The effect of vitamin C supplementation on coagulability and lipid levels in healthy male subjects.

Although dietary intake and plasma levels of vitamin C have been inversely associated with cardiovascular disease, the mechanism through which it may exert its effect has not been fully explained. Since thrombosis plays an important role in the onset of cardiovascular disease, we investigated the effect of vitamin C on measures of hemostasis that have been associated with cardiovascular risk. The effect of vitamin C on lipid levels was also evaluated. In a randomized, placebo-controlled, crossover study, we determined the effect of 2 g daily of vitamin C supplementation on platelet adhesion and aggregation, levels of tissue plasminogen activator antigen, plasminogen activator inhibitor, fibrinogen, plasma viscosity, von Willebrand factor, and lipid levels in 18 healthy male volunteers with low normal vitamin C levels. No striking effects of vitamin C on the hemostatic measures were observed, although tissue plasminogen activator antigen levels were inversely related to Vitamin C levels. Von Willebrand factor levels were slightly higher with vitamin C, although within the normal range. Total cholesterol levels were 10% lower when subjects were receiving vitamin C compared to placebo (167+/-7 mg/dL vs. 184+/-7 mg/dL), P=0. 007), although the total cholesterol/HDL ratio was not significantly different. Higher levels of tissue plasminogen activator antigen, which in the present study were associated with lower vitamin C levels, have been shown in prospective studies to convey an increased risk of cardiovascular events. Further studies of the effect of vitamin C on hemostatic measures are required in higher risk populations or those with known cardiovascular disease.

Plasma lipoproteins and lipolytic enzyme activities during endurance training in sedentary men: changes in high-density lipoprotein subfractions and composition.

Eighteen healthy sedentary males took part in supervised bicycle training for 50 minutes three to five times a week. Twelve subjects (group A) trained for 6 weeks at heavy intensity, and six subjects (group B) trained for 12 weeks at moderate intensity. Maximal oxygen uptake increased by about 20% (P less than 0.01). Body weight and composition as well as diet remained unchanged. After 6 weeks plasma high-density lipoprotein (HDL) cholesterol concentrations had increased by 7% (P less than 0.05) in all subjects. The increase was most marked in group B at 14% (P less than 0.05) compared to 3% in group A (ns). Apolipoprotein AI (apo AI) increased by about 7% in both groups (P less than 0.01). After 12 weeks HDL cholesterol and apo AI levels had almost returned to initial values. Measurements of HDL components showed increases of 6% to 12% in free cholesterol, cholesteryl ester (P less than 0.05), and phospholipid (P less than 0.01); whereas, the minor triglyceride fraction decreased by 20% (P less than 0.01). Zonal ultracentrifugation in four subjects revealed a preferential rise of about 35% in the HDL2 subfraction, increasing the HDL2/HDL3 ratio by about 20%. In parallel, the composition of the lipoprotein classes changed. The protein moiety of all classes, except low-density lipoprotein (LDL), expanded at the expense of the core components cholesteryl ester and triglyceride. Hepatic lipase (HL) activity decreased by 6% (P less than 0.05), and lipoprotein lipase (LPL) activity in adipose tissue increased by about 50% (P less than 0.05) during the first 6 weeks of training, while LPL activity in postheparin plasma and skeletal muscle did not change. The transient rise in HDL cholesterol levels was correlated (P less than 0.05) to the elevation of adipose tissue LPL activity. The alterations in HDL concentration were also related to changes in body composition and diet, especially to an increase in fat intake.

In-hospital exercise therapy in patients with severe angina pectoris.

The authors evaluated physiologic, psychologic and metabolic effects of a nine-week in-hospital training program on 14 men with severe disabling angina pectoris. The exercise program consisted of intensive interval training on an ergometer bicycle for two 30 min sessions daily. The physical performance increased by about 40% (p less than 0.001). Plasma insulin levels were reduced and glucose tolerance improved significantly. There was a decrease in plasma triglyceride and low-density lipoprotein (LDL) cholesterol levels, but no change in high-density lipoprotein (HDL) cholesterol, apolipoprotein AI and B concentrations. Plasma triglyceride (p less than 0.05) and LDL cholesterol (p less than 0.05) levels remained low three weeks after completion of the training period and the physical performance remained improved (p less than 0.01) even six months post-training. Four of the patients who had been disabled for at least five months were able to return to work. The authors suggest that comparatively short and intensive in-hospital rehabilitation of patients with coronary heart disease may be an attractive alternative to prolonged training on an outpatient basis, especially in patients with severe angina pectoris.

Alterations in plasma proteins and lipoproteins in acute myocardial infarction: effects on activation of lipoprotein lipase.

Plasma lipoprotein concentrations were followed in 21 men with acute myocardial infarction. HDL and LDL cholesterol concentrations showed similar time-courses with average maximal decreases of about 20%, 10-14 days after onset of symptoms. The decrease in HDL levels (measured as HDL cholesterol and apolipoprotein AI) was significantly correlated to the inflammatory response, as reflected by plasma orosomucoid concentrations, and to the extent of myocardial injury, as mirrored by serum activities of lactate dehydrogenase. In samples drawn 10 days after myocardial infarction we found marked changes in the ability of the patients' sera to enhance the activity of purified lipoprotein lipase. The maximal activating ability (at saturating serum concentrations) increased by about 30%; however, at suboptimal serum concentrations, the activating ability of the patients' sera declined (50% higher serum concentrations were required to reach half maximal reaction rate). The altered activation characteristics were correlated to the changes in HDL concentrations. By affecting the activity of lipoprotein lipase and thereby the rate of intravascular lipoprotein metabolism, this phenomenon may contribute to the lipoprotein alterations seen after myocardial infarction.

Comparison of left ventricular ejection fraction assessed by radionuclide angiocardiography, echocardiography and contrast angiocardiography.

The left ventricular ejection fraction (EF) obtained by first pass radionuclide angiocardiography was compared with that determined by contrast angiocardiography in 49 patients. In 35 of the patients a comparison with the EF obtained by M-mode echocardiography was also made. The EF echo was determined in two ways, from the standard cube formula and the regression equation suggested by Teichholz for left ventricular volume calculations. The latter formula gave an average EF closer to the average EF obtained by isotope technique and cineangiography and was therefore used in the comparison study. Measurements of EF by isotope technique and echocardiography correlated well (r = 0.78). The correlation between these two noninvasive methods for EF determination and their cineangiographic counterpart was almost identical (r = 0.72--0.74).

High-density lipoprotein concentrations increase after stopping smoking.

Concentrations of plasma lipoproteins in 10 men who were habitual smokers were monitored for six weeks after they stopped smoking and related to changes in diet and body weight. The energy intake increased by 10% (p less than 0.05) owing to a higher consumption of carbohydrates and fat, and body weight increased by 2% (p less than 0.01). Plasma triglyceride, cholesterol, and low-density lipoprotein cholesterol concentrations did not change significantly. The most prominent finding was a rapid and pronounced increased in high-density lipoprotein concentrations. From comparatively low values (mean 0.82 mmol/1) they rose by 29% (p less than 0.01) within two weeks and remained at this value throughout the observation period. In three subjects who resumed smoking after the end of the study they again fell to initial values six weeks later. The initial increase in concentration could be accounted for mainly by an increase in the esterified fraction and only to a lesser extent in the free cholesterol fraction. The changes in concentrations were accompanied by similar but less pronounced rises in high-density lipoprotein phospholipid and in apolipoprotein AI concentrations (p less than 0.01), whereas high-density lipoprotein phospholipid and in apolipoprotein AI concentration (p less than 0.01), whereas high-density lipoprotein triglyceride concentrations did not change significantly. These findings confirm and extend those of earlier cross-sectional studies which showed low concentrations of high-density lipoproteins in cigarette smokers, A significant correlation between the rise in high-density lipoprotein cholesterol concentrations and the increase in fat consumption after stopping smoking indicate that the changes in high-density lipoprotein concentrations may be partly due to nutritional factors.

The use of thallium-201 myocardial scintigraphy for the diagnosis of previous infarction.

The ability of thallium-201 scintigraphy to detect previous infarction (greater than 6 months ago) was studied in 43 patients with coronary artery disease, 39 with valvular heart disease, and 5 with cardiomyopathy or myocarditis. All patients had undergone selective coronary arteriography and left ventricular angiography. Thallium-201 scintigraphy at rest proved a very sensitive method for detecting previous infarction, also clinically silent. Scintigraphy was more sensitive than a recent ECG. However, scintigraphy can give falsely positive results.