Enhancement of contrast echocardiography by image variability analysis.

BACKGROUND: Although there have been recent advances in echocardiography, many studies remain suboptimal due to poor image quality and unclear blood-myocardium border. We developed a novel image processing technique, cardiac variability imaging (CVI), based on the variance of pixel intensity values during passage of ultrasound microbubble contrast into the left ventricle chamber, with the aim of enhancing endocardial border delineation and image quality. METHODS AND RESULTS: CVI analysis was performed on simulated data to test and verify the mechanism of image enhancement. Then CVI analysis was applied to echocardiographic images obtained in two different clinical studies, and still images were interpreted by expert reviewers. In the first study (N = 15), using contrast agent EchoGen, the number of observable wall segments in end-diastolic images, for example, was significantly increased by CVI (4.93) as compared to precontrast (3.28) and contrast images (3.36), P < 0.001 for both comparisons to CVI. In the second study (N = 8), using contrast agent Optison, interobserver variability of manually traced end-diastolic volumes was significantly decreased using CVI (22.3 ml) as compared to precontrast (63.4) and contrast images (49.0), P < 0.01 for both comparisons to CVI. CONCLUSION: CVI can substantially enhance endocardial border delineation and improve echocardiographic image quality and image interpretation.

Magnesium dynamics and relation to left ventricular function in acute myocardial infarction.

The present study investigated the serial changes in serum magnesium (Mg) and erythrocyte concentration of Mg in patients with acute myocardial infarction (AMI) and the relationship between these changes and left ventricular ejection fraction (LVEF) at 1 month after the onset of infarction. The study group comprised 26 patients with AMI (mean age, 57.9+/-8.9 years). Serum Mg and erythrocyte Mg were measured on hospital days 1, 2, 4, 7 and 21. The change in erythrocyte Mg during the acute phase was calculated as a ratio: [(erythrocyte Mg at day 2)-(erythrocyte Mg at day 1)]/(erythrocyte Mg at day 1). The change in serum Mg was calculated similarly. The following results were obtained. (1) Serum Mg tended to increase from the onset of myocardial infarction (day 1: 1.86+/-0.19, day 2: 1.93+/-0.22, day 4: 2.17+/-0.23; day 7: 2.25+/-0.20; day 21: 2.12+/-0.15 mg/dl). (2) Erythrocyte Mg on day 2 and day 4 showed a significant decrease compared with day 1 (day 1: 2.45+/-0.40, day 2: 2.09+/-0.41, day 4: 2.07+/-0.37, day 7: 2.22+/-0.33, day 7: 2.34+/-0.28 mg/dl per 400x10(4)/mm3 cells). (3) A significant positive correlation was observed between the change in serum Mg and LVEF (r=0.55, p<0.05), and a significant negative correlation was observed between the change in erythrocyte Mg and LVEF (r=-0.57, p<0.05). Thus, it was concluded that an extracellular shift in intracellular Mg occurred during the first 2 days after the onset of myocardial infarction. This responsive increase in the extracellular Mg level may be an important factor for maintaining left ventricular function in patients 1 month after the onset of AMI.

Physiological role of endothelin-1 in nonworking muscles during exercise in healthy subjects.

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. However, the role of ET-1 in exercise-induced physiological responses is still to be investigated. The purpose of the present study was to investigate in healthy volunteers whether the ET-1 plasma concentration in nonworking muscles is changed by exercise and to investigate the physiological role of ET-1 during exercise. Bicycle ergometer cardiopulmonary exercise tests were performed in 36 healthy men (mean age, 22.5 years). Blood samples for measuring ET-1 were drawn from the cubital vein during rest and immediately after the exercise test. The ET-1 change ratio was calculated as ET-1 immediately following exercise/ET-1 during the resting state. Cardiac output (CO) was measured during the exercise test by the impedance method. Arterial venous oxygen difference (AVO2D) when CO reached 10L/min or 15L/min was calculated as AVO2D = VO2/CO. Results were as follows: (1) the ET-1 change ratio correlated inversely with exercise time at the anaerobic threshold (r = -0.37, p = 0.03) and peak exercise time (r = -0.35, p = 0.04); (2) the ET-1 change ratio tended toward an inverse correlation with deltaVO2/deltawork rate (r = -0.29, p = 0.09); (3) the ET-1 change ratio correlated positively with AVO2D when CO reached 10L/min (r = 0.42, p = 0.02) and tended toward a positive correlation with AVO2D when CO reached 15 L/min (r = 0.32, p = 0.08). These results indicate that an increase in ET-1 in nonworking muscles may participate in the exercise-induced redistribution of blood flow and in increasing the blood flow to working muscles.

Exercise-induced changes in plasma atrial natriuretic peptide and brain natriuretic peptide concentrations in healthy subjects with chronic sleep deprivation.

Recent observations have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) correlate with cardiac function or prognosis in heart failure patients. However, relatively little is known about changes in their plasma concentration during commonly occurring physiological states such as fatigue. Therefore, this study was designed to examine the physiological changes of plasma ANP and BNP concentrations using a chronic sleep-deprivation model. Bicycle ergometer cardiopulmonary exercise tests were performed in 10 healthy volunteers (mean age: 22.7 years). Blood samples for measuring ANP and BNP were drawn during the resting state and immediately after each exercise test. Cardiac output (CO) was measured during the exercise test by the impedance method. The study conditions were designed as follows: (A) a day following a period of normal sleep (control state) and (B) a day preceded by 1 month during which sleep lasted <60% of normal (chronic sleep-deprived state). Results were as follows. (1) Peak oxygen uptake and peak CO decreased during the sleep-deprived state compared with the control state. (2) There was no difference between peak heart rates measured during exercise under the 2 conditions. (3) Plasma ANP concentration during exercise increased significantly during the control state, whereas only a tendency toward increase was observed during the sleep-deprived state. (4) Plasma BNP concentration during exercise tended to increase in the control state compared with the resting state, whereas there was no difference in plasma BNP between after exercise and resting state in the sleep-deprived state. These results indicate that changes of ANP or BNP induced by exercise tended to be decreased by chronic sleep deprivation.

Efficacy of oral magnesium administration on decreased exercise tolerance in a state of chronic sleep deprivation.

We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.

[Mechanism of increase in exercise tolerance in patients with acute myocardial infarction].

The contribution of cardiac output reserve and the skeletal muscle to exercise capacity was investigated in 24 patients with acute myocardial infarction. Symptom-limited exercise tests with a cycle ergometer were performed at 1 week, 3 weeks, and 3 months after the onset of the first infarction. Ventilatory gas was analyzed throughout the testing, and peak oxygen uptake (peak VO2) and anaerobic threshold (AT) were determined. During the test, the cardiac index (CI) was measured by the dye dilution method and the change in CI during exercise (delta CI) was calculated as an index of cardiac output reserve. The cross-sectional area of the thigh muscles (CSA) at the level of 10 cm above the patella was measured using computed tomography. Peak VO2 and AT increased significantly from 1 week to 3 months after the onset of infarction. delta CI increased significantly from 1 week to 3 weeks, and CSA increased significantly from 3 weeks to 3 months. Peak VO2 correlated significantly with both delta CI and CSA at each measurement point, as was AT with delta CI and CSA. Change in peak VO2 correlated with change of delta CI from 1 week to 3 weeks, and also with both delta CI and CSA from 3 weeks to 3 months. These results suggest that both cardiac output reserve and peripheral factors contribute to the exercise capacity up to 3 months after the onset of myocardial infarction. In particular, peripheral factors such as muscle volume are important to improve exercise capacity from 3 weeks to 3 months.

[Factors affecting exercise capacity after coronary bypass grafting].

In order to determine the contribution of cardiac reserve and the peripheral muscle to exercise capacity in patients after Coronary Artery Bypass Grafting (CABG), 19 patients (18 males, 1 female, mean age 63.3 +/- 7.1 years, mean numbers of grafting 2.5 +/- 0.8) performed exercise tests at 1 week, 3 weeks, and 3 months after CABG. Ventilatory gas was analyzed throughout the testing and anaerobic threshold (AT) and peak oxygen uptake (peak VO2) was determined. During exercise testing, the cardiac index (CI) was measured, and the change in CI during exercise, delta CI = (CI at peak exercise) (CI at rest), was calculated. O2 delivery was derived from the product of CO and the oxygen content of arterial blood at peak exercise. The sectional area of the thigh muscles at the level of 10 cm above the patella was measured using a computed tomography before each test. Average peak VO2 at 1 week after CABG was 867 +/- 171 ml/min and it increased to 1,214 +/- 246 ml/min at 6 months. Average AT did not change from 1 week to 3 weeks, however, it increased significantly from 665 +/- 122 ml/min at 3 weeks to 873 +/- 181 ml/min at 6 months. The muscle area of the thigh increased significantly from 170 +/- 24 cm2 at 3 weeks after CABG to 186 +/- 27 cm2 at 3 months. delta CI showed a tendency to increase from 6.6 +/- 1.2 l/min/m2 at 1 week after CABG to 7.3 +/- 1.3 l/min/m2 at 3 weeks, and also showed a tendency to increase from 3 weeks to 6 months. Peak VO2 and AT correlated to delta CI at 1 weeks and also it correlated significantly to both the muscle area of the thigh and delta CI at 3 weeks, 3 months, and 6 months after CABG. The delta value of peak VO2 from 1 week to 3 weeks showed a significant correlation to those of delta CI and O2 delivery. Moreover, the delta values of peak VO2 and AT from 3 weeks to 3 months showed a correlation to those of delta CI and O2 delivery. These results suggest that both cardiac reserve and peripheral factors contribute to the exercise capacity up to 3 months after CABG, and, in particular, O2 delivery are important to increase exercise capacity.

Erythrocyte magnesium and prostaglandin dynamics in chronic sleep deprivation.

BACKGROUND AND HYPOTHESIS: The mechanism of sudden cardiac death occurring in patients with chronic fatigue is controversial. This study was designed to define a hypothesis that coronary arterial spasm and thrombus formation can occur during chronic fatigue. METHODS: For evaluating the feasibility of coronary arterial spasm, erythrocyte magnesium (Mg) was measured. Blood coagulability was evaluated by the change of prostaglandin concentration. Subjects included 16 healthy male volunteers (mean age 21.6 +/- 2.5 years). Test conditions were as follows: (A) control state: a day following a night of good sleep; (B) temporary sleep deprivation: a day preceded by < 3 h of sleep; (C) chronic sleep deprivation: a day preceded by a month during which sleep lasted < 60% of that in condition (A) above. The erythrocyte Mg concentration was measured by the atomic absorption method. The plasma concentration of thromboxane B2 and 6-keto-prostaglandin F1 alpha were measured in eight subjects by radioimmunoassay method. RESULTS: (1) Mean erythrocyte Mg concentration was significantly less in chronic sleep deprivation (1.1 +/- 0.4 mg/dl) than in the control state (1.8 +/- 0.4 mg/dl, p < 0.01) or in temporary sleep deprivation (1.6 +/- 0.4, p < 0.01). (2) The level of thromboxane B2 was significantly higher during chronic sleep deprivation than under control conditions (104.4 +/- 78.0 vs. 20.4 +/- 9.0 pg/ml, p < 0.05). (3) There were no significant intergroup differences in 6-keto-prostaglandin F1 alpha level. CONCLUSION: These findings could support the hypothesis that coronary arterial spasm and thrombus formation occur in chronic sleep deprivation.

[Relationship between ischemic ST depression and oxygen uptake kinetics during ramp exercise test in patients with effort angina].

The relationship between ischemic ST depression and oxygen uptake kinetics was examined during cardiopulmonary exercise test using the ramp protocol in 22 patients (17 males and 5 females, mean age 61.4 +/- 8.1 years) with ischemic ST change (horizontal or down sloping ST depression over 1 mm) during a previous multi-stage exercise test (Bruce method). Patients were classified into three groups according to coronary angiographic findings: absence of significant stenosis group (control, n = 7), single-vessel disease group (n = 7) and multivessel disease (MVD) group (n = 8). Peak exercise time, peak heart rate, peak systolic blood pressure, anaerobic threshold, peak oxygen uptake (peak Vo2), exercise time, heart rate, systolic blood pressure, and oxygen uptake at appearance of ischemic ST change were measured. The ratio of oxygen uptake increase at appearance of ischemic ST change was calculated. Peak Vo2 was lower in the MVD group than in the control group (20.9 +/- 6.2 vs 27.3 +/- 3.3 ml/min/kg, p < 0.05), and exercise time from the beginning of ramp exercise to the appearance of ischemic ST depression was shorter in the MVD group than in the control group (5.2 +/- 2.1 vs 8.2 +/- 1.9 ml/min/kg, p < 0.05). The ratio of oxygen uptake increase was smaller in the MVD group than in the control group (0.7 +/- 0.3 vs 1.2 +/- 0.2, p < 0.01). These results could be caused by impaired increase of cardiac output due to myocardial ischemia occurring during exercise. In the clinical setting, these phenomena could be used as a parameter for differentiating ischemic from non-ischemic ST depression or evaluating the sensitivity of ischemic heart disease.