Longitudinal blood glucose level and increased silent myocardial infarction: a pooled analysis of four cohort studies.

BACKGROUND: Fasting glucose (FG) demonstrates dynamic fluctuations over time and is associated with cardiovascular outcomes, yet current research is limited by small sample sizes and relies solely on baseline glycemic levels. Our research aims to investigate the longitudinal association between FG and silent myocardial infarction (SMI) and also delves into the nuanced aspect of dose response in a large pooled dataset of four cohort studies. METHODS: We analyzed data from 24,732 individuals from four prospective cohort studies who were free of myocardial infarction history at baseline. We calculated average FG and intra-individual FG variability (coefficient of variation), while SMI cases were identified using 12-lead ECG exams with the Minnesota codes and medical history. FG was measured for each subject during the study's follow-up period. We applied a Cox regression model with time-dependent variables to assess the association between FG and SMI with adjustment for age, gender, race, Study, smoking, longitudinal BMI, low-density lipoprotein level, blood pressure, and serum creatinine. RESULTS: The average mean age of the study population was 60.5 (sd: 10.3) years with median fasting glucose of 97.3 mg/dL at baseline. During an average of 9 years of follow-up, 357 SMI events were observed (incidence rate, 1.3 per 1000 person-years). The association between FG and SMI was linear and each 25 mg/dL increment in FG was associated with a 15% increase in the risk of SMI. This association remained significant after adjusting for the use of lipid-lowering medication, antihypertensive medication, antidiabetic medication, and insulin treatment (HR 1.08, 95% CI 1.01-1.16). Higher average FG (HR per 25 mg/dL increase: 1.17, 95% CI 1.08-1.26) and variability of FG (HR per 1 sd increase: 1.23, 95% CI 1.12-1.34) over visits were also correlated with increased SMI risk. CONCLUSIONS: Higher longitudinal FG and larger intra-individual variability in FG over time were associated in a dose-response manner with a higher SMI risk. These findings support the significance of routine cardiac screening for subjects with elevated FG, with and without diabetes.

Preventing new-onset heart failure: Intervening at stage A.

Heart failure (HF) prevention is an urgent public health need with national and global implications. Stage A HF patients do not show HF symptoms or structural heart disease but are at risk of HF development. There are no unique recommendations on detecting Stage A patients. Patients in Stage A are heterogeneous; many patients have different combinations of risk factors and, therefore, have markedly different absolute risks for HF. Comprehensive strategies to prevent HF at Stage A include intensive blood pressure lowering, adequate glycemic and lipid management, and heart-healthy behaviors (adopting Life's Essential 8). First and foremost, it is imperative to improve public awareness of HF risk factors and implement healthy lifestyle choices very early. In addition, recognize the HF risk-enhancing factors, which are nontraditional cardiovascular (CV) risk factors that identify individuals at high risk for HF (genetic susceptibility for HF, atrial fibrillation, chronic kidney disease, chronic liver disease, chronic inflammatory disease, sleep-disordered breathing, adverse pregnancy outcomes, radiation therapy, a history of cardiotoxic chemotherapy exposure, and COVID-19). Early use of biomarkers, imaging markers, and echocardiography (noninvasive measures of subclinical systolic and diastolic dysfunction) may enhance risk prediction among individuals without established CV disease and prevent chemotherapy-induced cardiomyopathy. Efforts are needed to address social determinants of HF risk for primordial HF prevention.Central illustrationPolicies developed by organizations such as the American Heart Association, American College of Cardiology, and the American Diabetes Association to reduce CV disease events must go beyond secondary prevention and encompass primordial and primary prevention.

Highlights in ASCVD Primary Prevention for 2021.

This review examines key studies published in 2021 that are related to primary prevention of atherosclerotic cardiovascular disease (ASCVD). Major randomized clinical trials (RCTs) concerning traditional risk factors or ASCVD events, meta-analyses, and key observational studies related to primary prevention of ASCVD were considered. The review includes interventions for weight loss, cardiometabolic and renal disease, blood pressure control, diet, and the occurrence of cardiovascular disease events. A few studies considered both primary and secondary prevention populations. The review is not exhaustive. We did not include studies that focused on heart failure or clinical presentations that may be difficult to classify, such as acute or chronic ischemic cardiovascular disease without myocardial infarction. Our purpose was to highlight recent research that will help the reader stay abreast of the changing field of cardiovascular prevention.

Relation of glycemic status with unrecognized MI and the subsequent risk of mortality: The Jackson Heart Study.

Background: Almost 1/3 to 1/2 of initial myocardial infarctions (MI) may be silent or unrecognized (UMI), which forecasts future clinical events. Further, limited data exist to describe the potential risk for UMI in African-Americans. The relationship of glucose status with UMI was examined in the Jackson Heart Study: a cohort of African-American individuals. Methods and results: At baseline, there were 5,073 participants with an initial 12-lead electrocardiogram (ECG) and fasting glucose measured. Of these participants, 106(2.1%) had a UMI, and 268(4.2%) had a recognized MI. This population consisted of 3,233 (63.7%) participants with normal fasting glucose (NFG), 533 (10.5%) with IFG, and 1,039 (20.4%) with DM. Logistic regression investigated the relationship between glucose status and UMI. Cox proportional hazard models determined the significance of all-cause mortality during follow-up by MI status. The sample was 65% female with a mean age of 55.3 ± 12.9 years. Over a mean follow-up of 10.4 years, there were 795 deaths. Relative to NFG, the crude odds ratio (OR) estimates for UMI at baseline with IFG and DM were 1.00(95% CI:0.48-2.14) and 3.22(2.15-4.81), respectively. With adjustment, DM continued to be significantly associated with UMI [2.30 (1.42-3.71)]. Overall, participants with a baseline UMI had an adjusted Hazard ratio (HR) of 2.00(1.39-2.78) of death compared to no prior MI. Compared to those with no MI, those with a recognizedMI had an adjusted HR of 1.70(1.31-2.17) for mortality. Conclusions: DM is associated with UMI in African-Americans. Further, a UMI carried similar risk of death compared to those with a recognized MI.

Abnormal Fasting Glucose Increases Risk of Unrecognized Myocardial Infarctions in an Elderly Cohort.

OBJECTIVES: To investigate glucose levels as a risk factor for unrecognized myocardial infarctions (UMIs). DESIGN: Cohort SETTING: Cardiovascular Health Study. PARTICIPANTS: Individuals aged 65 and older with fasting glucose measurements (N=4,355; normal fasting glucose (NFG), n = 2,041; impaired fasting glucose (IFG), n = 1,706; DM: n = 608; 40% male, 84% white, mean age 72.4 ± 5.6). MEASUREMENTS: The relationship between glucose levels and UMI was examined. Participants with prior coronary heart disease (CHD) or UMI on initial electrocardiography were excluded. Using Minnesota codes, UMI was identified according to the presence of pathological Q-waves or minor Q-waves with ST-T abnormalities. Crude and adjusted hazard ratios (HRs) were calculated. Analyses were adjusted for age, sex, body mass index (BMI), hypertension, antihypertensive and lipid-lowering medication use, total cholesterol, high-density lipoprotein cholesterol, and smoking status. RESULTS: Over a mean follow-up of 6 years, there were 459 incident UMIs (NFG, n=202; IFG, n=183; DM, n=74). Participants with IFG were slightly more likely than those with NFG to experience a UMI (hazard ratio (HR)=1.11, 95% confidence interval (CI)=0.91-1.36, p = .30), and those with DM were more likely than those with NFG to experience a UMI (HR=1.65, 95% CI=1.25-2.13, p < .001). After adjustment HR for UMI in IFG those with IFG were no more likely than those with NFG to experience a UMI (HR=1.01, 95% CI=0.82-1.24, p = .93), whereas those with DM were more likely than those with NFG to experience a UMI (HR=1.37, 95% CI=1.02-1.81, p = .03). The 2-hour oral glucose tolerance test was not statistically significantly associated with UMI. CONCLUSION: Fasting glucose status, particularly in the diabetic range, forecasted UMI during 6 years of follow-up in elderly adults. Further studies are needed to clarify the level of glucose at which risk is greater. J Am Geriatr Soc 67:43-49, 2019.

The 4th Report of the Working Group on ECG diagnosis of Left Ventricular Hypertrophy.

The 4th Report provides a brief review of publications focused on the electrocardiographic diagnosis of left ventricular hypertrophy published during the period of 2010 to 2016 by the members of the Working Group on ECG diagnosis of Left Ventricular Hypertrophy. The Working Group recommended that ECG research and clinical attention be redirected from the estimation of LVM to the identification of electrical remodeling, to better understanding the sequence of events connecting electrical remodeling to outcomes. The need for a re-definition of terms and for a new paradigm is also stressed.

Prediabetes and the association with unrecognized myocardial infarction in the multi-ethnic study of atherosclerosis.

BACKGROUND: With one-quarter of initial myocardial infarctions (MI) being unrecognized MI (UMI), recognition is critical to minimize further cardiovascular risk. Diabetes mellitus is an established risk factor for UMI. If impaired fasting glucose (IFG) also increased the risk for UMI, it would represent a significant public health challenge due to the rapid worldwide increase in IFG prevalence. We compared participants with IFG to those with normal fasting glucose (NFG) to determine if IFG was associated with UMIs. METHODS: We performed cross-sectional analyses from the MESA, a population-based cohort study. There were 6,814 participants recruited during July 2000 to September 2002 from the general community at 6 field sites. After excluding those with diabetes mellitus or missing variables, 5,885 participants were included. At baseline, there were 4,955 participants with NFG and 930 participants with IFG. The main outcome was an UMI defined by the presence of pathological Q waves or minor Q waves with ST-T abnormalities on initial 12-lead electrocardiogram. Logistic regression was used to generate crude ORs and adjust for covariates. RESULTS: There was a higher prevalence of UMI in those with IFG compared with those with NFG [3.5% (n = 72) vs 1.4% (n = 30)]. After adjustment for multiple risk factors, there was a higher odds of an UMI among those with IFG compared with those with NFG [OR: 1.60 (95% CI: 1.0-2.5); P = .048]. CONCLUSIONS: Impaired fasting glucose is associated with unrecognized myocardial infarctions in a multi-ethnic population free of baseline cardiovascular disease.

Emerging risk factors as markers for carotid intima media thickness scores.

AIMS: Cardiovascular disease (CVD) remains the number one cause of mortality in the Western world. This study aims to determine which lifestyle factors are associated with mean carotid intima media thickness (IMT), a safe and reliable predictor of future CVD risk. METHODS AND RESULTS: A prospective cross-sectional analysis of 592 subjects. Measures were made of body composition, anthropometric measures, fitness, diet (measured with a 3-day food diary), laboratory results, and mean carotid IMT. Multivariate analyses show that higher mean IMT values are associated with increasing age (p < 0.0001), male gender (p = 0.0002), higher systolic blood pressure (BP; p = 0.0008), higher body mass index (BMI; p = 0.0005), and lower intake of zinc (p = 0.0001). Bivariate analyses controlling for age and gender, with and without statin use, showed that higher mean IMT scores were statistically associated with higher diastolic BP (p = 0.007), higher total cholesterol/high-density lipoprotein (HDL) ratio (p < 0.0001), higher triglyceride/HDL ratio (p = 0.0001), lower aerobic capacity measures (p = 0.0007), higher body fat percentage and waist circumference (p < 0.0001), higher fasting glucose level (p = 0.028), and lower intake of magnesium (p = 0.019), fish (p = 0.007), and fiber (p = 0.02). Other factors that were not associated with mean IMT include total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-sensitivity C-reactive protein (hs-CRP); intake of saturated fat, potassium, calcium, sodium, or vitamin K; percentage of calories from protein, fat, or carbohydrate; measures of strength (assessed with push-up and sit-up testing); and reported exercise. CONCLUSIONS: Aerobic fitness and dietary intake of fiber, fish, magnesium, and zinc are inversely associated with carotid IMT scores. Of the traditional CVD risk factors, only systolic BP, fasting glucose, body composition, and total cholesterol/HDL ratio have a direct relationship with mean carotid IMT.

Electrocardiographic left ventricular strain pattern: everything old is new again.

Electrocardiographic left ventricular hypertrophy (LVH) has many faces with countless features. Beyond the classic measures of LVH, including QRS voltage and duration, the left ventricular (LV) strain pattern is an element whereby characteristic R-ST depression is followed by a concave ST segment that ends in an asymmetrically inverted T wave. The LV strain pattern generally appears in states of increased systemic blood pressure and must be differentiated from similar but not identical ST-T waves indicating ischemia. The LV strain pattern has been found in population studies to be associated with poor prognosis and increased risk of adverse cardiovascular outcomes. Regression of LV strain pattern parallels decline in systemic BP during clinical trials of anti-hypertensive therapies but does not indicate or serve as a surrogate for decrease in LV mass. Newer techniques in data collection and processing may allow the process of strain to be studied in more detail to determine the ways in which electrical remodeling of the left ventricle as characterized by LVH with 'repolarization abnormalities' indicates how CV risk might be managed by using LV strain pattern as an electrocardiographic biomarker.

Exercise and pharmacological treatment of depressive symptoms in patients with coronary heart disease: results from the UPBEAT (Understanding the Prognostic Benefits of Exercise and Antidepressant Therapy) study.

OBJECTIVES: The aim of this study was to assess the efficacy of exercise and antidepressant medication in reducing depressive symptoms and improving cardiovascular biomarkers in depressed patients with coronary heart disease. BACKGROUND: Although there is good evidence that clinical depression is associated with poor prognosis, optimal therapeutic strategies are currently not well defined. METHODS: One hundred one outpatients with coronary heart disease and elevated depressive symptoms underwent assessment of depression, including a psychiatric interview and the Hamilton Rating Scale for Depression. Participants were randomized to 4 months of aerobic exercise (3 times/week), sertraline (50-200 mg/day), or placebo. Additional assessments of cardiovascular biomarkers included measures of heart rate variability, endothelial function, baroreflex sensitivity, inflammation, and platelet function. RESULTS: After 16 weeks, all groups showed improvement on Hamilton Rating Scale for Depression scores. Participants in both the aerobic exercise (mean -7.5; 95% confidence interval: -9.8 to -5.0) and sertraline (mean -6.1; 95% confidence interval: -8.4 to -3.9) groups achieved larger reductions in depressive symptoms compared with those receiving placebo (mean -4.5; 95% confidence interval: -7.6 to -1.5; p = 0.034); exercise and sertraline were equally effective at reducing depressive symptoms (p = 0.607). Exercise and medication tended to result in greater improvements in heart rate variability compared with placebo (p = 0.052); exercise tended to result in greater improvements in heart rate variability compared with sertraline (p = 0.093). CONCLUSIONS: Both exercise and sertraline resulted in greater reductions in depressive symptoms compared to placebo in patients with coronary heart disease. Evidence that active treatments may also improve cardiovascular biomarkers suggests that they may have a beneficial effect on clinical outcomes as well as on quality of life. (Exercise to Treat Depression in Individuals With Coronary Heart Disease; NCT00302068).

The effects of a tailored cardiac rehabilitation program on depressive symptoms in women: A randomized clinical trial.

BACKGROUND: Depression is known to co-occur with coronary heart disease (CHD). Depression may also inhibit the effectiveness of cardiac rehabilitation (CR) programs by decreasing adherence. Higher prevalence of depression in women may place them at increased risk for non-adherence. OBJECTIVE: To assess the impact of a modified, stage-of-change-matched, gender-tailored CR program for reducing depressive symptoms among women with CHD. METHODS: A two-group randomized clinical trial compared depressive symptoms of women in a traditional 12-week CR program to those completing a tailored program that included motivational interviewing guided by the Transtheoretical Model of behavior change. Women in the experimental group also participated in a gender-tailored exercise protocol that excluded men. The Center for Epidemiological Studies Depression (CES-D) Scale was administered to 225 women at baseline, post-intervention, and at 6-month follow-up. Analysis of Variance was used to compare changes in depression scores over time. RESULTS: Baseline CES-D scores were 17.3 and 16.5 for the tailored and traditional groups, respectively. Post-intervention mean scores were 11.0 and 14.3; 6-month follow-up scores were 13.0 and 15.2, respectively. A significant group by time interaction was found for CES-D scores (F(2, 446)=4.42, p=.013). Follow-up tests revealed that the CES-D scores for the traditional group did not differ over time (F(2, 446)=2.00, p=.137). By contrast, the tailored group showed significantly decreased CES-D scores from baseline to post-test (F(1, 223)=50.34, p<.001); despite the slight rise from post-test to 6-month follow-up, CES-D scores remained lower than baseline (F(1, 223)=19.25, p<.001). CONCLUSION: This study demonstrated that a modified, gender-tailored CR program reduced depressive symptoms in women when compared to a traditional program. To the extent that depression hinders CR adherence, such tailored programs have potential to improve outcomes for women by maximizing adherence. Future studies should explore the mechanism by which such programs produce benefits.