Longitudinal blood pressure patterns and cardiovascular disease risk

Abstract

Observational and interventional studies have unequivocally demonstrated that “present”, i.e. single-occasion, blood pressure is one of the key determinants of cardiovascular disease risk. Over the past two decades, however, numerous publications have suggested that longitudinal blood pressure data and assessment of long-term blood pressure exposure provide incremental prognostic value over present blood pressure. These studies have used several different indices to quantify the overall exposure to blood pressure, such as time-averaged blood pressure, cumulative blood pressure, blood pressure trajectory patterns, and age of hypertension onset. This review summarises existing research on the association between these indices and hard cardiovascular outcomes, outlines the strengths and weaknesses of these indices, and provides an overview of how longitudinal blood pressure changes can be measured and used to improve cardiovascular disease risk prediction.

• KEY MESSAGES

• Numerous recent publications have examined the relation between cardiovascular disease and long-term blood pressure (BP) exposure, quantified using indices such as time-averaged BP, cumulative BP, BP trajectory patterns, and age of hypertension onset.

• This review summarises existing research on the association between these indices and hard cardiovascular outcomes, outlines the strengths and weaknesses of these indices, and provides an overview of how longitudinal BP changes can be measured and used to improve cardiovascular disease risk prediction.

• Although longitudinal BP indices seem to predict cardiovascular outcomes better than present BP, there are considerable differences in the clinical feasibility of these indices along with a limited number of prospective data.

     

Relation between diabetes related distress and glycemic control: The mediating effect of adherence to treatment

AimsDiabetes related distress (DRD) is a negative emotional reaction to stresses associated with diabetes mellitus (DM) and its management. This study estimated the burden of DRD and self-reported adherence to treatment (SRAT) among patients with DM and investigated their relationship with glycemic control.MethodsA cross sectional study of consented 157 diabetics was conducted using the17-item Diabetes Distress Scale (DDS). It measures distress at four subscales: Emotional Burden (EB), Physician-related (PD), Regimen-related (RD) and Interpersonal Distress (ID). SRAT was assessed using Morisky’s scale. Glycemic control was assessed using the most recent HbA1c results. Multivariable linear regression analysis was used for adjustment of confounders and bootstrap Confidence Interval was used to test for the occurrence of mediating effect.ResultsAverage age was 44.5 ± 16.0 years, 65% were females, 79% had type 2 DM and nearly 55% has had DM for more than 7 years and the average HbA1c was 8.9 ± 2.2%. Clinically significant DRD was reported by 37% of the participants, EB and RD in 40.8%, PD in 46.5%, and ID among 32.5%. Younger patients showed higher level of stress compared to older participants and patients with type 1 DM showed higher level of stress in all DRD domains. Only 46% of patients were defined as having satisfactory SRAT and improvement of SRAT significantly enhanced the glycemic control (r = ?0.32, p < 0.01). DRD and low SRAT negatively correlated with HbA1c; increasing the DRD by one point may increase the HbA1c on average by 0.41 (C.I. 0.02–0.80) and will indirectly raise the HbA1c by 0.24 (C.I. 0.04–0.47) through the mediating effect of low SRAT.ConclusionDRD and low SRAT are commonly reported among DM patients and both are indirectly correlated. The mediating effect of low SRAT highlights the clinical role of DRD and clarifies the process by which distress affect the outcome of DM management.     

Young drivers who continue to drive while sleepy: What are the associated sleep‐ and driving‐related factors?

Crashes due to sleepiness account for a substantial proportion of road crash incidents. The purpose of the current study was to examine several sleep‐related factors and driving‐related factors for their association with self‐reports of continuing to drive while sleepy. In total 257 young drivers aged 18–25 years completed an online survey that assessed factors such as sleep quality, sleep duration and consistency, excessive daytime sleepiness, experiences with sleepiness and their driving‐related behaviours. The results demonstrate that being older, having a perceived ability to overcome sleepiness, committing more highway code violations and having experienced a sleep‐related close call were positively associated with an increased likelihood of continuing to drive while sleepy. The obtained results highlight the acceptance of risky driving behaviours among some younger drivers. Younger drivers’ risky driving behaviour is certainly a road safety concern given the impairment associated with sleepiness and their over‐representation in road crash incidents.     

Early signal from the hippocampus for memory encoding

The mediotemporal lobe (MTL), including the hippocampus, is involved in all stages of episodic memory including memory encoding, consolidation, and retrieval. However, the exact timing of the hippocampus' involvement immediately after stimulus encounter remains unclear. In this study, we used high‐density 156‐channel electroencephalography to study the processing of entirely new stimuli, which had to be encoded, in comparison to highly overlearned stimuli. Sixteen healthy subjects performed a continuous recognition task with meaningful pictures repeated up to four consecutive times. Waveform and topographic cluster analyses of event‐related potentials revealed that new items, in comparison to repetitions, were processed significantly differently at 220–300 ms. Source estimation localized activation for processing new stimuli in the right MTL. Our study demonstrates the occurrence of a transient signal from the MTL in response to new information already at 200–300 ms poststimulus onset, which presumably reflects encoding as an initial step toward memory consolidation.     

Prostaglandin D2 synthase modulates macrophage activity and accumulation in injured peripheral nerves

We have previously reported that prostaglandin D2 Synthase (L-PGDS) participates in peripheral nervous system (PNS) myelination during development. We now describe the role of L-PGDS in the resolution of PNS injury, similarly to other members of the prostaglandin synthase family, which are important for Wallerian degeneration (WD) and axonal regeneration. Our analyses show that L-PGDS expression is modulated after injury in both sciatic nerves and dorsal root ganglia neurons, indicating that it might play a role in the WD process. Accordingly, our data reveals that L-PGDS regulates macrophages phagocytic activity through a non-cell autonomous mechanism, allowing myelin debris clearance and favoring axonal regeneration and remyelination. In addition, L-PGDS also appear to control macrophages accumulation in injured nerves, possibly by regulating the blood–nerve barrier permeability and SOX2 expression levels in Schwann cells. Collectively, our results suggest that L-PGDS has multiple functions during nerve regeneration and remyelination. Based on the results of this study, we posit that L-PGDS acts as an anti-inflammatory agent in the late phases of WD, and cooperates in the resolution of the inflammatory response. Thus, pharmacological activation of the L-PGDS pathway might prove beneficial in resolving peripheral nerve injury.     

A novel SNCA E83Q mutation in a case of dementia with Lewy bodies and atypical frontotemporal lobar degeneration

In this case report, we discuss a patient presenting with parkinsonism followed by a non-amnestic dementia with aphasic clinical features, as well as frontal dysexecutive syndrome. There was a family history of dementia with an autopsy diagnosis of “Pick's disease” in the proband's father. Neuroimaging of the patient revealed focal and severe temporal lobe and lesser frontoparietal lobe atrophy. At autopsy, there was severe frontotemporal lobar degeneration. Histologic evaluation revealed an absence of tau or transactivation response DNA-binding protein of 43 kDa (TDP) pathology but rather severe Lewy body deposition in the affected cortices. Genetic phenotyping revealed a novel missense mutation (p.E83Q) in exon 4 of the gene encoding α-synuclein (SNCA). This case study presents a patient with a novel SNCA E83Q mutation associated with widespread Lewy body pathology with prominent severe atrophy of the frontotemporal lobes and corresponding cognitive impairment.