European Journal of Preventive Cardiology

Increased pulse pressure is associated with structural target organ damage, especially in elderly patients, increasing cardiovascular risk.

In this analysis, we investigated whether high pulse pressure retains a prognostic effect also when common markers of target organ damage are taken into account.

We analysed an unselected cohort of treated hypertensive patients from the Campania Salute Network registry (n = 7336). Participants with available cardiac and carotid ultrasound were required to be free of prevalent cardiovascular disease, with ejection fraction ≥50%, and no more than stage III Chronic Kidney Disease. The median follow-up was 41 months and end-point was occurrence of major cardiovascular events (i.e. fatal and non-fatal stroke or myocardial infarction and sudden death). Based on current guidelines, pulse pressure ≥60 mm Hg was classified as high pulse pressure (n = 2356), at the time of the initial visit, whereas pulse pressure <60 mm Hg was considered normal (n = 4980).

High pulse pressure patients were older, more likely to be women and diabetic, while receiving more antihypertensive medications than normal pulse pressure (all p < 0.0001). High pulse pressure exhibited greater prevalence of left ventricular hypertrophy, and carotid plaque than normal pulse pressure (all p < 0.0001). In Cox regression, high pulse pressure patients had 57% increased hazard of major cardiovascular events, compared to normal pulse pressure (hazard ratio = 1.57; 95% confidence interval: 1.12–2.22, p = 0.01), an effect that was independent of significant prognostic impact of older age, male sex, diabetes, left ventricular hypertrophy, carotid plaque and less prescription of anti-renin–angiotensin system therapy.

High pulse pressure is a functional marker of target organ damage, predicting cardiovascular events in hypertensive patients, even independently of well-known structural markers of target organ damage.

Although psychological interventions are recommended for the management of coronary heart disease (CHD), there remains considerable uncertainty regarding their effectiveness.

Systematic review and meta-analysis of randomised controlled trials (RCTs) of psychological interventions for CHD.

The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, CINAHL and PsycINFO were searched to April 2016. Retrieved papers, systematic reviews and trial registries were hand-searched. We included RCTs with at least 6 months of follow-up, comparing the direct effects of psychological interventions to usual care for patients following myocardial infarction or revascularisation or with a diagnosis of angina pectoris or CHD defined by angiography. Two authors screened titles for inclusion, extracted data and assessed risk of bias. Studies were pooled using random effects meta-analysis and meta-regression was used to explore study-level predictors.

Thirty-five studies with 10,703 participants (median follow-up 12 months) were included. Psychological interventions led to a reduction in cardiovascular mortality (rfcelative risk 0.79, 95% confidence interval [CI] 0.63 to 0.98), although no effects were observed for total mortality, myocardial infarction or revascularisation. Psychological interventions improved depressive symptoms (standardised mean difference [SMD] –0.27, 95% CI –0.39 to –0.15), anxiety (SMD –0.24, 95% CI –0.38 to –0.09) and stress (SMD –0.56, 95% CI –0.88 to –0.24) compared with controls.

We found that psychological intervention improved psychological symptoms and reduced cardiac mortality for people with CHD. However, there remains considerable uncertainty regarding the magnitude of these effects and the specific techniques most likely to benefit people with different presentations of CHD.

This study examined the association between cardiac structure and function and the deterioration in activities of daily living (ADLs) in an age-homogenous, community-dwelling population of patients born in 1920–1921 over a five-year follow-up period.

Longitudinal cohort study.

Patients were recruited from the Jerusalem Longitudinal Cohort Study, which has followed an age-homogenous cohort of Jerusalem residents born in 1920–1921. Patients underwent home echocardiography and were followed up for five years. Dependence was defined as needing assistance with one or more basic ADL. Standard echocardiographic assessment of cardiac structure and function, including systolic and diastolic function, was performed. Reassessment of ADLs was performed at the five-year follow-up.

A total of 459 patients were included in the study. Of these, 362 (79%) showed a deterioration in at least one ADL at follow-up. Patients with functional deterioration had a significantly higher left ventricular mass index and left atrial volume with a lower ejection fraction. There was no significant difference between the diastolic parameters the groups in examined. When the data were examined categorically, a significantly larger percentage of patients with functional decline had an abnormal left ventricular ejection fraction and left ventricular hypertrophy. The association between left ventricular mass index and functional decline remained significant in all multivariate models.

In this cohort of the oldest old, an elevated left ventricular mass index, higher left atrial volumes and systolic, but not diastolic dysfunction, were predictive of functional disability.

Elderly patients have been underrepresented in secondary cardiovascular prevention programmes. This study aimed to ascertain the effects of a secondary coronary disease prevention programme in these patients.

Open randomised intervention study with parallel groups.

One hundred and twenty-seven patients aged ≥70 years with a recent acute coronary syndrome were randomised to a protocolised clinical intervention plus usual care (intervention group, n = 64) or to usual care alone (control group, n = 63). Patients were assessed at baseline and after 12 months. The main outcome was the percentage of patients with optimal risk factor control after 12 months of follow-up. Secondary outcomes included changes in Mediterranean diet adherence, quality of life and functionality. Mortality was evaluated three years after the end of the intervention.

One hundred and six patients (83.4%) completed 12 months of follow-up (54 in the intervention group and 52 in the control group). At the end of intervention, 34.2% more patients in the intervention group had achieved optimal risk factor control with a number needed to treat of 3 (relative risk 2.18, 95% confidence interval 1.36 to 3.50). The intervention group improved adherence to the Mediterranean diet (p = 0.013) and functionality assessed by the Short Physical Performance Battery (p = 0.047). No differences between groups were found in quality of life (Short-Form 36 Health Survey) or mortality after three years (hazard ratio 1.19, 95% confidence interval 0.41 to 3.45).

A secondary coronary disease prevention programme in elderly patients with a recent acute coronary syndrome improved risk factor control, Mediterranean diet adherence and functionality.

To assess the association between health-related quality of life (HRQL) and a composite outcome including incident coronary heart disease (CHD) and cerebrovascular events in a large general population-based cohort.

Prospective analysis on 17,102 men and women (mean age 53 ± 11) free from cardiovascular disease at time of enrolment in the Moli-sani cohort (2005–2010).

HRQL was assessed by the 36-Item Short Form Health Survey. Hazard ratios with 95% confidence intervals (95% CIs) were calculated using multivariable Cox-proportional hazard models.

At the end of follow-up (median 4.2 years), 237 new events occurred (coronary heart disease n = 197, cerebrovascular disease n = 42). In a multivariable model adjusted for socioeconomic factors, chronic disease and health-related behaviours, both mental and physical HRQL were inversely associated with the risk of the composite outcome (hazard ratio = 0.57; 0.39–0.84 and hazard ratio = 0.62; 0.40–0.94, respectively; highest vs. lowest quartile). Further adjustment for C-reactive protein marginally modified the association with physical HRQL (hazard ratio = 0.67; 0.43–1.02). Similar findings were obtained when only CHD events were analysed (hazard ratio = 0.63; 0.41–0.96 for highest versus lowest mental HRQL) although results with physical HRQL were no longer significant (hazard ratio = 0.65; 0.40–1.04 for highest versus lowest quartile). Associations with incident cerebrovascular disease showed a trend toward protection (hazard ratio = 0.50; 0.22–1.17 and hazard ratio = 0.51; 0.22–1.23 for highest versus lowest tertile of mental and physical HRQL, respectively).

HRQL is an independent predictor of composite CHD/cerebrovascular outcomes in an adult population. The magnitude of the association was not affected either by socioeconomic factors, health conditions or health-related behaviours. Improvement of quality of life may be a major factor in targeting appropriate prevention strategies for cardiovascular health.

Myocardial infarction-triggered acute stress disorder (ASD) and subclinical inflammation associate with the development of posttraumatic stress disorder, and worsen the prognosis of myocardial infarction patients. We examined the relationship between ASD severity and C-reactive protein levels in patients with acute myocardial infarction.

We assessed 190 patients (median age 59 years; 83% men) with a verified myocardial infarction within 48 h of an acute coronary intervention. Circulating levels of C-reactive protein were categorized according to their prognostic risk for cardiovascular disease: 0 to <5, 5 to <10, 10 to <20, and ≥ 20 mg/l. Patients completed the ASD-Scale (ASDS) for myocardial infarction-triggered symptoms and questionnaires for demographic factors, health behaviours, cardiac-related variables and psychosocial characteristics.

The ASDS sum score was positively associated with C-reactive protein categories in the bivariate analysis (r = 0.20, p < 0.01). Significant relationships with C-reactive protein also emerged for dissociation (r = 0.25, p < 0.001) and avoidance (r = 0.19, p < 0.01), but not for arousal and re-experiencing. Similarly, C-reactive protein levels ≥ 20 mg/l versus < 20 mg/l were predicted by the ASDS sum score, and the dissociation, avoidance and arousal subscores (all p-values < 0.05) in the fully adjusted binary regression analyses. C-reactive protein levels ≥ 20 mg/l were also independently predicted by male gender, body mass index, lower education, and lower left ventricular ejection fraction and higher white blood cell count.

Higher levels of myocardial infarction-triggered ASD symptoms associate with a greater inflammatory response in patients with acute myocardial infarction independently of important covariates. The findings suggest a link between myocardial infarction-triggered ASD symptoms and a heightened acute phase response with a potential impact on cardiovascular disease prognosis.

The association between cardiorespiratory fitness, physical activity and coronary artery calcium (CAC) is unclear, and whether higher levels of fitness attenuate CAC prevalence in subjects with metabolic syndrome is not fully elucidated. The present study aims to: a) investigate the independent association of fitness on the prevalence of CAC, after adjustment for moderate-to-vigorous physical activity and sedentary time, and b) study the possible attenuation of increased CAC by higher fitness, in participants with metabolic syndrome.

Cross-sectional.

In total 678 participants (52% women), 50–65 years old, from the SCAPIS pilot study were included. Fitness (VO₂max) was estimated by submaximal cycle ergometer test and moderate-to-vigorous physical activity and sedentary time were assessed using hip-worn accelerometers. CAC score (CACS) was quantified using the Agatston score.

The odds of having a significant CACS (≥100) was half in participants with moderate/high fitness compared with their low fitness counterparts. Further consideration of moderate-to-vigorous physical activity, sedentary time and number of components of the metabolic syndrome did only slightly alter the effect size. Those with metabolic syndrome had 47% higher odds for significant CAC compared with those without metabolic syndrome. However, moderate/high fitness seems to partially attenuate this risk, as further joint analysis indicated an increased odds for having significant CAC only in the unfit metabolic syndrome participants.

Being fit is associated with a reduced risk of having significant CAC in individuals with metabolic syndrome. While still very much underutilized, fitness should be taken into consideration in everyday clinical risk prediction in addition to the traditional risk factors of the metabolic syndrome.

Acute vascular effects of high intensity physical activity are incompletely characterized. Circulating microparticles are cellular markers for vascular activation and damage.

Microparticles were analysed in 99 marathon runners (49 ± 6 years, 22% female) of the prospective Berlin Beat of Running study. Blood samples were taken within three days before, immediately after and within two days after the marathon run. Endothelial-derived microparticles were labelled with CD144, CD31 and CD62E, platelet-derived microparticles with CD62P and CD42b, leukocyte-derived microparticles with CD45 and monocyte-derived microparticles with CD14.

Marathon running induced leukocytosis (5.9 ± 0.1 to 14.8 ± 0.3 10⁹/l, p < 0.0001) and increased platelet counts (239 ± 4.6 to 281 ± 5.9 10⁹/l, p < 0.0001) immediately after the marathon. Blood monocytes increased and lymphocytes decreased after the run (p < 0.0001). Endothelial-derived microparticles were acutely increased (p = 0.008) due to a 23% increase of apoptotic endothelial-derived microparticles (p = 0.007) and returned to baseline within two days after the marathon. Thrombocyte-derived microparticles acutely increased by 38% accompanied by an increase in activated and apoptotic thrombocyte-derived microparticles (p ≤ 0.0001) each. Both monocyte- and leukocyte-derived microparticles were decreased immediately after marathon run (p < 0.0001) and remained below baseline until day 2. Troponin T increased from 12 to 32 ng/l (p < 0.0001) immediately after the run and returned to baseline after two days.

Circulating apoptotic endothelial- and thrombocyte-derived microparticles increased after marathon running consistent with an acute pro-thrombotic and pro-inflammatory state. Exercise-induced vascular damage reflected by microparticles could indicate potential mechanisms of post-exertional cardiovascular complications. Further studies are warranted to investigate microparticles as markers to identify individuals prone to such complications.

The risk of cardiovascular disease is closely connected to adipose tissue inflammation. The links between cardiovascular risk predictors and pro and anti-inflammatory macrophages in human adipose tissue were analysed to gain an insight into the pathophysiology of cardiovascular disease.

Subcutaneous and visceral adipose tissues were obtained from 79 subjects, 52 living kidney donors (during nephrectomy) and 27 patients with peripheral artery disease (during arterial tree reconstruction).

Macrophage subsets were isolated from adipose tissues and analysed by flow cytometry using CD14, CD16, CD36 and CD163 monoclonal antibodies. The mutually adjusted differences of phagocytic pro-inflammatory (CD14 + CD16 + CD36^high), anti-inflammatory (CD14 + CD16-CD163+) and transitional subsets of macrophages were analysed in relation to cardiovascular predictors (sex, age, body mass index, smoking, hypercholesterolaemia, hypertension and statin treatment).

Age, male sex and hypercholesterolaemia were closely positively associated with the phagocytic pro-inflammatory macrophage subset in visceral adipose tissues. Interestingly, the proportion of phagocytic pro-inflammatory macrophages was relevantly decreased by statin therapy. A strong positive association of body mass index to the phagocytic pro-inflammatory subset was found in subcutaneous adipose tissues only. A minor transitional subpopulation, CD14 + CD16 + CD36^lowCD163+, increased with age in both adipose tissues. This transitional subpopulation was also negatively associated with obesity and hypercholesterolaemia in visceral adipose tissues.

An effect of cardiovascular risk predictors on adipose tissue macrophage subpopulations was revealed. Interestingly, while age, male sex and hypercholesterolaemia were connected with the pro-inflammatory macrophage subpopulation in visceral adipose tissues, body mass index had a prominent effect in subcutaneous adipose tissues only. A decreasing effect of statins on these pro-inflammatory macrophages was documented.