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Biomedical subjects

A Hamsten

Publications and source records attributed to A Hamsten.

At least 217 records · Page 12Linked to original sources
PubMed1987

Risk factors for coronary artery disease in families of young men with myocardial infarction.

Familial clustering of coronary artery disease (CAD) and familial influences on various clinical and metabolic risk factors were investigated in 85 male survivors of acute myocardial infarction younger than 45 years. The study also involved 85 age-matched men randomly selected from the general population and the first-degree relatives of both patients and control subjects. Presence of CAD was assessed by an angina questionnaire and from rest and exercise electrocardiograms. There was an apparent aggregation of premature CAD in 38% of the case families. A familial clustering of hyperlipoproteinemia was present in 58% of the case families and 15% of the control families. Systemic hypertension and cigarette smoking also were clustered in the case families. Multivariate statistical analyses of clinical and metabolic risk indicators in patients with and without a family history of CAD and in control subjects indicated that familial aggregation of CAD is independently related to MI at a young age. Degree and extent of coronary atheromatosis and number and severity of hemodynamically significant stenoses did not differ between young patients with and without a familial aggregation of CAD. The absence of a relation between the family history and severity of CAD implies that other underlying mechanisms are involved.

Adult↗
PubMed1987

Glucose tolerance and insulin response to glucose in nondiabetic young male survivors of myocardial infarction.

Intravenous and oral glucose tolerance, as well as insulin response to glucose ingestion and a glucose infusion test, were investigated in 104 male nondiabetic survivors of myocardial infarction under the age of 45 years and in 100 matched control subjects randomly selected from the general population. Reduced oral glucose tolerance and hyperinsulinemic responses to both oral glucose challenge and to a glucose infusion test were present in a substantial number of the young patients. The very low density lipoprotein triglyceride concentration tended to rise progressively with increasing severity of glucose intolerance in both patients and control subjects. The magnitude of the early insulin response during the glucose infusion test, along with the high density lipoprotein cholesterol concentration, correlated inversely and independently with degree and extent of coronary atheromatosis, whereas the low density lipoprotein cholesterol level showed a positive correlation with severity of coronary atheromatosis. The present data argue against the concept of direct atherogenic action of high plasma insulin levels. In contrast, a low and delayed early insulin response might be a marker of enhanced liability to evolution of severe diffuse coronary atheromatosis.

Administration, Oral↗
PubMed1987

Psychosocial work conditions before myocardial infarction in young men.

All male patients in the greater Stockholm area who had survived a myocardial infarction below the age of 45 were examined with regard to medical and psychosocial risk factors 3-6 months after the onset of the infarction. For each patient, a male control subject was randomly selected after matching with regard to age and residence area. In the patient group, coronary angiograms were performed and rated with regard to degree of coronary atherosclerosis. The psychosocial variables were not correlated with degree of coronary atherosclerosis. Excessive work demands combined with boredom at work ("variety" and "intellectual discretion") were significantly more often reported by the patients after adjustment had been made for life style factors. In the multivariate analysis a high LDL/HDL cholesterol ratio, a high cumulative tobacco consumption, high demands in relation to variety at work as well as high demands in relation to influence over work and finally a low alcohol consumption were significant independent predictors of case status. Excessive work demands in themselves did not differentiate cases from controls.

Adult↗
PubMed1986

Antibodies to cardiolipin in young survivors of myocardial infarction: an association with recurrent cardiovascular events.

Antibodies to cardiolipin were measured in 62 survivors of myocardial infarction under age 45 at 3, 12, and 36 months after the acute event. 13 patients (21%) had raised anticardiolipin antibody levels on at least two of the three sampling occasions. Risk-factor profiles and coronary angiographic findings did not differ between the anticardiolipin-positive group and the rest of the patients. No correlation was found between cardiolipin and anti-DNA antibody levels. 8 of the 13 patients with raised anticardiolipin antibody levels experienced additional cardiovascular events during a follow-up of 36-64 months after the first myocardial infarction: cerebral infarction developed in 2, arterial occlusion of the lower limb in 2, new myocardial infarction in 3, pulmonary emboli in 1, and deep-vein thrombosis in 1. These 8 patients had cardiolipin antibody titres of 5 times the mean for voluntary blood donors. Antibodies to cardiolipin are common in young post-infarction patients and should be interpreted as markers of high risk for recurrent cardiovascular events.

Adult↗
PubMed1986

Repeated exercise and redistribution thallium-201 scintigrams in patients with myocardial infarction treated with timolol or placebo.

Repeat exercise thallium-201 scintigrams were performed 2 weeks, 3 months, and 6 months in 27 patients following their first myocardial infarction. All patients were treated with timolol or matching placebo, administered intravenously starting within 5 hours of onset of chest pain. The extent of transient perfusion defects in 15 timolol-treated patients increased significantly between 2 weeks and 3 months compared to a decrease in 12 placebo-treated patients (p less than 0.05). Between 3 and 6 months the extent of transient defects did not change in the two groups, and there was no difference between the groups. The extent of permanent defects was not significantly different between the timolol- and placebo-treated patients on any occasion. However, patients in the timolol group had a decrease in permanent defects with time in contrast to patients in the placebo group (p less than 0.05). Thus, early intervention with timolol in the acute phase of myocardial infarction may have consequences for the postinfarction phase, as reflected in repeat thallium-201 scintigrams.

Adult↗
PubMed1986

Serum lipoproteins and apolipoproteins in young male survivors of myocardial infarction.

Concentrations of serum lipoprotein lipids and apolipoproteins A-I, A-II and B were determined 3-6 months after myocardial infarction in 116 males below the age of 45 and in 116 age-matched controls. Among single variables the sum of cholesterol concentration in VLDL and LDL divided by the HDL cholesterol level was the best discriminator between patients and controls. The concentrations of serum triglycerides, apolipoprotein B, VLDL triglycerides and cholesterol, serum cholesterol, HDL cholesterol and LDL triglycerides, in that order, were better discriminators than was LDL cholesterol level. Among variables reflecting HDL concentration and composition HDL cholesterol was the best discriminator followed by HDL2 cholesterol, apolipoprotein A-I and the HDL cholesterol/apolipoprotein A-I ratio. Multivariate analysis indicated independent significance of elevated VLDL lipid and LDL cholesterol concentrations, and a decreased HDL cholesterol concentration, in relation to MI. The present data suggest that a disturbed triglyceride metabolism, in addition to elevated LDL and decreased HDL cholesterol levels, has an independent and pathogenetic significance for MI at a young age.

Adult↗
PubMed1986

Increased platelet-derived mitogenic activity in plasma of young patients with coronary atherosclerosis.

The early state of atherosclerosis is characterized by a nodular proliferation of smooth muscle cells in the arterial intima. It has been suggested that this proliferation is initiated by platelet-derived growth factor (PDGF) released from aggregating platelets in connection with endothelial injury. In the present study platelet reactivity and mitogenic activity of plasma and serum were compared in young male survivors of myocardial infarction with angiographically demonstrable coronary atherosclerosis and in healthy subjects of similar age. Young post-infarction patients with coronary atherosclerosis had lower ED50 values of ADP-induced platelet aggregation. Furthermore plasma and serum from the patients contained increased amounts of mitogenic activity. Experiments using antibodies against platelet-derived growth factor indicated that the increase in mitogenic activity represented elevated concentrations of free PDGF growth factor in plasma. The results raise the possibility of a connection between increased levels of free PDGF and the proliferative reaction that characterizes early lesion progression.

Adenosine Diphosphate↗
PubMed1986

Genetic and cultural inheritance of serum lipids, low and high density lipoprotein cholesterol and serum apolipoproteins A-I, A-II and B.

The genetic and cultural heritability of serum cholesterol and triglyceride concentrations, as well as of the concentrations of low and high density lipoprotein cholesterol and serum apolipoproteins A-I, A-II and B, were estimated by path analysis in families selected through probands with premature myocardial infarction and in families randomly selected from the general population. Genetic heritability was high for serum cholesterol (0.64) and low density lipoprotein cholesterol (0.67) concentrations, whereas it was lower for high density lipoprotein cholesterol level (0.42). Cultural inheritance was of less importance than genetic inheritance for all cholesterol variables. For serum triglyceride concentration genetic (0.33) and cultural (0.23) heritability was of similar significance. The results for serum apolipoproteins A-I and A-II parallelled those for HDL cholesterol. A marked intergenerational difference was found in the genetic heritability for apolipoprotein B concentration. The parental genetic heritability was 0.14, whereas the genetic heritability was 0.51 among siblings.

Adult↗
PubMed1986

Type A behaviour, education and psychosocial work characteristics in relation to ischemic heart disease--a case control study of young survivors of myocardial infarction.

The interaction of Type A behaviour, psychosocial work environment and education in relation to medical risk factors for IHD was analyzed in a case-control study of male and female post-MI-patients under age 45. In multivariate analysis LDL/HDL-cholesterol ratio and smoking (explaining 27 and 6% of the variance) emerged as the two most important discriminators of patients from control subjects. The third factor, variety of work tasks, explained 5% of the variance. Type A behaviour ranked as factor no. 7, explaining only 2% of the variance and educational level did not reach statistical significance as an independent explanatory factor. When the sample was divided into men and women with high and low education, most of the patient-control difference in Type A and psychosocial work characteristics was found among highly educated men on one hand and women with a low level of education on the other. Thus Type A behaviour seems to be less important and psychosocial work environment more important in adding psychosocial risk to the medically established risk of IHD.

Achievement↗
PubMed1986

Haemostatic function in myocardial infarction.

Coagulation factor VIII, von Willebrand factor, antithrombin, fibrinogen, plasminogen activator capacity, and inhibitors of fibrinolysis, including a recently discovered fast inhibitor of tissue plasminogen activator, were measured three to six months after myocardial infarction in 116 male and 32 female patients aged less than 45 and in 136 age and sex matched random controls. Plasma concentrations of fibrinogen and the fast inhibitor of tissue plasminogen activator were raised in male patients (with or without correction for orosomucoid levels, blood group distribution, tobacco and alcohol consumption, and weight/height index) and plasminogen activator capacity was reduced. In female patients the concentrations of factor VIII, von Willebrand factor, the fast inhibitor of tissue plasminogen activator, alpha 2-antiplasmin, and C1 inhibitor were significantly increased. The increase in factor VIII concentrations depended strongly on a persisting inflammatory response. Multivariate analysis indicated that a combination of fibrinogen and tissue plasminogen activator inhibitor concentrations gave the best independent discrimination between male patients and controls. For female patients the best combination was von Willebrand factor and tissue plasminogen activator inhibitor. Male patients with multiple vessel atheromatosis at coronary angiography had higher fibrinogen concentrations than those with atheromatosis of a single vessel. Atheromatosis was defined as sharp-edged, plaque-like, or irregular indentations, often multiple, into the vessel lumen without features suggesting fibromuscular hyperplasia.

Adult↗
PubMed1986

Relationship of angiographically defined coronary artery disease to serum lipoproteins and apolipoproteins in young survivors of myocardial infarction.

The relationship of serum lipoprotein and apolipoprotein concentrations to angiographically determined coronary artery disease was investigated in 105 consecutive male survivors of myocardial infarction under the age of 45. Concentrations and composition of lipoproteins, lipid indexes, and nonlipid risk factors (tobacco consumption, hypertension, reduced glucose tolerance, and obesity) were related to a recently developed scoring system for semiquantitative estimation of diffuse coronary atheromatosis, as well as to the number and severity of significant coronary artery stenoses. The concentrations of cholesterol in very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL), in combination with serum triglyceride or VLDL triglyceride level, comprised the best set of independent discriminatory lipid variables between patients and control subjects. In the patients, LDL cholesterol and apolipoprotein B levels showed strong relationships to the extent and severity of coronary atheromatosis but not to the number and severity of distinct coronary stenoses. HDL2 cholesterol concentration correlated inversely with the coronary atheromatosis score, whereas other variables reflecting HDL concentration and composition or VLDL lipids were not independently related to any of the coronary scores. The LDL triglyceride level, an index of intermediate-density lipoprotein (IDL) accumulation, was significantly correlated to the coronary atheromatosis score in univariate analysis. Nonlipid risk factors were correlated neither to coronary atheromatosis nor to severity of stenoses. Stepwise multiple regression analyses of data adjusted for age, cumulative tobacco consumption, and weight indicated that 18% of the variation in the coronary atheromatosis score could be accounted for by levels of apolipoprotein B. Addition of other lipoprotein variables or the nonlipid variables hypertension and glucose tolerance did not significantly increase the value of R2. When ratios of lipoprotein lipids and apolipoproteins were included in the regression model, the highest multiple correlation coefficient was obtained with the LDL/HDL cholesterol ratio alone (R2 = .22). The present data demonstrate the importance of elevated LDL cholesterol and apolipoprotein B concentrations for the development of coronary atheromatosis in young male survivors of myocardial infarction. The lack of correlations between the levels of lipoprotein lipids and serum apolipoproteins and the severity of coronary stenoses suggests that mechanisms other than disturbances of lipoprotein metabolism may be involved in the progression of more advanced coronary lesions.

Adult↗
PubMed1985

Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction.

Certain risk factors for myocardial infarction have been linked with disturbances in fibrinolytic activity. The recent development in our laboratory of new sensitive and specific methods for determination of tissue plasminogen activator (t-PA) activity and antigen, as well as the discovery of a new rapid inhibitor of this enzyme, enabled us to study fibrinolytic function in detail in a representative population of postinfarction patients. Seventy-one patients (62 men and 9 women) who had survived a myocardial infarction before the age of 45 were compared with 50 healthy subjects of similar age, three years after the infarction. Low t-PA activity after venous occlusion, mostly explained by high plasma levels of the t-PA inhibitor and to some extent by impaired release of t-PA from the vessel wall, was a frequent finding in the patients. The level of t-PA inhibitor was positively and significantly correlated with levels of serum triglycerides. Our data suggest that reduced fibrinolytic capacity due to increased plasma levels of a rapid inhibitor of t-PA may have pathogenetic importance in myocardial infarction, particularly in patients with hypertriglyceridemia.

Adult↗
PubMed1985

Shortened megakaryocyte-platelet regeneration time in young survivors of myocardial infarction.

Megakaryocyte-platelet regeneration time (MPRT) was determined 6 to 12 months after myocardial infarction in 42 patients below the age of 45 years (mean age +/- SD = 39.4 +/- 4.6, range 23 to 44) and in 11 healthy control subjects by measurement of the reappearance rate of platelet cyclooxygenase activity after oral aspirin. In the young post infarction patients, MPRT was correlated to pertinent metabolic, angiographic, and clinical findings. MPRT for all patients tended to be shorter than in control subjects (t1/2 = 4.53 +/- 1.15 vs 5.22 +/- 0.52; p less than 0.10). Age, present tobacco consumption, serum lipoprotein lipid concentrations, and glucose tolerance, as well as other measured risk factors, did not correlate significantly with MPRT. A marked difference in MPRT, independent of risk factor profile, was present between patients with and without hemodynamically significant stenoses in the coronary angiogram (4.06 +/- 0.92 vs 5.22 +/- 1.07; p less than 0.001). It is suggested that a shortened platelet survival in young post infarction patients is secondary to platelet activation by high-velocity flow and shear forces at the sites of proximal coronary artery stenoses.

Adrenergic beta-Antagonists↗
PubMed1984

Comparative study of echo- and angiocardiographically determined regional left ventricular wall motion in recent myocardial infarction.

We have studied regional left ventricular (LV) wall motion with M-mode, cross-sectional (2D) echocardiography and LV angiography in 50 patients with a recent myocardial infarction. Regional LV wall motion was evaluated according to a 9-segment model. 2D echocardiography permitted information from all, M-mode echocardiography from 8 and angiocardiography from 6 segments. Wall motion was visually classified according to a 5-grade scale. Systolic mean wall velocity (V mean) and its deviation from normal values was calculated from M-mode registrations. 2D echo- and angiocardiography were evaluated in 35 patients and M-mode echo- and angiocardiography in 37. Total agreement in segmental wall motion was seen in 61% when comparing 2D echo- with angiocardiography, and a further 35% showed 1-grade and 4% a 2-grade difference. Corresponding values for comparisons between M-mode echo- and angiocardiography were 59%, 32% and 9%, respectively. Discrepant wall motion grading from the 2D echo- and angiocardiography comparison was seen in 94 of 243 (38%) segments. Approximately one quarter of the discrepancies were either due to minor differences in evaluation or due to wall motion scoring. Discrepancies were seen in 83 of 202 (41%) segments when M-mode echo- and angiocardiography were compared. In 42 (21%) these were attributed to obvious M-mode errors and in 8 (4%) to left ventricular angiography. In 20 further segments, nonidentical subsegmental evaluations were the probable cause of discrepancies, and in 8 (10%) ischaemia during the angiocardiography. Five segmental discrepancies remained unexplained.

Adult↗
PubMedDate not supplied

Secretion of plasminogen activator inhibitor-1 from cultured human umbilical vein endothelial cells is induced by very low density lipoprotein.

Clinical studies have demonstrated an impaired fibrinolytic function in patients with angiographically ascertained coronary artery disease or previous myocardial infarction. This decreased fibrinolytic function is to a major extent explained by the presence of high plasma levels of plasminogen activator inhibitor-1 (PAI-1) and is most common in patients with hyperlipoproteinemias type IIB and IV. To further investigate the association between hypertriglyceridemia and elevated plasma levels of PAI-1, cultured human umbilical vein endothelial cells were exposed to purified lipoproteins isolated from normo- and hypertriglyceridemic (NTG and HTG) individuals. We found that very low density lipoprotein (VLDL) from both NTG and HTG subjects stimulated the secretion of PAI-1 from endothelial cells in a dose-dependent manner. HTG-VLDL at a concentration of 100 micrograms/ml gave rise to a 73% increase in PAI-1 secretion as compared to control cultures, whereas NTG-VLDL only gave rise to a 30% increase (p less than 0.05), indicating that HTG-VLDL is a more potent stimulus to PAI-1 secretion than is NTG-VLDL. Experiments in which endothelial cells were exposed to VLDL subfractions indicated that large VLDL particles, in particular, induce PAI-1 release. Binding experiments demonstrated a specific cellular binding of both NTG- and HTG-VLDL to the cells, but HTG-VLDL bound about four times more effectively than NTG-VLDL. Exposure of the endothelial cells to an LDL receptor antibody was found to block 75% (p less than 0.005) of the VLDL-induced secretion of PAI-1 from the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies↗