Search

The responses of sympathetic nerve activity to transient stress can be exaggerated in salt-sensitive (SS), hypertensive subjects. Cardiac and renal interstitial norepinephrine (iNE) levels during and after transient hypercapnia were investigated in conscious SS rats. Dahl SS and salt-resistant (SR) 6-wk-old rats were fed a high-salt diet, and at 12 wk iNE levels in the heart and kidney were determined using microdialysis with probes inserted in the left ventricular (LV) wall and kidney. A telemetry system determined blood pressure and heart rate (HR) in separate animals. After recovery from the operation, data were collected before, during, and after exposure to normoxic 10% CO2 for 25 min under unanesthetized conditions. The plasma NE concentrations at baseline did not differ between the two strains. Both cardiac and renal iNE levels were much higher in SS rats than in SR rats at baseline as well as during hypercapnic stress. After stress, the markedly increased iNE levels of SS rats were prolonged in the LV as well as in the kidney. During hypercapnic stress, HR decreased in both SS and SR rats, while sudden increases in HR immediately after the withdrawal from stress were followed by its slower reduction in SS rats compared with SR rats. In conclusion, transient hypercapnic stress causes exaggerated and prolonged elevation of iNE levels in the heart as well as in kidneys of SS animals. [ABSTRACT FROM AUTHOR]

The present study was designed to develop a method to continuously measure Holter electrocardiogram (ECG) and physical activity in term of metabolic costs to examine circadian dynamics of RR intervals and physical activity in patients with heart failure. A total of 7 healthy subjects and 3 heart failure patients performed cardiopulmonary exercise test using four-stage graded treadmill walking at 0% grade to examine whether the acceleration signals in the vertical direction could reflect actual body energy expenditure during physical activity. Then, using this new method, 24-hr monitoring of ECG and physical activity were performed in 24 inpatients with heart failure while they were allowed to walk around freely. Our results showed the integral of rectified acceleration signals was closely correlated with actual metabolic cost in all subjects. Instantaneous changes in heart rate were quite concordant with physical activity. As compared with the asymptomatic patients (n = 12), the symptomatic patients (n = 12) had lower energy expenditure during 8-hr daytime periods but higher mean heart rate. Furthermore, a more prominent ultradian rhythm of circadian changes in heart rate and physical activity was found in 50% of all subjects studied. The simultaneous analysis of Holter ECG and physical activity as the same time series revealed that in patients with heart failure, sympathovagal balance shifted toward sytnpathotonic conditions and their physical activity could become subject to intrinsic ultradian dynamics of body s homeostasis. [ABSTRACT FROM AUTHOR]

The upper limit of incidence of muscle sympathetic neural bursts can lead to underestimation of sympathetic activity in patients with severe heart failure. This study aimed to evaluate the pulse-synchronous burst power of muscle sympathetic nerve activity (MSNA) as a more specific indicator that could discriminate sympathetic activity in patients with heart failure. In 54 patients with heart failure, the pulse-synchronous burst power at the mean heart rate was quantified by spectral analysis of MSNA. Thirteen patients received a central sympatholytic agent (guanfacine) for 5 days to validate the feasibility of this new index. Both burst incidence and plasma norepinephrine level showed no significant difference between patients in New York Heart Association functional class III (94 ± 6 per 100 heartbeats and 477 ± 219 pg/ml, respectively) and class II (79 ± 14 per 100 heartbeats and 424 ± 268 pg/ml, respectively). In contrast, the burst power was useful for discriminating patients in class III from those in class II (61 ± 8% vs. 39 ± 10%; P < 0.05). Inhibition of sympathetic nerve activity by guanfacine was mom sensitively reflected by the change of burst power (-36 ± 25%) than by that of burst incidence (-12 ± 14%; P < 0.001). The sympathetic burst power reflects both burst frequency and amplitude independently of the absolute values and provides a sensitive new index for interindividual comparisons of sympathetic activity in patients with heart failure. [ABSTRACT FROM AUTHOR]

Study objectives: The prevalence of thromboembolism might be higher than previously recognized in patients with atrial flutter (AFL) based on findings of transesophageal echocardiography (TEE). To evaluate the potential prothrombotic state in patients with AFL, TEE findings and hemostatic markers were compared among patient groups with AFL, normal sinus rhythm (NSR) and chronic nonvalvular atrial fibrillation (AF). Design and settings: Cross-sectional study at a university hospital. Methods: In 28 patients (mean age, 63 years) with AFL, 58 patients (mean age, 66 years) with AF, and 27 patients (mean age, 61 years) with NSR who underwent TEE, plasma levels of markers for platelet activity (platelet factor 4 and β-thromboglobulin [β-TG]), thrombotic status (thrombinantithrombin III complex and prothrombin fragments 1 and 2) and fibrinolytic status (d-dimer and plasmin-α[sub 2]-plasmin inhibitor complex) were determined. Results: Left atrial appendage (LAA) blood flow velocity in patients with AFL was higher (p < 0.05) than that in patients with AF, but was lower (p < 0.05) than that in patients with NSR (AF, 25 ± 2; AFL, 44 ± 4; NSR, 60 ± 4 cm/s). Dense left atrial spontaneous echo contrast (SEC) was found in 4 patients (14%) with AFL and 16 patients (28%) with AF. There was no significant difference in plasma levels of hemostatic markers between the AFL group and the NSR group. AFL patients with impaired LAA function (LAA flow < 30cm/s, dense SEC, or both), however, showed higher level of d-dimer and β-TG than those without impaired LAA function (d-dimer, 1.9 ± 0.6 µg/mL vs 0.4 ± 0.1 µg/mL; β-TG, 73 ± 17 ng/mL vs 33 ± 5 ng/mL, p < 0.05). Conclusions: Patients with AFL as a whole are not in the prothrombotic state as compared with those with AF. However, patients with AFL and impaired LAA function are at potentially high risk for thromboembolism and might require anticoagulation. [ABSTRACT FROM AUTHOR]

Objectives: To determine the relationship between spontaneous echocardiographic contrast (SEC) in the descending thoracic aorta and plasma levels of hemostatic markers in patients with nonrheumatic atrial fibrillation (AF).Design and Settings: A cross-sectional study at a university hospital.Patients and Measurements: In 91 consecutive patients (mean +/- SE age, 70 +/- 1 years; 68 men) with nonrheumatic AF who underwent transesophageal echocardiography, plasma levels of markers for platelet activity (platelet factor 4 [PF4] and beta-thromboglobulin [beta-TG]), thrombotic status (thrombin-antithrombin III complex [TAT]), and fibrinolytic status (D-dimer and plasmin-alpha(2)-plasmin inhibitor complex [PIC]) were determined.Results: Forty-three patients who had aortic SEC (AoSEC) were older (72 years vs 68 years; p < 0.05) and had a higher prevalence of chronic AF (88% vs 52%; p < 0.05) than 48 patients without AoSEC. TAT, PIC, and D-dimer levels were significantly higher in patients with AoSEC than in those without AoSEC, whereas PF4 and beta-TG levels were not different between the two groups. Although the prevalence of cerebral embolism did not differ between the two groups (23% vs 29%), the prevalence of peripheral embolism was higher in patients with AoSEC than in those without AoSEC (10% vs 0%; p < 0.05). Multivariate analysis revealed mitral regurgitation (odds ratio, 7.53; p < 0.02), SEC in the left atrium (odds ratio, 2.14; p < 0.02), and aortic atherosclerosis (odds ratio, 1.87; p < 0.04) emerged as independent predictors of AoSEC.Conclusions: Patients with nonrheumatic AF who have AoSEC appear to have enhanced coagulation activity but not platelet activity. Intensive anticoagulation treatment might be required for these patients. [ABSTRACT FROM AUTHOR]

Study objectives: Atrial fibrillation (AF) becomes an increasingly important cause of stroke as patients get older. The aim of the study was to determine whether risk factors of cerebral embolism among elderly patients with AF differed from those of younger patients by using transesophageal echocardiography (TEE). Design and setting: Cross-sectional study at a university hospital. Methods: Cardiovascular lesions with the potential for thromboembolism in patients with AF were investigated using TEE. Left atrial spontaneous echocardiographic contrast (SEC), peak flow velocity in the left atrial appendage (LAA-flow), and aortic atherosclerosis of the thoracic aorta were assessed in 67 elderly (≥ 70 years old) and 135 younger (< 70 years old) patients. All patients underwent either brain CT (n = 54) or MRI (n = 148) to assess presence of cerebral infarction. Results: Cerebral infarction due to embolism was noted in 113 patients with AF. There was a higher prevalence of cerebral embolism in elderly patients when compared with younger patients (78% vs 45%; p < 0.001). Cerebral embolism found in younger patients was associated with high grade of SEC and lower LAA-flow (p < 0.05). In addition to these TEE findings, aortic atherosclerosis was more severe in elderly patients with cerebral embolism than in those without cerebral embolism (p < 0.0001). By multivariate logistic analysis, LAA-flow was an independent predictor of cortical infarction in younger patients, but not in elderly patients, whereas aortic atherosclerosis was a useful marker in predicting embolic risk in elderly patients. Conclusions: TEE findings indicative of left atrial blood stasis were useful to identify the embolic risk of younger patients with AF, while atherosclerosis of the thoracic aorta appears to be an important marker for cerebral embolism in elderly patients. [ABSTRACT FROM AUTHOR]

Objectives: The plasma status of vitamin E has been suggested to be linked to the activity of coronary artery spasm. This study was designed to determine whether vitamin E is actually consumed in the coronary circulation in patients with active variant angina having repetitive spasm-induced transient myocardial ischemia and reperfusion. Methods: Blood samples were obtained simultaneously from the aortic root, coronary sinus and right atrium in 12 patients with variant angina due to spasm of the left coronary artery, nine patients with stable effort angina and nine control subjects. Plasma vitamin E (α- and γ-tocopherol) concentrations were determined by use of high-performance liquid chromatography and plasma lipid peroxides were measured as thiobarbituric acid-reactive substances (TBARS). Results: At baseline, both plasma α- (p<0.01) and γ- (p<0.05) tocopherol levels were significantly lower in the coronary sinus (5.50±0.50 and 0.55±0.07 mg/l, mean±SEM) than in the aortic root (6.63±0.57 and 0.63±0.08 mg/l) and also in the right atrium (6.44±0.61 and 0.63±0.09 mg/l) in the variant angina group. The TBARS level was significantly (p<0.05) higher in the coronary sinus than in the aortic root in this group. In contrast, these levels were not significantly different between the samples from the coronary sinus and the aortic root or the right atrium in the control group and also in the stable effort angina group. The coronary sinus–aortic difference in plasma vitamin E levels in the variant angina group was not significantly altered after left coronary artery spasm induced by intracoronary injection of acetylcholine. Also, the plasma vitamin E levels in the aortic root, coronary sinus and right atrium all remained unchanged in the stable effort angina group after pacing-induced angina and in the control group after intracoronary administration of acetylcholine. Conclusions: Transcardiac reduction in plasma vitamin E concentrations concomitant with lipid peroxide formation was demonstrated in patients with active variant angina, suggesting actual consumption of this major endogenous antioxidant. Oxidative stress and vitamin E exhaustion may be involved in the pathogenesis of coronary artery spasm. [ABSTRACT FROM PUBLISHER]

The static mechanical properties of major branches of the human arteries (common carotid artery, abdominal aorta, femoral artery, and brachial artery) were studied in 39 subjects, aged 6-81 years, using an ultrasonic phase locked echo tracking system that allows continuous transcutaneous measurement of the diameter of the artery. The stiffness indices were calculated from the relation between systemic blood pressure and arterial diameter. With advancing age there was a significant increase in the diameter of all arteries associated with a reduction in percentage change in diameter. The stiffness index increased with age in all arteries; however, in the brachial and femoral arteries there was considerable variation in the individual values for a given age. The age associated increase in stiffness was statistically significant only in the common carotid artery and the abdominal aorta. Although the mechanical properties of the peripheral arteries were significantly influenced by the measuring environment, the calculated stiffness indices were less vulnerable to these stimuli in the central arteries. These results indicate that the stiffness indices of the peripheral muscular arteries are modified appreciably by vasoactive stimuli and that the mechanical properties of the deeper elastic arteries provide sufficiently reliable information about changes caused by aging and arteriosclerosis. The new ultrasonic method used appears to be suitable for this analysis. [ABSTRACT FROM PUBLISHER]

Objective: The aim of this study was to investigate whether the role of nitric oxide (NO) in regulating blood flow (BF) to working skeletal muscle is impaired in chronic heart failure (CHF). Methods: The effect of NG-nitro-l-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, was studied in conscious rats with and without CHF due to myocardial infarction (MI). BF to the hindquarter musculature was measured with radiolabelled microspheres during exercise after 4 min of treadmill running (10% grade, 20 m/min) before and after L-NAME (20 mg/kg i.a.) administration. Results: Before L-NAME administration, BF measured in the total hindquarter musculature was less (P < 0.05) during exercise in rats with a large MI (MI size; 44 ± 2% of the left ventricular endocardial circumference; n = 8) when compared with sham-operated rats (SHAM; n = 10) and rats with a small MI (MI size; 25 ± 4%; n = 5). The BF measured during exercise following L-NAME administration was similar between the 3 groups. Of the 28 individual hindquarter muscles, BF was reduced in 23 and 19 muscles following the administration of L-NAME for the SHAM rats and rats with a small MI, respectively. In comparison, BF was reduced to only 4 of 28 muscles in rats with a large MI. Conclusions: These results suggest that the contribution of the NO pathway to the hyperaemic BF responses found in the hindquarter muscles during exercise could be attenuated in rats with CHF. This attenuation of the NO pathway may be associated with the impairment of skeletal muscle BF distribution during exercise in CHF. [ABSTRACT FROM PUBLISHER]