22 research outputs found

    Quantification of valvular regurgitation by cardiac blood pool scintigraphy: correlation with catheterization

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    The diagnosis of valvular regurgitation (R) is usually based on clinical signs. Quantification conventionally requires catheterization (C). We have quantified R with cardiac blood pool scintigraphy (CBPS) and compared the results with those obtained by C. Regurgitant fraction (RF) determined by C was calculated with the technique of Dodge. Forward output was measured by thermodilution or cardiogreen dilution. The RF at CBPS was obtained by the stroke index ratio (SIR) minus 1.2 divided by SIR, where SIR is the ratio of the stroke counts of left venticle over those of the right ventricle. Stroke counts are calculated directly from the time-activity curves. Each time-activity curve was obtained by drawing one region of interest around each diastolic image. The correction factor (1.2) was calculated from a large normal population. 22 patients had aortic R, 7 mitral R, 12 both, 8 patients had no evidence of regurgitation. RF of the patients with R varied from 27 to 71% (x = 42%) at C and from 26 to 74% (Y = 41%) at CBPS. Linear regression shows a good correlation coefficient (r = 0.82). The regression equation is y = 0.93x + 1.8. No correlation was found between RF (CBPS or C) and the severity of R assessed visually from angiography. In conclusion: CBPS, a non-invasive method, allows easy and repeatable determination of RF and correlates well with data obtained at catheterizatio

    Evaluation of right-ventricular function by gated blood-pool scintigraphy.

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    The purpose of this paper is to review several modalities that can be helpful in evaluating right-ventricular (RV) function. We have investigated the role of functional imaging in analysis of regional RV function and in selection of RV region of interest (ROI). From this we have derived a method to determine the RV ejection fraction using a single RV ROI. The analysis is performed in a modified LAO projection; Fourier phase and amplitude functional images are used to help trace the ROI and study wall-motion abnormalities. This method is compared with the double-ROI technique of Maddahi. Values of RV ejection fraction obtained with one ROI correlate well with those obtained using two ROIs (r = 0.95). The regression equation is used to correct for the single-ROI underestimation. The inter- and intra-observer variability is better for the single- than for the double-ROI technique. RV function studies are performed in normal volunteers and in patients with a variety of cardiac disorders. Changes in RV ejection fraction caused either by direct alteration of RV function or by altered loading conditions are documented. Analysis of regional RV function demonstrates RV free wall as well as septal perturbations, further characterizing the extent of dysfunction and providing some etiologic information. We conclude that: 1. RV ejection fraction can be measured by the use of an adequate single diastolic ROI; and 2. A simple equilibrium gated technique can provide detailed information about global and regional RV function that should be systematically added to the analysis of the parameters for left-ventricular function

    Prognostic value of thallium-201 stress myocardial scintigraphy with exercise ECG after myocardial infarction.

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    The prognostic value of stress electrocardiogram and thallium-201 stress myocardial scintigraphy was analyzed in 224 patients 3 months after a myocardial infarction; both techniques allowed an adequate stratification based on the presence of ST depression or multivessel disease. Combining stress electrocardiogram and stress myocardial scintigraphy data improved the prognostic ability, particularly in patients who associated multivessel disease and ST depression

    Prognostic significance of electrocardiographic findings in angina at rest. Therapeutic implications.

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    Ninety-five patients with angina at rest were observed in the coronary care unit. Eighty-one per cent presented concomitantly or had previously presented some other manifestations of coronary artery disease. These patients were divided into two subgroups. In subgroup 1 (40 patients), episodes of non-exertional angina were associated with a pattern of hyperacute subepicardial injury and, frequently, with ventricular arrhythmias. In subgroup 2 (55 patients), the episodes of angina at rest were attended by horizontal ST depression, isolated T wave inversion, or trivial ST-T changes. Coronary angiographic findings were similar in both subgroups. Symptoms regressed in only 9% of patients in subgroup 1 while they were receiving beta-receptor antagonists, whereas amiodarone alone or amiodarone with nifedipine was successful in 58%. Of these patients, 25% developed a myocardial infarction shortly after admission. In subgroup 2 patients, beta-blockers were successful in 61%. Amiodarone isolated or associated with nifedipine was successful in 55% of the patients in whom it was tried. Only 5% of patients in this subgroup developed a myocardial infarction during their hospital stay. It is concluded that: (1) observation of the electrocardiogram during spontaneous angina in patients with known atherosclerotic coronary heart disease may be of prognostic significance and may influence therapeutic decision. (2) Amiodarone by virtue of its anginal and antiarrhythmic properties may be particularly useful in the treatment of non-exertional angina

    Active components from Cassia abbreviata prevent hiv-1 entry by distinct mechanisms of action

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    Cassia abbreviataC. abbreviata is widely used in Sub-Saharan Africa for treating many diseases, including HIV-1 infection. We have recently described the chemical structures of 28 compounds isolated from an alcoholic crude extract of barks and roots ofC. abbreviata, and showed that six bioactive compounds inhibit HIV-1 infection. In the present study, we demonstrate that the six compounds block HIV-1 entry into cells: oleanolic acid, palmitic acid, taxifolin, piceatannol, guibourtinidol-(4α→8)-epiafzelechin, and a novel compound named as cassiabrevone. We report, for the first time, that guibourtinidol-(4α→8)-epiafzelechin and cassiabrevone inhibit HIV-1 entry (IC50 of 42.47 µM and 30.96 µM, respectively), as well as that piceatannol interacts with cellular membranes. Piceatannol inhibits HIV-1 infection in a dual-chamber assay mimicking the female genital tract, as well as HSV infection, emphasizing its potential as a microbicide. Structure-activity relationships (SAR) showed that pharmacophoric groups of piceatannol are strictly required to inhibit HIV-1 entry. By a ligand-based in silico study, we speculated that piceatannol and norartocarpetin may have a very similar mechanism of action and efficacy because of the highly comparable pharmacophoric and 3D space, while guibourtinidol-(4α→8)-epiafzelechin and cassiabrevone may display a different mechanism. We finally show that cassiabrevone plays a major role of the crude extract of CA by blocking the binding activity of HIV-1 gp120 and CD4

    New paradigms in chemokine receptor signal transduction: Moving beyond the two-site model.

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    Chemokine receptor (CKR) signaling forms the basis of essential immune cellular functions, and dysregulated CKR signaling underpins numerous disease processes of the immune system and beyond. CKRs, which belong to the seven transmembrane domain receptor (7TMR) superfamily, initiate signaling upon binding of endogenous, secreted chemokine ligands. Chemokine-CKR interactions are traditionally described by a two-step/two-site mechanism, in which the CKR N-terminus recognizes the chemokine globular core (i.e. site 1 interaction), followed by activation when the unstructured chemokine N-terminus is inserted into the receptor TM bundle (i.e. site 2 interaction). Several recent studies challenge the structural independence of sites 1 and 2 by demonstrating physical and allosteric links between these supposedly separate sites. Others contest the functional independence of these sites, identifying nuanced roles for site 1 and other interactions in CKR activation. These developments emerge within a rapidly changing landscape in which CKR signaling is influenced by receptor PTMs, chemokine and CKR dimerization, and endogenous non-chemokine ligands. Simultaneous advances in the structural and functional characterization of 7TMR biased signaling have altered how we understand promiscuous chemokine-CKR interactions. In this review, we explore new paradigms in CKR signal transduction by considering studies that depict a more intricate architecture governing the consequences of chemokine-CKR interactions
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