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Biomedical subjects

M K Heng

Publications and source records attributed to M K Heng.

At least 19 recordsLinked to original sources
PubMed1992

Changes in cardiovascular function during inversion.

Although inversion therapy is used increasingly as a therapy for musculoskeletal back disorders, its effects on cardiovascular function have not been systematically determined. Heart rate, blood pressure and echocardiographic measurements were performed in 20 normal male volunteers before, during and after bent-knee inversion. Compared to control measurements in the supine position, inversion significantly increased heart rate, systolic and diastolic blood pressure, rate-pressure product, systemic vascular resistance and left ventricular (LV) wall stress. Inversion also resulted in a significant decrease in LV diastolic volume, cardiac output and ejection fraction. Thus inversion produces an increase in LV afterload and myocardial oxygen demand concomitantly with a decrease in LV preload and global systolic function, and may be contraindicated in patients with cardiovascular disease.

Adult↗
PubMed1992

Expression of the L-fucose moiety on infrainfundibular follicular keratinocytes of terminal follicles, its decreased expression on vellus and indeterminate follicles of androgenetic alopecia, and re-expression in drug-induced hair regrowth.

The distribution of various glycoprotein molecules on the surface of follicular keratinocytes was studied with a panel of lectins with specificity for various sugar moieties on biopsy specimens from both bald/balding scalp and normal occipital scalp, of 23 patients with androgenetic alopecia as well as on biopsies of normal forearm skin of four patients. The most significant differences between bald and normal scalp biopsy were noted with Ulex europaeus agglutinin I (UEA I). We noted an increased (91.8% +/- 3.1; mean +/- SE) expression of UEA I binding sites on the infra-infundibular follicular keratinocytes in anagen terminal scalp hairs, compared to 28.5% +/- 5.2 in the indeterminate (anagen) hairs of balding scalps, and 23.2% +/- 6.3 in the anagen follicles of vellus fore-arm hairs. By contrast, the telogen hairs demonstrated minimal UEA I staining: 4.0% +/- 0.8, mean +/- SE in telogen scalp hairs, 1.8% +/- 0.5 in telogen hairs of balding scalps (0% in completely bald scalps, in which all the hairs were in the telogen phase), and 1.9% +/- 0.2 in telogen forearm hairs. The percentage of UEA I staining correlated with the length of the infra-infundibular follicles in all cases studied. In three cases of hair regrowth after hair growth promotors, the UEA I staining increased to 80.6% +/- 6.1 in anagen hairs and correlated with increased length of infra-infundibular follicles. Our data indicate that there are 1) marked differences between anagen and telogen follicles in UEA I binding to infra-infundibular follicular keratinocytes; 2) the percentage of UEA I staining reflects the size (length) of the infra-infundibular hair follicle; and 3) the anagen follicles of balding scalps (indeterminate hairs) show UEA I staining resembling that exhibited by anagen follicles of vellus hairs.

Adult↗
PubMed1991

Focal endothelial cell degeneration and proliferative endarteritis in trauma-induced early lesions of necrobiosis lipoidica diabeticorum.

Microangiopathy is an essential component in diabetic vascular pathology. We report ultrastructural observations of ballooning degeneration involving isolated endothelial cells of cutaneous capillaries, while leaving adjacent endothelial cells relatively intact in six diabetic patients with early lesions of necrobiosis lipoidica induced by trauma. Focal proliferation of endothelial cells encroaching upon the vascular lumina (obliterative endarteritis) was also observed. Lectin studies on biopsy specimens of older lesions of necrobiosis lipoidica revealed paucity of dermal blood vessels. These observations enable us to gain further insight into the pathophysiological mechanisms that underlie diabetic microvascular disease.

Aged↗
PubMed1990

Beta, partial agonists to treat heart failure: effects of xamoterol upon cardiac function and clinical status.

The presence of systolic dysfunction, diastolic dysfunction, or both is an important consideration in selecting the optimal pharmacologic approach to the treatment of congestive heart failure in an individual patient. Cardiac glycosides and arterial vasodilators act only on systolic function, whereas beta 1-adrenoceptor-stimulating agents, such as beta 1 full and partial agonists, have both inotropic and lusitropic activity. Acute and chronic administration of xamoterol, a new beta 1 partial agonist, to patients with congestive heart failure has been shown to improve myocardial contractility, as indicated by increases in the peak rate of rise in left ventricular pressure, left ventricular ejection fraction, and cardiac output. Improvement in ventricular relaxation and filling, reflected by increases in the peak rate of decline in left ventricular pressure, reductions in the time constant of the decrease in isovolumic pressure, improved left ventricular compliance, and increases in the atrial contribution to diastolic filling, are other beneficial effects of xamoterol on diastolic function. Exercise capacity increases in response to xamoterol therapy, while heart rate at maximum exercise declines. Relief of the signs and symptoms of congestive heart failure and improvement in functional status have also been demonstrated in xamoterol-treated patients. The undesirable effects of beta 1 full agonists, such as tachycardia, arrhythmias, increased myocardial oxygen consumption, and effects on the peripheral vasculature, are not seen with xamoterol. The beta 1 partial agonist also causes no beta-adrenoreceptor down-regulation, a finding that may account for its sustained effectiveness with long-term therapy.

Adrenergic beta-Agonists↗
PubMed1989

Healing of necrobiotic ulcers with antiplatelet therapy. Correlation with plasma thromboxane levels.

Necrobiosis lipoidica in diabetics has been considered to be a cutaneous manifestation of diabetic microangiopathy. Seven diabetic patients with necrobiotic ulcers of recent onset that healed after administration of acetylsalicylic acid and dipyridamole had elevated thromboxane levels. Healing was associated with depression of the elevated thromboxane levels in all seven patients.

Adult↗
PubMed1989

The value of Holter monitoring in evaluating the elderly patient who falls.

Ambulatory cardiac (Holter) monitoring is often recommended in the routine evaluation of patients who fall; however, the prevalence of arrhythmias in old people is high, and the usefulness of such monitoring is unproven. As part of a large study of institutionalized elderly fallers, we compared Holter findings of fallers (N = 51) with a group of nonfallers (N = 27) having similar medical and demographic characteristics. Prevalence of ventricular arrhythmias was 82% in each group, and all patients had supraventricular arrhythmias. The mean number of ventricular and supraventricular couplets and runs did not differ between groups. There was no difference in severity of arrhythmias between fallers and nonfallers; in fact, fallers had slightly fewer Lown 4B arrhythmias than nonfallers (10% vs 18%, NS). Prevalence of heart disease was 78% in both groups and was associated with increased ventricular ectopy in the form of runs and couplets (P less than .05). No symptoms were reported during the Holter monitoring. We conclude that Holter monitoring should not be a routine part of the work-up of the patient who falls.

Accident Prevention↗
PubMed1988

Beta-adrenoceptor antagonist-induced psoriasiform eruption. Clinical and pathogenetic aspects.

A number of beta-adrenoceptor blocking drugs have been reported to induce a papulosquamous eruption which resembles psoriasis. We report distinctive clinical, histopathologic, immunocytochemical, and electron microscopic features in beta-blocker-induced psoriasiform eruptions that differentiate this syndrome from psoriasis. Preliminary data suggest that biopsy specimens from eruptions caused by beta 1-selective adrenoceptor blocking agents (metoprolol and atenolol) were characterized by excessive degranulation of the neutrophils in the dermis, while the nonselective beta blockers (propranolol, nadolol, and sotalol) were marked by excessive release of proteolytic enzymes from macrophages, which are thought to possess beta 2-adrenergic receptors. Surprisingly, excessive release of enzymes by lymphocytes were noted in both the beta 1-selective and in the nonselective induced syndromes. It is believed that excessive lysosomal enzyme release by neutrophils, lymphocytes, and macrophages is responsible for the presence of basal keratinocyte herniations, which have previously been shown to correlate with hyperproliferation and psoriasiform changes, as well as with the presence of excessive proteolytic enzymes in the skin. It is postulated that the beta-blocker-induced syndrome may result from enhanced proliferation, motility, and activity of lymphocytes, neutrophils, and cells of the macrophage-Langerhans cell series, stemming from depressed intracellular cyclic adenosine monophosphate levels caused by the beta blockade.

Adrenergic beta-Antagonists↗
PubMed1986

Blood pressure and electrocardiographic response to dental treatment with use of local anesthesia.

The incidence of ST segment depression during tooth extraction was significantly higher in patients with cardiac disease than it was in patients without cardiac disease, indicating that the cardiac patients experienced myocardial ischemia. The almost equivalent incidence of ST segment depression during anesthetic administration and surgery suggests that the administration of local anesthetic is as stressful as tooth extraction for cardiac patients. Medical consultation before dental treatment and use of stress-reduction techniques may be indicated for patients with or suspected to have cardiac disease.

Adult↗
PubMed1979

Regional 99m technetium diphosphonate uptake in experimental dog heart infarct: relation to duration and severity of ischaemia.

Regional uptake of 99mTechnetium diphosphonate was compared with regional myocardial blood flow 6, 12 and 24 h after the onset of myocardial infarction in dogs, and with regional creatine kinase depletion 24 h after the onset. Uptake of the imaging agent increased from 6 to 24 h, but no consistent relationship could be demonstrated between regional myocardial blood flow and regional uptake of the diphosphonate nor between uptake and regional creatine kinase depletion at the centre or border of the infarct. In addition, inappropriately high levels of 99m Technetium uptake could be demonstrated in the epicardial layer of the normal tissue surrounding the infarct. We conclude that diphosphonate uptake is not quantitatively related to the severity of ischaemia, and that use of this substance for imaging may over-estimate myocardial infarct size.

Animals↗
PubMed1979

Cross-sectional echocardiography. I. Analysis of mathematic models for quantifying mass of the left ventricle in dogs.

Cross-sectional echocardiography was used to quantify left ventricular mass noninvasively in 21 dogs. Short- and long-axis cross-sectional images of the left ventricle were reproducibly traced at endocardial and epicardial borders during stop-motion video-tape replay. We used area, length and diameter measurements to calculate left ventricular mass by seven mathematic models, including the standard formulas used with M-mode echocardiography and cineangiography. Calculated mass was compared with excised weight of the left ventricle by regression and percent error analyses. Formulas using short-axis areas and long-axis length resulted in higher correlation coefficients (0.94--0.95) and lower mean errors (6--7%) than for standard formulas. Since short-axis areas account for regional left ventricular irregularities, noninvasive quantification of left ventricular mass by cross-sectional echocardiography in dogs is most accurate with formulas using short-axis areas.

Animals↗
PubMed1978

The effect of glucose-insulin-potassium on experimental myocardial infarction in the dog.

The effect of glucose-insulin-potassium (GIK) infusions was studied in 45 dogs after left anterior descending coronary artery ligation. GIK caused a modest increase in lactate concentration in small veins draining the infarct but did not affect glucose uptake. No effect on creatine kinase activity in the infarct was seen from GIK, although there was a slight increase in blood flow to the centre of the infarct. We concluded that GIK did not reduce infarct size in this experimental model.

Animals↗
PubMed1978

Failure of high doses of propranolol to reduce experimental myocardial ischemic damage.

Myocardial creatine phosphokinase (CPK) activity and myocardial blood flow (MFB, 15 +/- mu microspheres) were measured at 24 hours after ligation of the left anterior descending coronary artery in nine untreated anesthetized dogs, in eight dogs pretreated with intravenous propranolol 5 mg/kg and in eight which had both pretreatment as well as infusion of propranolol (1.25 mg/kg/hour) after occlusion. Loss of CPK activity from the border and center zones of the myocardial infarct was similar in extent in dogs which had pretreatment but no infusion of propranolol as it was in the control group. Loss of CPK from the center zone was greater (P less than 0.005) in dogs receiving pretreatment followed by constant infusion of the drug. Propranolol had no significant effect on collateral blood flow to the border or center zone of the infarct. In separate experiments, there was no important difference in hemodynamic measurements, except a slower heart rate (P less than 0.01), when pretreated dogs were compared with control dogs up to 2 hours after coronary ligation. We conclude that propranolol given in this dose does not influence nyocardial damage, on the basis of regional myocardial blood flow or tissue CPK depletion values at 24 hr after coronary occlusion.

Animals↗
PubMed1978

Reduction of enzyme levels by propranolol after acute myocardial infarction.

The effect of propranolol (0.1 mg/kg intravenously followed by 320 mg given over 27 hour orally) on serum levels of creatine kinase enzyme was studied in a randomized trial involving 95 patients seen within 12 hours of onset of symptoms of uncomplicated myocardial infarction. In 15 patients who were treated with propranolol within 4 hours of onset, and who eventually developed pathological Q waves, peak measured enzyme levels were 27% (P less than 0.0125) lower than in 19 control patients who were also seen within 4 hours of the onset but had no specific treatment. Total calculated enzyme appearance was also lower in the treated patients (reduced 25%, P less than 0.05) as was the calculated rate of the appearance (33%, P less than 0.005). No significant difference was found for treated compared with control patients entering the trial more than 4 hours after the onset of chest pain. This evidence suggests that propranolol may reduce the size of uncomplicated infarctions if it is given intravenously within 4 hours of the onset.

Acute Disease↗
PubMed1977

Derangements of myocardial metabolism preceding onset of ventricular fibrilliation after coronary occlusion.

To determine alterations in myocardial metabolism and and hemodynamics that occur within the first 30 minutes after coronary arterial occlusion, before the onset of ventricular fibrillation, measurements were compared in two series of dogs. Series A, 90 dogs that did not manifest ventricular fibrillation after coronary occlusion, were considered a control group. Series B consisted of 28 dogs that had ventricular fibrillation within 30 minutes after occlusion. All had similar comprehensive measurements completed preceding the onset of ventricular fibrillation. The animals in series B (subseuqnt fibrillation) had significantly higher heart rates before and after coronary occlusion. In this series cardiac metabolism of the occluded segment judged by transmyocardial lactate extraction, potassium balance, sodium/potassium ratio and blood pH because grossly more abnormal after coronary occlusion than in series A. In 5 animals whose measurements were obtained within 5 minutes of the onset of ventricular fibrillation, a sudden massive lactate production, potassium loss and increased acidosis of the occluded portion supervened minutes before the onset of the fatal arrhythmia. Animals with ventricular fibrillation had higher intracoronary S-T segment elevation that persisted until the onset of ventricular fibrillation. Measurements of abnormal hemodynamic function (left ventricular end-diastolic pressure, peak systolic pressure and first derivative of left ventricular pressure [DP/dt]) were not associated with an increased incidence of ventricular fibrillation. The study indicates that animals that manifest ventricular fibrillation within 30 minutes after coronary occlusion have higher preocclusion heart rates, a more severe metabolic disorder of the coronary occluded segment and more persistent intracoronary S-T segment elevation compared with animals that do not manifest ventricular fibrillation.

Animals↗
PubMed1977

Isolated mitral replacement with stent-mounted antibiotic-treated aortic allograft valves.

The results of valve replacement with a stent-mounted antibiotic-treated aortic allograft valve are reported in 129 patients with isolated mitral valve disease. Of these patients, 70 per cent were in N.Y.H.A. Class IV. The hospital mortality rate was 3.9 percent. The cumulative complication-free rate at 5 years was only 37 percent as 21 percent died late, a further 15 percent were alive following reoperation, 4 percent had an embolic episode, 4 percent were alive with important incompetence, and 20 percent had unimportant incompetence. Proved valve failure was due mainly to detachment of the aortic wall remnant of the valve from the pillar of the rigid metal stent (16 percent incidence at 5 years) and methods for preventing this complication are discussed. Because of these complications the use of this device in the mitral position has been discontinued.

Adolescent↗
PubMed1976

Regional differences in lactate concentration in experimental myocardial infarction.

Lacate concentrations were measured in blood from (a) coronary veins within ischaemic myocardium and (b) veins nearer to the coronary vein, for periods of up to 2 1/2 hours after ligation of the left anterior descending artery in dogs. Concentrations at (a) were three to four times higher than at (b), while blood sampled simultaneously from two veins at (a) yielded similar concentrations of lactate. At 2 1/2 hours after ligation the veno-arterial difference of lactate concentration in blood from (a) was about one half of the difference at 15 minutes. Lactate concentration at (a) was approximately twice as great when the area of ischaemic myocardium drained by the vein was large (18 not equal to 1% of heart weight) than when it was small (6 not equal to 1% of heart weight). No close correlation was apparent between the height of epicardial ST-segment elevation and the level of lactate release. These experiments extend previous observations that changes in lactate concentration at a given site may reflect changes in venous dilution, rather than in the rate of production of lactate, and emphasize that caution is necessary in interpretation of changes in concentrations of metabolites in coronary sinus blood after acute myocardial infarction in man.

Animals↗
PubMed1976

Failure of ST segment elevation to predict severity of acute myocardial infarction.

Praecordial ST segment elevation was measured at 35 electrode positions in each of 40 patients admitted to a coronary care unit after acute transmural anterior myocardial infarction. Serial praecordial electrocardiographic maps were recorded to determine (a) the time course as well as reproducibility of measurements of ST segment alterations, and (b) the degree of correlation between the magnitude of ST segment elevation and the severity of infarction, as assessed clinically or by sequential estimations of serum creatine kinase activity. Large variations in ST segment elevation were found in different patients with a comparable degree of myocardial damage, and at intervals of as little as four hours in the same patient. These variations were greater than could be explained by technical factors, and were not related to apparent changes in the patients' clinical status. The patterns of release of myocardial creatine kinase showed that the time course of ST segment elevation was longer than the period of myocardial necrosis. No correlation was found between the myocardial infarct size as determined by enzyme release and the highest levels of ST segment elevation recorded. The findings suggest that ST segment elevation as measured by praecordial electrocardiographic mapping does not constitute a reliable index of the size or severity of myocardial infarcts in man.

Adult↗