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Biomedical subjects

A Sniderman

Publications and source records attributed to A Sniderman.

53 records · Page 3Linked to original sources
PubMed1980

Transfer of cholesterol esters between human high density lipoproteins and triglyceride-rich lipoproteins controlled by a plasma protein factor.

A protein factor from the d greater than 1.25 g/ml plasma fraction controls the transfer of cholesterol esters between high density lipoproteins and very low density lipoproteins. This transfer is time-dependent, and follows saturation kinetics relative to the concentration ratio of acceptor to donor lipoproteins. Although the process is reversible, the transfer rates are faster from high density to very low density lipoproteins and result in a net increase of cholesterol esters in the very low density lipoproteins. Under the same conditions, there is also a net mass transfer of cholesterol esters from high density lipoproteins to chylomicrons. This constitutes the first demonstration of cholesterol ester mass transfer between isolated lipoproteins and contrasts with the equilibrium of cholesterol esters between HDL and LDL which we previously demonstrated [4]. The apparent maximum transfer rate of cholesterol esters from high density to very low density lipoproteins was calculated to be about 80 nmoles cholesterol esters/h/ml plasma, which is very similar to the initial rate of reaction of lecithin:cholesterol acyltransferase in plasma. It is concluded that cholesterol ester formation in high density lipoproteins and their transfer to triglyceride-rich lipoproteins may be closely coupled.

Adult↗
PubMed1980

Association of coronary atherosclerosis with hyperapobetalipoproteinemia [increased protein but normal cholesterol levels in human plasma low density (beta) lipoproteins].

Most patients with coronary artery disease do not have elevated plasma or low density lipoprotein (LDL) cholesterol. To test whether the protein moiety of LDL, LDL B, might be a parameter to identify ischemic heart disease, the plasma cholesterol, triglyceride, LDL cholesterol, and LDL B were measured in 100 consecutive patients undergoing cardiac catheterization. On the basis of coronary angiography, these patients were divided into two groups: group I, 31 patients without, and group II, 59 patients with significant coronary artery disease. Although cholesterol, triglyceride, and LDL cholesterol levels were all significantly higher in group II, discriminant analysis indicated that LDL B concentrations most clearly separated the two groups. In group I (noncoronary), LDL B was 82 +/- 22 mg/100 ml, whereas in group II, LDL B was 118 +/- 22 mg/100 ml. The B protein level in group I was similar to other normal groups studied (35 asymptomatic male physicians, 83 +/- 11 mg/100 ml; 90 normolipidemic medical students, 72 +/- 17 mg/100 ml). The results therefore indicate that not only does LDL B better separate coronary and noncoronary groups than other lipid parameters studied, but also, among those with coronary artery disease, there exists a group with normal LDL cholesterol but with levels of LDL B protein similar to those observed in type II hyperlipoproteinemia. The explanation for the altered LDL composition observed in this group remains to be elucidated.

Apolipoproteins↗
PubMed1980

Causes of perioperative myocardial infarction: their identification and prevention.

Despite major technical advances in coronary bypass surgery and myocardial preservation, perioperative infarction remains a serious problem. The authors review the pathogenesis of the two different types of myocardial injury, occlusion necrosis and reperfusion necrosis. These two entities can be distinguished clinically by radioisotope scanning. Experimental studies have demonstrated that reperfusion necrosis can be prevented pharmacologically. Since the majority of perioperative infarcts are probably due to reperfusion, the importance of distinguishing between these two entities is evident.

Animals↗
PubMed1979

Fallibility of the epicardial electrocardiogram in quantitation of myocardial necrosis.

Estimation of infarct size utilising the epicardial electrocardiogram has been the subject of considerable controversy. The present study re-examines this technique in a dog model. It demonstrates that epicardial Q waves and S-T elevation are qualitative markers of local necrosis with different degrees of reliability; neither, however, is quantitatively related in a simple linear fashion to extent of necrosis. Conclusions from previous studies have been influenced both by different mathematical analyses of data and the inclusions of nonhomogenous sites in linear regression models.

Animals↗
PubMed1978

Cholesterol ester exchange between human plasma high and low density lipoproteins mediated by a plasma protein factor.

Although unesterified cholesterol and phospholipids exchange freely, a protein factor from the d greater than 1.25 g/ml plasma fraction was found to be necessary for cholesterol esters to transfer from HDL to LDL. This transfer was reversible, time-dependent and a function of the concentration of the d greater than 1.25 fraction, but independent of lecithin : cholesterol acyltransferase reaction. The transfer represented an equilibration of molecules, but no net mass transfer of cholesterol esters could be demonstrated from HDL to LDL.

Blood Proteins↗
PubMed1978

The posterior left atrial echocardiogram of mitral regurgitation.

The motion of the posterior wall of the normal left atrium has not been studied systematically. The superoposterior portion of the left atrium is adynamic throughout the cardiac cycle, whereas the inferoposterior portion is displaced posteriorly with left atrial filling during ventricular systole. In the present study, the left atrial diameter (LAD), the left atrial systolic motion (LASM) and the left atrial systolic velocity (LASV), were determined in the following groups of patients: 34 normals; eight patients with either coronary artery disease or aortic stenosis; six patients with aortic insufficiency; and three patients with ventricular septal defect. The results obtained were compared to 15 patients with angiographically documented mitral regurgitation. In the last group, the LAD (4.2 +/- .19 cm) and LASV (12.3 +/- 1.23 cm) and LASM (1.2 +/- 0.4 cm) were significantly greater reflecting the early accentuated filling of the left atrium induced by mitral regurgitation. As well, the product of these three parameters was greater in the mitral regurgitation group (63.2 +/- 7.34 cm3/sec) than in the other groups and patients with mild to moderate regurgitation had a significantly lower value than those with moderate to severe regurgitation (45.7 +/- 4.1 vs 78.5 +/- 10.9, P less than 0.02). The left atrial echocardiogram, therefore, is an aid in the diagnosis of mitral regurgitation and provides a rough index of the severity of the lesion.

Adult↗
PubMed1978

Low density lipoprotein. A metabolic pathway for return of cholesterol to the splanchnic bed.

The mechanism(s) by which cholesterol returns to the splanchnic bed from peripheral tissues are not well understood. To study this phenomenon in fasting man, lipoproteins were isolated from plasma obtained from hepatic vein and aorta. Cholesterol content of each lipoprotein class was determined and arteriovenous (AV) differences could be calculated for each patient. The results in the first 24 patients indicated splanchnic secretion of very low density lipoprotein cholesterol (mean AV difference - 3 mg/100 ml, P < 0.01), but not significant AV difference for total cholesterol, high density lipoprotein cholesterol, or low density lipoprotein (LDL) B protein. In contrast, for LDL (d 1.006-1.063 g/ml), there was significant uptake of cholesterol across the AV bed +8 mg/100 ml, P < 0.0002). In a further 15 patients, similar samples were obtained and intermediate density lipoprotein isolated at d 1.006-1.019 g/ml and LDL at 1.019-1.063 g/ml. The AV difference previously noted could now be localized to the 1.019-1.063 cholesterol ester moiety (+8 mg/100 ml, P < 0.0005). In the final 14 patients, the LDL cholesterol AV difference was again confirmed and shown to be unrelated to heparin. As well, there was secretion of triglyceride in the hepatic vein LDL. These quantitative data obtained in man raise the possibility that LDL rather than high density lipoprotein transports cholesterol ester to the splanchnic bed.

Apolipoproteins↗
PubMed1976

The significance of early changes of positive and negative dP/dt following contrast ventriculography.

The contrast agents used for cardiac angiography have pharmacologic effects on the myocardium and on peripheral and coronary circulations. These effects are a stress to the left ventricle. We have studied the sequential changes in heart rate, LVEDP, positive and negative dP/dt in 34 patients following left ventriculography. These patients were divided into three groups: nine normal patients, 14 patients with valvular or coronary artery disease and abnormal left ventricular function at rest, and 11 patients with significant coronary artery stenosis but normal left ventricular function at rest. Changes in dP/dt most clearly defined the normal and abnormal response. In the normal group the mean positive dP/dt rose abruptly at 30 sec after the ventriculogram, whereas the abnormal group showed a mean decrease. The extent of change varied, however, for patients within each group. Negative dP/dt decreased in both groups but more so in the abnormal group. As did the other groups, patients with coronary artery disease but with normal ventricular function showed individual variation in response. Their mean changes in positive and negative dP/dt were intermediate. Positive dP/dt decreased at 30 sec (similar to, but less than, the group with abnormal ventricular function) and negative dP/dt also diminished at 30 sec with a mean value between the normal and abnormal groups. The results of this study support the concept that left ventricular dysfunction may be elicited by the stress of contrast injection. More importantly, such dysfunction seen both with abnormal and normal left ventricles at rest, may be reflected by the relatively simple measurement of positive dP/dt after ventriculography.

Blood Circulation↗
PubMed1976

Myocardial infarction after aortocoronary bypass: etiologic factors.

To ascertain the frequency and probable determinants of myocardial infarction after aortocoronary bypass, two groups of patients were studied: a group of 20 patients who underwent valve replacement of repair of congenital anomalies and a group of 24 patients who underwent aortocoronary bypass. Postoperative myocardial infarction was diagnosed by an increase in serum creatine phosphokinase concentration to a minimum of 1200 IU in two consecutive samples. The frequency of myocardial infarction differed between the groups, being only 5% in group 1 but 20.4% in group 2. In the patients undergoing coronary artery surgery, the duration of bypass, the aortic cross-clamp time and the vent site did not influence the rate of infarction. However, the incidence of myocardial necrosis did correlate with the number of vessels bypassed. In no case was the clinical course influenced by the infarction. Our results suggest that the frequency of perioperative infarction is higher in coronary artery surgery than in other adult cardiac surgery, and that the most important determining factor is the number of diseased vessels.

Cardiopulmonary Bypass↗
PubMed1975

Determination of B protein of low density lipoprotein directly in plasma.

Quantitation of the apoprotein constituents of lipoproteins has extended our knowledge of plasma lipid transport. Previously, B protein content of low density lipoprotein could be measured by radial immunodiffusion only after ultracentrifugation. However, if performed in 1.5% agarose gel with standards and measured at 18 hr rather than at equilibrium, low density lipoprotein B protein can be measured directly in plasma, eliminating the need to separate very low density lipoprotein.

Apoproteins↗
PubMedDate not supplied

Hyperapobetalipoproteinemia. Plasma lipoprotein responses to oral fat load.

To better define lipid transport in patients with hyperapobetalipoproteinemia (HyperapoB), the response to an oral fat load was studied in six normotriglyceridemic patients with the disorder. Plasma triglycerides; Sf greater than 400, and Sf 20 to 400 triglycerides; Sf greater than 20 B100; total HDL and HDL subfractions (HDL2 and HDL3) were measured serially for a 7-hour period after an oral fat load and changes in these parameters were compared to those observed in six normolipidemic controls. In addition, plasma triglyceride levels and HDL2 and HDL3 cholesterol were also determined in seven patients with Type IV hyperlipoproteinemia: three with normal LDL apo B levels and four with HyperapoB. When the two normotriglyceridemic groups were compared, the patients with HyperapoB had significantly higher fasting levels of SF greater than 400 lipoproteins and higher fasting VLDL and LDL levels than the normal patients. After the fat load, Sf 20 to 400 triglycerides and Sf greater than 20 B100 levels increased in both groups. Plasma triglycerides rose to a higher level in the HyperapoB patients than in the normal group, but more strikingly, remained elevated in the HyperapoB patients, an elevation due principally to a persistant increase in Sf greater than 400 triglycerides. On the other hand, HDL2 cholesterol dropped substantially in the HyperapoB patients but not in the normal patients. Finally, in the hypertriglyceridemic group, after the fat load, HDL2 cholesterol levels did not change in the patients with normal LDL apo B levels but did decrease in those with elevated plasma LDL apo B.

Adult↗
PubMedDate not supplied

Hyperapobetalipoproteinemia in a kindred with familial combined hyperlipidemia and familial hypercholesterolemia.

A child showed a type IIb lipoprotein pattern and triglyceride-enriched cutaneous xanthomas before 1 year of age. The proband and 9 of 18 relatives had elevated plasma levels of low density lipoprotein (LDL) B protein; of these nine relatives, four had elevated LDL of increased density while five had elevated LDL of normal density. Compared with normal LDL, LDL of increased density had less cholesteryl ester and free cholesterol, more apolipoprotein B and triglyceride, and a lower molecular weight and flotation rate (Sf degrees). Patients with LDL of increased density had higher mean plasma levels of triglycerides, very low density lipoproteins, and intermediate density lipoproteins, but lower levels of high density lipoproteins than those with elevated LDL of normal density. Multiple lipoprotein patterns in the father's family suggested the presence of familial combined hyperlipidemia (FCH). The mother of the proband and two of her relatives had type IIa lipoprotein patterns and tendon xanthomas, compatible with familial hypercholesterolemia (FH). High affinity binding, internalization, and degradation of 125I LDL in cultured fibroblasts from the proband and his mother were reduced two- to threefold compared with normal cells, while LDL receptor activity in the proband's father was normal. This unusual proband has apparently inherited both FCH and FH.

Apolipoproteins A↗