Association of urinary albumin-to-creatinine ratio with cardiometabolic risk markers and pre-diabetes in adults with normoglycemia, normoalbuminuria, and normotension with parental type 2 diabetes.

INTRODUCTION: This is a post hoc analysis of urinary albumin-to-creatinine ratio (uACR) within the normoalbuminuric range in relation to cardiometabolic risk factors among initially normoglycemic, normotensive participants in the Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) Study. RESEARCH DESIGN AND METHODS: 308 healthy African American (AA) and European American (EA) participants in the POP-ABC Study underwent baseline assessments, including oral glucose tolerance test, anthropometry, urinary albumin-to-creatinine ratio (uACR), lipids, adipocytokines, insulin sensitivity and secretion. Participants were followed quarterly for 5.5 years (mean 2.62 years) for the primary outcome of incident pre-diabetes. RESULTS: The cohort's mean fasting glucose was 92.1±6.90 mg/dL, 2-hour plasma glucose was 123±25.0 mg/dL, systolic blood pressure was 123±15.9 mm Hg, and diastolic blood pressure was 74±8.80 mm Hg. Baseline uACR levels (range 1-29 mg/g) were similar in AA versus EA participants (6.40 mg/g±4.80 vs 6.80±5.40 mg/g, p=0.52), higher in women than men (7.30 mg/g±5.30 vs 4.60±3.90 mg/g, p<0.0001), and showed significant associations with cardiometabolic risk factors, including age, insulin sensitivity, high-density lipoprotein cholesterol, and adiponectin levels (p=0.03-0.004). During 5.5 years of follow-up, 104 participants developed pre-diabetes and 204 maintained normoglycemia. Baseline uACR quartiles were associated with incident pre-diabetes (r=0.19, p=0.0011). CONCLUSIONS: Baseline uACR levels were associated with cardiometabolic risk markers and incident pre-diabetes risk among adults with normoglycemia, normoalbuminuria and normotension with parental diabetes.

Changes in heart rate variability of depressed patients after electroconvulsive therapy.

Objective. As few, small studies have examined the impact of electroconvulsive therapy (ECT) upon the heart rate variability of patients with major depressive disorder (MDD), we sought to confirm whether ECT-associated improvement in depressive symptoms would be associated with increases in HRV linear and nonlinear parameters. Methods. After providing consent, depressed study participants (n = 21) completed the Beck Depression Index (BDI), and 15-minute Holter monitor recordings, prior to their 1st and 6th ECT treatments. Holter recordings were analyzed for certain HRV indices: root mean square of successive differences (RMSSD), low-frequency component (LF)/high-frequency component (HF) and short-(SD1) versus long-term (SD2) HRV ratios. Results. There were no significant differences in the HRV indices of RMSDD, LF/HF, and SD1/SD2 between the patients who responded, and those who did not, to ECT. Conclusion. In the short term, there appear to be no significant improvement in HRV in ECT-treated patients whose depressive symptoms respond versus those who do not. Future studies will reveal whether diminished depressive symptoms with ECT are reliably associated with improved sympathetic/parasympathetic balance over the long-term, and whether acute changes in sympathetic/parasympathetic balance predict improved mental- and cardiac-related outcomes.

Platelet thromboxane A2 secretion in patients with major depression responsive to electroconvulsive therapy.

OBJECTIVE: To determine a) whether clinical response to electroconvulsive therapy (ECT) is associated with decreased platelet activation in patients with major depressive disorder (MDD) and b) if any medical/demographic characteristics predict response to ECT or changes in platelet activation. Increased platelet activation may underlie the increased risk of coronary artery disease (CAD) in patients with MDD. METHODS: Before their first and sixth ECT treatments, study patients (n = 44) completed the Beck Depression Inventory (BDI) to assess the severity of depressive symptoms. Activity of the platelet thromboxane (TBX) A(2) pathway was assessed by measuring the morning spot urinary concentrations of 11-dehydroxy-thromboxane B(2) (11-D-TBX B(2)), a major metabolite of platelet-derived TBX A(2). RESULTS: Multivariate logistic regression analyses revealed that improvement on the BDI was significantly more likely in patients without a history of hypertension (p = .02) and in patients who were prescribed a greater number of "platelet-altering" medications (p = .03). During a course of ECT, a decrease in urinary 11-D-TBX B(2) was significantly more likely to occur in ECT nonresponders (p = .01) and younger patients (p = .02). CONCLUSIONS: Clinical response to ECT coadministered may not be associated with decreases in platelet-derived TBX. Future studies will confirm which somatic "antidepression" treatments offer optimal thrombovascular benefits for depressed patients with multiple risk factors for, or clinically evident, cerebral disease or CAD.