Cardiovascular reactivity and mental stress-induced myocardial ischemia in patients with coronary artery disease

This report evaluates the relationships of hemodynamic reactivity and determinants of myocardial oxygen demand to myocardial ischemia during mental stress in coronary artery disease patients. Thirty-nine patients and 12 controls were studied by radionuclide ventriculography during three mental tasks (arithmetic, Stroop task, and simulated public speaking). Patients were subdivided into three groups based on the severity of ischemic wall motion responses to the mental stressors. Results revealed that systolic blood pressure (SBP) levels during the mental tasks and SBP reactivity (increases) to stress were highest for the severely ischemic group, lowest for controls, with the mild-moderate ischemic and nonischemic patients in between. Severely ischemic patients started out with lower double product (heart rate x SBP) levels, and reached higher levels during the Stroop and speech tasks. There were no reliable group effects for diastolic blood pressure, heart rate, or left ventricular end-diastolic volumes. Among severely ischemic patients, the most potent task in eliciting ischemia (the speech) was associated with higher cardiovascular levels and elicited greater heart rate, double product, and ventricular volume responses. The present data indicate a relationship between cardiovascular levels and reactivity and the magnitude of ischemia induced by mental stress.     

Increases in lipids and immune cells in response to exercise and mental stress in patients with suspected coronary artery disease: effects of adjustment for shifts in plasma volume

This study examined the role of shifts in plasma volume on lipid and immune reactions to stress. Lipid, immune, rheological, and cardiovascular reactions to exercise and mental stress in 51 patients with suspected coronary artery disease were determined. Blood pressure and heart rate were measured during and blood samples taken at the end of each rest and task. Lipids (total cholesterol, triglycerides, HDL, LDL) and immune cells (lymphocytes, monocytes, granulocytes) increased with exercise, whereas cholesterol, LDL, and lymphocytes increased with mental stress. Plasma volume decreased by 1 and 5% following mental and exercise stress, respectively. The task-induced increases in lipids were no longer statistically significant following adjustment for changes in plasma volume, whereas the increases in immune cell numbers survived such correction. This study provides evidence that, in coronary artery disease patients, exercise and mental stress-induced increases in lipids but not immune cells can be largely accounted for by shifts in plasma volume.     

Mental stress-induced ischemia in patients with coronary artery disease: echocardiographic characteristics and relation to exercise-induced ischemia

Objective The aims of this study were to investigate the incidence and parameters associated with myocardial ischemia during mental stress (MS) as measured by echocardiography and to evaluate the relation between MS-induced and exercise-induced myocardial ischemia. Methods Study participants were 79 patients (63 men; mean [M] [standard deviation {SD}] age = 52 [8] years) with angiographically confirmed coronary artery disease and previous positive exercise test result. The MS protocol consisted of mental arithmetic and anger recall task. The patients performed a treadmill exercise test 15 to 20 minutes after the MS task. Data of post-MS exercise were compared with previous exercise stress test results. Results The frequency of echocardiographic abnormalities was 35% in response to the mental arithmetic task, compared with 61% with anger recall and 96% with exercise (p < .001, exercise versus MS). Electrocardiogram abnormalities and chest pain were substantially less common during MS than were echocardiographic abnormalities. Independent predictors of MS-induced myocardial ischemia were: wall motion score index at rest (p = .02), peak systolic blood pressure (p = .005), and increase in rate-pressure product (p = .004) during MS. The duration of exercise stress test was significantly shorter (p < .001) when MS preceded the exercise and in the case of earlier exercise (M [SD] = 4.4 [1.9] versus 6.7 [2.2] minutes for patients positive on MS and 5.7 [1.9] versus 8.0 [2.3] minutes for patients negative on MS). Conclusions Echocardiography can be successfully used to document myocardial ischemia induced by MS. MS-induced ischemia was associated with an increase in hemodynamic parameters during MS and worse function of the left ventricle. MS may shorten the duration of subsequent exercise stress testing and can potentiate exercise-induced ischemia in susceptible patients with coronary artery disease.     

冠脉搭桥患者血浆肾上腺髓质素和内皮素-1的变化

肾上腺髓质素(adrenomedullin,AM)是具有多种生物学效应,参与许多心血管系统疾病的病理过程,与疾病的严重程度相关[1-2].内皮素-1(endothelin-1,ET-1)与AM共同调节基础状态下的血管紧张度,引起血管的自主收缩及扩张.有关影响AM和ET-1分泌的因素很多,但心外科冠脉搭桥术对其影响尚未见报道,我们探讨体外和非体外循环两种冠脉搭桥方式对血浆AM及ET-1的影响.     

Heart rate variability at rest and during mental stress in patients with coronary artery disease: Differences in patients with high and low depression scores

This study tested the hypothesis that coronary artery disease (CAD) patients with high depressed mood scores differ in sympatho-vagal balance during mental stress compared to patients with low depressed mood scores. Using electrocardiographic monitoring, heart variability data from spectral analysis and hemodynamic parameters were obtained prior to and during mental stress from 34 men and 7 women. A public speaking task was used as the mental stressor. Patients were grouped by a median split of their Minnesota Multiphasic Personality Inventory-Depression score. During mental stress, patients with higher depression scores had greater changes in peak heart rate (p > .05) and low frequency to high frequency power ratio (p > 0.05) than patients with lower scores suggesting a shift toward more sympathetic activity during mental stress. These findings may be related to the reported relation between depression and survival risk in patients with CAD. This study was supported by Grant 1-R01-HL-47477 from the National Heart, Lung and Blood Institute, General Clinical Research Center Grant RR00046 from the National Institutes of Health, and Cooperative Agreement CR817643 from the Environmental Protection Agency.     

Changes in plasma lipid concentrations and risk of coronary artery disease in army veterans suffering from chronic posttraumatic stress disorder

Aim

To test the differences in serum lipid concentrations between veterans with chronic posttraumatic stress disorder (PTSD) and veterans without PTSD.

Methods

We determined plasma lipid parameters and calculated risk factors for 50 veterans in the PTSD group and 50 veterans in the non-PTSD group. Trauma exposure, coping strategies, and quality of life were assessed with Life Stressor List, Manchester Short Assessment of Quality of Life Scale, and Folkman-Lazarus Coping Strategies Questionnaire.

Results

There was no difference between the groups in the exposure to combat trauma. PTSD group had significantly lover education than non-PTSD group (10.6 ± 1.8 vs 12.4 ± 2.6 years, P = 0.007) and lower monthly income per family member (€67.8 ± 51.3 vs €281.9 ± 208.2, P < 0.001). PTSD group had significantly higher levels of all plasma lipid parameters (cholesterol: 6.54 ± 1.24 vs 5.40 ± 1.09 mmol/L, P < 0.001; triglycerides: 2.55 ± 0.68 vs 1.73 ± 0.77 mmol/L, P < 0.001; very low density lipoprotein-cholesterol: 1.14 ± 0.32 vs 0.78 ± 0.35 mmol/L, P < 0.001; low density lipoprotein-cholesterol: 4.49 ± 1.06 vs 3.46 ± 0.93 mmol/L, P < 0.001). High-density lipoprotein cholesterol concentration was significantly lower in PTSD group (0.96 ± 0.18 vs 1.15 ± 0.24 mmol/L, P < 0.001). Established risk factor for arteriosclerosis (6.96 ± 1.19 vs 4.71 ± 0.88, P < 0.001) and Adult Treatment Panel III ten years risk for coronary disease (19.44 ± 7.27% vs 9.74 ± 4.10%, P < 0.001) were significantly higher in the PTSD group. Secondary traumatization was significantly more frequent in the PTSD group (3.8 ± 5.7 vs 1.3 ± 4.7 events; P < 0.001).

Conclusions

Chronic PTSD is associated with dyslipidemia, leading to an increased risk of coronary artery disease. Environmental factors and coping strategies should be considered as important factors for the occurrence and persistence of PTSD.“The body keeps the score: memory and the evolving psychobiology of post traumatic stress” by Bessel van der Kolk (1) was published in the Harvard Review of Psychiatry in 1994. Although it may not be the first article on neurobiology of posttraumatic stress disorder (PTSD), the strong metaphor contained in the first part of its title summarizes the research results in this field. Studies looking for biological causes of a disorder that is clearly precipitated by environmental or man-made causes were largely outnumbered by studies on the psychosocial nature of the disorder decades after the delayed first recognition of PTSD in the diagnostic manuals – 1980 in Diagnostic and Statistical Manual of Mental Disorders III (DSM III) (2) and 1990 in the International Classification of Diseases-10 (ICD-10) (3). A small number of studies appeared in literature in parallel with the recognition of the disorder, but the number of biological studies since September 11, 2001 has grown 5-fold and keeps growing (4).Research interest mainly focused on alterations of neuroendocrine regulation (5,6) and neuroanatomical (7) and neuroimmunological alterations (8,9). From the neuroendocrine point of view, in PTSD there is an increased noradrenergic activity in absence of shutdown by serum cortisol that has been found to be decreased in this disorder due to dysregulation of the hypothalamo-pituitary-adrenal axis (10-12). Studies on changes in serum lipid concentrations were based on clinical observations and the results of epidemiological studies indicating increased cerebrovascular and cardiovascular morbidity and mortality in survivors of prolonged traumatic and combat stress (13-17). Kagan’s pioneer study (18) of changes in lipid status of Vietnam veterans was published in 1999 and was followed by the work of other researchers who confirmed its results (19-23).The population of Bosnia and Herzegovina suffered massive and prolonged traumatization in the 1992-1995 war (24-26). Increase in the prevalence and incidence of PTSD in comparison with the period before the war, as well as the increase in trauma-related disorders in overall psychiatric morbidity, represents a logical consequence of these events (27). In our work with people suffering from chronic PTSD, we had frequently noticed alterations of serum lipids, associated with an increased risk of cardiovascular diseases. This is consistent with our clinical observation of increased cardiovascular and cerebrovascular morbidity in patients who had been treated in the Unit for Trauma-related Disorders of the Department of Psychiatry of the University Clinical Center in Sarajevo and the literature (13-17). Therefore, we aimed to explore the differences in concentrations of serum cholesterol, triglycerides, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), very low density lipoprotein cholesterol (VLDL-C), index of arteriosclerosis, established risk factor for arteriosclerosis (ERF), and 10 years-risk for coronary disease according to Adult Treatment Panel III (ATP III) (28) between veterans with the diagnosis of chronic PTSD and veterans without the diagnosis of PTSD. Our second aim was to compare and analyze the differences between the two groups in socio-demographic characteristics, trauma exposure measures, secondary traumatization (after the war), PTSD symptoms, coping strategies, and quality of life, to obtain information on the factors influencing the development and persistence of PTSD in veterans with combat stress exposure.There are divided opinions in literature whether this disorder develops in individuals with certain predisposing factors or all people have equal chances of developing PTSD (29-32). There is also a question whether biological markers of PTSD are trait markers or state markers, as well as whether PTSD can be explained by stress-diathesis model as schizophrenia (33). To explore these claims, we also compared socio-demographic characteristics of the sample, trauma events inventory, coping strategies, and quality of life indicators.     

Carotid artery stenting in patients with symptomatic coronary artery disease

Carotid artery stenting has been accepted as a potential alternative to carotid endarterectomy in patients with significant carotid artery stenosis. The objective of this study was to evaluate the feasibility, safety and long-term outcome of percutaneous stenting of carotid artery stenosis in patients with coexisting symptomatic coronary disease. Between May 1996 and May 1999, we performed carotid artery stenting at 48 lesions in 36 patients with carotid stenosis of 60% and symptomatic coronary artery stenosis. Twenty-one patients (58%) had neurologic symptoms. Carotid stenting was performed in 43 internal, 2 external and 3 common carotid lesions. We used Wallstent in 46 lesions, Palmaz stent in 2 lesions and Microstent II in 1 lesion. Staged or combined coronary intervention was performed in 18 patients (50%) and staged coronary artery bypass surgery was performed in 6 patients (17%). In the other 12 patients (33%), medical treatments were performed. Carotid stenting was successful in all lesions. Simultaneous bilateral carotid stenting was performed in 11 patients (31%). One major and 1 minor stroke developed during the procedure. There were no deaths during the procedures and within 30 days post-procedure. During the follow-up of 14 +/- 7 (3 to 40) months, there were no deaths or neurological events. On follow-up (6 +/- 1 months) angiography and/or duplex sonography of 44 eligible lesions in 32 patients, there were 2 cases of asymptomatic restenosis (4.5%) which developed in Palmaz stents implanted at the external carotid artery and the common carotid artery, respectively. In conclusion, carotid artery stenting in patients with coexistent carotid and coronary artery disease is feasible, safe and shows favorable follow-up outcomes.     

冠心病患者血浆神经降压素水平的变化及其临床意义

目的: 研究不同类型冠心病患者发病不同阶段血浆神经降压素(NT)水平的变化,探讨其与冠心病心肌缺血的关系。方法: 检测急性心肌梗塞,不稳定型心绞痛,稳定劳力型心绞痛,陈旧性心肌梗塞患者各30余例发病不同阶段血浆NT浓度,并选32例健康者作为对照组。结果: 急性心肌梗塞急性期(24 h),不稳定型心绞痛患者疼痛发作期血浆NT水平均明显高于对照组,稳定劳力型心绞痛患者,陈旧性心肌梗塞患者血浆NT水平与对照组比较差异无显著性。不稳定型心绞痛患者疼痛发作期血浆NT水平显著高于治疗2周后病情稳定期(P＜0.01)。急性心肌梗塞患者血浆NT水平在心梗早期即有上升趋势,至12 h明显升高,24 h达到高峰 ,48h后逐渐下降,72h后降至正常水平 。结论:冠心病患者出现心肌急性缺血时,血浆NT水平升高,提示NT参与了冠心病患者急性心肌缺血时的病理生理过程。     

Prevalence of coronary artery disease in patients with valvular heart disease

To evaluate the usefulness of preoperatie coronary angiography in patients undergoing preoperative investigation because of valvular heart disease, we performed coronary angiography in a consecutive series of 329 patients. The prevalence of significant coronary artery disease was 32%. Asymptomatic coronary artery disease was present in 13%. Angina pectoris proved to be a poor predictor of coronary artery disease in aortic valve disease. In mitral valve disease, however, the specificity was high. A cost-benefit calculation was carried out in order to assess what advantage routine coronary angiography might have. According to this, coronary angiography should be performed in all patients suffering from valvular heart disease with angina pectoris, whereas it can be omitted in younger patients without angina. A cut-off point of 60 years seems appropriate for aortic valve disease and 65 years for mitral valve disease.     

Platelet volume indices in patients with coronary artery disease and acute myocardial infarction: an Indian scenario

AIMS: To study platelet volume indices (PVI) in the spectrum of ischaemic heart diseases. METHODS: A total of 210 cases were studied; 94 patients had unstable angina (UA) or acute myocardial infarction (AMI) diagnosed on the basis of history, characteristic electrocardiographic changes, and increased cardiac enzyme activities. Seventy patients had stable coronary artery disease (stable CAD) or were admitted for a coronary angiography or coronary artery bypass graft procedure. The third group comprised 30 age and sex matched healthy controls with no history of heart disease and a normal electrocardiogram. RESULTS: All PVI-mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (P-LCR)-were significantly raised in patients with AMI and UA (mean MPV, 10.43 (SD, 1.03) fL; mean PDW, 13.19 (SD, 2.34) fL; mean P-LCR, 29.4% (SD, 7.38%)) compared with those with stable CAD (mean MPV, 9.37 (SD, 0.99) fL; mean PDW, 11.35 (SD, 1.95) fL; mean P-LCR, 22.55% (SD, 6.65%)) and the control group (mean MPV, 9.2 (SD, 0.91) fL; mean PDW, 10.75 (SD, l.42) fL; mean P-LCR, 20.65% (SD, 6.14%)). CONCLUSIONS: Larger platelets are haemostatically more active and are a risk factor for developing coronary thrombosis, leading to myocardial infarction. Patients with larger platelets can easily be identified during routine haematological analysis and could possibly benefit from preventive treatment. Thus, PVI are an important, simple, effortless, and cost effective tool that should be used and explored extensively, especially in countries such as India, for predicting the possibility of impending acute events.     

Changes in serum lipids, plasma fibrinogen and other haemostatic parameters induced by ciprofibrate action in hyperlipidemic patients with and without coronary artery disease

The effects of drugs with hypolipidemic properties in the prevention of the atherothrombotic vascular disease, go further than reducing serum lipids, suggesting that there are other nonlipid-related mechanisms involved; the maintenance of appropriate haemostatic balance being one of them. The objective of this investigation was a drug intervention with ciprofibrat in hyperlipidemic people with high level of plasmatic fibrinogen with the purpose of knowing the effects of the drug over these risk factors and other haemostatic parameters. Forty people, both sexes, 20 of them apparently healthy and the other 20 with clinical and angiographic evidence of coronary artery disease, were randomized to receive 100 mg of ciprofibrat or placebo during an average of 56 weeks. All of them had a clinical exam, EKG and stress test. Laboratory exams included lipid profile, plasma fibrinogen (Fg), VII factor, vonWillebrand factor, protein C (PC) and the tissue plasminogen activator with samples taken every 8 weeks. The Ciprofibrat group showed significant changes of lipids: cholesterol -23%, triglycerides -31%, high-density lipoprotein (HDLc) +24% and very low-density lipoprotein -23%, except low-density lipoprotein -24%. The haemostatic parameters in 40 weeks showed that Fg decreased 21% (p = 0.001), decreasing to 9% at the end of the follow-up. In the placebo group the HDLc showed a 10% increase (p = 0.02), PC reduced to 20% (p = 0.01) and Fg kept blood levels close to basal line, descending 10% at the end of the follow-up. In this study, the use of ciprofibrat in patients with high risk of developing atherothrombotic events, showed efficiency and security in handling hyperlipidemia, such as keeping and appropriate haemostatic balance.     

Characterization of aspirin allergies in patients with coronary artery disease

BackgroundAspirin prevents coronary thrombosis and is used extensively in cardiovascular prophylaxis. However, patients with a prior history of an aspirin “reaction” are routinely denied this medication.ObjectiveTo characterize the clinical presentation of a cohort of patients with coronary artery disease (CAD) and aspirin reactions.MethodsBetween 2009 and 2012, using a retrospective computer analysis, information was collected on all patients within a county-wide health care system presenting with CAD and a prior history of aspirin reactions.ResultsOf 9,565 patients with CAD, a prior history of aspirin reactions was recorded in 142 patients. Of these 142 patients, 30 (21%) had histories compatible with cutaneous and/or respiratory reactions. The other patients described adverse effects to aspirin, mostly gastrointestinal intolerance and bleeding. Aspirin-induced anaphylaxis was recorded in patients but may have been misdiagnosed, describing instead respiratory hypersensitivity reactions. Of the 142 patients, only 34 (24%) were receiving daily cardiovascular prophylaxis with aspirin. Of 108 patients not receiving aspirin, 25 (17.6%) were prescribed clopidogrel.ConclusionHistories of aspirin reactions in patients with CAD are uncommon, occurring in only 1.5% of our study population. The 21% of patients with histories compatible with aspirin hypersensitivities can be challenged and, if the results are positive, successfully desensitized. Moreover, almost all patients with gastric intolerance to aspirin can be treated with aspirin and a proton pump inhibitor. However, both approaches, which result in restoration of cardiovascular prophylaxis, were seriously underused in our study population.