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Biomedical subjects

R T Lee

Publications and source records attributed to R T Lee.

At least 109 records · Page 6Linked to original sources
PubMed1996

Circumferential stress and matrix metalloproteinase 1 in human coronary atherosclerosis. Implications for plaque rupture.

Atherosclerotic plaque rupture may occur when regions of weakened extracellular matrix are subjected to increased mechanical stresses. Since collagen is a major determinant of extracellular matrix strength, enzymes that degrade collagen may play an important role in destabilizing the atherosclerotic lesion. To test the hypothesis that matrix metalloproteinase 1 (interstitial collagenase, or MMP-1), which initiates degradation of fibrillar collagens, colocalizes with increased stress in the fibrous cap of the atherosclerotic lesion, 12 unruptured human coronary lesions were studied. Finite-element analysis was used to determine the distribution of stress in the lesion, with estimates of material properties from previous measurements of human tissues. A computerized image analysis system was used to determine the distribution of immunoreactive MMP-1 within the fibrous tissue of the lesion. There was a significant correlation between immunoreactive MMP-1 and circumferential tensile stress in the fibrous cap within a given lesion (median Spearman rank correlation coefficient, .36; interquartile range, -.02 to .81; P < .02). Within a given lesion, the highest-stress region had twofold greater MMP-1 expression than the lowest-stress regions. In unruptured human atherosclerotic coronary lesions, overexpression of MMP-1 is associated with increased circumferential stress in the fibrous plaque. Degradation and weakening of the collagenous extracellular matrix at these critical high-stress regions may play a role in the pathogenesis of plaque rupture and acute ischemic syndromes.

Collagenases↗
PubMed1996

Regulation of matrix metalloproteinases and plasminogen activator inhibitor-1 synthesis by plasminogen in cultured human vascular smooth muscle cells.

Plasmin and matrix metalloproteinases (MMPs) both participate in extracellular matrix remodeling. This study examined the effects of tumor necrosis factor-alpha (TNF-alpha) and plasminogen on collagenase, stromelysin, and plasminogen activator inhibitor-1 (PAI-1) synthesis of collagenase and stromelysin, which remained predominantly in proenzyme forms, as determined by Western analysis of culture media. In contrast, plasminogen and plasmin not only increased secretion of MMPs but also induced cleavage to their active forms. The serine protease inhibitor aprotinin inhibited this activation of MMPs by plasminogen and plasmin. TNF-alpha reduced plasminogen-induced activation of MMPs, suggesting induction of an inhibitor or plasmin generation, such as PAI-1. Enzyme-linked immunosorbent assay of culture media showed that TNF-alpha (10 ng/mL) increased PAI-1 secretion by 4.2 fold compared with control (105.5 +/- 9.6) versus 24.9 +/- 1.7 ng/mL, n = 3). Surprisingly plasminogen also increased PAI-1 secretion by vascular SMCs (3.6-fold over control). These results demonstrate coordination of cytokines and serine proteases in regulating MMP secretion and activation. In addition, the induction of PAI-1 by TNF-alpha and plasminogen suggests a negative feedback mechanisms limit both plasmin-mediated and MMP-mediated matrix degradation.

Cells, Cultured↗
PubMed1995

High affinity binding of the Entamoeba histolytica lectin to polyvalent N-acetylgalactosaminides.

Entamoeba histolytica trophozoites initiate pathogenic colonization by adherence to host glycoconjugates via an amebic surface lectin which binds to galactose (Gal) and N-acetylgalactosamine (GalNAc) residues. Monovalent and multivalent carbohydrate ligands were screened for inhibition of E. histolytica lectin-mediated human red cell hemagglutination, revealing that: (i) the synthetic multivalent neoglycoprotein GalNAc39BSA (having an average of 39 GalNAc residues linked to bovine serum albumin) was 140,000-fold more potent an inhibitor than monovalent GalNAc and 500,000-fold more potent than monovalent Gal; and (ii) small synthetic multivalent ligands which bind with high affinity to the mammalian hepatic Gal/GalNAc lectin do not bind with high affinity to the E. histolytica lectin. Radioligand binding studies revealed saturable binding of 125I-GalNAc39BSA to E. histolytica membranes (KD = 10 +/- 3 nM, Bmax = 0.9 +/- 0.08 pmol/mg membrane protein). Maximal binding required the presence of calcium chloride (300 microM) or sodium chloride (50 mM), and had a broad pH maximum (pH 6-9). GalNAc39BSA was 200,000-fold more potent than monovalent GalNAc in blocking radio-ligand binding. Among synthetic saccharide-derivatized linear polymers, the GalNAc beta and GalNAc alpha 3Gal beta derivatives were the most potent, with GalNAc alpha and GalNAc alpha 3(Fuc alpha 2)Gal beta derivatives much weaker. The data support a model in which a unique pattern of spaced multiple GalNAc residues are the highest affinity targets for the E. histolytica lectin.

Acetylgalactosamine↗
PubMed1995

The differences in structural specificity for recognition and binding between asialoglycoprotein receptors of liver and macrophages.

The Gal/GalNAc-specific lectin on the surface of rat peritoneal macrophages (macrophage asialoglycoprotein binding protein, M-ASGP-BP), which consists of a single polypeptide chain of 42 kDa, can form a homo-oligomeric receptor exhibiting high affinity for asialoorosomucoid (ASOR) [Ozaki K., Ii M., Itoh N., Kawasaki T. (1992) J Biol Chem 267: 9229-35]. In this study, the binding affinity of M-ASGP-BP was studied by using a series of synthetic or natural glycosides as inhibitors of 125I-ASOR binding to recombinant M-ASGP-BP expressed on COS-1 cells (rM-ASGP-BP), and the results were compared with those of human hepatic lectin (HHL) on Hep G2 cells. Clustering of multiple Gal (or GalNAc) residues increased the binding affinity to M-ASGP-BP as well as to HHL. In contrast to HHL and other mammalian hepatic lectins, rM-ASGP-BP bound Gal residues tighter than GalNAc residues. A galactose-terminated triantennary N-glycoside, having one N-acetyl-lactosamine unit on the 6 branch and two N-acetyl-lactosamine units on the 3 branch of the trimannosyl core structure, showed affinity enhancement of approximately 10(5) over a monovalent ligand for HHL, while the same glycopeptide showed enhancement of about 2000-fold for rM-ASGP-BP. These results suggest that spatial arrangements of sugar combining sites and subunit organization of macrophage and hepatic lectins are different.

Animals↗
PubMed1995

Cytokines regulate vascular functions related to stability of the atherosclerotic plaque.

The cytokines are multipotent mediators of inflammation and immunity that can affect key functions of vascular wall cells. Growing evidence suggests that cytokines participate as autocrine or paracrine mediators in atherogenesis, as cells in lesions can both produce and respond to these mediators. The functions of vascular wall cells regulated by cytokines may influence lesion initiation, progression, or complication. For example, cytokines can regulate the expression of adhesion molecules crucial to the recruitment of leukocytes to lesions, including vascular cell adhesion molecule-1 (VCAM-1). Cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) can regulate the production of monocyte chemoattractant protein-1 (MCP-1), a potential signal for directed migration of monocytes into the intima. Cytokines can also regulate genes that encode other growth factors and cytokines themselves. TNF-alpha can induce IL-1 mRNA in human endothelial (EC) and smooth-muscle cells (SMC). IL-1 and TNF-alpha can augment the production by vascular cells of macrophage-colony stimulating factor (M-CSF), which may promote growth and activation of mononuclear phagocytes. Cytokines can exert both pro-and antiatherogenic actions. Activated T cells in human atheroma may secrete the lymphokine IFN-gamma, an inhibitor of SMC proliferation. Cytokines influence vasomotor tone in arteries, e.g., by inducing a form of nitric oxide synthase, the enzyme that synthesizes the vasodilatory nitric oxide radical. The cytokines also modulate endothelial functions that govern the formation and stability of blood thrombi. Finally, in the late stages of the disease, matrix metalloproteinases derived from macrophages or smooth-muscle cells themselves may contribute to weakening of the fibrous cap in the vulnerable shoulder area, promoting plaque rupture and occlusive thrombosis, culminating in the dramatic clinical manifestations of atherosclerosis, including myocardial infarction and stroke. Thus, cytokines can influence multiple aspects of atherogenesis and provide new and interesting targets for therapeutic intervention.

Animals↗
PubMed1995

Human vascular smooth muscle cell-monocyte interactions and metalloproteinase secretion in culture.

Degradation of the atherosclerotic plaque extracellular matrix could destabilize the lesion, rendering it more prone to rupture. Both macrophages and vascular smooth muscle cells (SMCs) are potential sources of matrix metalloproteinases (MMPs), secreted enzymes that can digest vascular matrix. We explored interactions between human vascular SMCs and human monocytes that result in the secretion of interstitial collagenase (MMP-1) and stromelysin (MMP-3). Monocytes alone or those treated with SMC-conditioned media did not secrete these metalloproteinases as detectable by Western blot analysis. SMCs increased secretion of both MMP-1 and MMP-3 greater than 20-fold when cocultured with monocytes or when treated with monocyte-conditioned media. Addition of macrophage colony stimulating factor (< or = 1000 U/mL) to cocultures of monocytes and SMCs did not affect metalloproteinase secretion. Recombinant interleukin (IL)-1 receptor antagonist inhibited MMP-1 and MMP-3 induction in SMC cultures treated with monocyte-conditioned media (94% and 96% reduction, respectively), while a neutralizing antibody to tumor necrosis factor-alpha had no significant effect on metalloproteinase secretion. In contrast to the induction by monocyte-conditioned media of MMP-1 and MMP-3 secretion by SMCs, monocyte-conditioned media did not increase secretion of 72-kD gelatinase (MMP-2). Thus, monocytes induce MMP-1 and MMP-3 secretion by vascular SMCs through an IL-1-dependent mechanism. This response of SMCs to a defined macrophage product may contribute to plaque destabilization by mononuclear phagocytes in the lesion.

Cells, Cultured↗
PubMed1995

Integrin-mediated collagen matrix reorganization by cultured human vascular smooth muscle cells.

Vascular smooth muscle cells perform the important function of modulation of vascular extracellular matrix. Because integrins mediate many cell-matrix interactions, the role of integrins in reorganization of collagen by cultured human vascular smooth muscle cells was studied. Immunoprecipitation demonstrated that human vascular smooth muscle cells express multiple beta 1 integrins. Monoclonal antibody A2-IIE10 (a blocking anti-alpha 2 antibody) inhibited adhesion of smooth muscle cells to collagen by 31%. The blocking anti-alpha 1 antibody 1B3.1 inhibited adhesion by 40%, whereas a blocking anti-alpha 3 antibody had no effect on adhesion. When 1B3.1 and A2-IIE10 were both used, a 79% reduction in adhesion was observed, indicating that active alpha 1 and alpha 2 integrins cooperatively mediate adhesion. The blocking anti-beta 1 antibody Mab13 abolished smooth muscle cell-mediated gel contraction, and the alpha 2-blocking antibody A2-IIE10 had a dose-dependent partial inhibitory effect (37%). In contrast, blocking antibodies to alpha 1 and alpha 3 had no effect. When anti-alpha 1 (1B3.1) and anti-alpha 2 (A2-IIE10) monoclonal antibodies were combined, no synergistic effect on inhibition of gel contraction was observed. Surprisingly, collagen gel contraction was inhibited by 46% by an anti-beta 1 antibody (TS2/16) known for its stimulatory effect on cell adhesion. Thus, whereas alpha 1 beta 1 and alpha 2 beta 1 integrins both participate in adhesion of vascular smooth muscle cells to collagen, only alpha 2 beta 1 integrins mediate collagen reorganization. In addition, collagen reorganization appears to be a dynamic process, adversely affected by excessive adhesion strengthening.

Cell Adhesion↗
PubMed1995

Preoperative prediction of prosthetic aortic valve annulus diameter by two-dimensional echocardiography.

Echocardiography may allow preoperative selection of appropriately sized aortic homograft valves. This study compared measurement of aortic annulus diameter from the preoperative transthoracic two-dimensional echocardiogram with prosthetic valve annulus diameter in 178 consecutive patients under-going primary aortic valve replacement. Aortic annulus diameter was measured independently from the two-dimensional parasternal long axis view by two experienced observers blinded to the size of valve implanted. Mean annulus diameter from three end-diastolic frames was recorded. Of the 178 patients, 124 (70%) of Observer 1 measurements and 102 (57%) of Observer 2 measurements were within 2mm of valve annulus diameter (p < 0.0001 for both observers). Six percent of Observer 1 measurements and 12% of Observer 2 measurements were more than 4mm away from valve annulus diameter. The echocardiographic prediction of valve size corresponded to actual prosthetic valve annulus diameter in 69 patients (39%) for Observer 1 and 60 patients (34%) for Observer 2. The percentages of echocardiographic measurements within two millimeter of valve annulus diameter were significantly different for the two observers (p < 0.05). The percentages of echocardiographic measurements within two millimeter of valve annulus diameter in 39 patients without significant aortic valve calcification were not significantly different from the remaining 139 patients with calcified valves. The interobserver coefficient of variation was 6.2% and the intraobserver coefficient of variation was 4.3%. Although preoperative measurement of aortic annulus diameter from transthoracic echocardiography approximates prosthetic valve annulus diameter in the majority of patients undergoing primary aortic valve replacement, a significant minority of estimates may be inaccurate, even in the absence of heavy calcification.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Major lectin of alligator liver is specific for mannose/L-fucose.

We surveyed the calcium-requiring (C-type) lectins in alligator liver. The major lectin purified by affinity chromatography was termed alligator hepatic lectin (AHL) and was found to be specific for mannose/L-fucose. AHL contained approximately equal amounts of 21- and 23-kDa bands upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Binding characteristics of AHL were similar to those of hepatic lectins of other classes in that 1) only terminal monosaccharide was recognized, and 2) the affinity increased exponentially when neoglycoproteins containing increasing numbers of mannose or L-fucose were used as ligand. However, unlike mammalian and chicken hepatic lectins, which exist as hexamers in Triton-containing solutions, AHL was present mainly as monomers, although small amounts of dimer and higher oligomers were present in equilibrium. Mannose-binding proteins and mannose-specific lectins of macrophages bind N-acetylmannosamine, glucose, and N-acetylglucosamine in addition to mannose, indicating that the nature and orientation of the C-2 substituent are not important to these lectins. In contrast, AHL shows a strict requirement for the presence of an axial hydroxyl group at the C-2 position (i.e. mannose).

Alligators and Crocodiles↗
PubMed1994

The sugar-combining area of the galactose-specific toxic lectin of mistletoe extends beyond the terminal sugar residue: comparison with a homologous toxic lectin, ricin.

Viscumin (the major lectin of mistletoe extract), also known as ML-1, and ricin (RCA II) belong to a group of heterodimeric toxic lectins composed of an A chain, which inhibits protein synthesis, and a B chain, which mediates entry into the cell in a galactose-specific manner. Although most of the binding force for the association of viscumin with galactose-containing ligands is generated by the nonreducing terminal galactose residue, a particular hydroxyl group on the penultimate sugar also appears to participate in the binding, suggesting that viscumin has an extended combining site. In this paper, we give further examples of affinity enhancement by the hydroxyl group situated on the penultimate sugar next to the glycosidic linkage of the terminal galactose. The structure with highest affinity for viscumin thus far discovered is beta-D-Gal-(1-->2)-beta-D-Gal. In contrast to viscumin, ricin does not have this extended binding area, as none of the disaccharides tested exhibited significant affinity enhancement.

Carbohydrate Conformation↗
PubMed1994

Synthesis of allyl 3-deoxy- and 4-deoxy-beta-D-galactopyranoside and simultaneous preparations of Gal(1-->2)- and Gal(1-->3)-linked disaccharide glycosides.

Syntheses of galactose derivatives that are useful in probing the binding specificity of galactose-specific lectins are reported. These include allyl 3-deoxy- and 4-deoxy-beta-D-xylo-hexopyranoside and several disaccharide glycosides having Gal(1-->2) and Gal(1-->3) linkages. The beta-linked Gal disaccharide isomers were produced using 2,3,4,6-tetra-O-acetyl-alpha-D-galactopyranosyl bromide as glycosyl donor and the 4,6-O-benzylidene derivatives of allyl beta-D-galactopyranoside, alpha-D-glucopyranoside, alpha-D-mannopyranoside, and 2-acetamido-2-deoxy-alpha-D-galactopyranoside as acceptors. Only the Gal(1-->3)-linked disaccharide was obtained when the benzylidene derivatives of the mannopyranoside and 2-acetamido-2-deoxygalactopyranoside were used. Attempts at the preparation of Gal(alpha, 1-->2)Gal and Gal(alpha, 1-->3)Gal disaccharide glycosides were made using the same strategy, but employing the 1-trichloro-acetimidate or 1-N-methylacetimidate of 2,3,4,6-tetra-O-benzyl-D-galactopyranose as the glycosyl donor. The latter imidate produced a mixture of Gal(alpha, 1-->2)Gal and Gal(alpha, 1-->3)Gal derivatives as major products, but the former gave the Gal(beta, 1-->2)Gal isomer as the major product.

Carbohydrate Sequence↗
PubMed1994

Prognostic significance of right ventricular hypokinesis and perfusion lung scan defects in pulmonary embolism.

We studied the relation between right ventricular (RV) hypokinesis on echocardiography and defects on the initial perfusion lung scan among 90 hemodynamically stable patients with pulmonary embolism (PE). Of the 90, 38 had qualitative evidence of RV hypokinesis, with a mean RV end-diastolic area significantly larger than those with normal RV wall motion (40.0 +/- 10.2 cm2 vs 20.1 +/- 6.4 cm2; p < 0.001). The degree of the perfusion defect was greater in those patients with baseline RV hypokinesis (54% +/- 16% of the lung nonperfused) than in those patients with normal RV wall motion at baseline (30% +/- 18% nonperfused lung; p < 0.001). Receiver operating characteristic curve analysis showed that a perfusion lung scan defect score of 0.3 (i.e., 30% of the lung nonperfused) had a 92% sensitivity for predicting RV hypokinesis and carried a relative risk for observing RV hypokinesis of 6.8 times greater than among those patients with a perfusion scan score of < 0.3. Considering that all patients with recurrent symptomatic PE were in the subgroup with RV hypokinesis (13% vs 0% for those with normal RV wall motion; p = 0.01), a strategy of performing echocardiography in those patients with a perfusion scan defect score of > or = 0.3 appears to identify patients at increased risk for recurrent PE.

Chi-Square Distribution↗
PubMed1994

Diagnosis of cardiac tamponade after cardiac surgery: relative value of clinical, echocardiographic, and hemodynamic signs.

Early detection and treatment of cardiac tamponade is crucial in management of patients after cardiac surgery. Because of the atypical features of this condition and paucity of data on relative frequency of different signs, we evaluated the sensitivity of various clinical, echocardiographic, and hemodynamic signs. We retrospectively evaluated the relative frequency of clinical, echocardiographic, and hemodynamic signs in 29 patients with cardiac tamponade after cardiac surgery. In our study 66% had a localized, posterior pericardial effusion, and the other 34% had circumferential pericardial effusion. In the whole group 24% of patients had hypotension, and pulsus paradoxus was noted in 48%, right atrial collapse in 34%, right ventricular diastolic collapse in 27%, left ventricular diastolic collapse in 65%, and left atrial collapse in 13%. Elevation with equalization of pressures was noted in 81% patients. In the patient group with circumferential pericardial effusion and cardiac tamponade 40% patients were hypotensive and 50% patients had pulsus paradoxus. RA collapse was present in 70%, RV diastolic collapse in 70%, and LV diastolic collapse in 20%. Elevated diastolic pressures with equalization of these pressures was present in 71%. In the group with regional pericardial effusion and cardiac tamponade hypotension was present in 16% and pulsus paradoxus in 47%. RA collapse was present in 16%, RV diastolic collapse in 5%, LV diastolic collapse in 89%, and LA collapse in 21% of the patients with regional tamponade. Elevated diastolic pressures with equalization of these pressures was noted in 86% of the patients. Our observations indicate that among patients who have undergone cardiac surgery the presentation of cardiac tamponade is usually atypical.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Static circumferential tangential modulus of human atherosclerotic tissue.

The mechanical properties of atherosclerotic plaque may be of critical importance to the processes of plaque rupture, the most common antecedent of myocardial infarction. To investigate the effects of plaque structure and applied tensile stress on the static circumferential tangential modulus of atherosclerotic plaque, the stress-strain behavior of 26 human aortic intimal plaques was studied. Intimal plaques were collected during routine autopsies of 21 patients from the abdominal (n = 19) and thoracic (n = 2) aorta and were classified by histological analysis as cellular (n = 12), hypocellular (n = 9), and calcified (n = 5). At a physiologic applied circumferential tensile stress of 25 kPa, the tangential moduli of cellular, hypocellular, and calcified specimens were 927 +/- 468 kPa, 2312 +/- 2180 kPa, and 1466 +/- 1284 kPa, respectively. There was a nonsignificant difference in tangential modulus at 25 kPa stress between specimens classified as cellular and hypocellular (p = 0.098), cellular and calcified (p = 0.410), and hypocellular and calcified (p = 0.380). This is in marked contrast to the previously measured radial compressive behavior of plaque tissue, which showed that cellular, hypocellular, and calcified plaques were significantly different in their modulus. In tension, all 26 plaques tested demonstrated a statistically significant increase in tangential modulus with increasing applied circumferential stress. We conclude that the static circumferential tangential modulus of atherosclerotic plaque, unlike its radial compressive modulus, is not significantly affected by the degree of cellularity and calcification determined by histological characterization.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

High stress regions in saphenous vein bypass graft atherosclerotic lesions.

OBJECTIVES: Our aim was to test the hypothesis that maximal stresses in saphenous vein atherosclerotic stenoses are greater than those in native coronary artery stenoses. BACKGROUND: The patency of coronary artery saphenous vein bypass grafts decreases with time, usually because of thrombosis. Plaque rupture has been described as one mechanism of vein graft thrombosis. METHODS: Twenty-six nonruptured human lesions were studied. Fourteen lesions were from native coronary arteries, and 12 were from saphenous vein bypass grafts placed a mean +/- SD of 9.8 +/- 3.3 years before pathologic study. The finite element method was used to determine the distribution of stress in the lesion, using estimates of material properties from previous measurements of human tissues. RESULTS: Maximal circumferential stresses were significantly higher in the saphenous vein lesions (median 352 kPa [interquartile range 161 to 475]) than in the coronary artery lesions (median 104 kPa [interquartile range 75 to 185]) (p = 0.05). Thin-walled cylinder formulations predict that stresses are proportional to the radius of the vessel and inversely proportional to the minimal wall thickness. In this study, there was a good correlation between the maximal stress in the 26 lesions and the ratio of the square root of lumen area to minimal fibrous cap thickness (r = 0.83, p < 0.001). CONCLUSIONS: Maximal circumferential tensile stresses in saphenous vein bypass graft stenoses are higher than in native coronary artery atherosclerotic stenoses. These data suggest that strategies that decrease stresses in bypass graft atherosclerotic lesions, such as prevention of lipid accumulation, could reduce the probability of plaque rupture in bypass grafts.

Arteriosclerosis↗
PubMed1994

Vascular mechanics for the cardiologist.

Many common problems in clinical cardiology are due to disturbances in vascular mechanics. The terminology and basic principles of vascular mechanics, including fundamentals of the relation of stress and strain, are described in this review. Approaches to measuring vessel wall stiffness and the mechanical basis for vascular catastrophes are introduced.

Biomechanical Phenomena↗
PubMed1994

Echocardiographic correlates of survival in patients with chest pain.

OBJECTIVES: This study sought to identify echocardiographic predictors of survival in patients with chest pain and to assess the utility of qualitative echocardiographic data in the prognostic stratification of this cohort. BACKGROUND: The potential usefulness of echocardiographic data in prognostic stratification of patients with acute chest pain is unclear, in part because of the qualitative nature of routinely available echocardiographic readings. METHODS: The study group comprised 513 patients who underwent transthoracic two-dimensional and Doppler echocardiography within 1 month of emergency department visits for acute chest pain. Clinical and electrocardiographic (ECG) data were recorded for these patients at the time of their initial evaluations, and echocardiographic data were subsequently obtained from the official hospital reports. Follow-up survival rate data were obtained from medical records or the Massachusetts Bureau of Vital Statistics. RESULTS: A mean of 28.5 months after the index visit, 102 patients (20%) had died, including 58 (57%) for whom the primary cause of death was cardiovascular. In analysis of routinely available qualitative echocardiographic data, left ventricular size and function, the presence of regional wall motion abnormalities, mitral regurgitation and structural abnormalities of the mitral valve were significant univariate correlates of both overall mortality and death from cardiovascular causes. Severe left ventricular dysfunction (adjusted rate ratio 3.8, 95% confidence interval [CI] 1.9-7.5) and moderate or severe mitral regurgitation (adjusted rate ratio 2.4, 95% CI 1.5-3.7) were independent predictors of mortality in a multivariate Cox regression analysis that adjusted for clinical and ECG variables. Moderate or severe left ventricular dysfunction and mitral regurgitation were predictors of mortality in the subset of patients without acute myocardial infarction. CONCLUSIONS: Qualitative echocardiographic reports of left ventricular dysfunction and mitral regurgitation were independent correlates of prognosis in patients with acute chest pain, including patients without acute myocardial infarction. Further data are needed to assess the generalizability of these findings and the implications for use of this diagnostic technology.

Acute Disease↗