ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundModerate hyperhomocysteinemia is a risk factor for arterial vascular disease and venous thrombosis in adults. We performed a case-control study to assess a possible relation between moderate hyperhomocysteinemia and ischemic stroke in Dutch children (age range, 0 to 18 years).Methods and Results-We measured plasma total homocysteine levels (tHcy) in 45 patients with ischemic stroke and in 234 controls. Hyperhomocysteinemia was defined as a tHcy above the 95th percentile regression line for the respective age of the controls. Hyperhomocysteinemia was present in 8 (18%) of the 45 patients with ischemic stroke. The odds ratio was 4.4 (95% CI, 1.7 to 11.6).ConclusionsWe conclude that moderate hyperhomocysteinemia is a risk factor for ischemic stroke in children.(Circulation. 1999;99:2070-2072.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundIdentification of patients with acute coronary syndromes (ACS) among those who present to emergency departments with possible myocardial ischemia is difficult. Myocardial perfusion imaging with99mTc sestamibi and measurement of serum cardiac troponin I (cTnI) both can identify patients with ACS.or=to2.0 ng/mL in 74 (12%). Sensitivity for detecting myocardial infarction was not significantly different between perfusion imaging (92%) and cTnI (90%), and both were significantly higher than the initial cTnI (39%). Sensitivity for predicting revascularization or significant coronary disease was significantly higher for perfusion imaging than for serial cTnI, although specificity for all end points was significantly lower. Lowering the cutoff value of cTnI to 1.0 ng/mL did not significantly change the results.ConclusionsEarly perfusion imaging and serial cTnI have comparable sensitivities for identifying myocardial infarction. Perfusion imaging identified more patients who underwent revascularization or who had significant coronary disease, but it had lower specificity. The 2 tests can provide complementary information for identifying patients at risk for ACS. (Circulation. 1999;99:2073-2078.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundA growing body of evidence suggests a role for inflammation in acute coronary syndromes. The aim of this study was to assess the role of proinflammatory cytokines, their time course, and their association with prognosis in unstable angina.Methods and Results-We studied 43 patients aged 62 +/- 8 years admitted to our coronary care unit for Braunwald class IIIB unstable angina. In each patient, serum levels of interleukin-1 receptor antagonist (IL-1Ra), interleukin-6 (IL-6) (which represent sensitive markers of biologically active IL-1 beta and tumor necrosis factor-alpha levels, respectively), and troponin T were measured at entry and 48 hours after admission. Troponin T-positive patients were excluded. Patients were divided a posteriori into 2 groups according to their in-hospital outcome: group 1 comprised 17 patients with an uneventful course, and group 2 comprised 26 patients with a complicated in-hospital course. In group 1, mean IL-1Ra decreased at 48 hours by 12%, and IL-6 diminished at 48 hours by 13%. In group 2, IL-1Ra and IL-6 entry levels were higher than in group 1 and increased respectively by 37% and 57% at 48 hours (P<0.01).ConclusionsThese findings indicate that although they receive the same medical therapy as patients who do not experience an in-hospital event, patients with unstable angina and with complicated in-hospital courses have higher cytokine levels on admission. A fall in IL-1Ra and IL-6 48 hours after admission was associated with an uneventful course and their increase with a complicated hospital course. These findings may suggest novel therapeutic approaches to patients with unstable angina. (Circulation. 1999;99:2079-2084.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundPrevious studies in humans have indicated that there is less ischemic dysfunction during PTCA when ischemic preconditioning is elicited. However, the clinical relevance of these observations remains unclear. The present study design tests the hypothesis that PTCA performed to elicit the preconditioning response would result in less myocardial necrosis as assessed by postprocedure creatine kinase (CK) levelsMethods and Results-Patients (n=150) undergoing PTCA for unstable ischemic syndromes were randomly assigned to receive a previously validated approach to PTCA-mediated preconditioning (PC) or an unrestricted approach to balloon angioplasty (UC). CK levels were determined at 8, 12, and, if necessary, 24 hours. Clinical success rates were equivalent for the 2 groups. However, the frequency of any CK elevation was significantly higher in the UC group (25%) than in the PC group (7.1%) (P<0.005). Multivariable analysis confirmed a significant effect of preconditioning on CK release.ConclusionsA standardized protocol to elicit preconditioning during PTCA results in a significant reduction in the rate of CK elevation in a high-risk population. These observations support the clinical relevance of ischemic preconditioning in humans. (Circulation. 1999;99:2085-2089.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundAlthough adrenergic activation plays a major role in the initiation of experimental myocardial ischemia, the significance of alpha-adrenergic coronary constriction in humans has been questioned. The present study assessed the impact of selective alpha-adrenergic receptor activation in patients with normal or atherosclerotic coronary arteries.Methods and Results-In 39 patients, coronary blood flow (CBF, mL/min) was determined from combined angiography and Doppler measurements. In 8 patients with normal coronary arteries (group 1) and 9 with single coronary artery stenosis (group 2), doses of 1, 2.5, 5, and 10 mg IC of the alpha1-agonistmethoxamine (M) were injected. Identical doses of the alpha2-agonistBHT933 (B) were injected in 8 patients with normal coronary arteries (group 3) and 8 with single stenosis (group 4). In 6 additional patients with single stenosis (group 5), aortocoronary sinus lactate differences were measured in response to M and B. CBF remained unchanged in group 1. In contrast, CBF was decreased dose-dependently in group 2, with a maximum at 10 mg M (39.0 +/- 9.4 versus 15.2 +/- 7.0). In groups 3 and 4, CBF was also decreased dose-dependently, with a maximum at 10 mg B (63.3 +/- 24.8 versus 49.1 +/- 27.9 and 41.5 +/- 19.0 versus 12.7 +/- 8.0, respectively). In group 5, there was more net lactate production with B than with M (-0.34 +/- 0.11 versus -0.04 +/- 0.09 mmol/L).ConclusionsIn normal coronary arteries, alpha1-adrenergicactivation does not reduce CBF, whereas alpha2-adrenergicactivation reduces CBF by microvascular constriction. Both alpha1-and alpha2-adrenergicepicardial and microvascular constriction are augmented by atherosclerosis and can induce myocardial ischemia. (Circulation. 1999;99:2090-2097.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundRisk indexes for operative mortality after cardiac surgery are used for comparative profiling of surgeons or centers. We examined whether clinicians and managers should use an existing index without modification, recalibrate it for their populations, or derive a new model altogether.Methods and Results-Drawing on 7491 consecutive patients who underwent isolated CABG at 2 Toronto teaching hospitals between 1993 and 1996, we compared 3 strategies: (1) using a ready-made model originally derived and validated in our jurisdiction; (2) recalibrating the ready-made model to better fit the population; and (3) deriving a new model with additional risk factors. We assessed statistical accuracy, ie, area under a receiver-operator characteristic curve (ROC); precision, ie, statistical goodness-of-fit; and actual impact on both risk-adjusted operative mortalities (RAOM) and performance rankings for 14 surgeons. The new model was slightly more accurate than the ready-made model (ROC, 0.78 versus 0.76; P<0.05), albeit not different from the recalibrated model (ROC, 0.77). The ready-made model showed poor fit between the predicted and observed results (P<0.001), leading to significant underestimation of RAOM (1.6 +/- 0.2%) compared with the other strategies (2.5 +/- 0.2%; P=0.048). Remodeling also changed the performance rankings among half the surgeons with higher RAOM.ConclusionsPoorly calibrated risk algorithms can bias the calculation of RAOM and alter the results of surgeon-specific profiles. Any existing index used for risk assessment in cardiac surgery should be episodically recalibrated or compared with new models derived from local subjects to ensure that its performance remains optimal. (Circulation. 1999;99:2098-2104.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundCardiac glycosides initiate an increase in force of contraction by inhibiting the sarcolemmal sodium pump (Na+,K+-ATPase), thereby decreasing Ca2+extrusion by the Na+-Ca2+exchanger, which increases the cellular content of Ca2+. In patients with heart failure the sensitivity toward cardiac glycosides is enhanced.Methods and Results-Because the inotropic effect of cardiac glycosides may be a function of the sodium pump and Na+-Ca2+exchanger (NCE) expression levels, the present study aimed to investigate protein expression of both transporters (immunoblot with specific antibodies against the sodium pump catalytic alpha1-, alpha2-, alpha3-, and glycoprotein beta1-isoformsand against NCE) in left ventricle from failing (heart transplantations, New York Heart Association class IV, n=21) compared with nonfailing (donor hearts, NF, n=22) human myocardium. The density of3H-ouabain-binding sites (Bmax) and the Na+,K+-ATPaseactivity were also measured. In NYHA class IV, protein levels of Na+,K+-ATPasealpha1-(0.62 +/- 0.06 of control), alpha3-(0.70 +/- 0.09), and beta1-(0.61 +/- 0.04) but not alpha2-isoformswere significantly reduced (P<0.01), whereas levels of NCE (0.92 +/- 0.13 of control) and calsequestrin (0.98 +/- 0.06) remained unchanged. Both Na+,K+-ATPaseactivity (NF: 1.9 +/- 0.29; NYHA class IV: 1.1 +/- 0.17 [micro sign]mol ATP/min per milligram of protein) and the (3) H-ouabain binding sites (BmaxNF: 15.9 +/- 1.9 pmol/mg protein; NYHA class IV: 9.7 +/- 1.5) were reduced in NYHA class IV and correlated significantly to each other (r2=0.73; P<0.0001), as did beta1-subunitexpression. In left ventricular papillary muscle strips from NYHA class IV compared with nonfailing tissue the Na (+-channel) modulator BDF 9198 exerted an increase in force of contraction with unchanged effectiveness but enhanced potency.ConclusionsThe enhanced sensitivity of failing human myocardium toward cardiac glycosides may be, at least in part, attributed to a reduced protein expression and activity of the sarcolemmal Na+,K+-ATPasewithout a change in Na+-Ca(2+) exchanger protein expression. (Circulation. 1999;99:2105-2112.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID