| 阳's profile静水流深BlogListsNetwork |  Tools  Help |
|
2/23/2008 暂时闭版～节后病房又忙碌起来，经常加班到深夜。
忘忧草
周华健
让软弱的我们懂得残忍 狠狠面对人生每次寒冷 依依不舍的爱过的人 往往有缘没有份 谁把谁真的当真 谁为谁心疼 谁是唯一谁的人 伤痕累累的天真的灵魂 早已不承认还有什么神 美丽的人生 善良的人 心痛心酸心事太微不足道 来来往往的你我遇到 相识不如相望淡淡一笑 忘忧草忘了就好 梦里知多少 某天涯海角 某个小岛 某年某月某日某一次拥抱 轻轻河畔草 静静等天荒地老 2/15/2008 病例讨论病史特点：
患者，男性，60岁，经商，因“心悸，胸闷，出汗11小时，伴意识不清半小时”入院。 患者于11小时前中午饮酒后自感心悸，胸闷，并有少许出汗，因症状较轻，故当时未予重视。四小时前自觉心悸，胸闷症状加重，全身出汗较多，并有活动后胸痛，进行性四肢乏力，头晕，自行上床休息，未见明显改善。半小时前，出现意识不清，伴有全身出汗，家人呼之不应，遂急送至我院急诊。病程中无头痛，发热，无咳嗽咳痰，可咯血及痰中带血，无腹痛，腹泻，无恶心，呕吐，无口干多饮多尿，无大小便失禁。 既往有“高血压”病史20年，不规则服用降压药物，具体不详。有“糖尿病”病史11年，一直服用二甲双胍及格列本脲控制血糖较理想。 查体：T36.8，R18，P100，BP130/80，意识不清，浅昏迷，呼之不应，口唇无紫绀，颈静脉无怒张，颈无抵抗，肺部无异常，心界不大，心率110，心律不齐，第一心音强弱不等，未闻及病理性杂音，腹部无异常体征，四肢肌力不能测及，病理征阴性。 辅检：头颅CT示“右侧侧脑室体部旁及半卵园中心腔隙性脑梗塞，脑萎缩”，心电图“快速室率房颤，ST—T改变”表现。血常规无异常。电解质“K3.83，Na139，Cl101”。肾功能正常。心肌酶谱正常。入院急查末梢血糖2.4mmol/l。血PT，APTT正常。次日血脂分析：Tc3.65，TG0.67，LDL-CH2.2，HDL-CH1.36。肝功能正常。复查心肌酶谱仍不高。 入院初步诊断：低血糖症，急性冠脉综合症？心房纤颤，高血压病，2型糖尿病。 立即给予10%GS快速静滴，十余分钟后患者逐渐清醒，2小时后复查末梢血糖9.0mmol/l。并给予吸氧，阿司匹林 ，低分子肝素钙，抗血小板，抗凝，雅施达防治心室重构，倍他乐克控制心室率，降低心肌耗氧量，并给予硝酸酯类药物扩冠及他丁稳定粥样板块，抗炎等治疗。当时急诊医生，无法判断房颤是否为新发的阵发性房颤，还是持续时间长的持续性或永久性房颤，故未给予复律治疗。次日上午，复查心电图为窦律。 讨论： 1.患者早期出现的心悸，胸闷，出汗，是低血糖反应，还是阵发性房颤所致？ 2.该患者，是低血糖症诱发了房颤？还是房颤诱发了低血糖症？ 3.患者发生房颤时，心电图示ST段明显压低，但心肌酶谱不高，是否可以诊断急性冠脉综合症？ 4.患者逐渐出现的意识不清，应该是低血糖症所致，但当时并发房颤，且头颅CT有梗塞表现，是否可能合并存在突发性的脑血管血栓栓塞可能? 5.患者的房颤，未给予抗心律失常药物治疗便自行转复为窦律。是自身的作用，还是低血糖改善之后的作用，是否低血糖和房颤之间存在着某种相关性？另外，当时，使用了倍他乐克，还有他丁及硝酸酯类（硝酸甘油静滴，和单硝酸酯口服）药物扩冠，难道是这三者的作用？ 解答： 天将降大任于斯人也...今天是节后第一个白班，一来就收了11个病人，是“天将降大任于斯人也...” 还是与今年去天子殿烧的特大香烛有关？呵呵 2/12/2008 circulation 2008年2月5日Volume 117, Issue 5; February 5, 2008
Abstract 1 of 10 Epidemiology How Much of the Recent Decline in the Incidence of Myocardial Infarction in British Men Can Be Explained by Changes in Cardiovascular Risk Factors? Evidence From a Prospective Population-Based Study Background— The incidence of myocardial infarction (MI) in Britain has fallen markedly in recent years. Few studies have investigated the extent to which this decline can be explained by concurrent changes in major cardiovascular risk factors. Methods and Results— The British Regional Heart Study examined changes in cardiovascular risk factors and MI incidence over 25 years from 1978 in a cohort of 7735 men. During this time, the age-adjusted hazard of MI decreased by 3.8% (95% confidence interval 2.6% to 5.0%) per annum, which corresponds to a 62% decline over the 25 years. At the same time, after adjustment for age, cigarette smoking prevalence, mean systolic blood pressure, and mean non–high-density lipoprotein (HDL) cholesterol decreased, whereas mean HDL cholesterol, mean body mass index, and physical activity levels rose. No significant change occurred in alcohol consumption. The fall in cigarette smoking explained the greatest part of the decline in MI incidence (23%), followed by changes in blood pressure (13%), HDL cholesterol (12%), and non-HDL cholesterol (10%). In combination, 46% (approximate 95% confidence interval 23% to 164%) of the decline in MI could be explained by these risk factor changes. Physical activity and alcohol consumption had little influence, whereas the increase in body mass index would have produced a rise in MI risk. Conclusions— Modest favorable changes in the major cardiovascular risk factors appear to have contributed to considerable reductions in MI incidence. This highlights the potential value of population-wide measures to reduce exposure to these risk factors in the prevention of coronary heart disease. Abstract 2 of 10 Epidemiology Pericardial Fat, Visceral Abdominal Fat, Cardiovascular Disease Risk Factors, and Vascular Calcification in a Community-Based Sample The Framingham Heart Study Background— Pericardial fat may be an important mediator of metabolic risk. Correlations with cardiovascular disease risk factors and vascular calcification in a community-based sample are lacking. We sought to examine associations between pericardial fat, metabolic risk factors, and vascular calcification. Methods and Results— Participants free of cardiovascular disease from the Framingham Heart Study (n=1155, mean age 63 years, 54.8% women) who were part of a multidetector computed tomography study underwent quantification of intrathoracic fat, pericardial fat, visceral abdominal fat (VAT), coronary artery calcification, and aortic artery calcification. Intrathoracic and pericardial fat volumes were examined in relation to body mass index, waist circumference, VAT, metabolic risk factors, coronary artery calcification, and abdominal aortic calcification. Intrathoracic and pericardial fat were directly correlated with body mass index (r=0.41 to 0.51, P<0.001), waist circumference (r=0.43 to 0.53, P<0.001), and VAT (r=0.62 to 0.76, P<0.001). Both intrathoracic and pericardial fat were associated with higher triglycerides (P<0.0001), lower high-density lipoprotein (P<0.0001), hypertension (P<0.0001 to 0.01), impaired fasting glucose (P<0.0001 to 0.001), diabetes mellitus (P=0.0005 to 0.009), and metabolic syndrome (P<0.0001) after multivariable adjustment. Associations generally persisted after additional adjustment for body mass index and waist circumference but not after adjustment for VAT (all P>0.05). Pericardial fat, but not intrathoracic fat, was associated with coronary artery calcification after multivariable and VAT adjustment (odds ratio 1.21, 95% confidence interval 1.005 to 1.46, P=0.04), whereas intrathoracic fat, but not pericardial fat, was associated with abdominal aortic calcification (odds ratio 1.32, 95% confidence interval 1.03 to 1.67, P=0.03). Conclusions— Pericardial fat is correlated with multiple measures of adiposity and cardiovascular disease risk factors, but VAT is a stronger correlate of most metabolic risk factors. However, intrathoracic and pericardial fat are associated with vascular calcification, which suggests that these fat depots may exert local toxic effects on the vasculature. Abstract 3 of 10 Exercise Physiology Exercise Capacity and Mortality in Black and White Men Background— Exercise capacity is inversely related to mortality risk in healthy individuals and those with cardiovascular diseases. This evidence is based largely on white populations, with little information available for blacks. Methods and Results— We assessed the association between exercise capacity and mortality in black (n=6749; age, 58±11 years) and white (n=8911; age, 60±11 years) male veterans with and without cardiovascular disease who successfully completed a treadmill exercise test at the Veterans Affairs Medical Centers in Washington, DC, and Palo Alto, Calif. Fitness categories were based on peak metabolic equivalents (METs) achieved. Subjects were followed up for all-cause mortality for 7.5±5.3 years. Among clinical and exercise test variables, exercise capacity was the strongest predictor of risk for mortality. The adjusted risk was reduced by 13% for every 1-MET increase in exercise capacity (hazard ratio, 0.87; 95% confidence interval, 0.86 to 0.88; P<0.001). Compared with those who achieved <5 METs, the mortality risk was 50% lower for those with an exercise capacity of 7.1 to 10 METs (hazard ratio, 0.51; 95% confidence interval, 0.47 to 0.56; P<0.001) and 70% lower for those achieving >10 METs (hazard ratio, 0.31; 95% confidence interval, 0.26 to 0.36; P<0.001). The findings were similar for those with and without cardiovascular disease and for both races. Conclusions— Exercise capacity is a strong predictor of all-cause mortality in blacks and whites. The relationship was inverse and graded, with a similar impact on mortality outcomes for both blacks and whites. Abstract 4 of 10 Health Services and Outcomes Research Effect of Board Certification on Antihypertensive Treatment Intensification in Patients With Diabetes Mellitus Background— Regular recertification is mandatory to maintain board certification status in all specialties. However, the evidence that physicians’ performance decreases with time since initial certification is limited. We therefore carried out a study to determine whether the frequency of antihypertensive treatment intensification for diabetic patients changes with time since their physicians’ last board certification. Methods and Results— In this retrospective cohort study, we analyzed treatment of 8127 hypertensive patients with diabetes mellitus treated by 301 internists at primary care practices affiliated with 2 large academic hospitals. Patient visits with documented blood pressure 130/85 mm Hg between January 1, 2000, and August 31, 2005, were studied. The association between the number of years since the physician’s last board certification and the probability of pharmacological antihypertensive treatment intensification at a given visit was analyzed. Frequency of treatment intensification decreased from 26.7% for physicians who were board certified the previous year to 6.9% for physicians who were board certified 31 years before the visit. Treatment intensification rate was 22.5% for physicians certified 10 years ago versus 16.9% for physicians last certified >10 years ago (P<0.0001). Multivariable analysis adjusted for patient and visit characteristics and physician age showed that for every decade since the physician’s last board certification, the probability of treatment intensification decreased by 21.3% (P=0.0097). Conclusion— Physician intensification of pharmacological therapy for blood pressure levels above the recommended treatment goals decreases with time since the last board certification. This finding supports the current policy of mandatory recertification. Abstract 5 of 10 Imaging Performance of Delayed-Enhancement Magnetic Resonance Imaging With Gadoversetamide Contrast for the Detection and Assessment of Myocardial Infarction An International, Multicenter, Double-Blinded, Randomized Trial Background— The identification and assessment of myocardial infarction (MI) are important for therapeutic and prognostic purposes, yet current recommended diagnostic strategies have significant limitations. We prospectively tested the performance of delayed-enhancement magnetic resonance imaging (MRI) with gadolinium-based contrast for the detection of MI in an international, multicenter trial. Methods and Results— Patients with their first MI were enrolled in an acute (16 days after MI; n=282) or chronic (17 days to 6 months; n=284) arm and then randomized to 1 of 4 doses of gadoversetamide: 0.05, 0.1, 0.2, or 0.3 mmol/kg. Standard delayed-enhancement MRI was performed before contrast (control) and 10 and 30 minutes after gadoversetamide. For blinded analysis, precontrast and postcontrast MRIs were randomized and then scored for enhanced regions by 3 independent readers not associated with the study. The infarct-related artery perfusion territory was scored from x-ray angiograms separately. In total, 566 scans were performed in 26 centers using commercially available scanners from all major US/European vendors. All scans were included in the analysis. The sensitivity of MRI for detecting MI increased with rising dose of gadoversetamide (P<0.0001), reaching 99% (acute) and 94% (chronic) after contrast compared with 11% before contrast. Likewise, the accuracy of MRI for identifying MI location (compared with infarct-related artery perfusion territory) increased with rising dose of gadoversetamide (P<0.0001), reaching 99% (acute) and 91% (chronic) after contrast compared with 9% before contrast. For gadoversetamide doses 0.2 mmol/kg, 10- and 30-minute images provided equal performance, and peak creatine kinase-MB levels correlated with MRI infarct size (P<0.0001). Conclusions— Gadoversetamide-enhanced MRI using doses of 0.2 mmol/kg is effective in the detection and assessment of both acute and chronic MI. This study represents the first multicenter trial designed to evaluate an imaging approach for detecting MI. Abstract 6 of 10 Molecular Cardiology Impact of Salusin- and -β on Human Macrophage Foam Cell Formation and Coronary Atherosclerosis Background— Human salusins, related bioactive polypeptides with mitogenic effects on vascular smooth muscle cells and fibroblasts and roles in hemodynamic homeostasis, may be involved in the origin of coronary atherosclerosis. Macrophage foam cell formation, characterized by cholesterol ester accumulation, is modulated by scavenger receptor (cholesterol influx), acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1; storage cholesterol ester converted from free cholesterol), and ATP-binding cassette transporter A1 (cholesterol efflux). Methods and Results— Serum salusin- levels were decreased in 173 patients with angiographically proven coronary artery disease compared with 40 patients with mild hypertension and 55 healthy volunteers (4.9±0.6 versus 15.4±1.1 and 20.7±1.5 pmol/L, respectively; P<0.0001). Immunoreactive salusin- and -β were detected in human coronary atherosclerotic plaques, with dominance of salusin-β in vascular smooth muscle cells and fibroblasts. After 7 days in primary culture, acetylated low-density lipoprotein–induced cholesterol ester accumulation in human monocyte-derived macrophages was significantly decreased by salusin- and increased by salusin-β. Salusin- significantly reduced ACAT-1 expression in a concentration-dependent manner. In contrast, salusin-β significantly increased ACAT-1 expression by 2.1-fold, with a maximal effect at 0.6 nmol/L. These effects of salusins were abolished by G-protein, c-Src tyrosine kinase, protein kinase C, and mitogen-activated protein kinase kinase inhibitors. ACAT activity and ACAT-1 mRNA levels were also significantly decreased by salusin- and increased by salusin-β; however, neither salusin- nor salusin-β affected scavenger receptor A function assessed by [125I]acetylated low-density lipoprotein endocytosis or scavenger receptor class A and ATP-binding cassette transporter A1 expression. Conclusions— Our results indicate that the 2 salusin isoforms have opposite effects on foam cell formation in human monocyte-derived macrophages. Development of atherosclerosis may be accelerated by salusin-β and suppressed by salusin- via ACAT-1 regulation. Abstract 7 of 10 Pediatric Cardiology Fetal Hemodynamic Adaptive Changes Related to Intrauterine Growth The Generation R Study Background— It has been suggested that an adverse fetal environment increases susceptibility to hypertension and cardiovascular disease in adult life. This increased risk may result from suboptimal development of the heart and main arteries in utero and from adaptive cardiovascular changes in conditions of reduced fetal growth. The aim of the present study was to evaluate whether reduced fetal growth is associated with fetal circulatory changes and cardiac dysfunction. Methods and Results— This study was embedded in a population-based, prospective cohort study starting in early fetal life. Fetal growth characteristics and fetal circulation variables were assessed with ultrasound and Doppler examinations in 1215 healthy women. The fetal circulation was examined in relation to estimated fetal weight. Higher placental resistance indices were strongly associated with decreased fetal growth. Cerebral resistance showed a gradual decline with reduced fetal growth. Cardiac output, peak systolic velocity of the outflow tracts, and cardiac compliance showed a gradual reduction with diminished fetal growth, whereas intraventricular pressure gradually increased. Conclusions— Decreased fetal growth is associated with adaptive fetal cardiovascular changes. Cardiac remodeling and cardiac output changes are consistent with a gradual increase in afterload and compromised arterial compliance in conditions of decreased fetal growth. These changes have already begun to occur before the stage of clinically apparent fetal growth restriction and may contribute to the increased risk of cardiovascular disease in later life. Abstract 8 of 10 Transplantation Critical Role of Donor Tissue Expression of Programmed Death Ligand-1 in Regulating Cardiac Allograft Rejection and Vasculopathy Background— Allograft vasculopathy is a major limiting factor in the long-term success of cardiac transplantation. T cells play a critical role in initiation of cardiac allograft rejection and allograft vasculopathy. The negative T-cell costimulatory pathway PD-1: PDL1/PDL2 (programmed death-1:programmed death ligand-1/2) plays an important role in regulating alloimmune responses. We investigated the role of recipient versus donor PD-1 ligands in the pathogenesis of allograft rejection with emphasis on the role of tissue expression in regulating this alloimmune response in vivo. Methods and Results— We used established major histocompatibility complex class II– and class I–mismatched models of vascularized cardiac allograft rejection, blocking anti-PDL1 and anti-PDL2 antibodies, and PDL1- and PDL2-deficient mice (as donors or recipients) to study the role of the PD-1: PDL1/PDL2 pathway in chronic rejection. We also used PDL1-deficient and wild-type mice and bone marrow transplantation to generate chimeric animals that express PDL1 exclusively on either hematopoietic or parenchymal cells. PDL1 but not PDL2 blockade significantly accelerated cardiac allograft rejection in the bm12-into-B6 and B6-into-bm12 models. Although wild-type cardiac allografts survived long term, PDL1–/– donor hearts transplanted into wild-type bm12 mice exhibited accelerated rejection and vasculopathy associated with enhanced recipient T-cell alloreactivity. Interestingly, PDL1–/– recipients did not exhibit an accelerated tempo of cardiac allograft rejection. Using chimeric animals as donors, we show that PDL1 expression on cardiac tissue alone significantly prolonged graft survival compared with full PDL1–/– donor grafts in transplanted wild-type recipients. Conclusions— This is the first report to demonstrate that expression of the negative costimulatory molecule PDL1 on donor cardiac tissue regulates recipient alloimmune responses, allograft rejection, and vasculopathy. Abstract 9 of 10 Vascular Medicine Hypoxic Modulation of Exogenous Nitrite-Induced Vasodilation in Humans Background— It has been proposed that under hypoxic conditions, nitrite may release nitric oxide, which causes potent vasodilation. We hypothesized that nitrite would have a greater dilator effect in capacitance than in resistance vessels because of lower oxygen tension and that resistance-vessel dilation should become more pronounced during hypoxemia. The effect of intra-arterial infusion of nitrite on forearm blood flow and forearm venous volumes was assessed during normoxia and hypoxia. Methods and Results— Forty healthy volunteers were studied. After baseline infusion of 0.9% saline, sodium nitrite was infused at incremental doses from 40 nmol/min to 7.84 µmol/min. At each stage, forearm blood flow was measured by strain-gauge plethysmography. Forearm venous volume was assessed by radionuclide plethysmography. Changes in forearm blood flow and forearm venous volume in the infused arm were corrected for those in the control arm. The peak percentage of venodilation during normoxia was 35.8±3.4% (mean±SEM) at 7.84 µmol/min (P<0.001) and was similar during hypoxia. In normoxia, arterial blood flow, assessed by the forearm blood flow ratio, increased from 1.04±0.09 (baseline) to 1.62±0.18 (nitrite; P<0.05) versus 1.07±0.09 (baseline) to 2.37±0.15 (nitrite; P<0.005) during hypoxia. This result was recapitulated in vitro in vascular rings. Conclusions— Nitrite is a potent venodilator in normoxia and hypoxia. Arteries are modestly affected in normoxia but potently dilated in hypoxia, which suggests the important phenomenon of hypoxic augmentation of nitrite-mediated vasodilation in vivo. The use of nitrite as a selective arterial vasodilator in ischemic territories and as a potent venodilator in heart failure has therapeutic implications. Abstract 10 of 10 Vascular Medicine Endothelial Lipase Is Increased In Vivo by Inflammation in Humans Background— Endothelial lipase (EL) is a plasma lipase that we previously reported to be significantly correlated with all features of the metabolic syndrome in humans, including directly with measures of adiposity and inversely with high-density lipoprotein cholesterol levels. We hypothesized that inflammation associated with obesity results in upregulation of EL. We determined the relationship between inflammatory markers and EL levels in a cohort of healthy persons recruited on the basis of family history of coronary disease. Furthermore, we directly tested the hypothesis that plasma EL concentrations would increase with induction of an inflammatory state by low-dose endotoxin in humans. Methods and Results— High-sensitivity C-reactive protein, interleukin 6, soluble tumor necrosis factor receptor II, soluble intercellular adhesion molecule 1, leptin, and adiponectin were measured in plasma of 858 subjects. Significant direct correlations (P<0.001 for all) were found between EL concentrations and high-sensitivity C-reactive protein (r=0.28), interleukin-6 (r=0.22), soluble tumor necrosis factor receptor II (r=0.22), soluble intercellular adhesion molecule 1 (r=0.24), and leptin (r=0.20). An inverse correlation was present with adiponectin (r=–0.15, P<0.001). Adiponectin inhibited the tumor necrosis factor-–stimulated EL secretion from cultured human coronary endothelial cells in a dose-dependent manner. Experimental low-dose endotoxemia in 20 subjects resulted in a 2.5-fold increase in EL concentrations 12 to 16 hours after injection, which correlated temporally with decreases in both total and high-density lipoprotein phospholipid. Conclusions— In humans, plasma inflammatory markers are directly correlated with plasma EL concentrations, and experimental endotoxemia significantly increases plasma EL concentrations, proving that EL is upregulated by inflammation in humans. This mechanism may partially explain the low high-density lipoprotein cholesterol levels seen in obesity and metabolic syndrome. 翻译待续... 2/11/2008 心血管领域亟待实现五个转变胡大一教授提出目前心血管领域亟待实现的五个“转变”，即: 1.从心血管疾病的终末期干预转向疾病的早期预防； 2.从经验医学转向循证医学； 3.从不同学科干预不同的心血管危险因素转向相关学科广泛联盟、共同干预多重危险因素； 4.从以大医院为中心的危重急症救治、疑难杂症诊治，转向以社区和农村为中心的重视病前预防和病后的疾病管理； 5.从针对疾病转向重视健康（健康教育、健康管理、健康促进），改变“病前不防、病后不管、急性心肌梗死救治还太晚”的现状。 病例回顾：主动脉夹层病例：男，67岁，农民。间断性心前区疼痛1周，伴左上肢麻木、皮温低1小时入院 现病史：入院前1周因间断性心前区疼痛，时轻时重，反复发作，在当地乡医院作心电图提示“V4、V5、V6导联ST轻度下移”，诊断‘冠心病“，给予扩冠、抗血小板以及对症治疗，缓解出院。 1小时前，出现胸闷、冷汗、伴左侧上肢麻木、疼痛、皮肤温度降低。 既往体健。 查体：右上肢血压110/72,左上肢不能扪及脉搏，痛苦貌。心肺听诊没有明显阳性体征，腹软，无压痛。双侧股动脉和下肢动脉未见异常。 心电图和1周前对比，无明显改变。 心脏超声：各心腔大小正常，极轻微二尖瓣返流，心功能测值正常。心腔未见血栓征象。 左上肢彩超：肱动脉中远端可见血栓，其下游血流信号明显减弱。 血生化：血糖、电解质、肝肾功等正常。心肌酶谱无明显异常。 处理：因病情紧急，加上患者经济能力有限，没有作进一步检查。用50万单位尿激酶溶栓，然后低分子肝素抗凝、氯比格雷和阿司匹林抗血小板等治疗。 4小时后病情缓解，左上肢脉搏恢复80％左右，麻木和皮温下降等症状缓解。继续观察和对症治疗。 1天半以后出现阵发性腹部绞痛、解暗红色血样大便4次，每次50－100ml。大便隐血（＋），但是多次复查无血压下降和红细胞数目、血红蛋白下降的表现。 仔细查体：脐周压痛，轻度反跳痛，无肌紧张。听诊肠鸣活跃。 不解！！！。。。结合前面的上肢血栓栓塞。。。拟考虑：肠系膜动脉栓塞。继续抗血小板、低分子肝素治疗。 还是觉得矛盾：既然多处血栓栓塞，那么血栓的来源呢？心腔里没有，没有心腔增大，也没有房颤，实在无法解释！ 再过5小时，患者出现左下肢麻木，继续仔细查体，这次有了进一步发现： 1、左侧股动脉搏动减弱； 2、脐周偏左侧闻及血管杂音。 于是心中有数了，马上停低分子肝素。立即作胸、腹部主动脉核磁共振。 结果：主动脉夹层！ 最后，患者无钱继续治疗，仅给予保守药物治疗，仍给了阿司匹林，停氯比格雷，回家休息，嘱注意事项、并说明预后恶劣，家属仍坚持，签字后自动出院。2月后随访，患者仍存活，病情基本稳定，生活能自理。 本例经验教训： 1、查体比较仔细，并且不以入院的第一次查体为准，而不断追踪，所以发现病因； 2、入院时没有进一步完善检查（既有医生的原因，也有患者经济方面的原因）； 3、溶栓治疗是错误和危险的。顺便请教高手：在当时确实合并血栓的情况下，如何处理？血管外科手术取栓，恐怕更危险。如果知道病因（主动脉夹层），抗血小板的药物能不能用，如果不用，那血栓进展又怎么办？ 4、回头想来：患者的血栓应该是主动脉夹层引起血管内膜撕裂、内皮损伤，然后继发血栓形成。 布鲁戈登综合征Brugada综合征是导致青壮年猝死的主要原因，已引起临床医师关注。 Brugada综合征又称右束支传导阻滞-----多行性室速-----晕厥综合征、意外夜间猝死综合征，在中国、日本、泰国、菲律宾等东南亚地区已不少见，本病多发生于20-49岁的男性，多数在夏季发病，84%的猝死发生于夜间睡眠中，泰国学者对此研究了27例睡眼中猝死病例和11例心电图正常人群，发现前组病例中有16例出现右束支传导阻滞、ST段抬高，多数在夜间睡眠中出现心室颤动、停搏而死亡，据此认为右束支传导阻滞，V1-V3导联心电损伤是Brugada综合征心电标记之一。劳累后加重的夜间低氧血症、膜Na+/K+泵的缺陷、内分泌紊乱为其诱发因素。有关研究发现疑似Brugada综合征的病例多在艰苦呻吟数分钟内死亡，部分被救活的病例发现有心室颤动和诱发的多行性室速。本病有遗传及家族易感性，有家族史的同族兄弟发病率增加。临床如何诊断Brugada综合片：1、有恶性心律失常发生的家族史。2、平素体健的青壮年，无器质性心脏病的检查证据。3、心电图有右束支传导阻滞、V1-V3导联ST段抬高0.1mV。4、发作性室速、室颤或不明原因的晕厥。5、排除心肌缺血、电解质失调或代谢紊乱等。 Brugada综合征的防治：目前药物治疗不能有效防止心脏事件发生，发作室速、室颤时应采取相应救治措施，惟一有效防止猝死的方法及早置入心脏除颤器（ICD）。
2/6/2008 回首又见他其实,真的有些东西过去了就没有办法再回来了! 不只是,人或者事 . 丢失的还有当初的那份心情......... 或许还有些怀念 有些不舍 但是终究没有多少人有勇气去找回过往的一切. 因为自私.害怕或一些别的什么原因. 虽然心里依旧难以抗拒 但一切终究是过去了 过去了就代表再也回不来了 所以,有些东西作决定时还是别那么冲动. 有些东西一旦放手就再也回不来了............. 过去的就让它过去吧 因为再也回不来了 《回首又见他》的主题曲《yahyahyah》的歌词大意 YAH YAH YAH --------------------------- 作词：飞鸟 凉 作曲：飞鸟 凉 编曲：飞鸟 凉 & 十川 知司 --------------------------- 关于自己无论如何都想拿到手的东西 是绝对不能告诉别人的 至于那些数也数不清的甜美童话 总有一天我也想享用一次 不需要去吵闹着说什么爱与勇气 只要真的去做就行了 你是不是现在正握起了颤抖的拳头 因愤怒而说不出话来? 要是受伤了 便露出獠牙来吧 这是为了不失去自己的缘故 让我们现在就一起去 现在就一起去 好好地大干它一场吧! YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH 要是一定得受伤 那就痛痛快快地给我来上一刀吧 因为钝刀 反而更会让人感到疼痛 至于那些之后会留下的伤疤 也用不着刻意地去遮掩 用不着吵闹着说什么已经天亮了 只要把眼睛张开就行了 你觉得生存是件悲哀的事吗? 世上没有一句能让你相信的话吗? 只要还残存有一丝气力 无论何时都能把眼泪忘掉 让我们现在就一起去 现在就一起去 修理那家伙一顿吧! YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH hang in there! 用着健康的心 hang in there! 用着不变的心 把拳头用力地伸出来 用力地 用力地挥出去 就像是在把缠在颈子上的T恤用力脱掉般地那么强而有力 把拳头用力地伸出来 用力地 用力地挥出去 就像是紧抱住胸中的回忆般地那么强而有力 YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH YAH hang in there! 用着健康的心 YAH YAH YAH YAH YAH YAH YAH hang in there! 用着不变的心 2/3/2008 《肖申克的救赎》(Shawshank Redemption)《肖申克的救赎》(Shawshank Redemption)是我所看过令人震撼的一部电影之一。故事与其说讲述的是主人公安迪成功越狱、重获自由，倒不如说是安迪从灵魂到肉体获得拯救的过程。在我看来，这部电影所表现的深刻、玄奥的宗教、社会、人生哲理是该片受到赞扬的最重要的原因。也就是说这部片子触及到了人类灵魂最深处的东西，它反思的是一个关于体制化与反体制化、希望与绝望、灵魂救赎的深刻的主题。 institutionalized（体制化）、hope（希望）、redemption（救赎）是《肖》片中三个最为关键的灵魂性词语，理解了这三个词语，我们才能够很好的解读该片所探讨的主题。 第一个词语institutionalized（体制化），影片是通过瑞德（Mogran Freeman饰演）之口说出对这个词语的看法的。他说：“first you hate them ，then you get used to,enough time passes...you get so you depend on them 。That is instititutionalized（起初，你讨厌它，然后你逐渐的习惯它，足够的时间后你开始依赖他。这就是体制化）”。理解片中所谓的体制化，我们回顾一下老布（那个监狱的图书管理员）的一生就明白了。老布在监狱中也就是在一种体制下，渡过了50年，几乎就是一生的时间。可以想象，曾经年轻的布，在刚刚进入这种体制时，他肯定曾经像一切刚刚进入Shawshank的所有NEW fish（菜鸟）一样，愤世嫉俗，并试图反抗，然后和大部分的囚徒一样，他们逐渐发现：反抗等于徒劳，于是从对体制的反抗逐渐变为慢慢的接受然后学会适应体制，最后发展到对体制的严重依赖。可怜的老布，他的灵魂和肉体都已经完全体制化了，在垂暮之年却被放逐出体制之外，可以想象的到，老布在一个几乎完全陌生的体制下是根本无法存活的，此时老布与体制脱离无异于一个胎儿被斩断脐带，因此老布最终选择了结束自己的生命。 第二个词语hope(希望)。对这个词语的阐释是通过安迪和瑞德在午餐中的争论展开的。心存信念和希望的安迪说：“forget that there are ...places...in the world that aren't made out of stone， there is something ...inside...that they can't get to...that is hope （不要忘了这个世界上还有可以穿透一切高墙的东西，它就在我们的内心深处，他们无法达到，也触摸不到，那就是希望）”,然而睿智的瑞德马上反驳说：“let me tell you something my friend 。hope is a dangerous thing hope can drive a man insane it's got no use on the inside.you'd better get used to that idea （让我来告诉你什么是希望，我的朋友。希望一个危险的东西，它能够使人疯狂，我们心中的希望根本毫无用处。你最好习惯这个观念）” 安迪的救赎 ——个人和群体的灵魂拯救 理解了以上两个词语，体制化和反体制化、希望和绝望，我们的主人公安迪开始了影片的主题——灵魂的救赎（redemption）。在Shawshank这个世界中，我们可以把人们划分成两大群体：体制内群体和体制外群体。体制内包括像典狱长和狱警在内，他们是体制的缔造者、执行者和维护者，以典狱长和那个凶狠的狱警无疑是撒旦的化身、穷凶极恶的统治者。而Shawshank的囚徒无疑是属于体制外的人群，他们是体制的服从者、被同化者。体制外的囚徒可以分为四类，以安迪为代表的英雄（hero），以瑞德为代表的精英（elite），以老布等为代表的大众(the masses),和以被虐待致死的肥仔为代表的失败者（alsoran）。英雄在灵魂上是超越体制的，尽管他们的肉体不得不服从体制的约束，然而英雄却能够利用自己伟大的灵魂和伟大的行动不断改变体制、超越体制。精英属于对体制有深刻清醒认识、曾经试图反抗但是最终选择妥协的那一类人。精英和英雄的共同之处在于在灵魂深处，二者都有希望存在。精英和英雄的区别在于，英雄除了在精神上笃信希望外，而且在行动上试图改变体制，这种卓越智慧的努力，正是是英雄成为英雄的根本所在。精英虽然在灵魂中尚有对希望的信仰，然而在行动上他们已经完全放弃了反抗的可能，他们在灵魂上虽然没有被体制化，但在肉体上已经完全体制化了。其次，就是绝大多数的大众（就是你我这样的芸芸众生），他们也曾经试图反抗，但是在强大的体制化的力量之下，他们却不幸的从精神到肉体完全被体制化了。最后，就是那些被淘汰的失败者，他们成了体制的祭品，很快被淹没在体制化的漩涡之中。 当然，安迪通过自己的行动不仅改变了自己的命运，而且深深的影响了牢笼中的其他人：安迪在狱中扩建图书馆，帮助其他犯人读书识字，那个拿到同等学历的问题青年就是被拯救的典型，一个跨掉一代中的嬉皮士竟然能够被教化成一个绅士，我们不得不感叹于救赎的力量。因此安迪的拯救不单单是一个个体的行为，还是一个群体的行为，这完全符合基督教关救赎的定义。影片在阐释安迪反抗的过程时，用了一个宗教性很强的词语——redemption（救赎）。追述这个词语的宗教渊源，我们很容易想起耶稣灵魂拯救的故事，事实上，在片中不知一次的出现过《圣经》，以及对《圣经》的引用。具有讽刺意味的是，那个道貌岸然的典狱长，外表似乎是一个圣洁的圣徒而他的行为和内心却肮脏的像魔鬼。在他的办公室旁边又一个精致的隽语：主的审判将要降临，然而这末日的审判却最终降临到这个审判者身上。 因此，《肖》片最重要的贡献在于对历史观的一种寓言式的阐述和对个体救赎、群体救赎的宗教式的反思。 对该片的反思——救赎就在你我心中 不难理解，Shawshank不过是一个寓言而已，它事实上就存在于我们现实的生活中。现实中的每一个人，都在自觉不自觉的扮演着Shawshank中囚徒或者狱方的角色。我们中的大部分人，都将沦为老布那样的命运，逐渐地被体制化直到严重地依赖体制，终其一生不曾越规逾矩。任何一种组织、制度、社会都可以视Shawshank为缩影。比如，我们的大学，某种程度上就是一个Shawshank城堡，当我们离开这座城堡时，我们中的绝大多数是注定要被体制化的，即使进入社会，体制对人的侵蚀也一刻没有停止过，社会历史就是在体制化和反抗体制化的循环中不断前进的，然而救赎却完全在于我们自己的选择，正如安迪的选择一样，再强大的体制也永远无法剥夺我们选择救赎的权利，因为，救赎就存在于我们的心中，那是任何强权也无法到达的地方。to being，or not to being，选择救赎还是选择绝望，选择英雄还是选择大众，选择上帝还是选择撒旦，这一切都在你我心中...... 为了更好体味斯蒂芬.金的佳作，买了一本书。 |
|
|
