Comparative effects of propranolol, timolol and metoprolol on myocardial infarct size after experimental coronary artery occlusion.

The effects of equiblocking doses of three beta-adrenergic blocking agents, propranolol, timolol and metoprolol, on myocardial infarct size were evaluated in 28 dogs after acute experimental coronary artery occlusion. Heart rate, arterial pressure and arterial free fatty acid concentration were measured in an attempt to evaluate their effects on the extent of myocardial injury. The zone at risk of infarction in each dog 1 minute after left anterior coronary artery occlusion was assessed by injecting highly radioactive albumin microspheres into the left atrium, and the hypoperfused zone was determined by autoradiography. After 15 minutes, the dogs were randomized into four groups: control dogs (n = 7), propranolol-treated dogs (1.2 mg/kg intravenously, n = 7), timolol-treated dogs (0.2 mg/kg intravenously, n = 7) and metoprolol-treated dogs (1.2 mg/kg intravenously, n = 7). After 6 hours, the dogs were killed. The left ventricle was sliced and stained with triphenyl-tetrazolium chloride for measurement on infarct size. The same slices were then autoradiographed for measurement of the hypoperfused zone. The percent of hypoperfused zone that evolved to infarction (the ratio of infarct size to hypoperfused zone) was 90.4 +/- 1.9% in the control group, 72.4 +/- 2.4% in the propranolol-treated dogs (p less than 0.05 versus control group); 57.9 +/- 4.4% in the timolol-treated dogs (p less than 0.01 versus control group; p less than 0.05 versus propranolol) and 54.4 +/- 3.7% in the metoprolol-treated dogs (p less than 0.01 versus control group; p less than 0.05 versus propranolol). Thus, propranolol, timolol and metoprolol reduced myocardial infarct size in dogs by 20, 36 and 40%, respectively, after experimental coronary artery occlusion. Metoprolol and timolol protected the ischemic myocardium more effectively than did propranolol.

Compression ultrasonography in hospitalized patients with suspected deep venous thrombosis.

Compression ultrasonography was compared with contrast venography in 215 hospitalized patients (218 limbs) with suspected deep venous thrombosis. All scans were performed using a 5-MHz linear-array scanner. The calf veins were not assessed owing to their small caliber. Distribution of deep venous thrombosis was proximal in 113 of 215 patients (number of limbs with deep venous thrombosis being the same as the number of patients) and limited to the calf veins (distal) in 29 patients. Deep venous thrombosis was detected by compression ultrasonography in 101 of 113 patients (sensitivity, 89%) and falsely diagnosed in two of 76 limbs (73 patients) with negative venographic results (specificity, 97%). The method was less sensitive below the knee, where deep venous thrombosis of the distal popliteal vein was not detected in five of 10 patients as compared with seven of 103 patients with thrombus extension above the knee. Pelvic vein deep venous thrombosis (n = 34) was detected by compression ultrasonography in 71% of the patients. The results of this study indicate that venography may be omitted in patients where compression ultrasonography demonstrates proximal deep venous thrombosis. In patients with negative compression ultrasonographic results, however, venographic verification is needed since venography has a considerably higher sensitivity than compression ultrasonography in detecting isolated iliac and calf vein deep venous thrombosis.

Cellular lipid accumulation in different regions of myocardial infarcts in cats during beta adrenergic blockade with timolol.

The effects of non-selective beta adrenergic blockade on intracellular lipid accumulation in hearts with acute ischaemia were studied by electron microscopy of myocardial biopsy specimens using quantitative stereological techniques. Pentobarbital anaesthetised cats with coronary ligation were divided into eight controls and eight cats treated with timolol intravenously just before ligation. Biopsy specimens were collected from ischaemic, borderline, and normally perfused myocardium, defined by an in vivo injection of fluorescein and verified by regional myocardial blood flow measurements with 15 microns radiolabelled microspheres. During a 3 h occlusion period timolol treated cats had a lower heart rate, left ventricular dP/dt, and plasma free fatty acid concentration. In control cats the cytosolic volume fraction of lipids was 0.71 X 10(-3) in non-ischaemic myocardium, 2.63 X 10(-3) in central ischaemic tissue, and 6.53 X 10(-3) in borderline tissue. Timolol reduced the appreciable lipid accumulation in borderline tissue by 24% (to 4.97 X 10(-3)) compared with controls, whereas accumulation in central ischaemic tissue was not affected. Thus timolol diminished lipid accumulation in borderline myocardial tissue. The mechanism is most likely related to reduced ischaemic intensity and better preserved metabolic function.

Is reduced cardiac performance the only mechanism for myocardial infarct size reduction during beta adrenergic blockade?

Equal reductions in heart rate (44 beats X min-1) were obtained in cats by treatment with either the beta blocking agent timolol or alinidine, an agent claimed to cause bradycardia without interfering with beta adrenoceptor function. Infarct size was measured by staining with triphenyltetrazolium-chloride after 5 h of coronary occlusion and related to the area of hypoperfused myocardium as measured by autoradiography. Regional myocardial blood flow was measured by 15 micron radiolabelled microspheres. Compared with the control cats, in whom 87.4 (SEM 2.2)% of hypoperfused myocardium developed into necrosis, timolol reduced infarct size to 65.8 (SEM 2.6)% (p less than 0.001) and alinidine to 76.2 (SEM 3.1)% (p less than 0.01) of the hypoperfused area. Timolol reduced infarct size more than did alinidine (p less than 0.01). Necrosis was more extensive in the endocardium than in the epicardium in all groups. In the subendocardium timolol and alinidine reduced infarct size to the same extent, whereas timolol reduced infarct size more than alinidine in the subepicardium. Although heart rate proved to be the dominant haemodynamic predictor of infarct size, this study indicates that mechanisms other than reduced oxygen demand associated with bradycardia and cardiodepression are operating in the ischaemic myocardium during beta adrenergic blockade.

Kinetics of a sulfadiazine-trimethoprim combination.

The pharmacokinetics of a combination of sulfadiazine and trimethoprim has been studied in 16 patients with varying degrees of reduced renal function. In normal renal function, the serum half-life (t1/2) of active sulfadiazine, total sulfadiazine, and trimethoprim were quite close: 7.7, 9.6, and 12.1 hr, respectively. There was a gradual increase in serum t1/2 with reduction in renal function for both active and total sulfadiazine and for trimethoprim. With accurate determinations of endogenous renal clearance, t1/2 estimates may be made from regression curves presented. The relative distribution in the body was unrelated to renal function. It was similar for the two fractions of sulfonamide and higher for trimethoprim. The means were 0.371, 0.176, and 1.104 L/kg, respectively, for active and total sulfadiazine, and trimethoprim.

Effects of heart rate on myocardial thallium-201 uptake and clearance.

The effects of heart rate on the myocardial uptake and clearance of 201Tl were studied prospectively in seven healthy men, mean age 43 +/- 7 (s.d.) yr. Initial and delayed (3 hr) thallium images were obtained in three views after three bicycle exercise tests: to maximal, 80% and 60% of predicted maximal heart rate. The mean of three views initial myocardial 201Tl uptake was higher at maximal than at both 80% and 60% of predicted maximal heart rate, being 81% (p less than 0.01) and 60% (p less than 0.01) of maximal activity, respectively. The myocardial activity in the delayed images was identical. There was a linear relationship between heart rate and the initial myocardial activity, r = 0.86 (p less than 0.001). The mean (range) 201Tl clearance was 58% (51-65), 47% (34-56), and 34% (22-49) (all differences p less than 0.01), respectively. Concordance among the three individual views in estimating clearance was best for the highest exercise level. There was a linear relationship between heart rate and clearance, r = 0.80 (p less than 0.001). Clearance was altered by only 1.67 x 10%/heart bpm (0.024 hr/heart beat). Clearance in the liver, spleen and lungs increased at submaximal exercise levels. Thus, a linear relationship between heart rate and clearance is the result of changes in the initial exercise myocardial 201Tl activity. Submaximal exercise may reduce reproducibility of clearance estimation, and the change of myocardial clearance with heart rate seems less than previously suggested.

Influence of free fatty acids on myocardial oxygen consumption and ischemic injury.

Myocardial oxygen consumption (MVO2) is influenced by the substrate supply to the heart. Utilization of free fatty acids increases MVO2, and catecholamines sensitize the heart to the oxygen-wasting effect of free fatty acids. Alteration of myocardial metabolism from mainly free fatty acid to carbohydrate oxidation reduces the extent of myocardial ischemic injury. Within the ischemic myocardium, lipolysis is stimulated with breakdown of endogenous triglycerides to fatty free acids and glycerol. Antilipolytic agents seem to have a combined effect on myocardial metabolism partly through inhibition of lipolysis in adipose tissue with reduction of free fatty acid mobilization to plasma, and partly through a local inhibition of lipolysis in the ischemic myocardium. In patients with high sympathoadrenal activity, for example, patients with acute myocardial ischemia in unstable ischemic heart disease, elevation of free fatty acids might effect a critical increase in both myocardial oxygen requirement and infarct size.

Factors affecting Doppler echocardiographic valve area assessment in aortic stenosis.

Doppler echocardiographic assessment of the aortic valve area (AVA) using the continuity equation was performed before cardiac catheterization in 100 patients with suspected aortic stenosis. Doppler echocardiographic AVA correlated closely with AVA calculated by the Gorlin equation at catheterization (r = 0.96). However, Doppler echocardiography slightly but systematically underestimated the AVA (p less than 0.001) and did so most markedly in patients with mild stenosis (greater than 1.0 cm2). In multivariate analysis, the difference in AVA by the 2 techniques was positively associated with left ventricular (LV) stroke volume and inversely with the difference between mean catheterization and Doppler gradients, LV ejection fraction and LV outflow tract velocity. Furthermore, the AVA difference also was related to gender, being larger in women. Thus, overall Doppler echocardiography reliably assesses AVA, but the usefulness of the method is somewhat reduced by its underestimation of AVA in mild stenosis. This drawback, however, is usually overcome by taking patients' symptoms into account. Furthermore, lacking a "gold standard," this underestimation need not imply errors of the Doppler echocardiographic method alone, but also may reflect known inaccuracies of the catheterization technique.

Subclinical left ventricular abnormalities in young subjects with long-term type 1 diabetes mellitus detected by digitized M-mode echocardiography.

Noninvasive studies in patients with type 1 diabetes mellitus suggest subclinical left ventricular (LV) impairment, but the studies differ with regard to methods, patient selection and results. Thus, digitized M-mode echocardiograms were recorded in 24 persons younger than 50 years with long-term (more than 12 years) type 1 diabetes but without overt heart disease and in 28 control subjects. To improve accuracy, measurements were adjusted for body surface area, LV size and the influence of heart rate, as appropriate. Diabetics had a higher heart rate and systolic and diastolic blood pressure than control subjects. LV end-diastolic and stroke dimensions were smaller, duration of systole longer and preejection period/LV ejection time ratio higher than in control subjects, whereas fractional shortening and peak shortening rate were similar. In diabetics, diastole was shorter, peak filling rate was lower and the rapid filling period was prolonged, while percent filling during the rapid filling period and atrial contribution to filling were higher. Thus, in a well defined study population of relatively young persons with long-term type 1 diabetes, subclinical LV systolic and diastolic dysfunction were found. The diastolic abnormalities suggest reduced LV compliance, while those in systole may be secondary to an increased afterload or decreased myocardial contractility.

Effect of timolol on cardiopulmonary exercise performance in men after myocardial infarction.

The effect of the nonselective beta blocker timolol on maximal cardiopulmonary exercise performance was evaluated in 28 men with previous myocardial infarction without effort angina (mean age 63 +/- 8 years). Patients were randomized to placebo or timolol (10 mg twice daily) for 4 weeks and then crossed over to the alternative therapy in a double-blind manner. At the completion of each treatment period, patients underwent symptom-limited maximal cardiopulmonary exercise on a cycle ergometer. Exercise time, heart rate, oxygen consumption (VO2), oxygen (O2) pulse and respiratory exchange ratio were measured at peak exercise and at a submaximal exercise level defined at a respiratory exchange ratio of 1.00. Timolol treatment reduced peak heart rate from 153 +/- 11 to 102 +/- 14 beats/min (-33%, p less than 0.001). Exercise time decreased from 680 +/- 91 to 633 +/- 78 seconds (-7%, p less than 0.001). Peak VO2 decreased from 25.3 +/- 4.7 to 21.4 +/- 3.5 ml/min/kg (-15%, p less than 0.001). O2 pulse increased from 12.9 +/- 1.9 to 16.7 +/- 2.3 ml/beat (+29%, p less than 0.001). Peak respiratory exchange ratio did not change significantly, indicating comparable effort. At submaximal exercise, defined at a respiratory exchange ratio of 1.00, there was no difference in exercise time between placebo and timolol. Heart rate decreased with timolol compared with placebo, from 126 +/- 16 beats/min by 31% (p less than 0.001), VO2 decreased from 18.5 +/- 4.3 ml/min/kg by 10% (p less than 0.001), O2 pulse increased from 11.5 +/- 2.0 ml/beat by 30% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic effects of flecainide acetate in patients with sinus nodal dysfunction.

Flecainide acetate (R818) is a new antiarrhythmic agent for oral and intravenous use; it has predominantly class I properties and a long plasma half-life. Electrophysiologic effects were evaluated in 11 patients with sinus nodal dysfunction before administration of flecainide acetate and 15 to 60 minutes after intravenous administration of 1.5 mg/kg body weight of flecainide acetate given over 15 minutes. In 8 of 11 patients with maximal sinus nodal recovery time increased after flecainide acetate. However, the mean maximal sinus nodal recovery time was not statistically significantly increased from 1,929 +/- 184 (mean +/- standard error of the mean [SEM]) to 2,770 +/- 500 ms (p less than 0.10). The corrected sinus nodal recovery time increased from 875 +/- 181 before to 1,727 +/- 507 ms after administration of flecainide acetate (p less than 0.05). The sinus cycle length and sinoatrial conduction time were not significantly changed. Flecainide acetate induced a marked prolongation of the H-V interval (from 41 +/- 3 to 52 +/- 4 mg [p less than 0.01]) as well as a significant increase in the A-H interval, QRS duration, and QT100 interval. The effective and functional refractory periods of the atria increased by 12% (p less than 0.01) and 11% (p less than 0.01), respectively. The atrioventricular (AV) nodal functional refractory period increased significantly by 7% (p less than 0.01), whereas the 9% prolongation of the effective refractory period was not statistically significant. No side effects were observed. It is concluded that flecainide acetate prolongs atrial and ventricular conduction and refractoriness, and thus appears to be a potent antiarrhythmic agent. However, the sinus nodal function is depressed, and thus caution is advised in the use of flecainide acetate in patients with sinus nodal dysfunction.

Left ventricular function in myasthenia gravis.

Myasthenia gravis is an autoimmune disorder with autoantibodies to acetylcholine receptors of skeletal muscle. Left ventricular diastolic function was studied with M-mode and Doppler echocardiography in 25 patients with myasthenia and in a group of age- and heart rate-matched control subjects. In the patients, diastolic peak filling rate was reduced by 37%, and Doppler peak early filling velocity (E) was reduced by 12% compared with the control subjects (2.7 +/- 0.7 vs 4.2 +/- 1.0 s-1, and 76 +/- 8 vs 85 +/- 15 cm/s, respectively; p less than 0.05). Peak atrial filling velocity (A) was increased by 38% (68 +/- 17 vs 48 +/- 9 cm/s; p less than 0.01), and consequently the E:A ratio in the group of patients was reduced by 33% (1.22 +/- 0.40 vs 1.81 +/- 0.33; p less than 0.001). End-diastolic dimension was 5.0 +/- 0.5 cm in both groups, heart rate was 70 +/- 12 vs 68 +/- 16 beats/min (p = not significant [NS]), M-mode ejection fraction was 76 +/- 8 vs 79 +/- 5% (p = NS), M-mode peak ejection rate was -1.9 +/- 0.4 vs -2.1 +/- 0.3 s-1 (p = NS), and peak aortic outflow velocity was 109 +/- 18 vs 98 +/- 13 cm/s (p = NS). Twenty-three patients and 15 control subjects were studied before and after intake of the acetylcholine-esterase inhibitor pyridostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary effects of enprofylline. A xanthine with weak adenosine receptor antagonism in patients with severe chronic lung disease.

The acute cardiovascular effects of a new xanthine, enprofylline, were studied in patients with chronic lung disease. The studies were done during cardiac catheterization (n = 12) and by radionuclide ventriculography (n = 6). Enprofylline was given intravenously, 2 mg/kg, and measurements were done after ten and 30 min. Enprofylline reduced the mean pulmonary artery pressure from 30 +/- 10 to 26 +/- 7 mm Hg (p less than 0.05) and the mean systemic arterial pressure from 92 +/- 17 to 83 +/- 15 mm Hg (p less than 0.01), increased the heart rate from 89 +/- 15 to 100 +/- 18 beats/min (p less than 0.01) and reduced the stroke volume from 55 +/- 12 to 48 +/- 12 ml (p less than 0.05) after 30 min. Radionuclide ventriculography revealed unchanged ejection fraction of left and right ventricles after enprofylline. None of the patients experienced serious side effects of the drug. Thus, enprofylline induced modest acute cardiovascular effects with a chronotropic response together with a small vasodilation in pulmonary and systemic circulation.

Plasma cardiac natriuretic peptide determination as a screening test for the detection of patients with mild left ventricular impairment.

OBJECTIVE: To determine the usefulness of measuring the cardiac natriuretic peptides, atrial natriuretic factor, N-terminal pro-atrial natriuretic factor, and brain natriuretic peptide, as screening tests for identifying patients with mild left ventricular impairment. DESIGN: Cross-sectional evaluation of the diagnostic accuracy of the cardiac natriuretic peptides. SETTING: Cardiac catheterisation unit, Norwegian central hospital. PATIENTS: A consecutive series of 254 patients undergoing diagnostic left-sided cardiac catheterisation. One hundred and twenty eight of these patients had a history of previous myocardial infarction. MAIN OUTCOME MEASURES: The presence of normal and impaired left ventricular function, as evaluated by logistic regression analysis and estimation of the area under the receiver operating characteristic (ROC) curve (an index of overall diagnostic accuracy). Ventricular function was assessed by the measurement of left ventricular end diastolic pressure and angiographically determined left ventricular ejection fraction. RESULTS: Logistic regression analysis showed that plasma brain natriuretic peptide was the best predictor of increased left ventricular end diastolic pressure (> or = 15 mm Hg) (P < 0.001), decreased left ventricular ejection fraction (< or = 45%) (P < 0.001), and the combination of left ventricular ejection fraction < or = 45% and left ventricular end diastolic pressure > or = 15 mm Hg (P < 0.001). The areas under the ROC function for the detection of left ventricular dysfunction were 0.789 for brain natriuretic peptide, 0.665 for atrial natriuretic factor, and 0.610 for N-terminal pro-atrial natriuretic factor. CONCLUSIONS: Plasma brain natriuretic peptide seemed to be a better indicator of left ventricular function than plasma atrial natriuretic factor or N-terminal pro-atrial natriuretic factor. However, the overall diagnostic accuracy of circulating atrial natriuretic factor, N-terminal pro-atrial natriuretic factor, and brain natriuretic peptide as indicators of normal and impaired ventricular function in an unselected group of patients with coronary heart disease and a high frequency of previous myocardial infarction was relatively modest.

Strain rate imaging by ultrasonography in the diagnosis of coronary artery disease.

Regional strain rate in the left ventricle can be assessed in real time and color mapped. The method is termed strain rate imaging (SRI), and findings correspond well with 2-dimensional echocardiography. This study addresses SRI as a method for localizing coronary lesions, compared with standard echocardiography. Twenty patients with acute myocardial infarction who underwent coronary angiography for clinical reasons were examined with SRI and standard echocardiography. Wall motion was graded by SRI color and separately by wall thickening. Strain rate imaging and 2-dimensional echocardiography results agreed well. An infarct-related artery was identified from angiograms combined with electrocardiograms. Both methods identified an infarct-related artery in 19 possible cases and had equal sensitivity and specificity for wall segments affected by lesion. Combining the information from both methods did not change accuracy. The study validates SRI as a method for assessing regional wall function in coronary artery disease. The advantages of SRI are discussed and measurements of strain rates are given.

The value of ultrasonography in predicting autoimmune thyroid disease.

Ultrasonography (US) may demonstrate a diffuse reduction in thyroid echogenicity (low-amplitude echoes) in autoimmune thyroid disease (AITD), which includes chronic lymphocytic thyroiditis and Graves' disease, as well as in subacute thyroiditis. The reported occurrence of this finding in AITD varies from 19% to 95%. To assess the validity of diffuse reduction in thyroid echogenicity as a predictor of AITD, 3,077 patients referred for US of the thyroid were examined prospectively with regard to reduced versus normal thyroid echogenicity. The most frequent reasons for referral were goiter, thyroid dysfunction, neck discomfort, and/or difficulty in swallowing. Ultrasonography demonstrated diffuse reduction in thyroid echogenicity in 485 patients. Of these, 452 patients had available records of fine-needle aspiration biopsy (FNAB), and were included in the study. From the remaining patients, with normal thyroid echogenicity, 100 consecutive patients were selected as controls. In 411 of the 452 study patients (90.9%) there was at least one laboratory finding consistent with possible AITD: cytology indicating lymphocytic thyroiditis, 287 of 363 patients (79.1%) with diagnostic specimens; elevated levels of peroxidase antibodies (TPOAb), 225 of 337 (66.8%); elevated thyrotropin (TSH) levels, 290 of 450 (64.4%); or low TSH levels, 79 of 450 (17.6%). The final diagnosis was: chronic autoimmune (Hashimoto's) thyroiditis in 352 patients; Graves' disease in 47 patients; subacute (granulomatous) thyroiditis in 7 patients; toxic nodular goiter in 3 patients; and toxic adenoma in 2 patients. In the remaining 41 patients, those without laboratory results consistent with AITD, the final diagnosis was colloid goiter in 37 and thyroid cancer in 4 patients. In the 100 controls, laboratory results were consistent with possible AITD in 14 patients: elevated TPOAb levels in 5 of 49 patients with retrieved antibody results; lymphocytic thyroiditis in 2 patients; elevated TSH levels in 2 patients; and low TSH levels in 2 patients. In these controls, the final diagnosis was: chronic autoimmune thyroiditis in 7; toxic nodular goiter in 6 patients, and toxic adenoma in 1 patient. The corresponding positive and negative predictive values of reduced thyroid echogenicity as an indicator of AITD were 399 of 452 (88.3% [95% CI, 85% to 91%]), and 93 of 100 (93.0% [95% CI, 88% to 98%]), respectively. Thus, diffuse reduction in thyroid echogenicity was a valid predictor of AITD.

Detection of left ventricular ischemia during atrial pacing: simultaneous assessment by echocardiography and invasive hemodynamic measurements.

The ability of cross-sectional echocardiography to detect myocardial ischemia induced by atrial pacing was assessed during cardiac catheterization in 11 patients with coronary arterial disease. Angina pectoris was precipitated in all patients with increase in left ventricular end-diastolic pressure after pacing by 5 +/- 6 (mean +/- standard deviation) mm Hg (P less than 0.01). Regional left ventricular dysfunction occurred during pacing in all patients as determined by quantitative echocardiographic assessment of wall motion. Simultaneously, systolic reduction in parasternal short-axis area decreased (from 42 +/- 13 to 28 +/- 9%, P less than 0.01) with concomitant decrease in ejection fraction as determined in the apical four-chamber view (from 49 +/- 5 to 40 +/- 8%, P less than 0.01). In conclusion, echocardiography may detect pacing-induced myocardial ischemia through detection of regional and global left ventricular dysfunction. Inadequate regional perfusion may be indicated by echocardiography even in patients without apparent evidence of ischemia as determined by invasive hemodynamic measurements.

Physiological effects of short-term training after myocardial infarction.

The effects of a period of 4 weeks training on treadmill exercise performance were evaluated in 27 patients, mean +/- SD age 55 +/- 7 years, who had previously suffered a myocardial infarction (17 Q-wave) 3-24 months (mean 11 +/- 8). To ensure comparability of exercise levels only patients who obtained their predicted maximal heart rate in the initial test were included. All trained 3-4 hours daily 5 days a week at an average maximal intensity of 85% of their initial peak heart rate. They performed 2 maximal exercise tests before and 1 after the training course. Maximal oxygen consumption was 28.1 +/- 5.3 and 28.8 +/- 6.5 ml/kg/minute (NS) before, and increased by 16% to 33.4 +/- 7.2 after training (P less than 0.01). Treadmill exercise distance was 510 +/- 153 and 559 +/- 163 meters (10% increase, P less than 0.01) before, and increased by 14% to 638 +/- 156 after (P less than 0.01). Heart rate, ratio of respiratory gas exchange, and breathing frequency remained unchanged in all three tests at maximal exercise, but were significantly lower at identical submaximal levels after training, while the respiratory tidal volume increased. Resting heart rate decreased by 12% after (P less than 0.01). Thus, aerobic exercise performance is improved by short-term training after myocardial infarction. By the longitudinal design of the study, and the maximal initial exercise test, this physiological improvement can be differentiated from that of increased motivation, and of increased treadmill exercise distance due to improved exercise technique.

Diagnosis of small infrarenal aortic aneurysms by ultrasonography.

OBJECTIVE: Localized dilatation of the infrarenal aorta is currently assessed by comparison with the suprarenal aorta using a diameter ratio > 1.5 as an index of aneurysm. However, the bulging may be underestimated when there is concomitant enlargement of the suprarenal aorta and enhanced tapering of the aorta toward the bifurcation. Therefore, we studied an alternative reference point closer to the aneurysm. EXPERIMENTAL DESIGN: Prospective ultrasound study of localized infrarenal aortic dilation where its diameter is compared to 1) suprarenal aorta just above the orifices of the renal arteries and (2) infrarenal aorta at the upper margin of the aortic dilatation. PATIENTS: 91 consecutive ambulatory patients (66 men and 25 women, mean age 69 yrs) with a localized infrarenal aortic dilatation of > or = 3.0 cm in diameter. RESULTS: Mean diameter of the aortic bulges was 4.5 +/- 0.13 (SD) cm in males vs 4.0 +/- 0.73 cm in the females, (NS). The diameter ratio dilatation/suprarenal aorta exceeded 1.5 in 96% of the patients with an aortic bulging > or = 4.0 cm (n = 53) as compared to only 55% when the diameter was 3.0 to 3.9 cm (n = 38), p < 0.0001. However, when the aorta immediately above the dilated part was used as size reference the number of aortic bulges with a relative size of > 1.5 increased from 55% to 87% (p < 0.001). CONCLUSIONS: The degree of aortic bulging may be underestimated when the diameter of the dilated area is compared to that of the suprarenal aorta instead of the aorta immediately proximal to the dilatation, especially in small dilatations located near the aortic bifurcation.