Chest pain without coronary artery disease: An exploratory comparison with panic disorder

Recent reports have indicated similarities between patients with persistent chest pain of nonorganic origin and patients with panic disorder. In order to explore this association further, we administered a structured interview and three self-report measures (State-Trait Inventory, Beck Depression Inventory, and SCL90-R) to three subject groups: (1) a sample with persistent chest pain (CP; n=14) who had been screened and found to have normal coronary arteries, (2) a sample of patients with panic disorder (PD; n=14), and (3) a sample of matched normals (n=14). CP patients were considered to be free of coronary artery disease (CAD) following normal cardiac catheterization and/or normal thallium stress tests and were not diagnosed initially with panic disorder. PD patients were diagnosed with a standardized psychiatric interview and were free of organic causes of panic. Using an exploratory data analytic approach, the results indicated that both CP and PD samples reported increased levels of state and trait anxiety (p <.0001), depression (p <.01), and somatization (p <.0001) compared with normals. CP patients differed from PD patients in their less frequent use of anxiolytic medication (p <.01) and lower levels of reported panic anxiety and phobic avoidance (p <.0001). These data suggest that persistent chest pain in the absence of CAD shares some features with panic disorder, yet differs from panic in key ways as well. The results are discussed in light of the role of anxiety in contributing to symptom labeling.This research was supported by Grant 86G-491 from the American Heart Association, Texas Affiliate, to J.G.B. H.T. is the recipient of USPHS Research Career Development Award K04-HL-0122246.     

An empirical study of the diathesis-stress theory of disease

One thousand, one hundred and twenty-one Jewish concentration camp survivors were compared with 367 Jewish controls who had not been in a concentration camp, and had not lost any family members in such a camp. Of interest was the mortality of camp and comparison groups, on the hypothesis that the stress of being in a camp would adversely affect inmates. It was found that former camp inmates were over twice as likely to die of cancer, coronary heart diesease, or other causes as the comparison subjects of similar age and sex composition, and that severity of stress was correlated with mortality in the expected direction. Diathesis, determined by means of a special interviewer-administrated questionnaire, was found to interact synergistically with stress in producing high mortality.     

Cognitive function after open-heart surgery: Are postoperative neuropsychological deficits caused by cardiopulmonary bypass?

Despite the many technological developments in arterial perfusion and cardiac surgical procedures, open-heart surgery is still believed to pose a significant risk for cerebral injury. There are several potential causes of brain damage during open-heart surgery, including prolonged or severe arterial hypotension, as well as emboli emanating from the cardiopulmonary bypass circuit or the operative field. This article reviews the available neuropsychological studies of outcome following cardiac valve replacement and coronary artery bypass grafting. Because both procedures are life-saving operations, the research in this area has been quasi-experimental and fraught with methodological problems. Nonetheless, the findings converge to suggest that cognitive dysfunction occurs after open-heart surgery, and that the deficits are attributable, at least in part, to factors specific to the operation or to the patient being maintained on cardiopulmonary bypass. Preliminary findings suggest that embolization is the primary cause of perioperative deficits in uncomplicated operations. Studies have also consistently found preoperative deficits in this population, suggesting that neuropsychological dysfunction is caused by severe chronic cardiac disease as well as open-heart surgery.     

Effects of midbrain central gray lesions on spontaneous and electrically induced aggression in the rat

Large electrolytic lesions were placed in the midbrain central gray of male rats. Their effects on hypothalamically induced aggression, switch-off behaviour, and locomotion were investigated. A number of these animals were also tested for territorial intermale aggression in order to compare electrically induced and spontaneous aggression. Large lesions resulted in an increase of the current threshold to induce aggression by hypo-thalamic stimulation. Smaller, but still quite large, lesions decreased the threshold current for hypothalamic aggression. After the operation a decrease in the threshold for switch-off was present, both in the experimental and the control group. Current thresholds for locomotion were decreased after the lesions only in the experimental group. Spontaneous aggression was temporarily decreased after the lesion. No indication was found that other behavioural elements of the animal were distorted by the lesion. The parallel between the effects on spontaneous and electrically induced aggression makes it attractive to ascribe a role to the neural circuit of hypothalamus and central gray in territorial aggression. However, even with large lesions the animals were still capable of fighting, hence the central gray is not indispensable. An attempt was made to explain the differential effects that differently sized central gray lesions have on hypothalamic aggression.     

Frontal-Lobe Involvement in Spatial Memory: Evidence from PET,fMRI, and Lesion Studies

Many studies have identified the prefrontal cortex as the brain area that is critical for spatial memory, both in humans and in other primates. Other studies, however, have failed to establish this relation. Therefore, the aim of this paper was to review the literature regarding the role of the human prefrontal lobe in spatial memory. This was done by examining the evidence obtained from neuropsychological patients and from studies using brain-imaging techniques (PET and fMRI). Evidence supporting the notion that the prefrontal cortex is extensively involved in spatial working memory was found. The majority of these studies, however, suggests that frontal-lobe involvement is not related to the type of material that is being processed (e.g., spatial vs. nonspatial), but to process-specific functions, such as encoding and retrieval. Theoretically, these functions could be linked to the central executive within Baddeley's working-memory model, or to recent theories that emphasize the various processes that play a role in working memory. Also, methodological issues were discussed. Further research is needed to enhance our understanding of the precise interaction of domain-specific and general processes.     

Deficit in selective and divided attention associated with cholinergic basal forebrain immunotoxic lesion produced by 192-saporin; motoric/sensory deficit associated with Purkinje cell immunotoxic lesion produced by OX7-saporin

The immunotoxin 192-saporin, infused intracerebroventricularly into rats, destroys cholinergic neurons in the basal forebrain nuclei. Doses required for complete cholinergic loss also kill some Purkinje cells. The immunotoxin OX7-saporin, when infused intraventricularly into rats, destroys Purkinje cells in a pattern similar to that produced by 192-saporin, without affecting cholinergic neurons. Thus, we used OX7-saporin to distinguish behavioral effects of 192-saporin due to cerebellar damage versus those due to cholinergic cell loss. Three doses of 192-saporin (1.6, 2.6, and 3.3 micrograms/rat) were chosen along with a dose of OX7-saporin (2.0 micrograms/rat) that produced Purkinje loss equivalent to the two highest doses of 192-saporin. Groups of Fischer-344 rats were trained in the multiple choice reaction time task and retested with more complex tasks after lesioning. They were also tested in the water maze, passive avoidance, acoustic startle, and open field. The OX7-saporin group exhibited changes in many tests suggesting hypermotility and sensory deficits. The 192-saporin groups differed from the OX7-saporin group when they displayed deficits in multiple choice reaction time tasks in which novel challenges were introduced, including sessions with a noise distractor, shortened and lengthened intertrial intervals, and use of nine instead of five sources of light stimulus. The 192-saporin groups showed no impairment in the other tasks. The cholinergic basal forebrain lesion may mask some of the effects of cerebellar damage up to a threshold after which effects of Purkinje cell loss predominate when 192-saporin is administered intraventricularly.     

Depression Screening,Assessment, and Treatment for Patients with Coronary Heart Disease: A Review for Psychologists

Depression prevalence is between 15% and 20% in coronary heart disease patients, such as those with angina, or after a myocardial infarction or coronary artery bypass graft surgery. The presence of depression places a coronary heart disease patient at twofold higher risk for further major cardiac events and death, as well as poor quality of life and early exit from the labour force. As a consequence, several learned societies, including the National Heart Foundation of Australia, have published guidelines that recommend questionnaire screening to improve identification and management strategies for depression in coronary heart disease patients. Psychologists in hospitals, community settings, and private practice can have a key role in the realisation of the National Heart Foundation of Australia's aims. We review the recent guidelines and outline implications for psychologists to identify and manage depression in coronary heart disease patients. The evidence reviewed suggests that cognitive‐behavioural therapy and problem‐solving therapy are frontline non‐pharmacological interventions for depression in CHD patients.     

Narcotrend监测下右美托咪定对冠心病患者麻醉诱导期血流动力学的影响

观察Narcotrend监测下右美托咪定联合丙泊酚靶控输注用于冠心病患者非心脏手术麻醉诱导时对血流动力学的影响.合并冠心痛行非心脏手术患者40例,随机分为两组：Dex组（n=20,患者在诱导前静脉泵注右美托咪定0.5μg/kg,15min内输注完毕）,对照组（n=20,等量生理盐水,方法同Dex组）.记录给药前后及诱导期间患者的血流动力学变化.对照组在气管插管即刻以及气管插管3min后血流动力学指标值均高于插管前,气管插管5min后平均动脉压（MAP）低于插管前（P＜0.05）,Dex组无明显差异.麻醉诱导前15min静脉注射0.5μg/kg右美托咪定可以使冠心病患者丙泊酚靶控输注诱导期间血流动力学更加平稳.     

原发灶切除在转移性乳腺癌治疗中的地位

无论是国内还是世界其他国家,乳腺癌近年来已成为女性常患恶性肿瘤之首。早期乳腺癌通过手术、化疗、放疗及内分泌治疗等综合治疗后可以达到长期生存。然而对于晚期乳腺癌,特别是伴有远处转移的乳腺癌,疗效却不尽如人意。对于转移性乳腺癌,目前治疗优先选择毒性尽可能小的全身系统性治疗方案;而对于需要缓解症状或避免即将发生并发症（如皮肤溃疡、出血、真菌感染以及疼痛等）的情况可于全身治疗后行相应手术。然而对于转移性乳腺癌是否手术切除原发灶以及是否可从手术中获益,仍然充满争议。     

Type D personality,but not Type A behavior pattern,is associated with coronary plaque vulnerability

Personality traits are associated with major adverse coronary events (MACE) in patients with coronary artery disease (CAD). However, the link between personality traits and intravascular morphology in CAD patients is poorly understood. This study investigated the relationship between personality traits, specifically Type A behavior pattern and Type D personality, and plaque vulnerability. After adjustment for demographic and clinical factors, multivariable regression analysis showed no association between Type A and optical coherence tomography indices. However, Type D personality was independently associated with lipid plaque, thin cap fibroatheroma (TCFA), and fibrous cap thickness. More specifically, negative affectivity of Type D was related to lipid plaque, TCFA and fibrous cap thickness, and social inhibition was associated with plaque rupture. Our results show that Type D personality was associated with plaque vulnerability, independent of clinical factors. Measurement of negative affectivity and social inhibition will increase our understanding of the progressive phase of the plaque vulnerability, which can contribute to the early identification of high risk patients and reduce the incidence of MACE.