20 K), smoking, diabetes, and no regular exercise. The association of SCMI with age was more pronounced in Mexican Americans (p-value for interaction 0.03), whereas the associations of SCMI with smoking, no-regular exercise, and diabetes were stronger in Whites (p-value for interaction 0.04, 0.001, 0.007, respectively). CONCLUSIONS: Heterogeneity in the racial differences in the prevalence of SCMI risk factors exists, but they do not explain racial differences in SCMI. The stronger associations of smoking, diabetes, and no regular exercise with SCMI partially explain the higher prevalence of SCMI in Whites.

Electrocardiographic left atrial abnormality and risk of heart failure.

INTRODUCTION: The association and the racial differences of the electrocardiographic markers of left atrial abnormality (ECG-LAA) with heart failure (HF) are unclear. METHODS: We examined the cross-sectional association of ECG-LAA, defined as deep terminal negativity of P wave in V1 (DTNPV1) with HF in 8460 participants (51.5% women, 60.3 ± 13.5 age and 49.8% Whites) from the US Third National Health and Nutrition Examination Survey. We excluded participants without P-wave in their ECG or with ECG findings that interfere with measurements of P-wave. DTNPV1 was automatically measured from ECGs processed at a central lab. Values of DTNPV1 ≥ 100 µV were considered abnormal. Past medical history of HF was identified through health interviews. Multivariable logistic regression analysis was used to examine the associations of DTNPV1 with HF. RESULTS: Abnormal DTNPV1 was detected in 3.2% (n = 271) of the participants. HF was significantly more common in individuals with abnormal, compared to those with normal, DTNPV1 (14.7% vs. 4.8%, respectively; p-value <0.001). In a model adjusted for socio-demographics and cardiovascular risk factors, ECG-LAA was associated with 98% increased odds of HF (OR (95% CI): 1.98 (1.30-3.01), p < 0.001). This association was stronger in non-White (vs. White) participants (OR (95% CI): 3.14 (1.82-5.43) vs. 1.01 (0.51-1.97), respectively; interaction p-value =0.01), but consistent in subgroups stratified by age and sex. CONCLUSIONS: ECG-LAA, defined as abnormal DTNPV1, is associated with an increased risk of HF, underscoring the role of atrial disease in developing HF. Racial differences in this association exist, possibly suggesting considering ECG-LAA in personalized assessments of HF risk.

Association between weight variability, weight change and clinical outcomes in hypertension.

Objective: The effect of body weight variability (BWV) and body weight change (BWC) in high-risk individuals with hypertension, but without diabetes mellitus (DM) remains unclear. We examined the effect of BWV and BWC on the primary outcome [the composite of myocardial infarction (MI), other acute coronary syndromes, stroke, acute decompensated heart failure (HF), or cardiovascular (CV) death] and all-cause mortality in the Systolic Blood Pressure Intervention Trial (SPRINT). Methods: In this post-hoc analysis, we used multivariate Cox regression models to examine the risk associated with BWV and BWC for the primary outcome in SPRINT. BWV was defined as the intra-individual average successive variability (ASV). BWC was defined as baseline weight minus final weight. Results: A total of 8714 SPRINT participants (mean age 67.8 ± 9.4 years, 35.1 % women, 58.9 % Whites) with available data on body weight were included. The median follow-up was about 3.9 years (IQR, 3.3-4.4). In multivariable-adjusted Cox models, each 1 unit standard deviation (SD) of BWV was significantly associated with a higher risk for the primary outcome, all-cause mortality, HF, MI, and stroke [HR(95 % CI)]: 1.13 (1.07-1.19; p < 0.0001), 1.22 (1.14-1.30; p < 0.0001), 1.16 (1.07-1.26; p < 0.001), 1.10 (1.00-1.20; p = 0.047), and 1.15 (1.05-1.27; p = 0.005), respectively. Similarly, each 1 unit SD of BWC was significantly associated with a higher risk of the primary outcome, all-cause mortality, MI, and HF: 1.11(1.02-1.21; p = 0.017), 1.44 (1.26-1.65; p < 0.0001), 1.16 (1.01-1.32; p = 0.041) and 1.19 (1.02-1.40; p = 0.031) respectively. However, there was no significant association with CV death (for both BWV and BWC) or stroke (BWC). Conclusion: In high-risk hypertension, BWV and BWC were both associated with higher risk of the primary outcome and all-cause mortality. These results further stress the clinical importance of sustained weight loss and minimizing fluctuations in weight in hypertension.

Joint Association of Albuminuria and Left Ventricular Hypertrophy With Incident Heart Failure in Adults at High Risk With Hypertension: A Systolic Blood Pressure Intervention Trial Substudy.

Albuminuria and left ventricular hypertrophy (LVH) are independent predictors of heart failure (HF); however, to the best of our knowledge, their combined effect on the risk of HF has not yet been explored. Therefore, we examined the joint associations of albuminuria and electrocardiographic-LVH with incident acute decompensated HF (ADHF), and whether albuminuria/LVH combinations modified the effects of blood pressure control strategy in reducing the risk of ADHF. A total of 8,511 participants from the Systolic Blood Pressure Intervention Trial (SPRINT) were included. Electrocardiographic-LVH was present if any of the following criteria were present: Cornell voltage, Cornell voltage product, or Sokolow-Lyon. Albuminuria was defined as urine albumin/creatinine ratio ≥30 mg/g. ADHF was defined as hospitalization or emergency department visit for ADHF. Cox proportional hazard models were used to examine the association of neither LVH nor albuminuria (reference), either LVH or albuminuria, and both (LVH + albuminuria) with incident ADHF. Over a median follow-up of 3.2 years, 182 cases of ADHF occurred. In adjusted models, concomitant albuminuria and LVH were associated with greater risk of ADHF than either albuminuria or LVH in isolation (hazard ratio [95% confidence interval]: 4.95 [3.22 to 7.62], 2.04 [1.39 to 3.00], and 1.47 [0.93 to 2.32], respectively, additive interaction p = 0.01). The effect of intensive blood pressure in reducing ADHF was attenuated in participants with coexisting albuminuria and LVH without any interaction between treatment group assignment and albuminuria/LVH categories (interaction p = 0.26). In conclusion, albuminuria and LVH are additive predictors of ADHF. The effect of intensive blood pressure control in reducing ADHF risk did not vary significantly across albuminuria/LVH combinations.

Association of Empirical Dietary Inflammatory Potential with Mortality: Results from the Third National Nutrition Examination Survey.

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.

Joint Association of Albuminuria and Left Ventricular Hypertrophy with Incident Heart Failure in High-Risk Adults with Hypertension: a SPRINT substudy.

Background: Albuminuria and left ventricular hypertrophy (LVH) are independent predictors of heart failure (HF), however their combined effect on risk of HF has not been explored previously. Objectives: To examine the joint associations of albuminuria and electrocardiographic (ECG) LVH with incident acute decompensated HF (ADHF), and whether albuminuria/LVH combinations modified the effects of blood pressure control strategy in reducing the risk of ADHF. Methods: 8,511 participants from the SPRINT (Systolic Blood Pressure Intervention Trial) were included. ECG-LVH was present if any of the following criteria: Cornell voltage, Cornell voltage product, or Sokolow Lyon were present. Albuminuria was defined as urine albumin-creatinine ratio (UACR) ≥30 mg/g. ADHF was defined as hospitalization or emergency visit for ADHF. Cox proportional hazard models were used to examine the association of neither LVH, nor albuminuria (reference), either LVH or albuminuria, and both (LVH + albuminuria) with incident ADHF. Results: Over a median follow-up of 3.2 years, 182 cases of ADHF occurred. In adjusted models, concomitant albuminuria and LVH were associated with higher risk of ADHF than either albuminuria or LVH in isolation (HR (95% CI): 4.95 (3.22-7.62), 2.04 (1.39-3.00), and 1.47 (0.93-2.32), respectively (additive interaction p=0.01). The effect of intensive blood pressure in decreasing ADHF attenuated among participants with co-existing albuminuria and LVH without any interaction between treatment group assignment and albuminuria/LVH categories (interaction p-value= 0.26). Conclusions: Albuminuria and LVH are additive predictors of ADHF. The effect of intensive blood pressure control in decreasing ADHF risk did not vary significantly across albuminuria/LVH combinations.

Electrocardiographic markers of atrial cardiomyopathy and risk of heart failure in the multi-ethnic study of atherosclerosis (MESA) cohort.

Background: The association of electrocardiographic (ECG) markers of atrial cardiomyopathy with heart failure (HF) and its subtypes is unclear. Methods: This analysis included 6,754 participants free of clinical cardiovascular disease (CVD), including atrial fibrillation (AF), from the Multi-Ethnic Study of Atherosclerosis. Five ECG markers of atrial cardiomyopathy (P-wave terminal force in V1 [PTFV1], deep-terminal negativity in V1 [DTNV1], P-wave duration [PWD], P-wave axis [PWA], advanced intra-atrial block [aIAB]) were derived from digitally recorded electrocardiograms. Incident HF events through 2018 were centrally adjudicated. An ejection fraction (EF) of 50% at the time of HF was used to classify HF as HF with reduced EF (HFrEF), HF with preserved EF (HFpEF), or unclassified HF. Cox proportional hazard models were used to examine the associations of markers of atrial cardiomyopathy with HF. The Lunn-McNeil method was used to compare the associations in HFrEF vs. HFpEF. Results: 413 HF events occurred over a median follow-up of 16 years. In adjusted models, abnormal PTFV1 (HR (95%CI): 1.56(1.15-2.13), abnormal PWA (HR (95%CI):1.60(1.16-2.22), aIAB (HR (95%CI):2.62(1.47-4.69), DTNPV1 (HR (95%CI): 2.99(1.63-7.33), and abnormal PWD (HR (95%CI): 1.33(1.02-1.73), were associated with increased HF risk. These associations persisted after further adjustments for intercurrent AF events. No significant differences in the strength of association of each ECG predictor with HFrEF and HFpEF were noted. Conclusions: Atrial cardiomyopathy defined by ECG markers is associated with HF, with no differences in the strength of association between HFrEF and HFpEF. Markers of atrial Cardiomyopathy may help identify individuals at risk of developing HF.

Relationship between abnormal P-wave axis, chronic obstructive pulmonary disease and mortality in the general population.

BACKGROUND: It is unclear whether the presence of a vertical P-wave axis on electrocardiogram modifies the association of COPD with mortality. OBJECTIVE: To examine the association and interaction of abnormal P-wave axis and COPD with mortality. STUDY DESIGN AND METHODS: The analysis included 7359 with ECG data from the Third National Health and Nutrition Examination Survey (NHANES-III) who were free of cardiovascular disease (CVD) at enrollment. Abnormal P-wave axis (aPWA) was defined as values above 75°. COPD was self-reported as either a diagnosis of emphysema or chronic bronchitis. National Death Index was used to identify the date of death and cause of death. Using multivariable Cox proportional hazard analysis, we examined the association of COPD with all-cause mortality by aPWA status. RESULTS: Over a median follow-up of 14 years, 2435 deaths occurred. Participants with concomitant presence of aPWA and COPD experienced higher death rates (73.9 per 1000 person-years (PY)) compared to either COPD or aPWA alone (36.4 per 1000 PY and 31.1 per 1000 PY), respectively. In multivariable-adjusted models, a stronger association between COPD and mortality was noted in the presence compared to the absence of aPWA (HR 95% CI): 1.71 (1.37-2.13) vs. 1.22(1.00-1.49), respectively (interaction P-value = 0.02). Similarly, a stronger association between aPWA and mortality was observed in the presence compared to the absence of COPD (HR 95% CI): 1.66(1.26-2.19) vs. 1.18(1.06-1.31), respectively (interaction P-value = 0.02). Similar higher death rates and mortality risk was observed when spirometry-confirmed COPD and aPWA were present together than in isolation. CONCLUSION: The concomitant presence of aPWA and COPD leads to a significantly higher mortality rate compared to the presence either COPD or aPWA alone as a clinical variable. P-wave axis, reported routinely on ECG printout, can potentially identify patients with COPD who need intensive control of risk factors and disease management.

Interrelations between albuminuria, electrocardiographic left atrial abnormality, and incident atrial fibrillation in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort.

BACKGROUND: The objective of the study was to examine the joint associations of albuminuria and electrocardiographic left atrial abnormality (ECG-LAA) with incident atrial fibrillation (AF) and whether this relationship varies by race. METHODS: This analysis included 6670 participants free of clinical cardiovascular disease (CVD), including atrial fibrillation (AF), from the Multi-Ethnic Study of Atherosclerosis. ECG-LAA was defined as P-wave terminal force in V1 [PTFV1] >5000 µV × ms. Albuminuria was defined as urine albumin-creatinine ratio (UACR) ≥30 mg/g. Incident AF events through 2015 were ascertained from hospital discharge records and study-scheduled electrocardiograms. Cox proportional hazard models were used to examine the association of "no albuminuria + no ECG-LAA (reference)", "isolated albuminuria", "isolated ECG-LAA" and "albuminuria + ECG-LAA" with incident AF. RESULTS: Over a median follow-up of 13.8 years, 979 incident cases of AF occurred. In adjusted models, the concomitant presence of ECG-LAA and albuminuria was associated with a higher risk of AF than either ECG-LAA or albuminuria in isolation (HR (95% CI): 2.43 (1.65-3.58), 1.33 (1.05-1.69), and 1.55 (1.27-1.88), respectively (interaction p-value = 0.50). Effect modification by race was observed with a 4-fold greater AF risk in Black participants with albuminuria + ECG-LAA (HR (95%CI): 4.37 (2.38-8.01) but no significant association in White participants (HR (95% CI) 0.60 (0.19-1.92) respectively; (interaction p-value for race x albuminuria-ECG-LAA combination = 0.05). CONCLUSIONS: Concomitant presence of ECG-LAA and albuminuria confers a higher risk of AF compared to either one in isolation with a stronger association in Blacks than Whites.

Relationship between premature ventricular complexes and stroke mortality in the general population.

OBJECTIVES: Predictors for increased stroke mortality identify those who may need closer monitoring and better hospital care. While the link between premature ventricular complexes (PVCs) and incident ischemic stroke has been reported, studies on the association with fatal stroke are non-existent. MATERIALS AND METHODS: We examined the association of PVCs with stroke mortality in 8047 participants (56.5 ± 0.39 years, 53% women, 80.9% Non-Hispanic Whites) without prior history of stroke from the Third National Health and Nutrition Examination Survey. National Death Index was used to identify the date and cause of death. PVCs were detected from 12­lead standard electrocardiograms. Cox proportional hazard analysis was used to examine the association between any PVC with stroke mortality. RESULTS: Approximately 2.1% (n = 134) participants had PVCs at baseline. Over a median follow-up of 22 years, 337 fatal strokes occurred. More strokes occurred in participants with baseline PVCs compared to those without (unadjusted cumulative incidence of stroke 9.5% vs. 2.5% respectively, p-value 0.001). In a multivariable-adjusted model, the presence of PVC was associated with an increased risk of stroke mortality (HR (95%CI): 2.50 (1.15-5.43). This association was stronger in participants with coronary heart disease (CHD) than those without it (HR (95%CI): 5.98 (2.2-16.2) vs. 1.97 (0.75-5.1) respectively; interaction-p = 0.008). CONCLUSIONS: PVCs are associated with an increased risk of stroke mortality, especially among individuals with CHD. Whether improved hospital care or modifying PVCs could change outcomes should be examined in prospective studies.

Relation of Electrocardiographic Abnormal P-Wave Axis With Stroke Mortality in the General Population.

The link between abnormal P-wave axis (aPWA) and incident ischemic stroke is well established. However, studies examining the association between aPWA and fatal stroke are rare. We hypothesized that aPWA is associated with fatal stroke. We examined the association of abnormal aPWA with stroke mortality in 7,359 participants (60.0 ± 13.4 years, 51.9% women, 49.8% White) without cardiovascular (CV) disease (CVD) from the Third National Health and Nutrition Examination Survey. aPWA was defined as any value <0 or >75°. The National Death Index was used to identify the date and cause of death. Cox proportional hazard analysis was used to examine the association between baseline aPWA with stroke mortality. Over a median follow-up of 14 years, 189 stroke deaths occurred. During follow-up, stroke mortality was more common in those with aPWA than those without aPWA (3.5% vs 2.2%, respectively; p = 0.002). In a multivariable-adjusted model, aPWA was associated with a 44% increased risk of stroke mortality (hazard ratio [HR] 95% confidence interval [CI] 1.44 [1.05 to 1.99]). This association was stronger in men than in women (HR 95% CI 2.29 [1.42 to 3.67] vs 1.00 [0.64 to 1.55]), respectively; p-interaction = 0.04) and among non-Whites than Whites (HR 95% CI 2.20 [1.39 to 3.46] vs. 1.07 [0.68 to 1.69], respectively; p-interaction = 0.09). The annualized stroke death rates/1,000 participants across levels of CHA2DS2-VASc scores were higher in those with than without aPWA. In conclusion, aPWA, a marker of atrial cardiopathy, is associated with an increased risk of stroke mortality, especially among men and non-Whites. Whether intensive risk factor modifications in those with aPWA would reduce the risk of stroke and thus, stroke mortality needs further investigation.

Alcohol Consumption and Systemic Hypertension (from the Third National Health and Nutrition Examination Survey).

Epidemiological studies have established the association between excessive alcohol consumption and systemic hypertension (SH). However, there are conflicting reports of the association of low to moderate alcohol consumption with SH. The objective of the study was to examine the associations of alcohol consumption and blood pressure categories using the 2017 American College of Cardiology/American Heart Association high blood pressure guidelines. This analysis included 17,059 participants from the Third National Health and Nutrition Examination Survey. Alcohol consumption was ascertained by way of a questionnaire. Blood pressure (mm Hg) was measured during the in-home interview and the participant's visit to the mobile examination center. We used multivariable logistic regression models to examine cross-sectional associations of alcohol consumption and blood pressure categories based on new American College of Cardiology/American Heart Association High Blood Pressure guidelines. Models were adjusted for age, gender, income, and cardiovascular risk factors. Compared with never drinkers, moderate drinkers (7 to 13 drinks/week) had increased odds of prevalent stage 1 and stage 2 SH (odds ratio [95% confidence interval] 1.51 [1.22 to 1.87] and 1.55 [1.20 to 2.00]). Similarly, there were significantly higher odds of prevalent stage 1 and stage 2 SH among heavy drinkers (≥14 drinks/week) (odds ratio [95% confidence interval] 1.65 [1.33 to 2.05] and 2.46 [1.93 to 3.14]). We did not find any association between alcohol consumption and elevated blood pressure category. Response bias must be considered because alcohol consumption was self-reported. Our study indicates the need for further research to understand the potential mechanisms by which alcohol consumption increases the risk of SH. In conclusion, this analysis from a population-based survey showed an association between moderate and heavy alcohol consumption and a higher prevalence of SH.

Preventing Diabetes and Atherosclerosis in the Cardiometabolic Syndrome.

PURPOSE OF REVIEW: Cardiometabolic syndrome is characterized by abdominal adiposity, insulin resistance, hypertension, and dyslipidemia. There is a growing burden of cardiometabolic disease in many parts of the world. This review highlights the critical preventive and therapeutic measures that need to be implemented to reduce the impact of cardiometabolic syndrome on cardiovascular health. RECENT FINDINGS: Recent cardiovascular outcome trials demonstrated that newer glucose-lowering medications reduce cardiovascular and renal events in patients with type 2 diabetes mellitus (T2DM). These medications should be considered in patients with T2DM and atherosclerotic cardiovascular disease (ASCVD). These novel drugs may also play a role in primary prevention of cardiovascular disease (CVD) and renal disease in high-risk patients without T2DM. To manage dyslipidemia associated with cardiometabolic syndrome, in addition to lifestyle interventions and statin therapy, ezetimibe, and proprotein convertase subtilisin/Kexin type 9 (PCSK9), inhibitors can be used to reduce the risk of major adverse cardiovascular outcomes (MACE) especially in patients with T2DM and coronary artery disease (CAD). The residual risk of MACE in such a high-risk population can be further mitigated by treatment with an omega-3 fatty acid such as icosapent ethyl. Lifestyle modifications and the use of proven pharmacological therapies are essential for the prevention and progression of diabetes and ASCVD in those with the cardiometabolic syndrome.

Incidence, Predictors, and Prognosis of Acute Kidney Injury Among Cardiac Arrest Survivors.

BACKGROUND: Acute kidney injury (AKI) is common among cardiac arrest survivors. However, the outcomes and predictors are not well studied. METHODS: This is a cohort study of cardiac arrest patients enrolled from January 2012 to December 2016 who were able to survive for 24 hours post-cardiopulmonary resuscitation. Patients with anuria, chronic kidney disease (stage 5), and end-stage renal disease were excluded. Acute kidney injury (stage 1) or higher was defined using Kidney Disease: Improving Global Outcomes classification. Multivariable adjusted regression models were used to compute hazard ratio (HR) for association of AKI with risk of mortality and odds ratio (OR) with risk of poor neurological outcomes after adjusting for demographics, comorbidities, and medical therapy. Multivariable logistic regression model was used to compute OR for association of various predictors with AKI. RESULTS: Of 842 cardiac arrest survivors, 588 (69.8%) developed AKI. Among AKI patients, 69.4% died compared with 52.0% among non-AKI patients. In multivariable adjusted Cox proportional hazard model, development of AKI post-cardiac arrest was significantly associated with mortality (HR: 1.35; 95% confidence interval [CI]: 1.07-1.71, P = .01) and poor neurological outcomes defined as cerebral performance category >2 (OR: 2.27; 95% CI: 1.45-3.57, P < .001) and modified Rankin scale >3 (OR: 2.22; 95% CI: 1.43-3.45, P < .001). Postdischarge dialysis was also associated with increased risk of mortality (HR: 2.57; 95% CI: 1.57-4.23, P < .001). Use of vasopressors was strongly associated with development of AKI and continued need for postdischarge dialysis. CONCLUSIONS: Acute kidney injury was associated with increased risk of mortality and poor neurological outcomes. There is need for further studies to prevent AKI in cardiac arrest survivors.

Impact of low fasting plasma glucose on mortality in the general population.

BACKGROUND: While the association between hypoglycaemia and poor outcomes in diabetes is well established, it is unclear whether such an association is generalizable to those without diabetes. METHODS: A total of 8497 participants free of cardiovascular disease and diabetes from the Third National Health and Nutrition Examination Survey were included. We examined the relationship between baseline low (<80 mg/dL) and high (⩾126 mg/dL) fasting plasma glucose compared to normal levels (80-99 mg/dL). RESULTS: Over a median follow-up of 14 years, 2101 deaths occurred, of which 570 were due to cardiovascular disease. In a model adjusted for sociodemographic and cardiovascular disease risk factors, individuals with low fasting plasma glucose were at increased risk of cardiovascular disease and all-cause mortality [hazard ratio = 1.79 (95% confidence interval = 1.04-3.08) and hazard ratio = 1.35 (95% confidence interval = 1.02-1.78), respectively], compared to those with normal fasting plasma glucose. These associations were stronger among men than women for both cardiovascular disease mortality and all-cause mortality. CONCLUSION: Low fasting plasma glucose in individuals without diabetes is a risk factor for cardiovascular disease and all-cause mortality, especially in men.

Electrocardiographic myocardial injury and stroke mortality in the general population.

BACKGROUND: Recent evidence suggests a link between myocardial infarction and stroke risk, but it is unclear whether such risk exists with electrocardiographic myocardial injury in otherwise healthy individuals. Therefore, we explored the association of myocardial injury with stroke mortality in participants free of cardiovascular disease. METHODS: This analysis included 6017 participants (58.4 ± 13.4 years, 54.1% women, 50.3% white) from the Third National Health and Nutrition Examination Survey. Cardiac infarction/injury score (CIIS), a weighted scoring system composed of several electrocardiographic waveform components related to myocardial injury and ischemia, was used to define myocardial injury. Stroke mortality was ascertained using the National Death Index during follow-up. Multivariable adjusted Cox proportional hazard analysis was used to examine the association between baseline myocardial injury and risk of stroke mortality. RESULTS: Over a median follow-up of 14 years, 152 stroke deaths occurred. Stroke mortality was more common in those with than those without myocardial injury (3.8% vs. 2.1%, respectively; p = 0.0003). In a model adjusted for potential confounders, the myocardial injury was associated with a 44% increased risk of stroke mortality (HR (95%CI):1.44(1.02-2.03)). In a similar model, each 1 CIIS score point increase was associated with a 2% increase in the risk of stroke mortality (HR (95%CI):1.02 (1.00-1.04), p = 0.01). CONCLUSIONS: Electrocardiographic myocardial injury in cardiovascular disease-free adults is associated with an increased risk of stroke mortality suggesting a potential link between asymptomatic myocardial injury and risk of cardiac thromboembolism. Whether screening and management of myocardial injury would reduce such risk requires further investigation.