个回答天前router.get('/odds/:bid', (req,res,next) =& {
const mergeRecs = [];
const currOdds = [];
const openOdds = [];
const homeTeam = [];
});const mergRecs = [];
function badMiddleware() {
// mergRecs needs to be declared here
mergRecs.push('yes');
console.log(mergRecs);
badMiddleware(); // 1 yes
badMiddleware(); // 2 yes
badMiddleware(); // 3 yes24小时热门版块排行榜&&&&
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【求助/交流】如何计算log-odds matrix?
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知道motif 的proability matrix, 如何计算log-odds matrix？
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【进展翻译】circulation5月14日版
Arrhythmia/Electrophysiology 1、Inductionless or Limited Shock Testing Is Possible in Most Patients With Implantable Cardioverter- Defibrillators/Cardiac Resynchronization Therapy DefibrillatorsBackground― Implantable cardioverter-defibrillators and cardiac resynchronization therapy defibrillators have relied on multiple ventricular fibrillation (VF) induction/defibrillation tests at implantation to ensure that the device can reliably sense, detect, and convert VF. The ASSURE Study (Arrhythmia Single Shock Defibrillation Threshold Testing Versus Upper Limit of Vulnerability: Risk Reduction Evaluation With Implantable Cardioverter-Defibrillator Implantations) is the first large, multicenter, prospective trial comparing vulnerability safety margin testing versus defibrillation safety margin testing with a single VF induction/defibrillation. Methods and Results― A total of 426 patients receiving an implantable cardioverter-defibrillator or cardiac resynchronization therapy defibrillator underwent vulnerability safety margin or defibrillation safety margin screening at 14 J in a randomized order. After this, patients underwent confirmatory testing, which required 2 VF conversions without failure at 21 J. Patients who passed their first 14-J and confirmatory tests, irrespective of the results of their second 14-J test, had their devices programmed to a 21-J shock for ventricular tachycardia (VT) or VF 200 bpm and were followed up for 1 year. Of 420 patients who underwent 14-J vulnerability safety margin screening, 322 (76.7%) passed. Of these, 317 (98.4%) also passed 21-J confirmatory tests. Of 416 patients who underwent 14-J defibrillation safety margin screening, 343 (82.5%) passed, and 338 (98.5%) also passed 21-J confirmatory tests. Most clinical VT/VF episodes (32 of 37, or 86%) were terminated by the first shock, with no difference in first shock success. In all observed cases in which the first shock was unsuccessful, subsequent shocks terminated VT/VF without complication. Conclusions― Although spontaneous episodes of fast VT/VF were limited, there was no difference in the odds of first shock efficacy between groups. Screening with vulnerability safety margin or defibrillation safety margin may allow for inductionless or limited shock testing in most patients. Epidemiology 2、Brachial Flow-Mediated Dilation Predicts Incident Cardiovascular Events in Older Adults.
The Cardiovascular Health Study Background― The relationship between impaired brachial flow-mediated dilation (FMD) and subsequent clinical cardiovascular events is not well established, especially in older adults whose FMD is often diminished. We assessed the hypothesis that FMD predicts incident cardiovascular events in a population-based cohort of older adults. Methods and Results― FMD was measured at the 1997 to 1998 Cardiovascular Health Study clinic visit in 2792 adults aged 72 to 98 years (82.7% white, 58.6% women) recruited at 4 clinic sites in the United States. Log-rank test and Cox proportional hazard models were used to examine the association between FMD and adjudicated cardiovascular events. A total of 674 subjects (24.1%) had an adjudicated event over the 5-year follow-up period. Event-free survival rates for cardiovascular events were significantly higher in subjects with FMD greater than the sex-specific medians than in subjects with FMD less than or equal to the sex-specific medians (78.3% versus 73.6%, log-rank P=0.006). FMD remained a significant predictor of cardiovascular events after adjustment for age, gender, diabetes mellitus, cigarette smoking, systolic and diastolic blood pressure, baseline cardiovascular disease status, and total cholesterol (hazard ratio, 0.91 [95% CI, 0.83 to 0.99], P=0.02 per unit SD of FMD) but added only 1% to the prognostic accuracy of the best Cox model. Brachial artery diameter was also predictive of CV events in the adjusted Cox proportional hazard model (hazard ratio, 1.12 [95% CI, 1.02 to 1.28], P=0.025) and also added 1% to the accuracy of our best Cox model. Conclusions― FMD is a predictor of future cardiovascular events but adds very little to the prognostic accuracy of traditional cardiovascular risk scores/factors in older adults. FMD and brachial artery diameter may have similar predictive values for cardiovascular events in older adults. Health Services and Outcomes Research 3、Incremental Benefit and Cost-Effectiveness of High-Dose Statin Therapy in High-Risk Patients With Coronary Artery DiseaseBackground― Recent clinical trials found that high-dose statin therapy, compared with conventional-dose statin therapy, reduces the risk of cardiovascular events in patients with acute coronary syndromes (ACS) and stable coronary artery disease (CAD). However, the actual benefit and cost-effectiveness of high-dose statin therapy are unknown. Methods and Results― We designed a Markov model to compare daily high-dose with conventional-dose statin therapy for hypothetical 60-year-old cohorts with ACS and stable CAD over patient lifetime. Pooled estimates for major clinical end points (all-cause mortality, myocardial infarction, stroke, rehospitalization, and revascularization) from relevant clinical trials were incorporated. Incremental benefit was quantified as quality-adjusted life-years (QALYs). Threshold analyses determined at what price difference high-dose statins would yield incremental cost-effective ratios below $50 000, $100 000, and $150 000 per QALY gained. In ACS patients, a high-dose versus conventional-dose statin strategy resulted in a gain of 0.35 QALYs. In threshold analyses, a high-dose statin strategy consistently yielded incremental cost-effective ratios below $30 000 per QALY even under conservative model assumptions. In stable CAD patients, a high-dose statin strategy yielded a gain of only 0.10 QALYs and was sensitive to model assumptions about statin efficacy. The daily cost difference between a high- and conventional-dose statin would need to be &$1.70, $2.65, and $3.55 to yield incremental cost-effective ratios below $50 000, $100 000, and $150 000 per QALY. Conclusions― High-dose statin therapy is potentially highly effective and cost-effective in patients with ACS. In patients with stable CAD, however, the cost-effectiveness of high-dose statin therapy is highly sensitive to model assumptions about statin efficacy and cost. Use of high-dose statins can be supported on health economic grounds in patients with ACS, but the case is less clear for patients with stable CAD. Heart Failure 4、Development of a Ventilatory Classification System in Patients With Heart FailureBackground― Ventilatory efficiency, commonly assessed by the minute ventilation (E)Ccarbon dioxide production (CO2) slope, is a powerful prognostic marker in the heart failure population. The purpose of the present study is to refine the prognostic power of the E/CO2 slope by developing a ventilatory class system that correlates E/CO2 cut points to cardiac-related events. Methods and Results― Four hundred forty-eight subjects diagnosed with heart failure were included in this analysis. The E/CO2 slope was determined via cardiopulmonary exercise testing. Subjects were tracked for major cardiac events (mortality, transplantation, or left ventricular assist device implantation) for 2 years after cardiopulmonary exercise testing. There were 81 cardiac-related events (64 deaths, 10 heart transplants, and 7 left ventricular assist device implantations) during the 2-year tracking period. Receiver operating characteristic curve analysis revealed the overall E/CO2 slope classification scheme was significant (area under the curve: 0.78 [95% CI, 0.73 to 0.83], P&0.001). On the basis of test sensitivity and specificity, the following ventilatory class system was developed: (1) ventilatory class (VC) I: 29; (2) VC II: 30.0 to 35.9; (3) VC III: 36.0 to 44.9; and (4) VC IV: 45.0. The numbers of subjects in VCs I through IV were 144, 149, 112, and 43, respectively. Kaplan-Meier analysis revealed event-free survival for subjects in VC I, II, III, and IV was 97.2%, 85.2%, 72.3%, and 44.2%, respectively (log-rank 86.8; P&0.001). Conclusions― A multiple-level classificatory system based on exercise E/CO2 slope stratifies the burden of risk for the entire spectrum of heart failure severity. Application of this classification is therefore proposed to improve clinical decision making in heart failure. Imaging 5、Evidence for Microvascular Dysfunction in Hypertrophic CardiomyopathyNew Insights From Multiparametric Magnetic Resonance Imaging Background― Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) may create an ischemic substrate conducive to sudden death, but it remains unknown whether the extent of hypertrophy is associated with proportionally poorer perfusion reserve. Comparisons between magnitude of hypertrophy, impairment of perfusion reserve, and extent of fibrosis may offer new insights for future clinical risk stratification in HCM but require multiparametric imaging with high spatial and temporal resolution. Methods and Results― Degree of hypertrophy, myocardial blood flow at rest and during hyperemia (hMBF), and myocardial fibrosis were assessed with magnetic resonance imaging in 35 HCM patients (9 [26%] male/26 female) and 14 healthy controls (4 [29%] male/10 female), aged 18 to 78 years (mean±SD, 42±14 years) with the use of the American Heart Association left ventricular 16-segment model. Resting MBF was similar in HCM patients and controls. hMBF was lower in HCM patients (1.84±0.89 mL/min per gram) than in healthy controls (3.42±1.76 mL/min per gram, with a difference of C0.95±0.30 [SE] mL/ P&0.001) after adjustment for multiple variables, including end-diastolic segmental wall thickness (P&0.001). In HCM patients, hMBF decreased with increasing end-diastolic wall thickness (P&0.005) and preferentially in the endocardial layer. The frequency of endocardial hMBF falling below epicardial hMBF rose with wall thickness (P=0.045), as did the incidence of fibrosis (P&0.001). Conclusions― In HCM the vasodilator response is reduced, particularly in the endocardium, and in proportion to the magnitude of hypertrophy. Microvascular dysfunction and subsequent ischemia may be important components of the risk attributable to HCM. Interventional Cardiology 6、Incomplete Stent Apposition and Very Late Stent Thrombosis After Drug-Eluting Stent ImplantationBackground― Stent thrombosis may occur late after drug-eluting stent (DES) implantation, and its cause remains unknown. The present study investigated differences of the stented segment between patients with and without very late stent thrombosis with the use of intravascular ultrasound. Methods and Results― Since January 2004, patients presenting with very late stent thrombosis (&1 year) after DES implantation underwent intravascular ultrasound. Findings in patients with very late stent thrombosis were compared with intravascular ultrasound routinely obtained 8 months after DES implantation in 144 control patients, who did not experience stent thrombosis for 2 years. Very late stent thrombosis was encountered in 13 patients at a mean of 630±166 days after DES implantation. Compared with DES controls, patients with very late stent thrombosis had longer lesions (23.9±16.0 versus 13.3±7.9 P&0.001) and stents (34.6±22.4 versus 18.6±9.5 P&0.001), more stents per lesion (1.6±0.9 versus 1.1±0.4; P&0.001), and stent overlap (39% versus 8%; P&0.001). Vessel cross-sectional area was similar for the reference segment (cross-sectional area of the external elastic membrane: 18.9±6.9 versus 20.4±7.2 mm2; P=0.46) but significantly larger for the in-stent segment (28.6±11.9 versus 20.1±6.7 mm2; P=0.03) in very late stent thrombosis patients compared with DES controls. Incomplete stent apposition was more frequent (77% versus 12%; P&0.001) and maximal incomplete stent apposition area was larger (8.3±7.5 versus 4.0±3.8 mm2; P=0.03) in patients with very late stent thrombosis compared with controls. Conclusions― Incomplete stent apposition is highly prevalent in patients with very late stent thrombosis after DES implantation, suggesting a role in the pathogenesis of this adverse event. Interventional Cardiology 7、Pathological Correlates of Late Drug-Eluting Stent Thrombosis Strut Coverage as a Marker of Endothelialization Background― Late stent thrombosis (LST) after Cypher and Taxus drug-eluting stent placement has emerged as a major concern. Although the clinical predictors of LST have been reported, specific morphological and histological correlates of LST remain unknown. Methods and Results― From a registry totaling 81 human autopsies of drug-eluting stents, 46 (62 lesions) had a drug-eluting stent implanted &30 days. We identified 28 lesions with thrombus and compared those with 34 of similar duration without thrombosis using computer-guided morphometric and histological analyses. LST was defined as an acute thrombus within a coronary artery stent in place &30 days. Multiple logistic generalized estimating equations modeling demonstrated that endothelialization was the best predictor of thrombosis. The morphometric parameter that best correlated with endothelialization was the ratio of uncovered to total stent struts per section. A univariable logistic generalized estimating equations model of occurrence of thrombus in a stent section versus ratio of uncovered to total stent struts per section demonstrated a marked increase in risk for LST as the number of uncovered struts increased. The odds ratio for thrombus in a stent with a ratio of uncovered to total stent struts per section &30% is 9.0 (95% CI, 3.5 to 22). Conclusions― The most powerful histological predictor of stent thrombosis was endothelial coverage. The best morphometric predictor of LST was the ratio of uncovered to total stent struts. Heterogeneity of healing is a common finding in drug-eluting stents with evidence of LST and demonstrates the importance of incomplete healing of the stented segment in the pathophysiology of LST. Molecular Cardiology 8、Poly(ADP-Ribose) Polymerase Inhibition Reduces Atherosclerotic Plaque Size and Promotes Factors of Plaque Stability in Apolipoprotein ECDeficient MiceEffects on Macrophage Recruitment, Nuclear Factor-B Nuclear Translocation, and Foam Cell Death Background― Poly(ADP-ribose) polymerase (PARP) was suggested to play a role in endothelial dysfunction that is associated with a number of cardiovascular diseases. We hypothesized that PARP may play an important role in atherogenesis and that its inhibition may attenuate atherosclerotic plaque development in an experimental model of atherosclerosis. Methods and Results― Using a mouse (apolipoprotein E [ApoE]C/C) model of high-fat dietCinduced atherosclerosis, we demonstrate an association between cell death and oxidative stressCassociated DNA damage and PARP activation within atherosclerotic plaques. PARP inhibition by thieno[2,3-c]isoquinolin-5-one reduced plaque number and size and altered structural composition of plaques in these animals without affecting sera lipid contents. These results were corroborated genetically with the use of ApoEC/C mice that are heterozygous for PARP-1. PARP inhibition promoted an increase in collagen content, potentially through an increase in tissue inhibitor of metalloproteinase-2, and transmigration of smooth muscle cells to intima of atherosclerotic plaques as well as a decrease in monocyte chemotactic protein-1 production, all of which are markers of plaque stability. In PARP-1C/C macrophages, monocyte chemotactic protein-1 expression was severely inhibited because of a defective nuclear factor-B nuclear translocation in response to lipopolysaccharide. Furthermore, PARP-1 gene deletion not only conferred protection to foam cells against H2O2-induced death but also switched the mode of death from necrosis to apoptosis. Conclusions― Our results suggest that PARP inhibition interferes with plaque development and may promote plaque stability, possibly through a reduction in inflammatory factors and cellular changes related to plaque dynamics. PARP inhibition may prove beneficial for the treatment of atherosclerosis.认领第6篇，呵呵小弟是新手，翻译的不好，还请大家多多批评以求更大的进步。Incomplete Stent Apposition and Very Late Stent Thrombosis After Drug-Eluting Stent Implantation药物涂层支架植入后支架位置不当以及迟发血栓形成Background― Stent thrombosis may occur late after drug-eluting stent (DES) implantation, and its cause remains unknown. 背景－药物涂层支架植入后可发生迟发支架内血栓形成，其原因目前仍未知The present study investigated differences of the stented segment between patients with and without very late stent thrombosis with the use of intravascular ultrasound. 本研究采用冠脉内超声来研究伴或不伴有支架内迟发血栓患者支架部分的差异。Methods and Results― Since January 2004, patients presenting with very late stent thrombosis (&1 year) after DES implantation underwent intravascular ultrasound.方法和结果－选择2004年1月份以来临床证实有迟发血栓形成（超过1年）的患者均行冠脉内超声检查。 Findings in patients with very late stent thrombosis were compared with intravascular ultrasound routinely obtained 8 months after DES implantation in 144 control patients, who did not experience stent thrombosis for 2 years. 将有迟发血栓形成患者的冠脉内超声结果与144例对照组患者相比较，这些患者在药物涂层支架植入8个月后均行冠脉内超声检查，并且2年之内无支架内再狭窄。Very late stent thrombosis was encountered in 13 patients at a mean of 630±166 days after DES implantation.13例患者支架植入后发生晚期支架内血栓形成，平均天数是630±166 天。 Compared with DES controls, patients with very late stent thrombosis had longer lesions (23.9±16.0 versus 13.3±7.9 P&0.001) and stents (34.6±22.4 versus 18.6±9.5 P&0.001), more stents per lesion (1.6±0.9 versus 1.1±0.4; P&0.001), and stent overlap (39% versus 8%; P&0.001). 与对照组相比较，发生迟发血栓者血管受损长度更长（23.9±16.0 比 13.3±7.9 P&0.001）、支架长度更长（34.6±22.4 比18.6±9.5 P&0.001）、支架/损伤长度比更大（1.6±0.9 versus 1.1±0.4; P&0.001）、具有更高的支架重叠率（39% 比8%; P&0.001）。Vessel cross-sectional area was similar for the reference segment (cross-sectional area of the external elastic membrane: 18.9±6.9 versus 20.4±7.2 mm2; P=0.46) but significantly larger for the in-stent segment (28.6±11.9 versus 20.1±6.7 mm2; P=0.03) in very late stent thrombosis patients compared with DES controls. 两者之间相对应部分血管横断面积相似（外弹性膜横断面积：18.9±6.9 比 20.4±7.2 mm2; P=0.46）但支架内部分却具有显著差异（28.6±11.9 比20.1±6.7 mm2; P=0.03）Incomplete stent apposition was more frequent (77% versus 12%; P&0.001) and maximal incomplete stent apposition area was larger (8.3±7.5 versus 4.0±3.8 mm2; P=0.03) in patients with very late stent thrombosis compared with controls. 与对照组相比较，迟发血栓患者组具有更高的支架位置不当发生率（77% 比 12%; P&0.001），此外最大支架位置不当面积也高于对照组（8.3±7.5 比4.0±3.8 mm2; P=0.03）Conclusions― Incomplete stent apposition is highly prevalent in patients with very late stent thrombosis after DES implantation, suggesting a role in the pathogenesis of this adverse event. 药物支架植入后发生迟发血栓患者中支架位置不当发生率高，可能是造成该种不良事件的一个原因。Interventional Cardiology突然发现之前已经有站友发过了，呵呵，真是不好意思，不过我这个可是自己翻译的哦认领6和7。兄弟，这个好像不是这期的circulation吧，不过还是可以一起翻译学习的哦。认领第八篇好久未在这里翻译了，希望不当之处多多指点7、Pathological Correlates of Late Drug-Eluting Stent Thrombosis Strut Coverage as a Marker of Endothelialization 题目：晚发药物洗脱支架（DES）内血栓与作为内皮化的一个标志物的支架丝内皮覆盖程度的病理关系Background― Late stent thrombosis (LST) after Cypher and Taxus drug-eluting stent placement has emerged as a major concern. Although the clinical predictors of LST have been reported, specific morphological and histological correlates of LST remain unknown. 背景：晚发支架内血栓（LST）是Cypher和TAXUS支架置入后出现的一个主要问题，虽然已有临床LST的预测因子的报道，但是LST与形态学和组织学的相关性还不清楚。Methods and Results― From a registry totaling 81 human autopsies of drug-eluting stents, 46 (62 lesions) had a drug-eluting stent implanted &30 days. We identified 28 lesions with thrombus and compared those with 34 of similar duration without thrombosis using computer-guided morphometric and histological analyses. LST was defined as an acute thrombus within a coronary artery stent in place &30 days. Multiple logistic generalized estimating equations modeling /demonstrated that endothelialization was the best predictor of thrombosis. The morphometric parameter that best correlated with endothelialization was the ratio of uncovered to total stent struts per section. A univariable logistic generalized estimating equations model of occurrence of thrombus in a stent section versus ratio of uncovered to total stent struts per section demonstrated a marked increase in risk for LST as the number of uncovered struts increased. The odds ratio for thrombus in a stent with a ratio of uncovered to total stent struts per section &30% is 9.0 (95% CI, 3.5 to 22). 方法和结果：一项入选81例置入DES支架尸检注册研究，46例（62处病变）患者置入DES超过30天，28处发生血栓的病变和相似的时期的34例，未发生支架内血栓的患者对照，使用计算机进行形态学和组织学分析。晚期血栓的定义为支架置入后30天发生的急性血栓形成。多因素logistic回归分析结果显示内皮化是DES血栓的最佳预测因子，形态学上与内皮化最为相关的是每个节段未被内皮覆盖/总的支架丝覆盖的比值。单因素logistic回归分析结果显示：支架内血栓发生率与每个节段内未被内皮覆盖与整个支架丝比值升高明显增加LST的危险，在这个比值&30％的情况下发生支架内血栓的优势比为9（95％CI，3.5-22）Conclusions― The most powerful histological predictor of stent thrombosis was endothelial coverage. The best morphometric predictor of LST was the ratio of uncovered to total stent struts. Heterogeneity of healing is a common finding in drug-eluting stents with evidence of LST and demonstrates the importance of incomplete healing of the stented segment in the pathophysiology of LST. 结论：支架内血栓的最强的组织学预测因子是支架的内皮覆盖程度；最佳的LST形态学预测因子为未被内皮覆盖支架丝与总的支架丝的比值；内皮修复的不均一性在置入DES后发生LST的患者中是常见的，证明了支架节段内内皮覆盖不全在LST病理生理机制中的重要性。领第5篇Evidence for Microvascular Dysfunction in Hypertrophic Cardiomyopathy肥厚性心肌病微血管功能失调的研究证据New Insights From Multiparametric Magnetic Resonance Imaging 来自于多参数磁共振成像（MRI）的观察Background― Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) may create an ischemic substrate conducive to sudden death, but it remains unknown whether the extent of hypertrophy is associated with proportionally poorer perfusion reserve. Comparisons between magnitude of hypertrophy, impairment of perfusion reserve, and extent of fibrosis may offer new insights for future clinical risk stratification in HCM but require multiparametric imaging with high spatial and temporal resolution. 背景― 肥厚性心肌病（HCM）的微血管功能失调可产生缺血性基质，并导致猝死的发生，不过至今尚不知道心肌肥厚的程度是否与更少的血流储备成比例关系。比较心肌肥厚的大小、血流储备的减少以及心肌纤维化的程度将有助于指导HCM的临床危险分层，但这需要多参数的空间成像分析Methods and Results― Degree of hypertrophy, myocardial blood flow at rest and during hyperemia (hMBF), and myocardial fibrosis were assessed with magnetic resonance imaging in 35 HCM patients (9 [26%] male/26 female) and 14 healthy controls (4 [29%] male/10 female), aged 18 to 78 years (mean±SD, 42±14 years) with the use of the American Heart Association left ventricular 16-segment model. Resting MBF was similar in HCM patients and controls. hMBF was lower in HCM patients (1.84±0.89 mL/min per gram) than in healthy controls (3.42±1.76 mL/min per gram, with a difference of C0.95±0.30 [SE] mL/ P&0.001) after adjustment for multiple variables, including end-diastolic segmental wall thickness (P&0.001). In HCM patients, hMBF decreased with increasing end-diastolic wall thickness (P&0.005) and preferentially in the endocardial layer. The frequency of endocardial hMBF falling below epicardial hMBF rose with wall thickness (P=0.045), as did the incidence of fibrosis (P&0.001). 方法与结果――研究对象为35个HCM患者[其中男性9名（26％），女性26名]和14个健康对照组〔其中男性4名（29％），女性10名〕，年龄18－78岁，平均（42±14）岁。按照美国心脏病协会（AHA）制定的左室16 层法，以MRI来评价肥厚的程度、静息及充血时心肌血流灌注（hMBF）和心肌纤维化。结果静息时心肌血流灌注在HCM组和对照组之间无差异；调节多变量包括舒张末期节段性室壁厚度后，充血时心肌血流灌注HCM组低于健康对照组（1.84±0.89 mLmin/ g vs 3.42±1.76 mL/min/ P&0.001）。对于HCM患者，充血时心肌血流灌注降低，而舒张末期节段性室壁厚度却是增加的，尤其在心内膜层。心内膜hMBF减少的频率低于心外膜hMBF，最终引起心室壁增厚(P=0.045)及心肌纤维化的发生(P&0.001).Conclusions― In HCM the vasodilator response is reduced, particularly in the endocardium, and in proportion to the magnitude of hypertrophy. Microvascular dysfunction and subsequent ischemia may be important components of the risk attributable to HCM. 结论――对于HCM患者，血管舒张反应减退，尤其是在心内膜，而且这与心肌肥厚的程度成比例。微血管功能失调以及继发性心肌缺血也许是形成HCM危险因素的重要组成部分。恐怕问题很大
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