Epidemiology and the physiopathological link between depression and cardiovascular disease

none3noIn the future, cardiovascular disease, togetherwith depression,will be one of the leading causes of global disease in the Western World. It is well known that depression is independently associated with a poor prognosis in patients with ischemic heart disease. Epidemiological studies suggest that in patients with coronary artery disease, depression symptoms identify patients with higher risk of adverse cardiovascular outcomes, other studies maintain that depression symptoms might influence the progression of coronary and peripheral atherosclerosis. The defined pathophysiological pathways which link depression and cardiovascular outcomes are not well recognized although various mechanisms have been proposed to explain this association. Beyond traditional cardiovascular risk factors, autonomic nervous system, lowgrade of inflammation, platelet function, abnormal function of the hypothalamic–pituitary–adrenal axis and genetic factors can adversely impact the endothelium and arterial walls. Consequently, these mechanisms might be crucial factors in promoting and accelerating atherosclerosis and its complications due to plaque rupture and thrombosis. For these reasons, depression symptoms should be considered as a new cardiac risk factor in the general population and in patients with coronary artery disease.In the future, cardiovascular disease, together with depression, will be one of the leading causes of global disease in the Western World. It is well known that depression is independently associated with a poor prognosis in patients with ischemic heart disease.Epidemiological studies suggest that in patients with coronary artery disease, depression symptoms identify patients with higher risk of adverse cardiovascular outcomes, other studies maintain that depression symptoms might influence the progression of coronary and peripheral atherosclerosis.The defined pathophysiological pathways which link depression and cardiovascular outcomes are not well recognized although various mechanisms have been proposed to explain this association. Beyond traditional cardiovascular risk factors, autonomic nervous system, low grade of inflammation, platelet function, abnormal function of the hypothalamic-pituitary-adrenal axis and genetic factors can adversely impact the endothelium and arterial walls. Consequently, these mechanisms might be crucial factors in promoting and accelerating atherosclerosis and its complications due to plaque rupture and thrombosis. For these reasons, depression symptoms should be considered as a new cardiac risk factor in the general population and in patients with coronary artery disease.mixedPizzi, Carmine; Santarella, Luigi; Bugiardini, RaffaelePizzi, Carmine; Santarella, Luigi; Bugiardini, Raffael

Epidemiologia e legame fisiopatologico fra depressione e malattie cardiovascolari

Nel futuro, insieme alle malattie cardiovascolari, la depressione sarà una delle principali cause di malattie nel mondo occidentale. È ben noto che la depressione è indipendentemente associata ad una prognosi sfavorevole nel paziente con cardiopatia ischemica. Studi epidemiologici indicano che nei pazienti con malattia coronarica, i sintomi della depressione identificano quelli con più alto rischio durante il follow-up. I link fisiopatologici che legano la depressione agli eventi cardiovascolari non sono ben conosciuti, anche se vari meccanismi sono stati proposti per spiegare questa associazione. Al di là dei tradizionali fattori di rischio cardiovascolare, il sistema nervoso autonomo, l’infiammazione, l’aggregazione piastrinica, la disfunzione dell’asse ipotalamo-ipofisi-surrene e fattori genetici possono avere un impatto negativo sulla parete arteriosa e sull’endotelio, quindi, questi meccanismi potrebbero essere fattori cruciali per promuovere e accelerare l’aterosclerosi e le sue complicanze a causa della rottura della placca e la formazione della trombosi coronarica. Per queste ragioni, la depressione dovrebbe essere considerata come un nuovo fattore di rischio cardiovascolare nella popolazione generale e nei pazienti con malattia coronarica

Functional MRI (fMRI) Evaluation of Hyperbaric Oxygen Therapy (HBOT) Efficacy in Chronic Cerebral Stroke: A Small Retrospective Consecutive Case Series

Topics: Functional Magnetic Resonance Imaging (fMRI) evaluation of HyberBaric Oxygen Therapy (HBOT) effects on chronic cerebral stroke Patients (Pts). Introduction: Our aim was to evaluate with fMRI, in a 3 Tesla system, the functional effects of HBOT on the Central Nervous System (CNS) in four Pts with established ischaemic and haemorrhagic cerebral strokes (2 Pts each). To our knowledge, no author used fMRI technique for this purpose, till now. Methods: All four Pts underwent a fMRI study before and after 40 HBOT sessions, with a time window of a few days. They carried out two language (text listening, silent word-verb generation) and two motor (hand and foot movements) tasks (30 s On-Off block paradigms). Results: After HBOT, all Pts reported a clinical improvement, mostly concerning language fluency and motor paresis. fMRI analysis demonstrated an increase in both the extent and the statistical significance of most of the examined eloquent areas. Conclusions: These changes were consistent with the clinical improvement in all Pts, suggesting a possible role of fMRI in revealing neuronal functional correlates of neuronal plasticity and HBOT-related neoangiogenesis. Although only four Pts were examined, fMRI proved to be a sensitive, non-invasive and reliable modality for monitoring neuronal functional changes before and after HBOT

UNFRACTIONED HEPARIN/CLOPIDOGREL INTERACTION IN PATIENTS WITH STEMI NOT UNDERGOING REPERFUSION

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Depression symptoms and the progression of carotid intima-media thickness: A 5-year follow-up study

Objective: Only a few studies have investigated the changes in carotid intima-media thickness (IMT) over time, and uncertainties remain on the underlying mechanisms linking depression and subclinical atherosclerosis. We carried out a prospective cohort study to evaluate whether depression is associated with changes in carotid IMT in subjects with cardiac risk factors but free from coronary heart disease (CHD), and to what extent the atherogenicity of depression can be explained by inflammatory markers and autonomic nervous system dysfunction. Methods: During baseline and follow-up visits: all participants were asked to provide blood samples and compile a structured questionnaire; trained physicians assessed depression symptoms using Beck Depression Inventory (BDI); altered cardiac autonomic tone was measured using time-domain components of heart rate variability in 24h Holter recordings; measurements of carotid IMT were carried out using B-mode ultrasound image acquisition. Logistic and linear regression analyses were used to adjust for potential confounders and explore potential mediators. Results: A total of 381 subjects completed the 5-year follow-up. The mean carotid IMT significantly increased in all subjects but the amount of increase was significantly larger among subjects with depression symptoms: mean IMT increased by 0.16±0.14mm; 0.31±0.28mm and 0.61±0.54mm among the subjects with no, mild and moderate/severe depression, respectively (all p<0.01). The association between moderate/severe depression and IMT increase remained highly significant even after controlling for all the variables considered, however when both IL-6 and CRP were included in multivariate models the regression coefficient decreased by 42.3%. Some of the inflammation markers and autonomic nervous system dysfunction were also independently correlated with carotid IMT increase. Conclusion: Depression symptoms are independently associated with an accelerated progression of carotid IMT in subjects with CHD risk factors, and inflammation may substantially modulate the association between depression and carotid IMT progression. © 2014 Elsevier Ireland Ltd

Potential markers of healing from near infrared spectroscopy imaging of venous leg ulcer. A randomized controlled clinical trial comparing conventional with hyperbaric oxygen treatment

The aim of this study is to ascertain whether the simultaneous measurement of hemoglobin O2 saturation (StO2 ) and dimension of venous leg ulcers (VLU) by near infrared spectroscopy (NIRS) imaging can predict the healing course with protocols employing a conventional treatment alone or in combination with hyperbaric oxygen therapy (HBOT). NIRS 2D images of wound region were obtained in 81 patients with hard-to-heal VLU that had been assigned, in a randomized controlled clinical trial, to the following protocols: 30 HBOT sessions, adjunctive to the conventional therapy, either twice daily over 3 weeks (group A) or once daily over 6 weeks (group B), and conventional therapy without HBOT (group C). Seventy-three patients completed the study with a total of 511 NIRS images being analyzed. At the end of treatment, wound area was significantly smaller in all three groups. However, at the 3-week mark the wound area reduction tended to be less evident in group A than in the other groups. This trend continued up to the 6-week end-point when a significantly greater area reduction was found with group B (65.5%) and group C (56.8%) compared to group A (29.7%) (P &lt; .01). Furthermore, a higher incidence of complete healing was noted with group B (20%) than with group A (4.5%) and group C (3.8%). When using a final wound reduction in excess of 40% to distinguish healing from nonhealing ulcers, it was found that only the former present NIRS StO2 values abating over the study period both at center and edge of lesions. In conclusion, NIRS analysis of StO2 and wound area can predict the healing course of VLU. Adjunctive HBOT significantly facilitates VLU healing compared to the conventional treatment alone. This positive action, however, becomes manifest only with a longer and less intensive treatment schedule

Mice carrying an analogous heterozygous dynamin 2 K562E mutation that causes neuropathy in humans develop predominant characteristics of a primary myopathy

Some mutations affecting dynamin 2 (DNM2) can cause dominantly inherited Charcot–Marie–Tooth (CMT) neuropathy. Here, we describe the analysis of mice carrying the DNM2 K562E mutation which has been associated with dominant-intermediate CMT type B (CMTDIB). Contrary to our expectations, heterozygous DNM2 K562E mutant mice did not develop definitive signs of an axonal or demyelinating neuropathy. Rather, we found a primary myopathy-like phenotype in these mice. A likely interpretation of these results is that the lack of a neuropathy in this mouse model has allowed the unmasking of a primary myopathy due to the DNM2 K562E mutation which might be overshadowed by the neuropathy in humans. Consequently, we hypothesize that a primary myopathy may also contribute to the disease mechanism in some CMTDIB patients. We propose that these findings should be considered in the evaluation of patients, the determination of the underlying disease processes and the development of tailored potential treatment strategies.ISSN:0964-6906ISSN:1460-208