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      Effect of Combination Therapy on Cardiovascular Risk in the Pit Miners with Hypertension, Metabolic Syndrome and Depression

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          Abstract

          Background:

          Higher cardiovascular (CV) morbidity and mortality in depressed patient has demonstrated repeatedly.

          Aim:

          Determine the degree of occurrence of hypertension, metabolic syndrome (MetS) and depression in the pit miners and the impact of the six-month holistic treatment of all CV risk factors and depression in the overall CV risk in miners with hypertension, MetS and depression.

          Methods:

          From 492 pit miners was taken smoking status, measured blood pressure, waist circumference and body mass index. Analysis was done using the concentration of sugar in blood, triglycerides, total cholesterol, HDL, LDL cholesterol and determined total CV risk. All respondents filled self-assessment Beck's depression scale. Prevalence MetS hypertension and depression were determined. Group of 67 patients with joint hypertension, MetS and depression that is treated six months with psychotropic and somatotropin medication, was singled out. After six months, the effect of therapy on the risk factors and total CV was assessed.

          Results:

          Among 492 miners 67 (13,61%) of them had hypertension, MetS and depression. After six months treatment, it showed statistically significant reduction in blood pressure (p=0,0001), waist circumference (p=0,0001) ,total (p=0,002), HDL (p=0,007) and LDL cholesterol (p=0,003), smoking (p=0,002), Beck's scale results (p=0,007) and reduction in total CV risk.

          Conclusion:

          After six month of combine therapy in respondents has led to reduced CV risk and level of all factors, except BMI and triglycerides.

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          Most cited references28

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          Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

          Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.
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            Impact of the metabolic syndrome on mortality from coronary heart disease, cardiovascular disease, and all causes in United States adults.

            Mortality resulting from coronary heart disease (CHD), cardiovascular disease (CVD), and all causes in persons with diabetes and pre-existing CVD is high; however, these risks compared with those with metabolic syndrome (MetS) are unclear. We examined the impact of MetS on CHD, CVD, and overall mortality among US adults. In a prospective cohort study, 6255 subjects 30 to 75 years of age (54% female) (representative of 64 million adults in the United States) from the Second National Health and Nutrition Examination Survey were followed for a mean+/-SD of 13.3+/-3.8 years. MetS was defined by modified National Cholesterol Education Program criteria. From sample-weighted multivariable Cox proportional-hazards regression, compared with those with neither MetS nor prior CVD, age-, gender-, and risk factor-adjusted hazard ratios (HRs) for CHD mortality were 2.02 (95% CI, 1.42 to 2.89) for those with MetS and 4.19 (95% CI, 3.04 to 5.79) for those with pre-existing CVD. For CVD mortality, HRs were 1.82 (95% CI, 1.40 to 2.37) and 3.14 (95% CI, 2.49 to 3.96), respectively; for overall mortality, HRs were 1.40 (95% CI, 1.19 to 1.66) and 1.87 (95% CI, 1.60 to 2.17), respectively. In persons with MetS but without diabetes, risks of CHD and CVD mortality remained elevated. Diabetes predicted all mortality end points. Those with even 1 to 2 MetS risk factors were at increased risk for mortality from CHD and CVD. Moreover, MetS more strongly predicts CHD, CVD, and total mortality than its individual components. CHD, CVD, and total mortality are significantly higher in US adults with than in those without MetS.
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              Depression as a predictor for coronary heart disease. a review and meta-analysis.

              To review and quantify the impact of depression on the development of coronary heart disease (CHD) in initially healthy subjects. Cohort studies on depression and CHD were searched in MEDLINE (1966-2000) and PSYCHINFO (1887-2000), bibliographies, expert consultation, and personal reference files. Cohort studies with clinical depression or depressive mood as the exposure, and myocardial infarction or coronary death as the outcome. Information on study design, sample size and characteristics, assessment of depression, outcome, number of cases, crude and most-adjusted relative risks, and variables used in multivariate adjustments were abstracted. Eleven studies met the inclusion criteria. The overall relative risk [RR] for the development of CHD in depressed subjects was 1.64 (95% confidence interval [CI]=1.29-2.08, p<0.001). A sensitivity analysis showed that clinical depression (RR=2.69, 95% CI=1.63-4.43, p<0.001) was a stronger predictor than depressive mood (RR=1.49, 95% CI=1.16-1.92, p=0.02). It is concluded that depression predicts the development of CHD in initially healthy people. The stronger effect size for clinical depression compared to depressive mood points out that there might be a dose-response relationship between depression and CHD. Implications of the findings for a broader bio-psycho-social framework are discussed.
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                Author and article information

                Journal
                Mater Sociomed
                Mater Sociomed
                MSM
                Materia Socio-Medica
                AVICENA, d.o.o., Sarajevo (Bosnia and Herzegovina )
                1512-7680
                1986-597X
                11 April 2014
                April 2014
                : 26
                : 2
                : 112-115
                Affiliations
                [1 ]Public Health Centre Banovici, Department of Occupational Medicine, Banovici, Bosnia and Herzegovina
                [2 ]Internal Diseases Clinic, University and Clinical Centre Tuzla, Tuzla, Bosnia and Herzegovina
                [3 ]Department for Family Medicine, Public Health Centre Tuzla, Tuzla, Bosnia and Herzegovina
                Author notes
                Corresponding author: Munevera Becarevic, MD. Public Health Centre Banovici, Department for Occupational Medicine, Banovici, Bosnia and Herzegovina. Phone: 0038761 282 873; E-mail: b.munevera@ 123456gmail.com
                Article
                MSM-26-112
                10.5455/msm.2014.26.112-115
                4035143
                75599a37-a1ac-4320-a72c-48dc987f80be
                Copyright: © AVICENA

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 05 January 2014
                : 05 April 2014
                Categories
                Original Paper

                hypertension,cardiovascular risk,metabolical syndrome,depression,risk factor

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