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Biomedical subjects

J Hung

Publications and source records attributed to J Hung.

At least 73 records · Page 4Linked to original sources

Association of sleep apnoea with myocardial infarction in men.

To examine the hypothesis that sleep apnoea is a risk factor for ischaemic heart disease, overnight polysomnography was performed in 101 unselected male survivors of acute myocardial infarction (MI) aged less than 66 yr and in 53 male subjects of similar age without evidence of ischaemic heart disease. The apnoea index (AI, number of apnoea episodes per hour of sleep) was 6.9 (SEM 1.2) in the MI patients versus 1.4 (0.3) in the control subjects. After adjustment for age, body mass index, hypertension, smoking, and cholesterol level, multiple logistic regression analysis identified the top quartile of AI (greater than 5.3) as an independent predictor of MI patients. The relative risk for myocardial infarction between the highest and lowest quartiles of AI was 23.3 (95% confidence interval 3.9-139.9).

Adult↗

The effects of low density lipoproteins on uptake of Photofrin II.

The cellular uptake of Photofrin II (PII) was studied using fluorescence imaging and chemical extraction. The influence of serum and low density lipoproteins (LDL) was examined under a variety of experimental conditions employing cultured human cells of different origins as well as a subcutaneously SMT-F tumor implanted in mice. Results showed that serum inhibited PII uptake. In general, LDL also inhibits PII uptake with the exception of an initial increase in the first 10-30 min when the cellular concentration of PII was measured by fluorescence imaging instead of chemical extraction. Our results suggest a possible de-aggregation process occurring upon internalization or binding of PII to LDL.

Animals↗

Detection of early lung cancer using low dose Photofrin II.

Fluorescence imaging using hematoporphyrin derivative (HpD) or Photofrin II as a tumor marker has been used for localization of early bronchogenic carcinoma. Wider clinical application of HpD or Photofrin II as a cancer imaging agent has been hampered by the potentially serious and prolonged skin photosensitivity. Using a sensitive fluorescence bronchoscope system with a ratio fluorometer probe, carcinoma in situ was detected in four patients with low dose Photofrin II (0.25 mg/kg) with no apparent skin phototoxicity to 30 J/cm2 visible light on skin photosensitivity test.

Aged↗

Pericarditis associated with tick-borne Q fever.

A case of pericarditis associated with Q fever is described. Transmission was probably via an arthropod vector, which was most likely the kangaroo tick Amblyomma triguttatum. Complete recovery occurred in association with the use of non-steroidal anti-inflammatory agents only. This is a rare presentation of Q fever implicating transmission by a novel vector.

Acute Disease↗

Left heart involvement with cardiac shunt complicating carcinoid heart disease.

The manifestations of carcinoid heart disease are usually right heart failure due to pulmonary and tricuspid valve disease and sometimes high output failure due to peripheral vasodilation. Recently there has been one case report of progressive central cyanosis due to right to left shunting through a patent foramen ovale. We present a similar case where such a shunt developed and was also complicated by significant valvular disease affecting the left side of the heart.

Adult↗

Pharmacokinetics of diltiazem in patients with unstable angina pectoris.

The pharmacokinetics of diltiazem and its major metabolites, deacetyldiltiazem and N-monodemethyl-diltiazem, were studied after single and chronic oral administration in eight patients aged 45 to 69 years with unstable angina pectoris, treated by diltiazem, 120 mg t.i.d. After a single oral dose the time to peak plasma diltiazem concentration was 3.4 (2.1 to 5.0) hours and the elimination half-life was 6.6 hours (4.4 to 10.8 hours). These were unchanged after repeated oral administration (16 to 19 doses). The mean trough (8 hours after administration) plasma diltiazem level after six consecutive doses was 167 micrograms/L (63 to 286 micrograms/L) and was thereafter stable. With chronic administration the AUC increased by a factor of 2.24 +/- 0.31 (SEM; P less than 0.01). Plasma protein binding of diltiazem in these patients ranged from 83% to 93% whereas deacetyldiltiazem binding ranged from 58% to 75%. Plasma protein binding was independent of drug concentration and duration of treatment. Thus an average dose of 120 mg diltiazem given every 8 hours would appear to be a suitable regimen of treatment in most patients with angina pectoris, although users should be aware that there is a significant interpatient variability in steady-state diltiazem concentrations and that a significant accumulation of diltiazem occurs with chronic therapy.

Administration, Oral↗

An immunoreactive form of erythrocyte protein 4.9 is present in non-erythroid cells.

Using immunoblots and an affinity-purified antibody prepared against human erythrocyte protein 4.9, we have demonstrated and quantified the presence of an immunoreactive form of this protein in avian and bovine brain and lens tissues, avian heart, as well as in human platelets and mammalian, avian, piscine, and amphibian erythrocytes. Both the 48 kDa and the 52 kDa variants were observed in human erythrocytes, whereas 50 kDa and 54 kDa immunoreactive forms were observed in human platelets. As reported for erythroid protein 4.9, platelet protein 4.9 was phosphorylated in response to treatment with phorbol ester. Bovine brain showed five cross-reactive polypeptides in the 47 to 52 kDa range while avian brain and avian and bovine lens exhibited predominantly a 49-kDa band. Cross-reactivity was not observed in a number of cell lines and tissues including leukocytes, liver, kidney, pancreas, and skeletal muscle. Immunofluorescence indicated that protein 4.9 was present in cortical fiber cells of avian lens and in neurons of avian cerebrum.

Animals↗

Adaptation of human left ventricular volumes to the onset of supine exercise.

UNLABELLED: The purpose of this study was to measure the changes and rates of adaptation of left ventricular volumes at the onset of exercise. Eight asymptomatic subjects, in whom intramyocardial markers had been implanted 3-6 years previously during aortocoronary bypass surgery, exercised in the supine position at a constant workload of 73.6 W for 5 min. Six also exercised first at 16.4 W, and then against a workload which progressively increased by 8.2 W every 15 s. Cardiac volumes were measured by computer assisted analysis of the motion of the implanted markers. In the constant workload test, cardiac output increased rapidly from 5.7 +/- 1 min-1 to 10.3 +/- 1.9 1 min-1 by 2 min and then increased more slowly to 10.8 +/- 2.0 1 min-1 by 5 min. The cardiac output increase was mainly due to an increase in heart rate from 68 +/- 12 beats min-1 to 120 +/- 16 beats min-1 with minimal changes in stroke volume. The time constant for the early increase in cardiac output was 45s and for heart rate, 35s. With progressively increasing workloads, there was an almost linear increase of heart rate and cardiac output, but these increased at a slower rate than during the early phase of the constant load exercise test. IN CONCLUSION: rapid changes in cardiac output during supine exercise were produced by changes in heart rate; changes in stroke volume provided minor adjustments to cardiac output; the end-diastolic volume was almost constant.

Adaptation, Physiological↗

Differences in left ventricular function between anterior and inferior myocardial infarction of equivalent enzymatic size.

The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.

Aged↗

A logistic regression analysis of multiple noninvasive tests for the prediction of the presence and extent of coronary artery disease in men.

The incremental diagnostic yield of clinical data, exercise ECG, stress thallium scintigraphy, and cardiac fluoroscopy to predict coronary and multivessel disease was assessed in 171 symptomatic men by means of multiple logistic regression analyses. When clinical variables alone were analyzed, chest pain type and age were predictive of coronary disease, whereas chest pain type, age, a family history of premature coronary disease before age 55 years, and abnormal ST-T wave changes on the rest ECG were predictive of multivessel disease. The percentage of patients correctly classified by cardiac fluoroscopy (presence or absence of coronary artery calcification), exercise ECG, and thallium scintigraphy was 9%, 25%, and 50%, respectively, greater than for clinical variables, when the presence or absence of coronary disease was the outcome, and 13%, 25%, and 29%, respectively, when multivessel disease was studied; 5% of patients were misclassified. When the 37 clinical and noninvasive test variables were analyzed jointly, the most significant variable predictive of coronary disease was an abnormal thallium scan and for multivessel disease, the amount of exercise performed. The data from this study provide a quantitative model and confirm previous reports that optimal diagnostic efficacy is obtained when noninvasive tests are ordered sequentially. In symptomatic men, cardiac fluoroscopy is a relatively ineffective test when compared to exercise ECG and thallium scintigraphy.

Adult↗

Diltiazem and propranolol, alone and in combination, on exercise performance and left ventricular function in patients with stable effort angina: a double-blind, randomized, and placebo-controlled study.

Diltiazem and propranolol alone and in combination as antianginal agents were compared with placebo in 12 patients with stable exertional angina at Stanford University Medical Center. The patients performed symptom-limited, multi-stage upright bicycle ergometric exercise while undergoing radionuclide angiographic studies every two weeks while being treated with 90 mg of diltiazem four times daily, 60 mg of propranolol four times daily, a combination of 90 mg of diltiazem and 60 mg of propranolol four times daily, and placebo. Diltiazem, propranolol and a combination all significantly increased exercise duration compared to placebo (526 +/- 149, 525 +/- 115, and 549 +/- 129 vs 430 +/- 132 sec.). Although rate pressure product and heart rate decreased with diltiazem therapy at submaximal workloads, these values were unchanged at peak exercise in contrast to propranolol or the combination of propranolol or diltiazem. Diltiazem decreased the sub-maximal and maximal degree of exercise-induced ST segment depression by over 50% compared to placebo (P less than 0.01 vs placebo). Diltiazem resulted in a higher exercise left ventricular ejection fraction compared to placebo, propranolol or the combination of diltiazem or propranolol (all less than P less than 0.05). Sinus bradycardia or orthostatic hypertension occurred in four patients on the high-dose combination therapy and required dose reduction. We concluded that high-dose diltiazem, appeared to be even more effective than moderate-dose propranolol or the combination of diltiazem and propranolol in improving exercise tolerance, electrocardiographic evidence of myocardial ischaemia and left ventricular function in patients with stable effort angina due to occlusive coronary artery disease.

Aged↗

Changes in rest and exercise myocardial perfusion and left ventricular function 3 to 26 weeks after clinically uncomplicated acute myocardial infarction: effects of exercise training.

The effects of exercise training on exercise myocardial perfusion and left ventricular (LV) function in the first 6 months after clinically uncomplicated acute myocardial infarction (AMI) were assessed in 53 consecutive men aged 55 +/- 9 years. Symptom-limited treadmill exercise with thallium myocardial perfusion scintigraphy and symptom-limited upright bicycle ergometry with equilibrium gated radionuclide ventriculography were performed 3, 11 and 26 weeks after AMI by 23 men randomized to training and 30 randomized to no training. Peak cycle capacity increased in both groups between 3 and 26 weeks (p less than 0.01), but reached higher levels in trained than in untrained patients (803 +/- 149 vs 648 +/- 182 kg-m/min, p less than 0.01). Reversible thallium perfusion defects were significantly more frequent at 3 than at 26 weeks: 59% and 36% of patients, respectively (p less than 0.05), without significant inter-group differences. Values of LV ejection fraction at rest, submaximal and peak exercise did not change significantly in either group. The increase in functional capacity, i.e., peak treadmill or bicycle workload, that occurred 3 to 26 weeks after infarction was significantly correlated with the increase in peak exercise heart rate (p less than 0.001), but not with changes in myocardial perfusion or LV function determined by radionuclide techniques. Changes in myocardial perfusion or LV function do not appear to account for the improvement in peak functional capacity that occurs within the first 6 months after clinically uncomplicated AMI.

Coronary Circulation↗

Comparative value of maximal treadmill testing, exercise thallium myocardial perfusion scintigraphy and exercise radionuclide ventriculography for distinguishing high- and low-risk patients soon after acute myocardial infarction.

The prognostic value of symptom-limited treadmill exercise electrocardiography, exercise thallium myocardial perfusion scintigraphy and rest and exercise radionuclide ventriculography was compared in 117 men, aged 54 +/- 9 years, tested 3 weeks after a clinically uncomplicated acute myocardial infarction (MI). During a mean follow-up period of 11.6 months, 8 men experienced "hard" medical events (cardiac death, nonfatal ventricular fibrillation or recurrent MI) and 14 were hospitalized for unstable angina pectoris, congestive heart failure or coronary bypass surgery (total of 22 combined events). By multivariate analysis (Cox proportional hazards model), peak treadmill work load and the change in left ventricular ejection fraction (EF) during exercise were significant (p less than 0.01) predictors of hard medical events; these 2 risk factors and recurrent ischemic chest pain in the coronary care unit were also significantly predictive (p less than 0.001) for combined events. A peak treadmill work load of 4 METs or less or a decrease in EF of 5% or more below the value at rest during submaximal effort distinguished 22 high-risk patients (20% of the study population) from 89 low-risk patients. The rate of hard medical events within 12 months was 23% (5 of 22 patients), vs 2% (2 of 89 patients) in the high- and low-risk patient subsets, respectively (p less than 0.001). Thus, in patients who underwent evaluation 3 weeks after a clinically uncomplicated MI, exercise radionuclide ventriculography contributed independent prognostic information to that provided by symptom-limited treadmill testing and was superior to exercise thallium scintigraphy for this purpose.

Aged↗