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.

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.

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.

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.

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.

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.

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.