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End Diastolic Volume (end + diastolic_volume)

Distribution by Scientific Domains
Medical Sciences83%

Selected Abstracts

Right Ventricular Function in Congenital Heart Defects Assessed by Regional Wall Motion

CONGENITAL HEART DISEASE, Issue 3 2010
FSCAI, Michael R. Nihill MB
ABSTRACT Objectives., To develop a simple method to assess right ventricular function by angiography. Background., Conventional methods of evaluating right ventricular function are inaccurate, cumbersome, and expensive. Methods., We analyzed biplane right ventricular angiograms taken in the posterior,anterior and lateral projections using software to measure right ventricular volumes and regional wall motion in 78 patients with normal hearts (n = 29), atrial septal defects (ASD n = 13), pulmonary valve stenosis (PVS n = 21), and postoperative atrial switch patients (n = 15). We also measured the shortening fraction (SF) from the midtricuspid annulus to the septum and correlated various angiographic measurements with the right ventricular (RV) ejection fraction. Results., The volume-overloaded patients (ASD) had larger end diastolic volumes and increased SF compared with normal patients, while the pressure-loaded patients (PVS) had normal volumes and SF. The postoperative atrial switch patients had decreased systolic function and increased end diastolic volume. The SF for all of the patients correlated with the ejection fraction (r= 0.785, P, .0001). Conclusions., A simple measurement of the end diastolic and end systolic distance from the midtricuspid annulus to the septum (SF) provides a good index of RV function by angiography and correlates well with RV ejection fraction. [source]

Cardiovascular Response to Graded Lower Body Negative Pressure in Young and Elderly Man

EXPERIMENTAL PHYSIOLOGY, Issue 3 2001
R. van Hoeyweghen
Lower body negative pressure (LBNP) reduces central venous pressure (CVP) and cardiac output. The elderly are reported to have a limited capacity to increase cardiac output by increasing heart rate (HR), are especially dependent on end diastolic volume to maintain stroke volume and therefore should be especially vulnerable to LBNP. The present study compared the effects of LBNP in the young and old. Stroke volume was assessed non-invasively as stroke distance (SD) by aortovelography. Two groups of healthy male volunteers were studied: eight young (29.7 ± 2.0 years, mean ± S.E.M.) and nine old (70.1 ± 0.9 years). LBNP was applied progressively at 17.5, 35 and 50 mmHg in 20 min steps, with measurements taken during each steady state. There were similar, significant, falls in CVP in both groups. SD fell significantly in both groups from respective control values of 24.8 ± 1.6 and 16.6 ± 0.9 cm to 12.5 ± 1.3 and 8.9 ± 0.4 cm at a LBNP of 50 mmHg. Although SD in the elderly was significantly lower than in the young, the LBNP-induced changes were not different between groups. Both groups produced similar significant increases in vascular resistance, HR, plasma vasopressin (AVP) and noradrenaline. Mean arterial blood pressure (MBP) and plasma adrenaline did not change significantly. Therefore healthy old men respond to LBNP in a similar manner to the young, although MBP and SD are regulated around different baselines in the two groups. [source]

Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2002
ANTONIO FRANCO FOLINO
FOLINO, A.F., et al.: Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features. The identification of subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC) at higher risk for sudden death is an unresolved issue. An influence of the autonomic activity on the genesis of ventricular arrhythmias was postulated. Heart rate variability (HRV) analysis provides a useful method to measure autonomic activity, and is a predictor of increased risk of death after myocardial infarction. For these reasons, the aim of the study was to evaluate HRV and its correlations with ventricular arrhythmias, heart function, and prognostic outcome in patients with ARVC. The study included 46 patients with ARVC who were not taking antiarrhythmic medications. The diagnosis was made by ECG, echocardiography, angiography, and endomyocardial biopsy. Exercise stress test and Holter monitoring were obtained in all patients. Time-domain analysis of HRV was expressed as the standard deviation of all normal to normal NN intervals (SDNN) detected during 24-hour Holter monitoring. Thirty healthy subjects represented a control group for HRV analysis. The mean follow-up was 10.8 ± 1.86 years. SDNN was reduced in patients with ARVC in comparison with the control group (151 ± 36 vs 176 ± 34, P = 0.00042). Moreover, there was a significant correlation of this index with the age of the patients (r =,0.59, P < 0.001), with the left (r = 0.44, P = 0.002) and right (r = 0.47, P = 0.001) ventricle ejection fraction, with the right ventricular end diastolic volume (r =,0.62, P < 0.001), and with the ventricular arrhythmias, detected during the same Holter record used for HRV analysis (patients with isolated ventricular ectopic beats < 1,000/24 hours, 184 ± 34; patients with isolated ventricular ectopic beats > 1,000/24 hours and/or couplets, 156 ± 25; patients with repetitive ventricular ectopic beats (,3) and/or ventricular tachycardia, 129 ± 25; P < 0.001). During follow-up two patients showed a transient but significant reduction of SDNN and a concomitant increase of the arrhythmic events. In eight patients an episode of sustained ventricular tachycardia occurred, but the mean SDNN of this subgroup did not differ from the mean value of the remaining patients (152 ± 15 vs 150 ± 39; P = NS). Only one subject died after heart transplantation during follow-up (case censored). Time-domain analysis of HRV seems to be a useful method to assess the autonomic influences in ARVC. A reduction of vagal influences correlates with the extent of the disease. The significant correlation between SDNN and ventricular arrhythmias confirmed the influences of autonomic activity in the modulation of the electrical instability in ARVC patients. However, SDNN was not predictive of spontaneous episodes of sustained ventricular tachycardia. [source]

Left ventricular structure and function in patients with rheumatoid arthritis, as assessed by cardiac magnetic resonance imaging

ARTHRITIS & RHEUMATISM, Issue 4 2010
Jon T. Giles
Objective Heart failure is a major contributor to cardiovascular morbidity and mortality in patients with rheumatoid arthritis (RA), but little is known about myocardial structure and function in this population. This study was undertaken to assess the factors associated with progression to heart failure in patients with RA. Methods With the use of cardiac magnetic resonance imaging, measures of myocardial structure and function were assessed in men and women with RA enrolled in the Evaluation of Subclinical Cardiovascular Disease and Predictors of Events in Rheumatoid Arthritis study, a cohort study of subclinical cardiovascular disease in patients with RA, in comparison with non-RA control subjects from a cohort enrolled in the Baltimore Multi-Ethnic Study of Atherosclerosis. Results Measures of myocardial structure and function were compared between 75 patients with RA and 225 frequency-matched controls. After adjustment for confounders, the mean left ventricular mass was found to be 26 gm lower in patients with RA compared with controls (P < 0.001), an 18% difference. In addition, the mean left ventricular ejection fraction, cardiac output, and stroke volume were modestly lower in the RA group compared with controls. The mean left ventricular end systolic and end diastolic volumes did not differ between the groups. In patients with RA, higher levels of anti,cyclic citrullinated peptide (anti-CCP) antibodies and current use of biologic agents, but not other measures of disease activity or severity, were associated with significantly lower adjusted mean values for the left ventricular mass, end diastolic volume, and stroke volume, but not with ejection fraction. The combined associations of anti-CCP antibody level and biologic agent use with myocardial measures were additive, without evidence of interaction. Conclusion These findings suggest that the progression to heart failure in RA may occur through reduced myocardial mass rather than hypertrophy. Both modifiable and nonmodifiable factors may contribute to lower levels of left ventricular mass and volume. [source]

Right Ventricular Function in Congenital Heart Defects Assessed by Regional Wall Motion

CONGENITAL HEART DISEASE, Issue 3 2010
FSCAI, Michael R. Nihill MB
ABSTRACT Objectives., To develop a simple method to assess right ventricular function by angiography. Background., Conventional methods of evaluating right ventricular function are inaccurate, cumbersome, and expensive. Methods., We analyzed biplane right ventricular angiograms taken in the posterior,anterior and lateral projections using software to measure right ventricular volumes and regional wall motion in 78 patients with normal hearts (n = 29), atrial septal defects (ASD n = 13), pulmonary valve stenosis (PVS n = 21), and postoperative atrial switch patients (n = 15). We also measured the shortening fraction (SF) from the midtricuspid annulus to the septum and correlated various angiographic measurements with the right ventricular (RV) ejection fraction. Results., The volume-overloaded patients (ASD) had larger end diastolic volumes and increased SF compared with normal patients, while the pressure-loaded patients (PVS) had normal volumes and SF. The postoperative atrial switch patients had decreased systolic function and increased end diastolic volume. The SF for all of the patients correlated with the ejection fraction (r= 0.785, P, .0001). Conclusions., A simple measurement of the end diastolic and end systolic distance from the midtricuspid annulus to the septum (SF) provides a good index of RV function by angiography and correlates well with RV ejection fraction. [source]

Left ventricular structure and function in patients with rheumatoid arthritis, as assessed by cardiac magnetic resonance imaging

ARTHRITIS & RHEUMATISM, Issue 4 2010
Jon T. Giles
Objective Heart failure is a major contributor to cardiovascular morbidity and mortality in patients with rheumatoid arthritis (RA), but little is known about myocardial structure and function in this population. This study was undertaken to assess the factors associated with progression to heart failure in patients with RA. Methods With the use of cardiac magnetic resonance imaging, measures of myocardial structure and function were assessed in men and women with RA enrolled in the Evaluation of Subclinical Cardiovascular Disease and Predictors of Events in Rheumatoid Arthritis study, a cohort study of subclinical cardiovascular disease in patients with RA, in comparison with non-RA control subjects from a cohort enrolled in the Baltimore Multi-Ethnic Study of Atherosclerosis. Results Measures of myocardial structure and function were compared between 75 patients with RA and 225 frequency-matched controls. After adjustment for confounders, the mean left ventricular mass was found to be 26 gm lower in patients with RA compared with controls (P < 0.001), an 18% difference. In addition, the mean left ventricular ejection fraction, cardiac output, and stroke volume were modestly lower in the RA group compared with controls. The mean left ventricular end systolic and end diastolic volumes did not differ between the groups. In patients with RA, higher levels of anti,cyclic citrullinated peptide (anti-CCP) antibodies and current use of biologic agents, but not other measures of disease activity or severity, were associated with significantly lower adjusted mean values for the left ventricular mass, end diastolic volume, and stroke volume, but not with ejection fraction. The combined associations of anti-CCP antibody level and biologic agent use with myocardial measures were additive, without evidence of interaction. Conclusion These findings suggest that the progression to heart failure in RA may occur through reduced myocardial mass rather than hypertrophy. Both modifiable and nonmodifiable factors may contribute to lower levels of left ventricular mass and volume. [source]