Association between depression and development of coronary artery disease: pathophysiologic and diagnostic implications.

Depression and coronary artery disease (CAD) are both extremely prevalent diseases. In addition, compromised quality of life and life expectancy are characteristics of both situations. There are several conditions that aggravate depression and facilitate the development of CAD, as well as provoke a worse prognosis in patients with already established CAD: inferior adherence to medical orientations (medications and life style modifications), greater platelet activation and aggregation, endothelial dysfunction, and impaired autonomic dysfunction (lowered heart rate variability). Recent literature has shown that depression alone is becoming an independent risk factor for cardiac events both in primary and secondary prevention. As the diagnosis of depression in patients with heart disease is difficult, due to similarities of symptoms, the health professional should perform a careful evaluation to differentiate the clinical signs of depression from those related with general heart diseases. After a myocardial infarction, depression is an independent risk factor for mortality. Successful therapy of depression has been shown to improve patients' quality of life and cardiovascular outcome. However, multicentric clinical trials are needed to support this inference. A practical liaison between qualified professionals is necessary for the better management of depressed patients with excess risk in developing CAD. Accordingly, pathophysiological and clinical implications between depression and CAD are discussed in this article.

Subtle gray matter changes in temporo-parietal cortex associated with cardiovascular risk factors.

Vascular risk factors may play an important role in the pathophysiology of Alzheimer's disease (AD). While there is consistent evidence of gray matter (GM) abnormalities in earlier stages of AD, the presence of more subtle GM changes associated with vascular risk factors in the absence of clinically significant vascular events has been scarcely investigated. This study aimed to examine GM changes in elderly subjects with cardiovascular risk factors. We predicted that the presence of cardiovascular risk would be associated with GM abnormalities involving the temporal-parietal cortices and limbic structures. We recruited 248 dementia-free subjects, age range 66-75 years, from the population-based "São Paulo Ageing and Health Study", classified in accordance to their Framingham Coronary Heart Disease Risk (FCHDR) score to undergo an MRI scan. We performed an overall analysis of covariance, controlled to total GM and APOE4 status, to investigate the presence of regional GM abnormalities in association with FCHDR subgroups (high-risk, medium-risk, and low-risk), and followed by post hoc t-test. We also applied a co-relational design in order to investigate the presence of linear progression of the GM vulnerability in association with cardiovascular risk factor. Voxel-based morphometry showed that the presence of cardiovascular risk factors were associated with regional GM loss involving the temporal cortices bilaterally. Those results retained statistical significance after including APOE4 as a covariate of interest. We also observed that there was a negative correlation between FCHDR scores and rGM distribution in the parietal cortex. Subclinical cerebrovascular abnormalities involving GM loss may provide an important link between cardiovascular risk factors and AD.

A double-blind, placebo-controlled treatment trial of citalopram for major depressive disorder in older patients with heart failure: the relevance of the placebo effect and psychological symptoms.

BACKGROUND: Little is known about the treatment of depression in older patients with heart failure. This study was developed to investigate the effectiveness of antidepressant treatment for major depressive disorder (MDD) in the elderly with heart failure. METHODS: We enrolled 72 older outpatients with ejection fraction <50 and diagnosed with MDD by the structured clinical interview for DSM-IV. Thirty-seven patients, 19 on citalopram and 18 on placebo, initiated an 8-week double-blind treatment phase. Measurements were performed with the 31-item Hamilton Rating Scale for Depression (Ham-D-31), the Montgomery-Asberg rating scale (MADRS) and the Systematic Assessment for Treatment Emergent Effects (SAFTEE). A psychiatrist followed up the patients weekly, performing a consultation for about 20 min to field complaints after the measurements. RESULTS: A trend toward superiority of citalopram over placebo in reducing depression was observed in MADRS scores (15.05+9.74 vs 9.44+9.25, P=.082) but not on HAM-D scores. The depressive symptomatology significantly decreased in both groups (P < .001). The high rate of placebo response during the double-blind phase (56.3%) led us to conclude the study at the interim analysis with 37 patients. CONCLUSION: Citalopram treatment of MDD in older patients with heart failure is well-tolerated with low rates of side effects, but was not significantly more effective than placebo in the treatment of depression. Weekly psychiatric follow-up including counseling may contribute to the improvement of depression in this population. Scales weighted on psychological symptoms such as the MADRS are possibly better suited to measure depression severity and improvement in patients with heart failure.

Major depressive disorder and inflammatory markers in elderly patients with heart failure.

The authors evaluated levels of inflammatory markers in 34 chronic heart failure (CHF) out-patients age 65 years and over, with (N=18) and without (N=16) major depressive disorder (MDD), and healthy-control subjects (N=13). Patients with CHF had left-ventricular ejection fractions <0.40 and were in the New York Heart Association functional class II or III. The authors used the SCID DSM-IV to diagnosis MDD. High-sensitivity C-reactive protein levels were significantly higher in patients with CHF and MDD as compared with healthy-control subjects. No differences regarding tumor necrosis factor(alpha) or interleukin(6) were found among the three groups.

Depressão, estado emocional e doença arterial coronária / Depression, emotional state and coronary artery disease

A depressão e doença arterial coronariana (DAC) são duas doenças muito prevalentes. Além disso, o comprometimento da qualidade de vida e expectativa de vida são características de ambas as situações. Existem várias condições que, além de agravar a depressão e facilitar o desenvolvimento da DAC, ainda pioram o prognóstico em pacientes com DAC estabelecida. São elas: adesão inferior a orientações médicas (medicamentos e modificações no estilo de vida), maior ativação e agregação plaquetária, disfunção endotelial e disfunção autonômica (diminuição da variabilidade da frequência cardíaca). A literatura recente tem mostrado que a depressão por si só está se tornando um fator de risco independente para eventos cardíacos, tanto na prevenção primária e como na secundária. Como o diagnóstico de depressão em pacientes com doença cardíaca é difícil, devido às semelhanças dos sintomas, o profissional de saúde deve realizar uma avaliação cuidadosa para diferenciar os sinais clínicos de depressão daqueles relacionados com doenças cardíacas em geral. Tratamentos bem sucedidos da depressão têm mostrado melhora na qualidade de vida dos pacientes e nos resultados cardiovasculares. No entanto, estudos clínicos multicêntricos são necessários para apoiar essa inferência. Aligação prática entre profissionais qualificados é necessária para melhor gestão dos pacientes deprimidos com excessode risco no desenvolvimento de DAC. Assim, as implicações fisiopatológicas e clínicas entre depressão e DAC são discutidas neste artigo.

Depression and coronary artery disease (CAD) are both extremely prevalent diseases. In addition, compromised quality of life and life expectancy are characteristics of both situations.There are several conditions that aggravate depression and facilitate the development of CAD, as well as provoke aworse prognosis in patients with already established CAD:inferior adherence to medical orientations (medications and life style modifications), greater platelet activation and aggregation, endothelial dysfunction, and impaired autonomic dysfunction (lowered heart rate variability). Recent literature has shown that depression alone is becoming an independent risk factor for cardiac events both in primary and secondary prevention. As the diagnosis of depression in patients with heart disease is difficult, due to similarities of symptoms, the health professional should perform a careful evaluation to differentiate the clinical signs of depression from those related with general heart diseases. Successful therapy of depression has been shown to improve patients’quality of life and cardiovascular outcome. However, multicentric clinical trials are needed to support this inference. A practical liaison between qualified professionals is necessary for the better management of depressed patients with excess risk in developing CAD. Accordingly, pathophysiological and clinical implications between depression and CAD are discussed in this article.

Uso de tromboliticos no infarto agudo do miocardio / Thrombolytic use in the acute myocardial infarction

Nos paises industrializados,a isquemia miocardica e a principal causa de morte. Nos Estados Unidos da America do Norte, a incidencia anual e de 1500000 casos, onde 60% dos obitos ocorrem na primeira hora devido a fibrilacao ventricular.Com o melhor conhecimento fisiopatogenico e dos avancos tecnologicos, a mortalidade no infarto agudo do miocardio(IAM) vem diminuindo nas ultimas decadas, em consequencia da introducao das unidades coronarias,monitoracao das arritmias cardiacas, uso de drogas vasoativas e beta-bloqueadores ,tromboliticos, etc.

Comportamento dos níveis plasmáticos de proteína C-reativa, interleucina-6 e fator de necrose tumoral-alfa em idosos com insuficiência cardíaca compensada associada à depressão maior / Plasma levels of C-reactive protein, interleukin-6 and tumor necrosis factor-alpha in elderly with stable heart failure associated with major depression

A insuficiência cardíaca e a depressão maior são doenças prevalentes na população idosa. Evidências sugerem que a depressão está associada ao aumento da morbi- mortalidade cardiovascular. Em ambas as doenças, ocorre ativação do eixo hipotálamo-hipófise-adrenal e do sistema nervoso simpático, assim como aumento de marcadores inflamatórios como citocinas e proteína C-reativa. Este estudo investigou o papel dos marcadores inflamatórios na presença de depressão maior em idosos com insuficiência cardíaca compensada. Foram analisados os níveis plasmáticos do fator de necrose tumoral-alfa, interleucina-6 e proteína C-reativa em 18 pacientes idosos com insuficiência cardíaca compensada em classe funcional II ou III (NYHA) e fração de ejeção < 40 por cento e depressao maior (diagnosticada pelo PRIME-MD e Hamilton -31), 16 pacientes idosos com insuficiência cardíaca e 13 idosos sadios. Concluímos que em idosos com insuficiência cardíaca compensada, a presença de depressão maior não está associada ao aumento dos níveis plasmáticos do fator de necrose tumoral-α ou da interleucina-6 mas ao aumento dos níveis plasmáticos da proteína C-reativa, sugerindo uma exacerbação da resposta inflamatória / Heart failure and major depression are prevalent diseases in the elderly. Evidence indicates that depression is associated with increased cardiovascular morbidity and mortality. In both diseases, there is an hypothalamus-pituitary-adrenal axis and sympathetic hyperactivity and elevation of inflammatory markers, such as cytokines and C-reactive protein. This study investigates the behavior of inflammatory markers in the presence of major depression in compensated heart failure elderly patients.We analysed the plasma levels of tumor necrosis factor-alpha, interleukin-e and C-reactive protein in 18 elderly patients with stable NYHA functional class II or III heart failure with ejection fraction < 40 per cent and major depression (diagnosed PRIME-MD and Hamilton-31), 16 elderly patients with heart failure and 13 healthy elderly individuals. We concluded that in elderly patints with compensated heart failure, the presence of major depression didn’t show association with plasma levels of tumor necrosis factor and interleukin-6 but there was an elevation of the plasmatic levels of C-reactive protein supporing anexacrbation of the inflammatory response...