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Purpose: Effective cardiac rehabilitation interventions must provide adequate support to overcome psychosocial return-to-work (RTW) barriers. No validated instrument is available for this aim for cardiovascular patients. The Return-to-work Obstacles and Self-Efficacy Scale (ROSES) measures RTW obstacles workers perceive and the self-efficacy for overcoming them through 46 items and ten dimensions. This study aimed to adapt and validate ROSES for cardiovascular disease (CVD) in the Italian context., Methods: This prospective study involved 183 CVD working patients at baseline and 121 six months later. ROSES-CVD internal consistency, construct, and predictive validity was evaluated with Cronbach's α, Confirmatory factor analyses (CFA), and ANCOVAs., Results: CFAs adequately replicated the original ROSES model (CFI = .92-.96; TLI = .91-.94; RMSEA = .042-.057; SRMR = .046-.071) with α close or higher than .70 for all dimensions. Four ROSES-CVD dimensions significantly predicted the number of days to RTW controlling for age, gender, educational level, and surgery type. Workers who perceived salient RTW obstacles and low self-efficacy in any of these dimensions in mean returned to work from 38 to 53 days later., Conclusions: The study supported the validity and reliability of ROSES-CVD. This tool can be used in rehabilitation to detect CVD patients at risk of a longer RTW process and define appropriate cardiac rehabilitation intervention.IMPLICATIONS FOR REHABILITATIONVocational rehabilitation interventions should provide tailor-made support to overcome RTW barriers based on individual risk assessmentThe Italian translation of ROSES-CVD is a valid and reliable tool to measure psychosocial barriers to RTW among CVD working patientsThe use of ROSES-CVD would allow detection of CVD patients at risk of longer RTW processAdministering ROSES-CVD can help focus traditional vocational intervention on individually relevant obstacles to RTW.

Purpose: The study evaluated work experience changes and its determinants after return to work (RTW) in angioplasty or heart surgery patients., Methods: During a 1-year period (2014) in a Rehabilitation Hospital in northwestern Italy, we approached 253 patients (19.3% of inpatients). 199 patients consented to complete a survey on job characteristics, job satisfaction, job involvement, illness perception, depression, anxiety, adherence to therapy, and sociodemographic characteristics. The data were analysed with paired sample t tests and random intercept regression models., Results: 156 patients completed both the baseline and the 6-month follow-up assessments. After 6 months, 137 (88%) patients return to work (86% male, M age = 51.9 ± 8.1). The patients predominantly underwent angioplasty/bypass (46%) or valve replacement/repair (38%). Work hours (WO), job satisfaction (JS), and job involvement (JI) significantly decreased after RTW (WO: t (132)  = 2.07, p < 0.05; JS: t (134)  = 2.56, p < 0.05; JI: t (129)  = 4.14, p < 0.001). The decrease in work hours over time was associated with a within-subjects decrease in psychological job demands (β = 5.107, t (112.1 ) = 2.21, p < 0.05) and job satisfaction (β = 2.498, t (112.92)  = 2.265, p < 0.05) and an increase in physical job demands (β = - 1.314, t (112.07)  = - 2.416, p < 0.05). The decrease in job satisfaction over time was related to a within-subjects decrease in decision latitude (β = 0.505, t (116.43)  = 2.825, p < 0.01) and an increase in psychological job demand (β = - 0.586, t (116.78)  = - 3.141, p < 0.01). The decrease in job involvement over time was associated with a decrease in physical job demands (β = 0.063, t (117.19 ) = 2.157, p < 0.05) within-subjects., Conclusions: The study showed that many patients who RTW after angioplasty or heart surgery have poorer work experiences relative to changes in psychological and physical demands and more passive roles.

The cell adhesion molecule CD146 is normally located at the endothelial cell-to-cell junction and colocalizes with actin cytoskeleton. The soluble form of CD146 (sCD146) has been identified in the endothelial cell supernatant and in normal human plasma, and is increased in pathologic conditions with altered endothelial function. Soluble CD146 binding to monocytes promotes their transendothelial migration, which represents a central step in the development of atherosclerotic plaque. Since peripheral blood monocytes are characterized by a phenotypic and functional heterogeneity, with different transendothelial migration capacity, we hypothesized that monocyte subsets differently bind sCD146. Based on surface CD14 and CD16 expression monocytes were distinguished by flow cytometry (FACS) into three subsets: CD14++/CD16-, CD14++/CD16+ and CD14+/CD16+. CD16+ monocytes have been found to possess higher transendothelial migration ability. FACS analysis on blood monocytes from 30 healthy subjects revealed that higher percentages of CD14++/CD16+ (median, first and third quartile: 2.26, 1.62-3.87) and of CD14+/CD16+ (2.59, 1.28-4.80) were positive for CD146 (both p < 0.01), in comparison to CD14++/CD16- (0.66, 0.47-1.01). Moreover, in vitro treatment of ficoll separated monocytes with recombinant CD146 showed that both CD16+ subsets increased their percentage of CD146-positive events compared to CD16- monocytes (p < 0.01). Soluble CD146 levels were evaluated by ELISA in plasma samples of subjects from our study group and showed a correlation with percentage of CD146-positive CD14+/CD16+ monocyte subset. In this work we have demonstrated that monocyte subsets behave differently with regard to their sCD146 binding activity; because binding of CD146 influences transendothelial migration of monocytes, modulation of monocyte-CD146 interaction may represent a potential target to limit atherosclerotic plaque development.

Our aim was to define the distribution of monocyte subsets in a cohort of congestive heart failure (CHF) patients, to verify whether increased severity of CHF is linked to the expansion of specific monocyte subsets, and finally to investigate the relationship between monocyte subset relative frequencies, laboratory parameters of inflammation, and monocyte ACE expression. Thirty consecutive CHF patients and 26 healthy control subjects were evaluated for peripheral blood monocyte expression of CD14, CD16 and CD143 (ACE) by flow-cytometry, and for endothelial-derived soluble CD146 levels by ELISA. CD14++ CD16+ frequency was significantly higher in CHF patients than in Controls (%, median value and IQ) (12.3, 8.7-14.8 vs 5.9, 4.7-6.9, p< 0.05, CHF vs Controls), and it increased depending on how high NYHA class was, on worsening LV ejection fraction and on circulating pro-BNP values. Furthermore, it was associated with increasing creatinine and with decreasing GFR and albumin levels. Monocyte CD143 expression was significantly elevated in CHF patients as compared to Controls, and positively associated with CD14++ CD16+ levels. Frequencies of CD14+ CD16+ monocytes were significantly lower in CHF patients as compared to Controls, and negatively correlated with levels of soluble CD146 (r=-0.529; p 0.048). In conclusion, monocytic CD14++ CD16+ frequency and CD143 levels are increased and reflect disease status and progressive cardiac deterioration in CHF patients. The CD14+ CD16+ subset is depleted in CHF and is linked to endothelial damage in this group of patients. Although the question of whether differences in monocyte CD14CD16 expansion are causal or whether they represent a marker of HF progression which is potentially relevant for risk prediction remains unanswered, we believe that our data represent an important tool for exploring the role of selective inflammatory pathways in CHF progression.

Aims: Congestive heart failure (CHF) can be thought of as a state of chronic immune activation. Polymorphonuclear neutrophil (PMN) apoptosis is one of the mechanisms responsible for the resolution of inflammation. A reduced PMN apoptotic rate in CHF patients may generate a persistent inflammatory response and hence mediate tissue damage in this group of patients. We aimed to measure levels of spontaneous apoptosis of circulating PMNs in CHF patients and in controls, and to examine whether NYHA class, left ventricular ejection fraction (LV-EF), and laboratory parameters of inflammation, endothelial damage, and of liver and renal function, could predict the rate of PMN apoptosis in CHF patients., Methods and Results: A total of 29 CHF patients and 26 controls were studied. Propidium iodide and flow cytometry were used to assess PMN apoptosis. Delay in PMN apoptosis was expressed as percentage (expressed as median, first and third quartiles) of surviving PMNs in the study subjects. We found an increased percentage of surviving PMNs [38(27.1-47.1)] in CHF patients compared with controls [19.4 (15.8-25.2)] (P < 0.05). The PMN survival rate in the CHF group was correlated to NYHA class, and plasma levels of C-reactive protein and alkaline phosphatase, while it was inversely correlated to LV-EF and protein levels. A positive relationship between PMN survival and increased ex vivo endothelial apoptosis was found., Conclusion: Increased PMN lifespan in patients with worsening CHF could be used as a novel measurement of tissue and endothelial damage in this group of patients.

Unlabelled: The aims of this study were to assess the value of dobutamine echocardiography in identifying myocardial hibernation versus stunning and to elucidate the underlying pathophysiological mechanism of the contractile impairment., Methods: Twenty-one patients with isolated stenosis of the left anterior descending artery were evaluated 1 mo after thrombolysed acute anterior infarction. Regional function and blood flow were measured using echocardiography and PET at rest and during dobutamine administration (10 microg/kg/min)., Results: Defined by [18F]fluorodeoxyglucose uptake, 36 of 102 dyssynergic segments were necrotic, and 66 were viable. The latter segments were subdivided according to their [13N]ammonia flow distribution: 30 hibernating regions with perfusion defects (flow of <80% of maximum) and 36 stunned areas with preserved resting perfusion (flow of > or =80% of maximum). Resting flows were similar in necrosis and hibernation (0.43 +/- 0.18 versus 0.47 +/- 0.16 ml x min(-1) x g(-1); not significant), and both resting values were lower than those seen in stunning (0.79 +/- 0.24; p < 0.05). Flow response to dobutamine was markedly reduced in necrosis (dobutamine/resting flow = 1.16 +/- 0.27), whereas it was maintained in hibernation (1.65 +/- 0.54) and stunning (1.42 +/- 0.57). Dobutamine improved function in a higher number of stunned (55%) than hibernating (16%) or necrotic (11%) segments., Conclusion: Dobutamine improves function mainly in stunned myocardium and does not reliably identify hibernation. The lack of functional response in hibernation is not related to an exhausted vasodilating capacity.

After myocardial infarction, regional dysfunction can occur in viable myocardial regions because of the presence of baseline hypoperfusion. Recent evidence suggests that these areas may maintain a residual perfusion reserve. The aim of the present study was to evaluate whether oral nisoldipine can increase regional myocardial blood flow (MBF) in dyssynergic but viable myocardium after myocardial infarction. Patients with isolated left anterior descending coronary stenosis were studied 1 month after the first myocardial infarction. Patients underwent [18F]fluorodeoxyglucose imaging, and MBF was measured, using positron emission tomography and [13N]ammonia, at baseline and following dobutamine administration (10 micrograms/kg/min over 5 minutes). MBF measurements were repeated 24 hours after nisoldipine (10 mg twice daily). Preliminary results suggest that necrotic areas showed the largest reduction in baseline MBF. Dyssynergic-viable regions showed a reduced resting MBF but maintained a residual perfusion reserve in response to inotropic stimulation. Thus, nisoldipine selectively improved basal perfusion in dyssynergic-viable myocardium.

Silent myocardial ischaemia has been documented in various clinical entities. Exercise testing and ambulatory ECG monitoring are the most widely used tests for documenting silent ischaemia, and both exercise-induced and daily life ischaemia have the potential to trigger prolonged functional and structural changes. Numerous clinical investigations in apparently healthy subjects, in stable and unstable angina, in patients with a previous myocardial infarction indicate that ischaemia has an adverse prognostic influence, independent of whether the ischaemia is silent or symptomatic. Methods for documenting silent ischaemia lead to different considerations according to each clinical syndrome of coronary artery disease. This review deals with the different intervention strategies derived from the unique prognostic profiles offered by silent ischaemia in a variety of clinical entities.