Biomedical subjects

J G Nelson

Publications and source records attributed to J G Nelson.

At least 19 recordsLinked to original sources

PubMed1998

Platelet-derived growth factor inhibits insulin stimulation of insulin receptor substrate-1-associated phosphatidylinositol 3-kinase in 3T3-L1 adipocytes without affecting glucose transport.

Phosphatidylinositol 3-kinase (PI3K) activation is necessary for insulin-responsive glucose transporter (GLUT4) translocation and glucose transport. Insulin and platelet-derived growth factor (PDGF) stimulate PI3K activity in 3T3-L1 adipocytes, but only insulin is capable of stimulating GLUT4 translocation and glucose transport. We found that PDGF causes serine/threonine phosphorylation of insulin receptor substrate 1 (IRS-1) in 3T3-L1 cells, measured by altered mobility on SDS-polyacrylamide gel, and this leads to a decrease in insulin-stimulated tyrosine phosphorylation of IRS-1. The PI3K inhibitors wortmannin and LY294002 inhibit the PDGF-induced phosphorylation of IRS-1, whereas the MEK inhibitor PD98059 was without a major effect. PDGF pretreatment for 60-90 min led to a marked 80-90% reduction in insulin stimulatable phosphotyrosine and IRS-1-associated PI3K activity. We examined the functional consequences of this decrease in IRS-1-associated PI3K activity. Interestingly, insulin stimulation of GLUT4 translocation and glucose transport was unaffected by 60-90 min of PDGF preincubation. Furthermore, insulin activation of Akt and p70(s6kinase), kinases downstream of PI3K, was unaffected by PDGF pretreatment. Wortmannin was capable of blocking these insulin actions following PDGF pretreatment, suggesting that PI3K was still necessary for these effects. In conclusion, 1) PDGF causes serine/threonine phosphorylation of IRS-1, and PI3K, or a kinase downstream of PI3K, mediates this phosphorylation. 2) This PDGF-induced phosphorylation of IRS-1 leads to a significant decrease in insulin-stimulated PI3K activity. 3) PDGF has no effect on insulin stimulation of Akt, p70(s6kinase), GLUT4 translocation, or glucose transport. 4) This suggests the existence of an IRS-1-independent pathway leading to the activation of PI3K, Akt, and p70(s6kinase); GLUT4 translocation; and glucose transport.

3T3 Cells↗

PubMed1998

Association of the insulin receptor with phospholipase C-gamma (PLCgamma) in 3T3-L1 adipocytes suggests a role for PLCgamma in metabolic signaling by insulin.

Phospholipase C-gamma (PLCgamma) is the isozyme of PLC phosphorylated by multiple tyrosine kinases including epidermal growth factor, platelet-derived growth factor, nerve growth factor receptors, and nonreceptor tyrosine kinases. In this paper, we present evidence for the association of the insulin receptor (IR) with PLCgamma. Precipitation of the IR with glutathione S-transferase fusion proteins derived from PLCgamma and coimmunoprecipitation of the IR and PLCgamma were observed in 3T3-L1 adipocytes. To determine the functional significance of the interaction of PLCgamma and the IR, we used a specific inhibitor of PLC, U73122, or microinjection of SH2 domain glutathione S-transferase fusion proteins derived from PLCgamma to block insulin-stimulated GLUT4 translocation. We demonstrate inhibition of 2-deoxyglucose uptake in isolated primary rat adipocytes and 3T3-L1 adipocytes pretreated with U73122. Antilipolytic effect of insulin in 3T3-L1 adipocytes is unaffected by U73122. U73122 selectively inhibits mitogen-activated protein kinase, leaving the Akt and p70 S6 kinase pathways unperturbed. We conclude that PLCgamma is an active participant in metabolic and perhaps mitogenic signaling by the insulin receptor in 3T3-L1 adipocytes.

3T3 Cells↗

PubMed1998

Ligand-independent GLUT4 translocation induced by guanosine 5'-O-(3-thiotriphosphate) involves tyrosine phosphorylation.

To delineate the signaling pathway leading to glucose transport protein (GLUT4) translocation, we examined the effect of microinjection of the nonhydrolyzable GTP analog, guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS), into 3T3-L1 adipocytes. Thirty minutes after the injection of 5 mM GTPgammaS, 40% of injected cells displayed surface GLUT4 staining indicative of GLUT4 translocation compared with 55% for insulin-treated cells and 10% in control IgG-injected cells. Treatment of the cells with the phosphatidylinositol 3-kinase inhibitor wortmannin or coinjection of GST-p85 SH2 fusion protein had no effect on GTPgammaS-mediated GLUT4 translocation. On the other hand, coinjection of antiphosphotyrosine antibodies (PY20) blocked GTPgammaS-induced GLUT4 translocation by 65%. Furthermore, microinjection of GTPgammaS led to the appearance of tyrosine-phosphorylated proteins around the periphery of the plasma membrane, as observed by immunostaining with PY20. Treatment of the cells with insulin caused a similar phosphotyrosine-staining pattern. Electroporation of GTPgammaS stimulated 2-deoxy-D-glucose transport to 70% of the extent of insulin stimulation. In addition, immunoblotting with phosphotyrosine antibodies after electroporation of GTPgammaS revealed increased tyrosine phosphorylation of several proteins, including 70- to 80-kDa and 120- to 130-kDa species. These results suggest that GTPgammaS acts upon a signaling pathway either downstream of or parallel to activation of phosphatidylinositol 3-kinase and that this pathway involves tyrosine-phosphorylated protein(s).

3T3 Cells↗

PubMed1997

The small guanosine triphosphate-binding protein Rab4 is involved in insulin-induced GLUT4 translocation and actin filament rearrangement in 3T3-L1 cells.

Insulin's stimulation of glucose transport involves the translocation of vesicles containing the glucose transporter GLUT4 to the plasma membrane. Small GTP-binding proteins have been implicated in the regulation of vesicular traffic. We studied the effects of microinjection of wild-type Rab4 glutathione S-transferase fusion protein (WT Rab4), a GTP-binding defective mutant (Rab4 N121I), a guanosine triphosphatase-defective mutant (Rab4 Q67L), and a Rab4 antibody on insulin-induced GLUT4 translocation in 3T3-L1 adipocytes. Microinjection of Rab4 N121I and Rab4 antibodies had no effect on basal GLUT4 staining, but inhibited insulin-induced GLUT4 translocation by 50% compared with that in control IgG-injected cells. WT Rab4 and Rab4 Q67L microinjection had no effect on either basal or insulin-induced GLUT4 translocation. Premixing and coinjection of the Rab4 antibody with WT Rab4 almost completely abolished its inhibitory effect on insulin-induced GLUT4 translocation. In contrast, microinjection of an antibody directed against the highly conserved region of Rab3 proteins had no effect on insulin-induced GLUT4. These results point to a direct role of Rab4 in insulin-induced GLUT4 translocation, and that this effect is dependent on nucleotide binding to the protein. We also studied the effect of microinjection of the same proteins on insulin-induced actin filament rearrangement (membrane ruffling) in the same cell line. Microinjection of Rab4 N121I and Rab4 antibodies inhibited insulin-induced membrane ruffling by 40%, whereas WT Rab4 or a Rab3 antibody injection had no effect on cytoskeletal rearrangement. In summary, 1) Rab4 is a necessary component of the insulin/GLUT4 translocation signaling pathway; 2) the function of Rab4 in this pathway requires GTP binding; 3) Rab4 also participates in the process of insulin-induced membrane ruffling; and 4) Rab3 proteins do not seem to be involved in these processes.

3T3 Cells↗

PubMed1996

Evidence for an insulin receptor substrate 1 independent insulin signaling pathway that mediates insulin-responsive glucose transporter (GLUT4) translocation.

Interaction of the activated insulin receptor (IR) with its substrate, insulin receptor substrate 1 (IRS-1), via the phosphotyrosine binding domain of IRS-1 and the NPXY motif centered at phosphotyrosine 960 of the IR, is important for IRS-1 phosphorylation. We investigated the role of this interaction in the insulin signaling pathway that stimulates glucose transport. Utilizing microinjection of competitive inhibitory reagents in 3T3-L1 adipocytes, we have found that disruption of the IR/IRS-1 interaction has no effect upon translocation of the insulin-responsive glucose transporter (GLUT4). The activity of these reagents was demonstrated by their ability to block insulin stimulation of two distinct insulin bioeffects, membrane ruffling and mitogenesis, in 3T3-L1 adipocytes and insulin-responsive rat 1 fibroblasts. These data suggest that phosphorylated IRS-1 is not an essential component of the metabolic insulin signaling pathway that leads to GLUT4 translocation, yet it appears to be required for other insulin bioeffects.

3T3 Cells↗

PubMed1995

Insulin-stimulated GLUT4 translocation is mediated by a divergent intracellular signaling pathway.

Insulin stimulates glucose transport largely by mediating translocation of the insulin-sensitive glucose transporter (GLUT4) from an intracellular compartment to the plasma membrane. Using single cell microinjection of 3T3-L1 adipocytes, coupled with immunofluorescence detection of GLUT4 proteins, we have determined that inhibition of endogenous p21ras or injection of oncogenic p21ras has no effect on insulin-stimulated GLUT4 translocation. On the other hand, microinjection of anti-phosphotyrosine antibodies or inhibition of endogenous phosphatidylinositol 3-kinase by microinjection of a GST-p85 SH2 fusion protein markedly inhibits this biologic effect of insulin. These data suggest that the p21ras/mitogen-activated protein kinase pathway is not involved in this metabolic effect of insulin, whereas tyrosine phosphorylation and stimulation of phosphatidylinositol 3-kinase activity are critical components of this signaling pathway.

1-Methyl-3-isobutylxanthine↗

PubMed1987

A Podospora anserina longevity mutant with a temperature-sensitive phenotype for senescence.

A Podospora anserina longevity mutant was identified with a temperature-sensitive phenotype for senescence. This mutant, termed TS1, grew for over 3 m at 27 degrees C, but when shifted to 34 degrees C, it underwent senescence between 10 and 18 cm. A previously described senescence-associated plasmid, alpha senDNA, derived from the mitochondrial genome, was not detected in TS1 at 27 degrees C but was present in senescent cultures at 34 degrees C. A similar result was observed in progeny strains obtained by crossing the TS1 mutant with a wild-type strain. Other mitochondrial excision-amplification DNAs in addition to alpha senDNA were also observed in the senescent cultures. Most were derived from a specific region of the mitochondrial genome. These results provide evidence that alpha senDNA is involved in TS1 senescence and suggest that this plasmid may play a role in the formation of other mitochondrial excision-amplification plasmids.

Aging↗

PubMed1987

Hydrostatic theory and G protection using tilting aircrew seats.

A hydrostatic theory of blackout is generally supported in the acceleration literature, but there is disagreement as to the correct origin in the thorax for h, the hydrostatic distance to the eye. Our goal was to determine whether representative published data would preferentially support some particular origin for h. Based upon a reanalysis of published data (1) relating acceleration tolerance (T) to seat-back angle (theta), it was found that a simple hydrostatic model, with h measured from the aortic valve to the eye, yields an excellent fit. The nonlinear equation fitted was Ti = Tmin 1/cos(theta i-phi), where phi = correction to back angle. The value of phi derived from the 1975 data (1) (13.74 degrees) was the same as the independent estimate of phi for this same seat (13.06 degrees) derived from published values of h, which were measured by X-ray with h referenced to the aortic-valve and eye (2). The acceleration tolerance data for the other two seats of the 1984 study also strongly supported the model. Future studies should measure h (aortic valve-to-eye), use seat-back angles giving even spacing on a 1/h scale, and analyze data using the required nonlinear methods.

Acceleration↗

PubMed1986

Accurate noninvasive quantification of stenotic aortic valve area by Doppler echocardiography.

Laminar flow through a conduit is equal to the mean velocity times the cross-sectional area of the orifice. Therefore, volume is equal to the time-velocity integral multiplied by the cross-sectional area. In aortic stenosis, flow in the stenotic jet is laminar and the aortic valve area should be equal to the volume of blood ejected through the valve divided by the time-velocity integral of the aortic jet velocity recorded by continuous-wave Doppler echocardiography. To test whether this concept can be used to accurately determine aortic valve area noninvasively by the Doppler method, 39 patients (age 35 to 82 years, mean 63) underwent pulsed Doppler combined with two-dimensional echocardiography for measurement of stroke volume at the aortic, pulmonic, and mitral anulus as well as continuous-wave Doppler recording of the aortic jet. Aortic valve area determined at cardiac catheterization by the Gorlin equation ranged between 0.4 and 2.07 cm2 (mean 0.89 +/- 0.45). Doppler-derived valve area, determined with the stroke volume value from either the aortic, pulmonic, or mitral anulus, correlated well with the area determined at cardiac catheterization (r = .95, .97, and .96, respectively). A simplified method for measuring aortic valve area derived as the cross-sectional area of the aortic anulus times peak velocity just proximal to the aortic valve divided by peak aortic jet velocity correlated well with measurements obtained at cardiac catheterization (r = .94). An excellent separation between critical and noncritical aortic stenosis was seen using either one of the Doppler methods.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Value of multiple echocardiographic views in the evaluation of aortic stenosis in adults by continuous-wave Doppler.

Fifty-two adults referred for evaluation of aortic stenosis (AS) were studied using continuous-wave and pulsed Doppler echocardiography. Three windows were used to determine which approach (apical, right parasternal or suprasternal) yielded optimal results. Doppler-derived peak aortic valve gradients were compared with the peak gradients measured at cardiac catheterization in 23 patients. High-velocity jets were best recorded from the cardiac apex and less frequently from the right parasternal and suprasternal areas. However, gradients from the right parasternal area correlated best with cardiac catheterization findings, although recordings could be made from this window in only 49% of the patients. Velocities from the suprasternal window were significantly (p less than 0.01) lower than those from the apex or right parasternal areas. Gradient underestimation from the suprasternal window tended to increase with age of the patient (p less than 0.01). When the maximal Doppler derived gradient from any window was compared with catheterization measurements, the correlation coefficient was 0.86. Gradients derived from Doppler velocities accurately predicted severe (more than 50 mm Hg) gradients at catheterization. Thus, Doppler echocardiography is useful in evaluation of AS when several windows are used for optimal assessment of aortic valve gradient.

Adult↗

PubMed1985

Frequency of mitral valve dysfunction from mitral anular calcium as detected by Doppler echocardiography.

Doppler echocardiography is useful for detecting and quantifying mitral regurgitation (MR) and mitral stenosis (MS). To determine the prevalence of these abnormalities in patients with mitral anular calcium (MAC), 51 consecutive patients who had an echocardiographic diagnosis of MAC were examined by Doppler ultrasound. Transmitral flow was evaluated to determine the presence of MR or left ventricular inflow obstruction (MS) by continuous and pulsed-wave Doppler echocardiography. The severity of these hemodynamic abnormalities was quantitated by previously described techniques. Eleven patients (22%) had mild MR, 17 (33%) had moderate to severe MR and 4 (8%) had significant MS. Clinical findings such as a systolic murmur, evidence of congestive heart failure, and dyspnea on exertion were not helpful in distinguishing patients with no or mild MR from those who had moderate to severe MR. M-mode measured left atrial size was significantly larger (p less than 0.05) in patients with moderate to severe MR. This study suggests that MR is often associated with MAC, that MS is not a rare finding with MAC, and that Doppler echocardiography can quantitate these lesions in the elderly when symptoms are not specific and physical findings are inconclusive or absent.

Aged↗

PubMed1985

Clinical experience with two-dimensional echocardiography to guide endomyocardial biopsy.

Two-dimensional echocardiography was used to aid right ventricular endomyocardial biopsy during 163 procedures in 83 patients being evaluated for myocarditis, cardiac transplant rejection, or drug toxicity. Thirty procedures were performed using combined echocardiography and fluoroscopy and 133 using echocardiography alone. For 80 of the 83 patients (96%) the forceps could be adequately visualized entering the right atrium, crossing the tricuspid valve, and advancing to the right ventricular apex and free wall. The catheter could be guided to biopsy the septum and sample multiple, separate sites along the right ventricular walls. By opening the forceps prior to contact with the myocardium, the right ventricular free wall could be biopsied without perforation. We found two-dimensional echocardiography to be a useful and safe technique for forceps visualization and manipulation in the right ventricle.

Antibiotics, Antineoplastic↗

PubMed1984

Comparison of two-dimensional echocardiography with gated radionuclide ventriculography in the evaluation of global and regional left ventricular function in acute myocardial infarction.

Two-dimensional echocardiography and gated radionuclide ventriculography were performed in 93 patients (66 men, 27 women; mean age 61 years) with 95 episodes of acute myocardial infarction within 48 hours and at 10 days after infarction. Electrocardiographic sites of infarction were: 35 anterior, 49 inferoposterior and 11 nonlocalized. Abnormal motion of the anterior wall, septum or apex was seen in 97 and 100% of anterior infarctions by radionuclide ventriculography and echocardiography, respectively. Abnormal motion of an inferior or posterior wall segment was seen in 91% of inferoposterior infarctions by echocardiography versus 61% seen by radionuclide ventriculography. Ejection fractions determined by echocardiography and radionuclide ventriculography correlated well (r = 0.82) and did not change from the first 48 hours to 10 days after infarction (0.48 +/- 0.14). Similarly, wall motion score showed minimal change from the first 48 hours to 10 days. In-hospital mortality was 37 and 42% in patients with an ejection fraction of 0.35 or less by echocardiography and radionuclide ventriculography, respectively. No mortality was seen in patients with an ejection fraction above 0.40 by either test. The echocardiographic wall motion score was also predictive of mortality (40 versus 2%; score less than or equal to 0.50 versus greater than 0.50). The 1 year mortality rate in the 81 short-term survivors was 17%. Mortality was lowest in patients with an ejection fraction above 0.49 or wall motion score above (0.79 (2 to 5%) and worse in those with an ejection fraction below 0.36 or wall motion score below 0.51 (36 to 63%) by either technique. Thus in acute myocardial infarction, echocardiography and radionuclide ventriculography provide a comparable assessment of left ventricular function and wall motion in anterior infarction. Echocardiography appears more sensitive in detecting inferoposterior wall motion abnormalities. Both techniques are capable of identifying subgroups of patients with a high risk of death during the acute event and with an equally high mortality rate over a 1 year follow-up period.

Adult↗

PubMed1984

Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window.

Two methods of measuring stroke volume and cardiac output with pulsed Doppler two-dimensional echocardiography were developed and validated against the thermodilution technique in 39 patients, 33 of which were in an intensive care unit. With the use of the apical four-chamber view, a mitral inflow method combined the velocity of left ventricular inflow at the mitral anulus with the cross-sectional area of the anulus calculated from its diameter at middiastole (area = pi r2). From the apical five-chamber view a left ventricular outflow method combined the velocity of left ventricular outflow with the cross-sectional area of the aortic anulus calculated from its diameter during early systole (parasternal long-axis view). Measurements with the mitral inflow and left ventricular outflow methods were obtained in 35 of 39 (90%) and 39 of 39 (100%) patients, respectively. Validation of the mitral method excluded patients with mitral regurgitation (n = 11) and validation of the left ventricular outflow method excluded those with aortic regurgitation (n = 4). Good correlations were observed between thermodilution and Doppler measurements of stroke volume and cardiac output for both the mitral anulus method (R = .96 and .87, respectively) and the left ventricular outflow method (R = .95 and .91, respectively). The results of the two methods correlated well with each other in patients without regurgitant valve lesions. A greater interobserver variability was observed with the mitral anulus method, which was related solely to greater variability in measuring the annular diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1983

Cardiac echinococcal cyst: diagnosis by two-dimensional echocardiography.

A case of an intracardiac echinococcal cyst is presented. The diagnosis was made by two-dimensional echocardiography, which clearly identified a large multiseptated cystic structure in the right ventricular outflow tract. The findings were verified at surgery. It is suggested that two-dimensional echocardiography may be the procedure of choice in the diagnosis of cardiac echinococcal disease.

Adult↗

PubMed1983

Detection of coronary artery disease with exercise two-dimensional echocardiography. Description of a clinically applicable method and comparison with radionuclide ventriculography.

Two-dimensional echocardiography (2-D echo) was performed in 73 patients evaluated for coronary artery disease (CAD) and in four normal volunteers before and immediately after a maximal treadmill exercise test. Diagnostic images were obtained from the apical and parasternal windows. In 17 patients with normal coronary arteriograms, ejection fraction (EF) increased from 66 +/- 9% (+/- SD) at rest to 73 +/- 8% after exercise (p less than 0.001), while in 56 patients with proved CAD, EF fell from 56 +/- 13% at rest to 53 +/- 16% after exercise (p less than 0.01). The sensitivity of postexercise 2-D echo for detecting CAD (based on abnormal EF response and/or regional dyssynergy) was 91% (51 of 56 patients) and the specificity was 88% (15 of 17). Sensitivity for one-, two- and three-vessel disease was 64% (seven of 11), 95% (20 of 21) and 100%, respectively. Patients with multivessel disease showed a significant fall in a wall motion score index, from 0.79 +/- 0.25 to 0.63 +/- 0.26. Exercise radionuclide ventriculography (RNV) was also performed in 41 of the subjects (17 normals and 24 CAD patients) on a bicycle ergometer. The overall sensitivity of 2-D echo in this subgroup was 92%, compared with 71% for RNV. The sensitivity of 2-D echo for one-vessel disease (n = 4) was 50%, that for two-vessel disease (n = 12) was 100% and that for three-vessel disease (n = 12) was 100%. Respective values for RNV were 0%, 80% and 90%. The specificity of 2-D echo was 88% and that of RNV was 82%. A significantly higher peak heart rate response was observed on the treadmill than on the bicycle ergometer in both CAD patients and normal subjects. We conclude that postexercise 2-D echo is a clinically applicable technique for the diagnosis and evaluation of CAD patients and compares favorably with exercise RNV.

Adult↗

PubMed1982

Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic predictors of normalization of left ventricular dilatation after valve replacement in chronic aortic insufficiency.

To define and compare predictors of postoperative normalization of diastolic left ventricular dimension after aortic valve replacement, echocardiographic indexes of left ventricular size, function, degree of hypertrophy and systolic wall stress were examined in 43 patients with chronic and 14 with acute aortic insufficiency. In all of the latter 14 patients, left ventricular diastolic dimension returned to normal (mean 5.2 +/- 0.4 cm) in the postoperative follow-up period (mean 8.0 months). In contrast, of those with chronic insufficiency, 28 (group A) had postoperative normalization of diastolic dimension whereas the remaining 15 (group B) had persistent enlarged diastolic dimension. Preoperative end-systolic dimension, diastolic radius/thickness ratio, mean radius/thickness ratio, mean wall stress and end-systolic stress were 84 to 93 percent accurate in predicting normalization versus persistence of left ventricular dilatation postoperatively, and were superior to preoperative end-diastolic dimension and shortening fraction. Postoperatively, group A had complete normalization of end-systolic dimension and of mean and end-systolic wall stresses with persistence of a normal shortening fraction. Group B continued to have increases in end-systolic dimension, mean wall stress and end-systolic stress with a reduction in shortening fraction. Postoperatively there was a 43 and 29 percent incidence rate of heart failure and death by heart failure, respectively, in group B versus none in group A (p less than 0.01). These findings support the concept that inappropriate hypertrophy in chronic aortic insufficiency is associated with progressive increases in wall stress and end-systolic dimension and a reduction in shortening fraction that eventually result in irreversible cardiac dilatation and failure. Accurate and clinically relevant determination of reversible and irreversible alterations in left ventricular size and function may be obtained with these echocardiographic indexes.

Adolescent↗

PubMed1982

Effect of cardiac surgery on ventricular septal motion: assessment by intraoperative echocardiography and cross-sectional two-dimensional echocardiography.

Echocardiographic evidence of paradoxical septal motion frequently occurs after cardiac surgery. To assess possible etiologic factors 17 patients were studied preoperatively, intraoperatively, and 7 days after surgery. Preoperative septal motion was normal in 14 and paradoxical in three (two with previous cardiac surgery, one with atrial septal defect [ASD]). Intraoperative septal motion prior to surgical procedure was normal in 16 and paradoxical in one (ASD). Septal motion (excursion and thickening fraction) was normal in all patients prior to chest closure. Echocardiograms of adequate quality were obtained at 7 days post surgery in 15 patients; septal motion was paradoxical in nine (group A) and normal in six (group B). No significant differences were seen between the two groups in ischemic time or in the preoperative to postoperative change in left ventricular (LV) and right ventricular diastolic dimension, shortening fraction, or septal and posterior wall thickening fraction. A significant postoperative decrease in septal excursion was seen in group A but not in group B; significant postoperative increases in posterior wall excursion were seen in both groups. Cross-sectional two-dimensional echocardiograms performed in 20 patients (8 normal, 12 postoperative paradoxical septal motion) were analyzed. In normal controls no significant change was detected in the LV centroid position during systole. In contrast, the 12 postoperative patients showed significant anterior displacement of the LV centroid and right septum during systole. Thus, paradoxical septal motion after cardiac surgery appears to relate to excessive anterior cardiac mobility due to pericardiotomy rather than to myocardial ischemia resulting from cardiopulmonary bypass.

Adult↗