Ventricular pressure-volume curve indices change with end-diastolic pressure.
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Many indices have been proposed to describee the diastolic pressure-volume curve mathematically and permit quantification of the elastic properties of the myocardium itself in hopes that changes in the muscle caused by disease would b.e reflected in the diastolic pressure-volume curve. To date, none of the proposed indices has been shown convincingly to discriminate one group of patients from another. While this situation in part arises from the relatively large amount of noise introduced by the technical difficulties of measuring synchronous pressures and volumes during diastole in man, ther is a more fundamental difficulty. In practice, one can measure only a short segment of the entire pressure-volume curve, and the values of all diastolic pressure-volume curve parameters investigated change significantly when one uses different segments of the same pressure-volume curve to compute them. These results were derived from relatively noise-free pressure-volume curves obtained by filling nine excised dog left ventricles at a known rate and monitoring pressure-volume curve used to compute the parameter. Merely increasing measurement fidelity will not resolve this problem, because none of these parameters accurately characterizes the entire diastolic pressure-volume curbe from a segment like that which one can reasonably expect to obtain from humans. (+info)
2,3,7,8-Tetrachlorodibenzo-p-dioxin alters cardiovascular and craniofacial development and function in sac fry of rainbow trout (Oncorhynchus mykiss).
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Hallmark signs of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity in rainbow trout sac fry, are yolk sac edema, hemorrhage, craniofacial malformation, and growth retardation culminating in mortality. Our objective was to determine the role of cardiovascular dysfunction in the development of this toxicity. An embryotoxic TCDD dose (385 pg/g egg) caused a progressive reduction in blood flow in rainbow trout sac fry manifested first and most dramatically in the 1st and 2nd branchial arches and vessels perfusing the lower jaw. Blood flow was reduced later in the infraorbital artery and occipital vein of the head as well as segmental vessels and caudal vein of the trunk. Reduced perfusion occurred last in gill branchial arteries involved with oxygen uptake and the subintestinal vein and vitelline vein involved with nutrient uptake. Although heart rate throughout sac fry development was not affected, heart size at 50 days post-fertilization (dpf) was reduced far more than body weight or length, suggesting that the progressive circulatory failure caused by TCDD is associated with reduced cardiac output. Craniofacial development was arrested near hatch, giving rise to craniofacial malformations in which the jaws and anterior nasal structures were underdeveloped. Unlike the medaka embryo, in which TCDD causes apoptosis in the medial yolk vein, endothelial cell death was not observed in rainbow trout sac fry. These findings suggest a primary role for arrested heart development and reduced perfusion of tissues with blood in the early-life stage toxicity of TCDD in trout. (+info)
Left ventricular function in chronic renal failure.
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Left ventricular function was studied in 14 patients with end-stage chronic renal failure using non-invasive methods (echocardiography and systolic time intervals). Patients were divided into 3 groups. Group 1 consisted of 5 patients who were normotensive at the time of study and group 2 of 7 patients who were hypertensive when studied. Group 3 consisted of 2 patients: one was receiving propranolol and the other, studied 302 days after renal transplantation, was receiving digitalis for recurrent episodes of cardiac failure. All except the patient receiving propranolol had normal left ventricular function in systole with normal measurements of fractional fibre shortening (% delta S, EF) and normal measurements relating to the velocity of ventricular contraction (mean Vcf, mean velocity of posterior wall motion). Stroke volume and cardiac output were normal in some patients but were increased in patients with fluid overload. Early diastolic compliance of the left ventricle seemed to be normal except in the patient with recurrent cardiac failure. The study provided no evidence for the existence of a specific uraemic cardiomyopathy. (+info)
Fetal pulmonary venous flow into the left atrium relative to diastolic and systolic cardiac time intervals.
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OBJECTIVE: To establish the nature and gestational age dependency of the pulmonary venous flow velocity pattern into the left atrium relative to systolic and diastolic phases of the cardiac cycle. DESIGN: This was a cross-sectional study of Doppler measurements of fetal pulmonary venous inflow velocities, which were correlated with simultaneous recordings of transmitral and aortic flow velocity waveforms based on an equal cardiac cycle length (+/- 5%). RESULTS: Successful recordings were obtained in 28 out of 60 (47%) normal singleton pregnancies at 20-36 weeks of gestation. Reproducibility of waveform analysis of the various phases of the cardiac cycle was satisfactory, within-patient variance ranging between 1.7% and 6.5%. A statistically significant increase (p < 0.05) in pulmonary venous time average velocity and velocity integral with advancing gestational age was established. A statistically significant increase (p < 0.05) of the pulmonary flow velocity integral was also found when related to each of the systolic and diastolic segments of the cardiac cycle, with the exception of isovolemic relaxation time. The duration of each of the diastolic and systolic segments of the cardiac cycle, as well as the pulmonary venous velocity integral expressed as a percentage of the cardiac cycle, remained constant with advancing gestational age. CONCLUSIONS: The second half of pregnancy is characterized by pulmonary venous inflow into the left atrium throughout the cardiac cycle. Pulmonary venous inflow into the left atrium occurs predominantly during the filling and ejection phases of the cardiac cycle. Absolute cardiac diastolic and systolic time intervals as well as the percentage distribution of pulmonary venous flow velocity integrals between these cardiac time intervals remain unchanged with advancing gestational age. (+info)
Familial predisposition of left ventricular hypertrophy.
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OBJECTIVES: The study evaluated the contribution of familial predisposition to the risk of left ventricular hypertrophy (LVH). BACKGROUND: Left ventricular hypertrophy is a multifactorial condition that serves as an important predictor of cardiovascular mortality. At present it is unclear whether familial predisposition contributes to the manifestation of LVH. Thus, we determined whether siblings of subjects with LVH are at increased risk to present with an elevation of LV mass or an abnormal LV geometry. METHODS: Echocardiographic and anthropometric measurements were performed in 2,293 individuals who participated in the echocardiographic substudies of population-based MONICA Augsburg surveys. In addition, a total of 319 siblings of survey participants with echocardiographic evidence of LVH were evaluated. The risk of these siblings to present with LVH or abnormal LV geometry was estimated by comparison with 636 subjects matched for gender and age that were selected from the entire echocardiography study base. RESULTS: Blood pressure, body mass index, age, and gender (i.e., known determinants of LV mass) were comparable in LVH-siblings and the matched comparison group. However, septal and posterior wall thicknesses, relative wall thickness as well as LV mass index were significantly elevated in LVH-siblings (p < 0.001, each) whereas LV dimensions did not differ. Likewise, the prevalence of LVH was raised in LVH-siblings, as was the relative risk of LVH after adjustment for confounders (p < 0.05). More specifically, LVH-siblings displayed increased prevalences of concentric remodeling and concentric LVH (p < 0.05) but not of eccentric LVH. CONCLUSIONS: Familial predisposition appears to contribute to increased LV wall thickness, to the development of LV hypertrophy and abnormal LV geometry. (+info)
Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis.
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The aim of this study was to assess the relationship between subtle cardiovascular abnormalities and abnormal sodium handling in cirrhosis. A total of 35 biopsy-proven patients with cirrhosis with or without ascites and 14 age-matched controls underwent two-dimensional echocardiography and radionuclide angiography for assessment of cardiac volumes, structural changes and systolic and diastolic functions under strict metabolic conditions of a sodium intake of 22 mmol/day. Cardiac output, systemic vascular resistance and pressure/volume relationship (an index of cardiac contractility) were calculated. Eight controls and 14 patients with non-ascitic cirrhosis underwent repeat volume measurements and the pressure/volume relationship was re-evaluated after consuming a diet containing 200 mmol of sodium/day for 7 days. Ascitic cirrhotic patients had significant reductions in (i) cardiac pre-load (end diastolic volume 106+/-9 ml; P<0.05 compared with controls), due to relatively thicker left ventricular wall and septum (P<0.05); (ii) afterload (systemic vascular resistance 992+/-84 dyn.s.cm(-5); P<0. 05 compared with controls) due to systemic arterial vasodilatation; and (iii) reversal of the pressure/volume relationship, indicating contractility dysfunction. Increased cardiac output (6.12+/-0.45 litres/min; P<0.05 compared with controls) was due to a significantly increased heart rate. Pre-ascitic cirrhotic patients had contractile dysfunction, which was accentuated when challenged with a dietary sodium load, associated with renal sodium retention (urinary sodium excretion 162+/-12 mmol/day, compared with 197+/-12 mmol/day in controls; P<0.05). Cardiac output was maintained, since the pre-load was normal or increased, despite a mild degree of ventricular thickening, indicating some diastolic dysfunction. We conclude that: (i) contractile dysfunction is present in cirrhosis and is aggravated by a sodium load; (ii) an increased pre-load in the pre-ascitic patients compensates for the cardiac dysfunction; and (iii) in ascitic patients, a reduced afterload, manifested as systemic arterial vasodilatation, compensates for a reduced pre-load and contractile dysfunction. Cirrhotic cardiomyopathy may well play a pathogenic role in the complications of cirrhosis. (+info)
Patterns of body fat deposition in youth and their relation to left ventricular markers of adverse cardiovascular prognosis.
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The patterns of body fat deposition in healthy youth and their relation to future development of cardiovascular disease remain incompletely understood. To further evaluate these patterns, we measured indirect indexes of central and general fat deposition in healthy adolescents (mean age 15.4+/-2.3 years) with family histories of hypertension. We examined the relation between these indexes and echocardiographic markers of adverse prognosis as well as the effect of gender and ethnicity. All 225 subjects (64% black and 48% female) had > or =1 biologic parent and 1 grandparent with hypertension. Skinfold thicknesses, waist-to-hip girth ratio, Quetelet index, Ponderal index, conicity, and Z score weight - Z score height were measured. Left ventricular (LV) mass, indexed LV mass, relative wall thickness (RWT), and midwall fractional shortening (MFS) were determined using echocardiography. In both black and white subjects, the adiposity indexes were significantly correlated with posterior wall thickness, total LV mass, and indexed LV mass (p <0.05 for all). Additionally, in black subjects, central adiposity was inversely related to MFS and directly related to RWT and septal thickness. General adiposity independently predicted indexed and nonindexed LV mass, whereas central adiposity predicted MFS and RWT. Compared with subjects with normal LV geometry, those with abnormal geometry were heavier and fatter based on every index of obesity (p <0.03 for all). Thus, indexes of fat deposition are significantly correlated with LV markers of adverse prognosis in healthy youth. (+info)
Changes in left ventricular filling and left atrial function six months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy.
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OBJECTIVES: The purpose of this study was to evaluate changes in left ventricular (LV) filling, left atrial (LA) volumes and function six months after nonsurgical septal reduction therapy (NSRT) for hypertrophic obstructive cardiomyopathy (HOCM). BACKGROUND: Patients with HOCM frequently have enlarged left atria, which predisposes them to atrial fibrillation. Nonsurgical septal reduction therapy results in significant reduction in left ventricular outflow tract (LVOT) obstruction and symptomatic improvement. However, its effect on LV passive filling volume, LA volumes and function is not yet known. METHODS: Thirty patients with HOCM underwent treadmill exercise testing as well as 2-dimensional and Doppler echocardiography before and six months after NSRT. Data included clinical status, exercise duration, LVOT gradient, mitral regurgitant (MR) volume, LV pre-A pressure and LA volumes. Left atrial ejection force and kinetic energy (KE) were computed noninvasively and were compared with 12 age-matched, normal subjects. RESULTS: New York Heart Association (NYHA) class was lower and exercise duration was longer (p < 0.05) six months after NSRT. The LVOT gradient, MR volume and LV pre-A pressure were all significantly reduced. HOCM patients had larger atria, which had a higher ejection force and KE, compared with normal subjects (p < 0.01). After NSRT, LV passive filling volume increased (p < 0.01), whereas LA volumes, ejection force and KE decreased (p < 0.01). Reduction in LA maximal volume was positively related to changes in LV pre-A pressure (r = 0.8, p < 0.05) and MR volume (0.4, p < 0.05). Changes in LA ejection force were positively related to changes in LA pre-A volume (r = 0.7, p < 0.01) and KE (r = 0.81, p < 0.01). The increase in exercise duration paralleled the increase in LV passive filling volume (r = 0.85, p < 0.05). CONCLUSIONS: Nonsurgical septal reduction therapy results in an increase in LV passive filling volume and a reduction in LA size, ejection force and KE. (+info)