Psychosocial correlates of apparent treatment-resistant hypertension in the Jackson Heart Study.

This corrects the article DOI: 10.1038/jhh.2016.100.

Psychosocial correlates of apparent treatment-resistant hypertension in the Jackson Heart Study.

Apparent treatment-resistant hypertension (aTRH) is associated with adverse cardiovascular outcomes. aTRH is common and disproportionately affects African Americans. The objective of this study is to explore psychosocial correlates of aTRH in a population-based cohort of African Americans with hypertension. The sample included 1392 participants in the Jackson Heart Study with treated hypertension who reported being adherent to their antihypertensive medications. aTRH was defined as uncontrolled clinic BP (⩾140/90 mm Hg) with ⩾3 classes of antihypertensive medication or treatment with ⩾4 classes of antihypertensive medication, including a diuretic. Self-reported medication adherence was defined as taking all prescribed antihypertensive medication in the 24 h before the study visit. The association of psychosocial factors (chronic stress, depressive symptoms, perceived social support and social network) with aTRH was evaluated using Poisson regression with progressive adjustment for demographic, clinical and behavioural factors. The prevalence of aTRH was 15.1% (n=210). Participants with aTRH had lower social network scores (that is, fewer sources of regular social contact) compared with participants without aTRH (P<0.01). No other psychosocial factors differed between groups. Social network was also the only psychosocial factor that was associated with aTRH prevalence in regression analyses. In age-, sex-adjusted and fully adjusted models, one additional unique source of social contact was associated with a 19% (PR=0.81; 95% confidence interval (CI): 0.68-0.94, P=0.001) and a 13% (PR=0.87; 95% CI 0.74-1.0, P=0.041) lower prevalence of aTRH, respectively. Social network was independently associated with aTRH and warrants further investigation as a potentially modifiable determinant of aTRH in African Americans.

Ambulatory blood pressure monitoring phenotypes among individuals with and without diabetes taking antihypertensive medication: the Jackson Heart Study.

Ambulatory blood pressure monitoring (ABPM) can detect phenotypes associated with increased cardiovascular disease (CVD) risk. Diabetes is associated with increased CVD risk but few data are available documenting whether blood pressure (BP) phenotypes, detected by ABPM, differ between individuals with versus without diabetes. We conducted a cross-sectional analysis of 567 participants in the Jackson Heart Study, a population-based study of African Americans, taking antihypertensive medication to evaluate the association between diabetes and ABPM phenotypes. Two clinic BP measurements were taken at baseline following a standardized protocol. ABPM was performed for 24 h following the clinic visit. ABPM phenotypes included daytime, sustained, nocturnal and isolated nocturnal hypertension, a non-dipping BP pattern, and white coat, masked and masked isolated nocturnal hypertension. Diabetes was defined as fasting glucose ⩾126 mg dl-1, haemoglobin A1c ⩾6.5% (48 mmol mol-1) or use of insulin or oral hypoglycaemic medications. Of the included participants (mean age 62.3 years, 71.8% female), 196 (34.6%) had diabetes. After multivariable adjustment, participants with diabetes were more likely to have daytime hypertension (prevalence ratio (PR): 1.32; 95% confidence interval (CI): 1.09-1.60), masked hypertension (PR: 1.46; 95% CI: 1.11-1.93) and masked isolated nocturnal hypertension (PR: 1.39; 95% CI: 1.02-1.89). Although nocturnal hypertension was more common among participants with versus without diabetes, this association was not present after adjustment for daytime systolic BP. Diabetes was not associated with the other ABPM phenotypes investigated. This study highlights the high prevalence of ABPM phenotypes among individuals with diabetes taking antihypertensive medication.

Unmasking masked hypertension: prevalence, clinical implications, diagnosis, correlates and future directions.

'Masked hypertension' is defined as having non-elevated clinic blood pressure (BP) with elevated out-of-clinic average BP, typically determined by ambulatory BP monitoring. Approximately 15-30% of adults with non-elevated clinic BP have masked hypertension. Masked hypertension is associated with increased risks of cardiovascular morbidity and mortality compared with sustained normotension (non-elevated clinic and ambulatory BP), which is similar to or approaching the risk associated with sustained hypertension (elevated clinic and ambulatory BP). The confluence of increased cardiovascular risk and a failure to be diagnosed by the conventional approach of clinic BP measurement makes masked hypertension a significant public health concern. However, many important questions remain. First, the definition of masked hypertension varies across studies. Further, the best approach in the clinical setting to exclude masked hypertension also remains unknown. It is unclear whether home BP monitoring is an adequate substitute for ambulatory BP monitoring in identifying masked hypertension. Few studies have examined the mechanistic pathways that may explain masked hypertension. Finally, scarce data are available on the best approach to treating individuals with masked hypertension. Herein, we review the current literature on masked hypertension including definition, prevalence, clinical implications, special patient populations, correlates, issues related to diagnosis, treatment and areas for future research.

Higher leptin is associated with hypertension: the Multi-Ethnic Study of Atherosclerosis.

Adipokines are secreted from adipose tissue, influence energy homeostasis and may contribute to the association between obesity and hypertension. Among 1897 participants enrolled in the Multi-Ethnic Study of Atherosclerosis, we examined associations between blood pressure and leptin, tumor necrosis factor-α (TNFα), resistin and total adiponectin. The mean age and body mass index (BMI) was 64.7 years and 28.1, respectively, and 50% were female. After adjustment for risk factors, a 1-s.d.-increment higher leptin level was significantly associated with higher systolic (5.0 mm Hg), diastolic (1.9), mean arterial (2.8) and pulse pressures (3.6), as well as a 34% higher odds for being hypertensive (P<0.01 for all). These associations were not materially different when the other adipokines, as well as BMI, waist circumference or waist-to-hip ratio, were additionally added to the model. Notably, the associations between leptin and hypertension were stronger in men, but were not different by race/ethnic group, BMI or smoking status. Adiponectin, resistin and TNFα were not independently associated with blood pressure or hypertension. Higher serum leptin, but not adiponectin, resistin or TNFα, is associated with higher levels of all measures of blood pressure, as well as a higher odds of hypertension, independent of risk factors, anthropometric measures and other selected adipokines.

Negative impact of depression on outcomes in patients with coronary artery disease: mechanisms, treatment considerations, and future directions.

Depressive symptoms are common in coronary artery disease (CAD) patients, and are associated with increased cardiac risk. Although an important relation exists between depression and CAD prognosis, the underlying pathophysiological mechanisms are poorly understood. Additionally, evidence including the recently published ENRICHD (Enhancing Recovery in Coronary Heart Disease Patients) trial suggests that depression treatments do not lower recurrent cardiac risk. The reason for the observed lack of benefit with depression treatment in CAD patients is unclear. In this review, we discuss the impact of depression in CAD patients, the possible mechanisms involved, the studies that have examined the effects of psychological and antidepressant therapies on recurrent cardiac events, and the direction that future research should take.

Antithrombotic effects of S 18886, a novel orally active thromboxane A2 receptor antagonist.

Platelet activation and thrombus formation play a critical role in the onset of acute coronary syndromes. Thromboxane A2 (TxA2) is among the different chemical modulators released by activated platelets. TxA2 is considered one of the most powerful agonists for platelet activation. In addition, TxA2 exerts a vasoconstrictor effect by serving as an agonist of the thromboxane receptor (TP) on the vascular smooth muscle cell membranes. The putative effect of TxA2 on thrombosis is demonstrated by the clinical effectiveness of acetylsalicylic acid (ASA) in the prevention of acute coronary syndromes. Among the clinically used antiplatelet agents, clopidogrel has shown to be slightly more effective than ASA in the prevention of atherothrombotic events in patients with peripheral arterial disease, and is one of the most widely used after aspirin. The aims of the study were to study the antithrombotic effects of escalating doses of the TP-receptor antagonist, S 18886 and to compare its effects with those achieved by the administration of ASA (5 mg kg-1 day-1), and clopidogrel (3 mg kg-1 day-1). The study was undertaken at high and low shear rate conditions using the Badimon perfusion chamber in a porcine model. Antithrombotic effects were assessed as changes on platelet and fibrin(ogen) deposition. The doses of 30 and 100 micro g kg-1 day-1 were selected based on a previous platelet aggregation study. S 18886 shows a dose-dependent antithrombotic response. The dose of S-100 develops similar antithrombotic effects to those of clopidogrel and superior to those of aspirin. The antithrombotic effects were statistically significant at both studied shear rate conditions. Therefore, the orally active TP-receptor antagonist, S 18886, appears to be a new and effective agent to prevent atherothrombotic complications.

Testing platelet activation with a shear-dependent platelet function test versus aggregation-based tests: relevance for monitoring long-term glycoprotein IIb/IIIa inhibition.

BACKGROUND: Tests developed to monitor glycoprotein (GP) IIb/IIIa blockade do not properly reflect platelet function in vivo and need a baseline (pretreatment) value. Because GP IIb/IIIa is essential in platelet aggregation and thrombosis under shear conditions, a flow-dependent approach to monitor its inhibition can be used. METHODS AND RESULTS: We compared a test based on flow-dependent platelet deposition, the Cone and Platelet Analyzer (CPA), with in vitro platelet aggregometry and the Rapid Platelet Function Assay (RPFA) on platelet function after GP IIb/IIIa inhibition. In vitro, increasing concentrations of abciximab (0% to 100% receptor occupancy) were tested. Ex vivo, platelet function was monitored with the CPA and with aggregometry for up to 1 week after abciximab administration. The CPA was better correlated with the percentage of free GP IIb/IIIa receptors than was aggregometry or the RPFA. Only the RPFA, when expressed as a ratio over baseline (pretreatment), was comparable to the CPA. Ex vivo, the CPA, but not aggregometry, showed prolonged platelet inhibition with gradual recovery from GP IIb/IIIa receptor blockade in the first week after abciximab administration. CONCLUSIONS: Platelet function assessment by shear-induced deposition is a reliable test to monitor a wide range of GP IIb/IIIa inhibition. Its accuracy does not require a baseline reference. The effects of GP IIb/IIIa blockade on platelet function should be examined under high shear conditions.