ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTThe 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.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTChildren in the eastern part of Finland have higher serum total and low-density lipoprotein from the western part of the country showed the greatest differences. Prepubescent boys 3 to 12 years old living in the west but with grandparents from the east had total and LDL cholesterol levels similar to those of boys living in and descended of grandparents from the east, despite their diet being of the western type. Thus, although diet is known to be a major determinant of serum cholesterol level,genetic factors also seem to play a role.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTUsing phosphorous nuclear magnetic resonance, we have previously demonstrated that patients with heart failure often exhibit abnormal forearm muscle metabolism during forearm exercise. To determine if this altered metabolism is due to reduced muscle flow, we measured forearm blood flow with plethysmography and forearm muscle inorganic phosphate (P), phosphocreatine (PCr), and pH with 31P nuclear magnetic resonance spectroscopy at rest and during mild forearm exercise (0.2, 0.4, and 0.6 W) in 21 men with heart failure and in 12 aged-matched normal male subjects. The Pi/PCr ratio was correlated with power output and the slope of this relationship was used as an index of forearm metabolism. At rest, both groups had similar Pi/PCr ratios (normal subjects 0. 11 ±- 0.05; patients with heart failure 0.11 + 0.03; p = NS) and forearm blood flows (normal subjects 2.9 1.4 ml/min/100 ml; patients with heart failure 2.6 1.2 ml/min/100 ml; p = NS). In both groups, exercise resulted in a progressive increase in both Pi/PCr and forearm blood flow as power output increased. However, the patients exhibited a steeper slope of the Pi/PCr-to-power output relationship than did the normal subjects (normal subjects 1.4 + 0.6 Pi/PCr U/W; patients with heart failure 3.0 + 2.4 Pi/PCr U/W; p < .03). In contrast, forearm blood flow was similar in both groups during exercise (at 0.2 W, 6.3 + 3.3 and 6.8 ± 3.2 ml/min/100 ml in normal subjects and patients with heart failure, respectively; at 0.4 W, 8.7 ± 6.5 and 8.3 ± 3.3; at 0.6 W, 12.8 ± 7.9 and 12.0 ± 4.6; all p = NS). Nine of the 21 patients with heart failure had slopes of the Pi/PCr-to-power output relationship above the normal range. These nine patients also had forearm blood flows comparable to flows observed in the normal subjects. These data indicate that forearm muscle metabolism during forearm exercise is altered in a subpopulation of patients with heart failure. This metabolic alteration does not appear to be due to decreased muscle blood flow, suggesting that other mechanisms, such as alterations in mitochondrial population or substrate utilization, may be responsible.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTThe dynamic increase in oxygen uptake ('902) at the start of exercise reflects the circulatory adjustments to metabolic changes induced by the exercise. Because '902 measured at the lungs is the product of pulmonary blood flow and arteriovenous oxygen difference, pathologic conditions affecting the capacity of these factors to change would be expected to alter V02 kinetics. To determine whether measurement of VO2 kinetics can detect conditions in which the pulmonary blood flow response to exercise is abnormal,'02 was measured, breath-by-breath, during the transition from rest to exercise in 13 adults wth cyanotic congenital heart disease (central venoarterial shunting) and in nine normal subjects. The increase in V02 above baseline during the first 20 sec of exercise (phase I),reflecting the immediate increase in pulmonary blood flow, was diminished in the patients compared with that in normal subjects (14.8 10.9 vs. 49.8 19.2 ml of oxygen) (p < .001). The patients' phase I responses correlated with their reported physical activity tolerance (p < .01). In addition, the second phase of the '2 response kinetics was prolonged in patients compared with normal subjects (half-time = 63 13 vs 15 + 13 sec) (p < .001). We conclude that striking disturbances in -902 kinetics occur in patients with cyanotic congenital heart disease and that these measurements provide a useful noninvasive means of evaluating the degree to which the increase in pulmonary blood flow is constrained in response to exercise.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTInformation on the hemodynamic effects of vasopressin (AVP) in healthy humans is very limited despite its known importance in body fluid homeostasis and release in pathologic states such as hemorrhage and trauma. Although it is a potent vasoconstrictor in vitro, it does not cause the expected rise in arterial pressure when given systemically to animals with intact baroreflexes. It has been proposed that this is because AVP facilitates baroreflex control of the circulation. In this study, we assessed the effect of infusion of AVP on resting circulatory variables and on the baroreflex control of forearm vascular resistance and heart rate in healthy men. AVP in a dose of 0.4 ng/kg/min, which raised plasma level of AVP to 24 ± 4 pg/ml, a value known to have a significant antidiuretic effect, had little hemodynamic effect, producing only mild bradycardia and a slight increase in central venous pressure. Reflex changes in heart rate during neck suction (- 15 and -30 mm Hg) and neck pressure (+ 15 and + 30 mm Hg) were not altered. Reflex responses to lower body negative pressure and to its release were also unchanged by this dose of AVP. In contrast, a higher dose of AVP (4 ng/kg/min),which raised plasma levels to 290 ± 41 pg/ml, a concentration known to occur as a result of hemorrhagic hypotension and circulatory stresses, did cause hemodynamic changes. There was tachycardia (from 63 ± 2 to 68 ± 2 beats/min), a decrease in pulse pressure (from 62 ± 2 to 53 ± 2 mm Hg), an increase in central venous pressure (from 2.6 ± 0.5 to 4.1 0.4 mm Hg), and surprisingly in view of the known vasoconstrictor effect of AVP, an increase in forearm flow (from 4.4 0.7 to 5.9 ± 1.2 ml/min/100 ml tissue) and a decrease in forearm vascular resistance (from 24 ± 4 to 18 ± 3 U);there was no significant change in mean arterial pressure (from 83 ± 2 to 83 ± 3 mm Hg). Reflex changes in heart rate were unaltered. The maximal vasoconstrictor response in the forearm attained during lower body negative pressure was not influenced by AVP, but the reflex vasodilator response to the sudden release of lower body negative pressure was significantly augmented, vascular resistance falling to 23 ± 4 U before and 13 ± 2 U during AVP. The unanticipated findings in this study include the biphasic changes in heart rate with increasing doses of AVP, the absence of a pressor response, and the vasodilatation in forearm vessels. We speculate that the vasodilatation in the forearm is the result of an increase in central venous pressure and a facilitated baroreflex-mediated withdrawal of sympathetic tone.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTTo evaluate the relationship between plasma levels of immunoreactive atrial natriuretic hormone (IR-ANH) and different hemodynamic parameters in man, we studied 34 patients undergoing right heart catheterization. Plasma levels of IR-ANH in blood samples withdrawn from the femoral vein (n = 28), right ventricle (n = 27), and left ventricle (n = 17) were determined by radioimmunoassay. Right atrial pressure, pulmonary arterial wedge pressure, heart rate, and mean arterial pressure were found to be independent and significant predictors of IR-ANH plasma levels. The closest correlations were between right atrial pressure and either right ventricular IR-ANH levels (r = .78, p > .001) or femoral vein IR-ANH levels (r = .52, p < .006). Five patients with isolated left ventricular failure had elevated IR-ANH levels out of proportion to their right atrial pressure levels. Pulmonary arterial wedge pressure also correlated with right ventricular IR-ANH levels (r = .46, p < .002) and with femoral vein IR-ANH levels (r = .58, p < .002). A single patient with isolated right heart failure had markedly elevated IR-ANH levels despite normal pulmonary arterial wedge pressure. Right ventricular levels were twice femoral vein levels and were closely correlated (181 + 40 vs 90 + 20 pmol/liter; r = .90, p < .001). Right ventricular and left ventricular levels were almost identical (155 + 46 vs 146 43 pmol/liter; r = .99, p < .001). Patients with volume overload states had elevated IR-ANH levels. We conclude that distention of either atrium may act as a potent stimulus for IR-ANH release in man, although circulating levels may be clinically ineffective in producing diuresis and natriuresis. Further investigations into the mechanisms that regulate IR-ANH secretion in man should include atrial pressure measurements.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTLeft ventricular filling dynamics were investigated in 24 patients with aortic stenosis (AS). Biplane cineangiography was performed with simultaneous micromanometry in these 24 patients and in six control subjects. Twelve of the patients with AS had moderate hypertrophy with a left ventricular muscle mass index of less than 180 g/m2 (AS 1 group) and 12 had severe hypertrophy with an index of 180 g/m2 or more (AS2 group). Filling dynamics were also evaluated postoperatively in eight patients in the AS 1 and six patients in the AS2 group. Preoperatively, end-diastolic and end-systolic volume indexes were larger and ejection fraction was lower in the AS2 compared with the control or AS 1 group. Percent volume increase during the first half of diastole (%V 1) was smaller in the AS 1 than in the AS2 group. Peak filling rate in the first half of diastole (PFRl) was higher in the AS2 than in the control or in AS l group, while peak filling rate in the second half of diastole (PFR2) was considerably greater in the AS 1 group than in the other two groups. The time constant of left ventricular pressure decline, an index of the rate of relaxation, was prolonged in the AS2 group. In contrast, mitral valve opening pressure (MVOP) was significantly higher in this group than in the other two groups. The constant of left ventricular chamber stiffness was slightly but not significantly greater in both AS groups than in the control subjects. After surgery in patients in the AS 1 group, preoperatively reduced %V had increased and preoperatively enhanced PFR2 had decreased. In patients in the AS2 group, excluding one with a persistent low ejection fraction after surgery, preoperatively enhanced PFR1 decreased in association with a decrease in MVOP. Thus, left ventricular filling dynamics vary in patients with AS depending on the degree of left ventricular hypertrophy and systolic function. In patients with AS and moderate hypertrophy %V1 is slightly reduced but is compensated for by a forceful atrial contraction. In those with severe hypertrophy and systolic dysfunction increased driving pressure allows %VV1 to remain within normal limits, despite prolonged left ventricular relaxation and decreased elastic recoil. Both changes in left ventricular filling dynamics tend to normalize after surgery in association with a reduction in left ventricular hypertrophy and/or an improvement of systolic function.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID