Disease relevance of Cardiac Volume

• In 16 people with essential hypertension, heart rate (HR), blood pressure (BP) and relative cardiac volumes were measured at rest and during submaximal upright exercise before and after 10 mg of sublingual nifedipine using radionuclide ventriculography [1].
• We hypothesized that CPAP would cause greater reductions in cardiac volumes in CHF patients with idiopathic dilated cardiomyopathy (IDC) than in those with ischemic cardiomyopathy (IsC), because their ventricles are more compliant [2].
• The cardiac volume data of 49 normal children were compared with those of 23 with secundum atrial septal defect and 24 with patent ductus arteriosus [3].
• An antidiabetic thiazolidinedione induces eccentric cardiac hypertrophy by cardiac volume overload in rats [4].
• BACKGROUND: Secundum atrial septal defect is a common congenital heart defect that causes right heart volume overload and produces symptoms usually after the third decade of life [5].

High impact information on Cardiac Volume

• At 4 weeks, negative sodium balance was achieved (52 +/- 21 mmol/day; P < 0.01), despite continued systemic arterial vasodilatation, associated with significant increases in total central and cardiac volumes (P < 0.05) and normalization of serum aldosterone levels (P < 0.01) [6].
• Moreover, the low affinity of enalapril for cardiac ACE appears to lead to continuous angiotensin II generation in the heart and can thus explain the failure of enalapril to attenuate hypertrophic response of the heart induced by shunt despite decreasing cardiac volume overload [7].
• Cardiac volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats [8].
• CONCLUSIONS: Cardiac volume overload, even when accompanied by increased plasma renin activity, decreases LV collagen accumulation, suggesting that in contrast to the stimulatory effect of systolic wall stress, increased diastolic wall stress inhibits collagen accumulation [8].
• The effect of cardiac volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed [8].

Chemical compound and disease context of Cardiac Volume

• These results suggest that chronic cardiac volume load appears to determine the type of cardiac hypertrophy induced by a nonhemodynamic mechanism (possibly cardiac sympathetic activity) activated by minoxidil [9].

Biological context of Cardiac Volume

• The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation [10].
• Although various neurohormones at initial measurement confer prognostic value in heart failure and correlate with the left ventricular ejection fraction (EF) and cardiac volumes, the significance of their temporal changes (Delta) remains undetermined [11].
• Myocardial angiotensin receptor type 1 gene expression in a rat model of cardiac volume overload [12].
• Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce central blood volume shifts in ten cardiac and one heart-lung transplant recipients to assess the contribution of cardiac volume receptors in the control of ADH release during the initial acute phase of exposure to weightlessness [13].

Anatomical context of Cardiac Volume

• Measurements included conventional hemodynamic and echocardiographic variables of cardiac volume conditions and systolic function of the left ventricle (fractional area change [FAC], velocity of myocardial fiber shortening) using a transesophageal probe, arterial and mixed venous blood gas parameters, and serum thyroid hormone concentrations [14].
• A small balloon placed at the junction of the superior vena cava and right atrium was used to stimulate cardiac volume receptors in pentobarbital sodium-anesthetized male rats [15].

Associations of Cardiac Volume with chemical compounds

• One trophic factor may be cardiac angiotensin II generated via an angiotensin II-forming enzyme resistant to ACEI and possibly activated by cardiac volume overload [16].
• Verapamil, but not propranolol, increased (p less than .05) cardiac volumes of resting subjects; used in combination, no further increase in LV volume occurred [17].
• Therefore to explain the effect of nitroglycerin on exercise capacity additional economizing changes in myocardial performance (e.g., reduction of heart volume) are required [18].
• A high intravenous dose of norepinephrine (4 micrograms/kg/min for 60 minutes) to New Zealand Red rabbits produced patchy subendocardial damage (estimated stereologically in frozen sections) of about 5% of the heart volume 2 days after application [19].
• To investigate the possible contributions of cardiac volume overload and cardiac sympathetic hyperactivity in the effects of sodium on cardiac mass, we evaluated the effects of treatment with saline (1%) and deoxycorticosterone acetate + saline (DOCA/saline) for 10 days and 3 and 6 weeks on ventricular anatomy and intracardiac pressures [20].

Gene context of Cardiac Volume

• Plasma and cardiac ET-1 concentrations and ET-1 receptor regulation on both ventricular cell types are not altered in cardiac volume overload, suggesting that cardiac ET-1 may not play a significant role in this model [21].
• To investigate the regulation of the angiotensin receptor type 1 (AT1) in different organs in cardiac volume overload, we measured AT1 mRNA content in the atria, left and right ventricle, kidney and liver of rats with an aortocaval shunt, produced by infrarenal aortocaval puncture 4 weeks earlier [12].
• In the IHD group there was a significant positive correlation between heart volume and TH activity [22].
• Left heart volume characteristics following ventricular septal defect closure in infancy [23].
• The CT-based three-dimensional treatment-planning system (TMS) represents a valuable tool in identifying such patients; thus, treatment may be conformed to reduce the irradiated heart volume [24].

Analytical, diagnostic and therapeutic context of Cardiac Volume

• In 10 patients during cardiac catheterization hemodynamic parameters and cardiac volumes were obtained during baseline and after intravenous infusion of aminophylline [25].
• The cardiovascular effects of low-dose adrenomedullin (ADM, 1, 2 and 3 pmol kg-1 min-1 for 30 min each) were evaluated in six healthy subjects in a placebo controlled, cross-over study by determining cardiac volumes, systolic and diastolic function (echocardiography) and systemic haemodynamics before, during and after ADM or placebo [26].

References