Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy.

This study assesses how the newer modalities of tissue Doppler echocardiography and color M-mode flow propagation compare with respiratory variation of Doppler flow in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. We studied 30 patients referred for further evaluation of diastolic function who had a diagnosis of constrictive pericarditis or restrictive cardiomyopathy established by diagnostic tests, including clinical assessment, magnetic resonance imaging, cardiac catheterization, endomyocardial biopsy, and surgical findings. Nineteen patients had constrictive pericarditis and 11 had restrictive cardiomyopathy. We performed 2-dimensional transesophageal echocardiography combined with pulsed-wave Doppler of the pulmonary veins and mitral inflow with respiratory monitoring, tissue Doppler echocardiography of the lateral mitral annulus, and color M-mode flow propagation of left ventricular filling. Respiratory variation of the mitral inflow peak early (peak E) velocity of > or =10% predicted constrictive pericarditis with 84% sensitivity and 91% specificity and variation in the pulmonary venous peak diastolic (peak D) flow velocity of > or =18% distinguished constriction with 79% sensitivity and 91% specificity. Using tissue Doppler echocardiography, a peak early velocity of longitudinal expansion (peak Ea) of > or =8.0 cm/s differentiated patients with constriction from restriction with 89% sensitivity and 100% specificity. A slope of > or =100 cm/s for the first aliasing contour in color M-mode flow propagation predicted patients with constriction with 74% sensitivity and 91% specificity. Thus, the newer methods of tissue Doppler echocardiography and color M-mode flow propagation are equivalent and complimentary with Doppler respiratory variation in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. The additive role of the new methods needs to be established in difficult cases of constrictive pericarditis where respiratory variation may be absent or decreased.

Mechanisms of retarded apical filling in acute ischemic left ventricular failure.

BACKGROUND: We examined the hypothesis that retardation of apical filling as measured by color M-mode Doppler echocardiography in the diseased left ventricle (LV) reflects a decrease in the intraventricular mitral-to-apical pressure gradient. METHODS AND RESULTS: In 9 open-chest anesthetized dogs, micromanometers were placed near the mitral tip and in the apical region. From the color M-mode Doppler images, the time delay (TD) between peak velocity at the mitral tip and the apical region was determined as an index of LV flow propagation. Acute ischemic LV failure was induced by coronary microembolization. Induction of ischemia caused a marked increase in LV end-diastolic pressure and a decrease in LV ejection fraction. The time constant of LV isovolumic apical pressure decay (tau) increased from 31+/-8 to 49+/-16 ms (P<0.001). The peak early diastolic mitral-to-apical pressure gradient (DeltaPLVmitral-apex) decreased from 1.9+/-0.9 to 0.7+/-0.5 mm Hg (P<0.01), and TD increased from 5+/-3 to 57+/-26 ms (P<0.001). The slowing of flow propagation was limited to the apical portion of the LV cavity. The TD correlated with DeltaPLVmitral-apex (r=-0.94, P<0.01) and with tau (r=0.92, P<0.01). Before ischemia, the mitral-to-apical flow propagation velocity far exceeded the velocity of the individual blood cells, whereas during ischemia, flow propagation velocity approximated the blood velocity. CONCLUSIONS: Retardation of apical filling in acute ischemic failure was attributed to a decrease in the mitral-to-apical driving pressure, reflecting slowing of LV relaxation. The slowing of flow propagation appeared to represent a shift in apical filling from a pattern of column motion to a pattern dominated by convection.

Mechanics of intraventricular filling: study of LV early diastolic pressure gradients and flow velocities.

This study investigates mechanisms of left ventricular (LV) intracavitary flow during early, rapid filling. In eight coronary artery disease patients with normal LV ejection fraction we recorded simultaneous LV apical and outflow tract pressures and intraventricular flow velocities by color M-mode Doppler echocardiography. In five anesthetized dogs we also recorded left atrial pressure and LV volume by sonomicrometry. In patients, as the early diastolic mitral-to-apical filling wave arrived at the apex, we observed an apex-outflow tract pressure gradient of 3.5 +/- 0.3 mmHg (mean +/- SE). This pressure gradient correlated with peak early apex-to-outflow tract flow velocity (r = 0.75, P < 0.05). The gradient was reproduced in the dog model and decreased from 3.1 +/- 0.3 to 1.7 +/- 0.5 mmHg (P < 0.05) with caval constriction and increased to 4.2 +/- 0.5 mmHg (P < 0.001) with volume loading. The pressure gradient correlated with peak early transmitral flow (expressed as time derivative of LV volume; r = 0.95) and stroke volume (r = 0.97). In conclusion, arrival of the early LV filling wave at the apex was associated with a substantial pressure gradient between apex and outflow tract. The pressure gradient was sensitive to changes in preload and correlated strongly with peak early transmitral flow. The significance of this gradient for intraventricular flow propagation in the normal and the diseased heart remains to be determined.

Early diastolic intraventricular filling pattern in acute myocardial infarction by color M-mode Doppler echocardiography.

The aim of the present study was to investigate whether slowing of mitral-to-apical filling is present in patients with acute myocardial infarction (AMI). Twenty-eight patients with their first AMI were examined by color M-mode Doppler echocardiography. Twenty-eight age- and sex-matched healthy individuals served as control subjects. From the color M-mode Doppler images, we measured the time difference (TD) between occurrence of peak flow velocity at the mitral tip and in the apical region by a blinded analysis. The TD was increased in the AMI group compared with the control subjects (70 +/- 60 versus 40 +/- 30 msec, p = 0.02) and correlated with peak SGOT (r = 0.46, p = 0.02) and age (r = 0.57, p < 0.01). In the 15 patients with anterior AMI, the correlation between TD and SGOT was better (r = 0.68, p < 0.01). This study demonstrated slowing of early diastolic mitral-to-apical flow propagation in patients with AMI. Infarction size and age appear to be of importance for the retardation of mitral-to-apical flow propagation.

Results of intensive long-term treatment of familial hypercholesterolemia.

Fifty-seven patients with familial hypercholesterolemia (FH) with mean age of 48 years (range 30 to 69), participated in a follow-up examination 5.5 years after the completion of a 1-year trial with lovastatin, cholestyramine, probucol, or omega-3 fatty acids. The goals were to record quality of life, compliance to treatment, adverse effects, and clinical outcome. The quality of life was similar to that in a Norwegian reference population. The factors causing most distress to patients were keeping a diet low in saturated fats, taking medication, and fear of death. The medication was mostly prescribed in maximum dosages. At follow-up, the reduction in total cholesterol was 36% (p < 0.05), low-density lipoprotein (LDL) cholesterol 38% (p < 0.05), triglycerides 20% (p < 0.05) compared with being on diet therapy only. High-density lipoprotein (HDL) cholesterol increased 8% (p < 0.05). Intake of saturated and monounsaturated fat increased 1.5% and 1.7% (p < 0.05), respectively; polyunsaturated fat was unchanged. Three patients experienced myocardial infarction, of whom 2 died and 1 developed angina pectoris. Before the start of lovastatin treatment, 27 coronary events occurred per 1,000 patient-years in this group compared with 12 events per 1,000 patient-years thereafter. Of 28 patients reporting adverse events, 4 discontinued lovastatin and 3 discontinued cholestyramine. Several practical and psychological difficulties were associated with FH. Long-term intensive lipid-lowering therapy was possible in FH outpatients without loss of effect and with good compliance to therapy. Intensive therapy, today is, however, not sufficient for many FH patients to reach a therapeutic goal of LDL cholesterol < 4.0 mmol/L. More potent lipid-lowering agents are needed.

Increased risk of heart valve regurgitation after mediastinal radiation for Hodgkin's disease: an echocardiographic study.

OBJECTIVE: To assess by echocardiography the occurrence and degree of late cardiac sequelae after treatment for Hodgkin's disease by radiation and chemotherapy. PATIENTS AND METHODS: In Norway from 1980 to 1988, 129 patients < 50 years old with Hodgkin's disease had curative treatment with mediastinal radiation, with or without chemotherapy. 116 (90%) of these patients (mean (SD) age 37 (7) years, 67 males) were examined by echocardiography 5-13 years after treatment. 40 healthy individuals (mean (SD) age 40 (11), 20 males) were examined as controls. All those examined were in regular sinus rhythm. RESULTS: Grade > 1 (scale 0-3) aortic and/or mitral valvar regurgitation was found in 24% of the patients (15% aortic, 7% mitral, and 2% aortic+mitral), affecting 46% of the females v 16% of the males (P < 0.001). Female gender was a significant risk factor for aortic and mitral regurgitation (odds ratio 4.7, 95% confidence interval 2.0 to 11.2), whereas age, period of follow up, radiation dose, and chemotherapy were not. Thickened pericardium was diagnosed in 15% of the patients. No risk factors were identified. No cases of pericardial thickening or valvar regurgitation grade > 1 were recorded in the control group. Mean values for measured and calculated indices of systolic and diastolic function were within the normal range for patients and controls. The patients had reduced E/A ratio compared with the healthy controls (E/A 1.1 v 2.0, P < 0.001). CONCLUSIONS: Abnormal left sided valvar regurgitation was detected in one fourth of the patients, affecting the aortic valve in more than half of the cases. Females had an increased risk of valvar regurgitation. Echocardiographic screening after high-dose mediastinal radiation is recommended.

Intraventricular early diastolic velocity profile during acute myocardial ischemia: a color M-mode Doppler echocardiographic study.

The aim of the study was to investigate the effect of acute myocardial ischemia on the early diastolic mitral-to-apical velocity profile. Intraventricular filling velocities were measured by color M-mode Doppler echocardiography, which allows simultaneous measurements of velocities at multiple sites. Twenty patients were examined during angioplasty and eight dogs during transient coronary artery occlusion. Velocities at each 0.46 cm level from the mitral tip toward the apex were determined at the time of peak early transmitral velocity. Before angioplasty, early diastolic flow velocities decreased progressively from the mitral tip toward the apex. During angioplasty, intraventricular velocities showed a more abrupt decrease from the middle region toward the apex (p < 0.05). A similar change in the mitral-to-apical profile was found during myocardial ischemia in dogs (p < 0.05). Also, there was a decrease in peak early transmitral velocity (p < 0.01) and peak early transmitral pressure gradient (p = 0.06). Volume loading and constriction of the caval veins performed in the nonischemic ventricle did not appear to change the mitral-to-apical velocity profile. Regional myocardial ischemia was associated with a change in the mitral-to-apical velocity profile as measured by color M-mode Doppler echocardiography. The altered filling pattern could not be explained by changes in loading conditions and may reflect impaired relaxation of the ischemic ventricle.

Visual assessment of intra ventricular flow from colour M-mode Doppler images.

Left intra ventricular filling was studied by colour M-mode Doppler ultrasound to determine whether the flow pattern can be assessed visually, and explore its relation to left ventricular (LV) function. Patients with coronary artery disease (CAD) or dilated cardiomyopathy (DCM) were divided into three groups according to angiographically evaluated LV function. The groups were compared with a control group of 54 healthy volunteers. The mitral to apical delay of early diastolic flow was qualitatively assessed from printed colour M-mode images, twice by four independent observers blinded to the subject's status. The repeatability of the assessments as determined by the kappa statistic was good intra observer (kappa = 0.75) and moderate inter observer (kappa = 0.53). The CAD-group with angiographically normal LV function (n = 25) had flow patterns resembling those observed in the control group. The group with ejection fraction (EF) < 50% (n = 19) had flow patterns clearly different from the control group. Patients with regional wall motion abnormality (RWMA) but EF > 50% (n = 16) exhibited flow patterns intermediate between the control and the low EF group. Among the 50 CAD patients there was a negative correlation between EF and the presence of delay of apical peak velocity (Spearman's rs = -0.62, p < 0.0001). A visible delay of apical peak velocity had a sensitivity towards DCM of 83% and specificity of 75%. The sensitivity towards CAD with either RWMA or low EF was 55% and the specificity 75%. In conclusion, visual assessment of intra ventricular flow patterns was feasible and allowed discrimination between normal and diseased ventricles.

Intracavitary filling pattern in the failing left ventricle assessed by color M-mode Doppler echocardiography.

OBJECTIVES: The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade. BACKGROUND: Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle. METHODS: In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling. RESULTS: There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 +/- 6 (mean +/- SEM) to 101 +/- 17 ms (p < 0.05) and from 21 +/- 8 to 80 +/- 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 +/- 3 to 43 +/- 5 ms (p < 0.05) and from 31 +/- 1 to 39 +/- 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure however, peak apical filling velocity occurred 53 +/- 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution. CONCLUSIONS: Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardial ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.

Abnormalities of left ventricular filling in patients with coronary artery disease: assessment by colour M-mode Doppler technique.

In 54 healthy individuals and 107 patients with coronary artery disease, intraventricular early filling velocities were recorded by colour M-mode Doppler. The time difference between the occurrence of peak velocity in the apical region and at the mitral tip was calculated, and normalized by dividing it by the mitral to apical distance. Transmitral velocities were determined by the single pulsed Doppler technique. The patients were divided into groups according to systolic function as assessed by left ventriculography. The normalized time difference was similar in the reference group (12 +/- 8 ms.cm-1) and the patient group with no electrocardiographical signs of previous infarction and normal ventriculography (16 +/- 16 ms.cm-1). It increased significantly in the group with infarction and/or regional systolic dysfunction (43 +/- 21 ms.cm-1), and a further increase was present in the group with severely impaired ventricles (53 +/- 14 ms.cm-1). The ratio between peak early and late transmitral velocity fell significantly in the group with infarction and/or regional systolic dysfunction, but was normalized in the group with severely impaired ventricles. Colour M-mode Doppler shows that apical filling is delayed in patients with injured left ventricles due to coronary artery disease. This delay increases with progression of ventricular injury. The technique may be an important addition to transmitral pulsed Doppler in assessing left ventricular filling.

Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography.

BACKGROUND: Color M-mode Doppler echocardiography has been suggested as a new noninvasive technique for assessing left ventricular diastolic function. The present study investigated intraventricular filling pattern by color M-mode Doppler in patients during percutaneous transluminal coronary angioplasty (PTCA). In a dog model of myocardial ischemia, the color M-mode flow pattern was related to indices of global and regional myocardial function. METHODS AND RESULTS: From color M-mode images, the time difference (TD) between occurrence of peak velocity in the apical region and at the mitral tip was determined in 20 patients and eight anesthetized dogs during coronary occlusions. During PTCA, the timing of peak velocity was progressively delayed from mitral valve to apex. Consistent with this, the dog model showed delayed apical filling during coronary occlusion; TD increased from 18 +/- 4 to 71 +/- 9 milliseconds (P < .01). In the ischemic region, systolic shortening (sonomicrometry) decreased from 20 +/- 3% to -5 +/- 2% (p < .01). The one-third filling fraction decreased from 59 +/- 5% to 31 +/- 6% (P < .01) and correlated with TD (r = .85, P < .01). The time constant of isovolumic relaxation (tau) increased slightly and correlated with TD (r = .81, P < .01). Pacing tachycardia, caval constriction, and volume loading were performed to mimic the ischemia-induced changes in heart rate, stroke volume, and intracavitary filling pressure, respectively. There were no significant changes in TD or tau during these interventions. CONCLUSIONS: Color M-mode Doppler echocardiography showed a marked delay of apical peak filling velocity during PTCA. The experimental data suggest that this reflects retarded filling of the ischemic ventricle. Thus, color M-mode Doppler may provide a useful method for assessing diastolic dysfunction.

[Familial hypercholesterolemia--intensive diet therapy combined with drug therapy]. / Familiaer hyperkolesterolemi--intensiv kostbehandling i kombinasjon med medikamentell behandling.

The aim of the investigation was twofold: to study the effect of lovastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, alone and in combination with other lipid lowering drugs in an open 48 week single centre study, and to study if lipid lowering drugs influence adherence to diet in adult patients with familial hypercholesterolemia. Lovastatin monotherapy (80 mg daily) for 12 weeks reduced serum cholesterol, LDL-cholesterol and triglycerides levels by 36%, 44% and 24% respectively. HDL-cholesterol level was increased by 12%. The addition of 16 g cholestyramine daily further increased the reduction of total cholesterol and LDL-cholesterol levels by 17% and 24% respectively. Addition of 1 g probucol daily decreased total cholesterol, LDL-cholesterol and HDL-cholesterol levels by 9%, 5% and 27% respectively. Addition of omega-3-fatty acids (3.6 g daily) reduced total cholesterol, LDL-cholesterol and triglycerides levels by 10%, 12% and 20% respectively. Administration of potent lipid lowering agents did not influence adherence to a diet with a mean daily fat energy of 21% (CI: 20-22), cholesterol of 177 mg (CI: 157-196) and P/S ratio of 0.75 (CI: 0.66-0.84). A significant increase in liver enzymes was recorded in only one patient. One patient was withdrawn from the study because of myositis.

Correlations between left ventricular mass and systolic blood pressure at rest and during maximal exercise in moderately hypertensive men.

We examined 87 men with moderate hypertension (diastolic blood pressure, DPB, greater than or equal to 95 and less than 110 mmHg) (mean age 45, range 22-64, years) with echocardiography and maximal ergometer bicycle test. Left ventricular mass index (LVMI) was calculated according to the Penn convention. Mean LVMI was 126 (60-210) g/m2. The maximal systolic blood pressure (SBP) during exercise was on average 217 (155-260) mmHg. Linear regression analysis revealed a significant correlation between LVMI and SBP at rest (r = 0.48, P less than 0.001) and during exercise (r = 0.39, P less than 0.001). Multiple regression analysis correcting for differences in age, cumulative work and cholesterol level revealed a significant correlation between LVMI and SBP at rest (t = 4.07, P less than 0.0001) and during exercise (t = 3.25, P = 0.002). Thus in patients with established, moderate hypertension exercise SBP is not more predictable for LVMI than is SBP at rest.

Validity of the ECG diagnosis of left ventricular hypertrophy in normotensive and moderately hypertensive men when using the echocardiographic assessment of left ventricular mass index as reference.

The diagnostic validity of ECG criteria for left ventricular hypertrophy (LVH) was assessed in 100 men aged 22-64 (mean 47) years with moderate hypertension (Group 1) and 95 age-matched normotensive men (Group 2) using echocardiographic recordings of LV mass index (MI) as reference. A diagnosis of LVH was made in subjects with LVMI greater than or equal to 125 g/m2. Mean LVMI was 126 +/- 34 g/m2 in Group 1 vs. 100 +/- g/m2 in Group 2 (P less than 0.001), and the prevalence of LVH was 48% and 11% respectively (P less than 0.001). The mean ECG voltage according to Sokolow-Lyon (S-L) was 28 +/- 8 mm in Group 1 and 27 +/- 7 mm in Group 2 (NS); with 19% having LVH in Group 1 and 14% in Group 2 (NS). Using the Cornell criterion Group 1 had on average 15 +/- 6 mm vs. 12 +/- 5 mm in Group 2 (P less than 0.001), but only two Group 1 patients had LVH. In Group 2 a significant negative correlation between age and S-L voltage was found (r = 0.33, P less than 0.001). LVMI was not correlated with any of the two voltage criteria using linear regression analysis whereas multiple regression analysis revealed a weak, but significant correlation between LVMI and S-L voltage in Group 1 (t = 2.06, P = 0.04). No subject had LV strain pattern or LVH according to the Romhilt Estes point score system. In the assessment of possible LVH in normal or moderately hypertensive men less than 65-70 years of age, ECG has limited value.

Diurnal and monthly intra-individual variability of the concentration of lipids, lipoproteins and apoproteins.

Diurnal and monthly variability of the serum concentration of lipids, lipoproteins and apoproteins were examined in 11 healthy subjects aged 32-63 (mean 46) years. For diurnal measurements, blood samples were drawn at 0800, 1200, 1500, 1800, and 2100 hours. The variability over 1 month was assessed from four analyses taken weekly at 0800 hours after at least 8 h fast. The analytical variability expressed as mean coefficient of variation (CV) ranged from 0.95% for cholesterol to 7.6% for apoprotein B. The mean CVs for diurnal biological variability were 2.4% for cholesterol, 3.5% for HDL-cholesterol, 5.1% for LDL-cholesterol, 29.5% for triglycerides, 6.5% for apoprotein A and 6.5% for apoprotein B. The respective biological CVs for monthly variability were 4.2%, 4.1%, 5.2%, 20.7%, 9.4% and 9.7%. A repeated-measures ANOVA revealed a significant increase of triglycerides (p less than 0.01) and decrease of LDL-cholesterol (p less than 0.01) during the day. Within 1 month, apoprotein A tended to rise (0.05 less than p less than 0.10). Although the best reproducibility was found for cholesterol, the results obtained indicate that six tests have to be taken before and after intervention by drug or diet to detect a reduction of 10% in an individual with a probability of 0.95.

Is left ventricular mass in apparently healthy, normotensive men correlated to maximal blood pressure during exercise?

In 95 apparently healthy normotensive men aged 21-69 (mean 44) years with supine blood pressure (BP) less than 150/90 mmHg when less than 50 years, and less than 160/95 when greater than or equal to 50 years of age, left ventricular mass (LVM) was measured by M-mode echocardiography and related to maximal BP during a symptom-limited ergometer bicycle test. Mean LVM was 195 (+/- 43) g and LVM index (I) 101 (+/- 20) g m-2 body surface area (BSA). The subjects were subdivided into two groups: Group 1 = 28 subjects (29%) with LVM greater than or equal to 220 g, and Group 2 = 67 subjects (71%) with LVM less than 220 g. Group 1 had a slightly larger BSA (P less than 0.05), weight (P less than 0.05) and resting systolic BP (P less than 0.05). A higher prevalence of smokers (P less than 0.01) and serum cholesterol levels (P less than 0.05) were also noted among Group 1 subjects, who had a higher maximal systolic BP during exercise (P less than 0.0001). Using linear regression analysis, significant positive correlations were observed between LVM and systolic BP at rest (r = 0.20, P less than 0.05), and maximal exercise systolic BP (r = 0.32, P less than 0.001). When correcting for differences in age, weight, body surface area, physical performance, smoking and hours of exercise per week, multiple regression analysis revealed a significant between LVM and maximal systolic BP (t = 2.38, P = 0.020, Partial F = 5.64).(ABSTRACT TRUNCATED AT 250 WORDS)

[Serum cholesterol in a selected group of healthy individuals aged 20-70 years. Influence of age and sex]. / Serumkolesterol hos en selektert gruppe friske individer i alderen 20-70 år. Innflytelse av alder og kjønn.

Several epidemiological studies world-wide have shown that serum (s)-cholesterol is a major risk factor for development of atherosclerosis. The risk of coronary heart disease increases with increasing s-cholesterol, and the relationship is continuous and curvilinear, with an increase with s-cholesterol levels greater than or equal to 5.2 mmol/l (200 mg/dl). Therefore, the recommended s-cholesterol is below 5.2 mmol/l. The purpose of this study was to investigate the level of s-cholesterol in a group of apparently healthy Norwegians aged 20-70 years in 1987. 94 men and 93 women were examined. We found, as others have shown before, that s-cholesterol increases significantly with age both among men and among women. The intersexual differences are not statistically significant. 69% of the total group had s-cholesterol greater than or equal to 5.2 mmol/l. These findings should have consequences for dietary policy in Norway.

Influence of age on physical performance, heart rate and systolic blood pressure response during exercise in apparently healthy women.

In order to assess normal physical performance in women, a near-maximal ergometer bicycle test was performed in 95 healthy non-athletic women aged 24-65 years (mean 44 years). The starting load was 50 W and the load was increased by 50 W every 4 min until exhaustion. Physical performance was expressed as cumulative work in Watts (W). All subjects had normal two-dimensional, M-Mode and Doppler echocardiographic findings. Physical performance was similar in the age groups 24-29, 30-39 and 40-49 years. Mean cumulative work among subjects less than 50 years was 1208 (600-1800) W vs. 947 (500-1600) W (p less than 0.001) in those greater than or equal to 50 years. Physical performance was similar in the age groups 50-59 and 60-65 years (NS). An inverse correlation between maximal heart rate and age was found (r = 0.64, p less than 0.001). Systolic blood pressure increased more during exercise in the subjects greater than or equal to 50 years (p less than 0.001 vs. those aged less than 50 years). M-Mode echocardiographic measurements at rest were similar in all age groups. These findings may be related to reduction in beta-sympathetic stimulation during exercise in women greater than or equal to 50 years of age.

M-mode echocardiographic findings in apparently healthy, non-athletic Norwegians aged 20-70 years. Influence of age, sex and body surface area.

In order to assess M-mode echocardiographic recordings in a normal Norwegian population, 190 apparently healthy subjects (95 women and 95 men) aged 21-69 years were examined with an Irex Meridian system. Measurements were performed according to criteria recommended by the American Society of Echocardiography. Absolute values for all parameters except for left ventricular (LV) shortening fraction (SF) were greater in men (P less than 0.001). When corrected for body surface area (BSA), the differences between the two genders were far less pronounced. Women had greater left atrium (LA) (P less than 0.01) and LV end-diastolic diameter (EDD) (P less than 0.001), whereas the interventricular septum in end-diastole (IVS-ED) (P less than 0.05) and LV posterior wall (PW) in ED (P less than 0.001) were thicker in men. Only weak correlations between age and the various echocardiographic parameters with r-values less than or equal to 0.30 were observed. It is recommended that BSA corrected values should be preferred since the differences between men and women are negligible. When absolute values are used, different normal ranges for both sexes should be applied.