ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundPartial left ventriculectomy (PLV) is a novel surgical treatment for severe heart failure consisting of resection of a large wedge of myocardium to reduce wall stress and restore the normal mass-volume ratio. Although ejection fraction (EF) has been shown to improve after PLV, few other physiological data describing its immediate effects on left ventricular (LV) performance are available.Methods and Results-Eight patients, 58 +/- 5 years old, with severe clinical heart failure and EF of 12 +/- 3% were studied before and immediately after PLV. LV performance was assessed by the predominantly load-insensitive measures of pressure-area relations with high-fidelity pressure catheters and transesophageal automated echocardiographic measures of cross-sectional area as a surrogate for volume. LV end-diastolic volume decreased from 200 +/- 60 to 89 +/- 17 mL, EF increased from 12 +/- 3% to 41 +/- 8%, and right ventricular (RV) fractional area change increased from 24 +/- 12% to 37 +/- 16% (all P <.05 versus before). Changes in pressure-area relations were variable: end-systolic elastance, 6.5 +/- 3.4 to 4.3 +/- 2.5 mm Hg/cm2and preload recruitable stroke work, 33 +/- 16 to 34 +/- 19 mm Hg (P = NS versus before). End-diastolic stiffness increased from 0.13 +/- 0.06 to 0.19 +/- 0.07 mm Hg/cm2(P < .05 versus before). Improvement in LV performance was inversely correlated with semiquantitative histological assessment of myocardial fibrosis and positively correlated with nuclear enlargement and hyperchromasia, indicative of myocyte hypertrophy. No long-term follow-up data were available.ConclusionsPLV resulted in reductions in LV volumes, increases in EF and RV ejection, but increases in LV stiffness. Estimates of LV performance revealed variable results associated with the degree of myocardial fibrosis. Further study of these effects in relation to patient outcome is warranted. (Circulation. 1998;97:839-842.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundNew high-energy collimators for single photon emission computed tomography (SPECT) cameras have made imaging of positron-emitting tracers, such as [(18) F]fluorodeoxyglucose (18) FDG), possible. We examined differences between SPECT and PET technologies and between18FDG and thallium tracers to determine whether18FDG SPECT could be adopted for assessment of myocardial viability.Methods and Results-Twenty-eight patients with chronic coronary artery disease (mean left ventricular ejection fraction [LVEF] = 33 +/- 15% at rest) underwent18FDG SPECT,18FDG PET, and thallium SPECT studies. Receiver operating characteristic curves showed overall good concordance between SPECT and PET technologies and thallium and18FDG tracers for assessing viability regardless of the level of18FDG PET cutoff used (40% to 60%). However, in the subgroup of patients with LVEF <or= to 25%, at 60%18FDG PET threshold value, thallium tended to underestimate myocardial viability. In a subgroup of regions with severe asynergy, there were considerably more thallium/(18) FDG discordances in the inferior wall than elsewhere (73% versus 27%, P <.001), supporting attenuation of thallium as a potential explanation for the discordant observations. When uptake of18FDG by SPECT and PET was compared in 137 segments exhibiting severely irreversible thallium defects (scarred by thallium), 59 (43%) were viable by18FDG PET, of which 52 (88%) were also viable by18FDG SPECT. However, of the 78 segments confirmed to be nonviable by18FDG PET, 57 (73%) were nonviable by18FDG SPECT (P < .001).ConclusionsAlthough18FDG SPECT significantly increases the sensitivity for detection of viable myocardium in tissue declared nonviable by thallium (to 88% of the sensitivity achievable by PET), it will occasionally (27% of the time) result in falsely identifying as viable tissue that has been identified as nonviable by both PET and thallium. (Circulation. 1998;97:843-850.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundPatients with essential hypertension have impaired endothelial NO activity, but the mechanism underlying this abnormality is unknown.Methods and Results-To investigate whether the endothelial dysfunction of hypertensive patients is related to a selective defect in NO synthesis, we studied the forearm blood flow responses to intra-arterial infusion of acetylcholine (7.5 to 30 micro gram/min), an endothelial agonist linked to NO synthase through the Ca2+signaling pathway, and isoproterenol (50 to 200 ng/min), a beta-adrenoceptor agonist that stimulates NO production by increasing intracellular cAMP, in 12 normotensive subjects and 12 hypertensive patients. The infusion of isoproterenol was repeated during the concurrent blockade of NO synthesis by NG-monomethyl-L-arginine (L-NMMA; 4 micro mol/min). The vasodilator response to acetylcholine was significantly reduced in hypertensives compared with normotensives (maximum blood flow: 10.4 +/- 4.6 versus 14.4 +/- 3.7 mL [center dot] min-1[center dot] dL-1; P = .008). However, the vasodilator effect of isoproterenol was similar in normotensives and hypertensives (maximum blood flow: 14.4 +/- 5.4 versus 13.5 +/- 5 mL [center dot] min-1[center dot] dL-1; P = .56) and was significantly (both P < .01) and equally blunted by L-NMMA in both groups (maximum blood flow: 11 +/- 3 mL [center dot] min-1[center dot] dL-1in normotensives versus 10.8 +/- 3.9 mL [center dot] min (-1) [center dot] dL-1in hypertensives; P = .77). The vasodilator response to sodium nitroprusside (0.8 to 3.2 micro gram/min), an exogenous NO donor, was similar in both groups and was not modified by L-NMMA.ConclusionsHypertensive patients have impaired endothelium-dependent vasodilation in response to acetylcholine but preserved NO activity in response to beta-adrenergic stimulation. These findings suggest that the endothelial dysfunction in essential hypertension is due to a selective abnormality of NO synthesis, probably related to a defect in the phosphatidylinositol/Ca2+signaling pathway. (Circulation. 1998;97:851-856.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundThe clinical and angiographic demographics of patients requiring unplanned coronary stent deployment and the optimal adjunct pharmacotherapy in this population are not well described. This report details the EPILOG trial experience with unplanned coronary stent deployment and the effect of abciximab platelet glycoprotein IIb/IIIa blockade to improve clinical outcomes during 6 months of follow-up.10 mm (P = .002), lesion eccentricity (P = .027), irregular lesion contour (P = .001), and bifurcation involvement (P = .019) than nonstented patients. Unplanned stents were required less often in patients treated with abciximab and low-dose, weight-adjusted heparin than in patients receiving placebo and standard-dose heparin (9.0% versus 13.7%; P = .001). Although adverse clinical outcomes including target-vessel revascularization and bleeding events were more frequent in patients requiring unplanned coronary stent deployment, abciximab therapy reduced adverse outcomes in these patients at 30 days and 6 months to a greater extent than was observed in patients not requiring stent placement. Among stented patients, abciximab therapy did not increase bleeding events.ConclusionsPatients requiring unplanned coronary stent deployment have more complex coronary lesion morphology and a more complicated clinical course after coronary intervention. Abciximab therapy both reduces the need for unplanned stent deployment and confers clinical benefit to patients requiring an unplanned stent, without increasing bleeding complications. (Circulation. 1998;97:857-864.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Bachground-Arginine vasopressin (AVP) not only acts directly on blood vessels through V1receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins.Methods and Results-Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (3 x 10-9mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.87 x 10-7to 1.04 x 10-7mol/L; P < .05). The V1vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10-6mol/L) prevented the potentiation evoked by AVP. The selective V1receptor agonist [Phe2, Orn8]-vasotocin (3 x 10-9mol/L) induced potentiation of electrical stimulation-evoked responses, which was also inhibited in the presence of the V1receptor antagonist (10-6mol/L). In contrast, the V2receptor agonist desmopressin (10-9to 10-7mol/L) did not modify neurogenic responses, and the V2receptor antagonist [d(CH2)5, D-Ile2, Ile4, Arg8]-vasopressin (10-8to 10-6mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (10-6mol/L) did not affect the potentiating effect of AVP.ConclusionsThe results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated. (Circulation. 1998;97:865-870.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundPatients with a mutation in the LDL receptor gene (familial hypercholesterolemia, or FH) are characterized by substantial elevations in plasma LDL cholesterol and are at higher risk of developing coronary artery disease (CAD). Correlates of abdominal obesity may also contribute to the risk of ischemic cardiac events. Whether the hyperinsulinemic-insulin-resistant state of abdominal obesity affects coronary atherosclerosis among FH patients has not been determined.95 cm) and hyperinsulinemic FH patients (odds ratio, 12.9; P = .0009). This increase in risk remained significant even after adjustment for LDL cholesterol or apolipoprotein B concentrations.ConclusionsResults of the present study provide support for the notion that the hyperinsulinemic-insulin-resistant state of abdominal obesity is a powerful predictor of CAD in men, even in a group of patients with raised LDL cholesterol concentrations due to FH. (Circulation. 1998;97:871-877.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundLesion composition, rather than size or volume, determines whether an atherosclerotic plaque will progress, regress, or rupture, but current techniques cannot provide precise quantitative information about lesion composition. We have developed a technique to assess the pathological state of human coronary artery samples by quantifying their chemical composition with near-infrared Raman spectroscopy.Methods and Results-Coronary artery samples (n = 165) obtained from explanted recipient hearts were illuminated with 830-nm infrared light. Raman spectra were collected from the tissue and processed to quantify the relative weights of cholesterol, cholesterol esters, triglycerides and phospholipids, and calcium salts in the examined artery location. The artery locations were then classified by a pathologist and grouped as either nonatherosclerotic tissue, noncalcified plaque, or calcified plaque. Nonatherosclerotic tissue, which included normal artery and intimal fibroplasia, contained an average of [nearly =] 4 +/- 3% cholesterol, whereas noncalcified plaques had [nearly =] 26 +/- 10% and calcified plaques [nearly =] 19 +/- 10% cholesterol in the noncalcified regions. The average relative weight of calcium salts was 1 +/- 2% in noncalcified plaques and 41 +/- 21% in calcified plaques. To make this quantitative chemical information clinically useful, we developed a diagnostic algorithm, based on a first set of 97 samples, that demonstrated a strong correlation of the relative weights of cholesterol and calcium salts with histological diagnoses of the same locations. This algorithm was then prospectively tested on a second set of 68 samples. The algorithm correctly classified 64 of these new samples, thus demonstrating the accuracy and robustness of the method.ConclusionsThe pathological state of a given human coronary artery may be assessed by quantifying its chemical composition, which can be done rapidly with Raman spectroscopic techniques. When Raman spectra are obtained clinically via optical fibers, Raman spectroscopy may be useful in monitoring the progression and regression of atherosclerosis, predicting plaque rupture, and selecting proper therapeutic intervention. (Circulation. 1998;97:878-885.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundReduced cGMP production caused by increased superoxide has been proposed as a mechanism of nitrate tolerance during continuous nitrate therapy. This study was designed to evaluate the effects of ascorbate, an antioxidant, on the development of nitrate tolerance during continuous nitrate therapy in patients with congestive heart failure.Methods and Results-Twenty patients with congestive heart failure were randomized to receive intravenous infusion of nitroglycerin concomitantly with placebo (placebo group, n = 10) or intravenous ascorbate (vitamin C group, n = 10). After baseline measurements were obtained, dose titration was started by the infusion of nitroglycerin at a rate of 0.5 micro gram/kg per minute (titration period). Measurements of hemodynamic parameters and blood sampling were performed serially at 0, 6, 12, 18, and 24 hours after the titration period. At baseline, mean pulmonary artery pressure (MPAP, mm Hg), mean pulmonary capillary wedge pressure (PCWP, mm Hg), plasma vitamin E level (micro mol/L), and platelet cGMP level (pmol/109platelets) were comparable in the two groups (placebo group: MPAP, 48 +/- 6; PCWP, 24 +/- 4; cGMP, 0.76 +/- 0.12; vitamin E, 18.2 +/- 1.2; vitamin C: MPAP, 49 +/- 7; PCWP, 24 +/- 4; cGMP, 0.71 +/- 0.16; vitamin E, 18.6 +/- 1.3). In both groups, at 6 hours after the titration period, MPAP and PCWP were significantly decreased (placebo group: MPAP, 26 +/- 5; PCWP, 15 +/- 4; vitamin C: MPAP, 26 +/- 4; PCWP, 16 +/- 4), and platelet cGMP was significantly increased (placebo group: 2.42 +/- 0.24; vitamin C: 2.26 +/- 0.26). However, at 18 hours after titration, in the placebo group, MPAP (44 +/- 5) and PCWP (23 +/- 4) were increased, and platelet cGMP (0.85 +/- 0.20) and plasma vitamin E levels (12.4 +/- 1.4) were significantly decreased. In contrast, in the vitamin C group, MPAP (31 +/- 6), PCWP (17 +/- 5), platelet cGMP (2.49 +/- 0.23), and plasma vitamin E levels (17.6 +/- 1.4) were maintained for 18 hours after the titration period.ConclusionsThese findings indicate that ascorbate, an antioxidant, may prevent the development of nitrate tolerance during continuous nitrate therapy in patients with congestive heart failure. (Circulation. 1998;97:886-891.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundLarge transmural myocardial infarction (MI) leads to maladaptive cardiac remodeling and places patients at increased risk of congestive heart failure. Angiotensin II, endothelin, and alpha1-adrenergic receptor agonists are implicated in the development of cardiac hypertrophy, interstitial fibrosis, and heart failure after MI. Because these agonists are coupled to and activate Gqalpha protein in the heart, the aim of the present study was to investigate Gqalpha expression and function in cardiac remodeling and heart failure after MI.Methods and Results-MI was produced in rats by ligation of the left coronary artery, and Gqalpha protein concentration, localization, and mRNA abundance were noted in surviving left ventricle remote from the infarct and in border and scar tissues from 8-week post-MI hearts with moderate heart failure. Immunohistochemical staining localized elevated G (q) alpha expression in the scar and border tissues. Western analysis confirmed significant upregulation of Gqalpha proteins in these regions versus controls. Furthermore, Northern analysis revealed that the ratios of Gqalpha/GAPDH mRNA abundance in both scar and viable tissues from experimental hearts were significantly increased versus controls. Increased expression of phospholipase C (PLC)-beta1and PLC-beta3proteins was apparent in the scar and viable tissues after MI versus controls and is associated with increased PLC-beta1activity in experimental hearts. Furthermore, inositol 1,4,5-tris-phosphate is significantly increased in the border and scar tissues compared with control values.ConclusionsUpregulation of the Gqalpha/PLC-beta pathway was observed in the viable, border, and scar tissues in post-MI hearts. Gqalpha and PLC-beta may play important roles in scar remodeling as well as cardiac hypertrophy and fibrosis of the surviving tissue in post-MI rat heart. It is suggested that the Gqalpha/PLC-beta pathway may provide a possible novel target for altering postinfarct remodeling. (Circulation. 1998;97:892-899.)

ISSN:0009-7322    

出版商:OVID    

年代:1998

数据来源: OVID