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PubMed1986

Echocardiographic assessment of cardiac function in open chest dogs.

Echocardiographic parameters of left ventricular function were compared with standard parameters in 5 open chest dogs. Cardiac output by echo compared with thermodilution showed a close correlation of r = 0.952. Peak rate of decrease of left ventricular diameter (RDD) correlated with dp/dtmax r = 0.826, and "normalized" RDD with dp/dtmax r = 0.873. The peak rates of increase of LV diameter (RID) and "normalized" RID correlated less with dp/dtmin, r = 0.610 and r = 0.642 respectively. Because of significant differences between the dogs, and because the results from all dogs induced into different hemodynamic states during the investigation were all pooled, the method proved reliable even under borderline conditions. We therefore think it may also be used in clinical situations.

Animals↗
PubMed1991

Effects of antihypertensive treatment on cardiac hypertrophy and cardiac function in elderly hypertensive patients.

The effects of antihypertensive treatment with calcium antagonists or angiotensin-converting enzyme (ACE) inhibitors on the reversal of left ventricular hypertrophy and the left ventricular function in elderly hypertensive patients were examined. Twenty-four elderly hypertensive patients with cardiac hypertrophy, aged from 65 to 79 years (mean +/- SEM of 71 +/- 1 years), were treated with a calcium antagonist (nifedipine or nicardipine) or ACE inhibitor (captopril or enalapril) for 3 months. Thirteen patients had essential hypertension [EH: systolic blood pressure (SBP) greater than or equal to 160 mm Hg and diastolic blood pressure (DBP) greater than or equal to 90 mm Hg, aged 70 +/- 1 years] and 11 had isolated systolic hypertension (ISH:SBP greater than or equal to 160 mm Hg and DBP less than 90 mm Hg, aged 74 +/- 2 years). All patients underwent M-mode echocardiography to assess left ventricular mass index (LVMI) and left ventricular function (ejection fraction, EF) before and after 3 months of treatment. BP significantly decreased from 174 +/- 3/97 +/- 1 to 144 +/- 5/84 +/- 2 mm Hg in EH and from 167 +/- 3/82 +/- 2 to 144 +/- 4/74 +/- 2 mm Hg in ISH. The LVMI was also significantly reduced from 204 +/- 14 to 174 +/- 16 g/m2 in EH and from 179 +/- 14 to 156 +/- 12 g/m2 in ISH. EF showed no significant changes with treatment in either group. In elderly hypertensive patients, the antihypertensive treatment with calcium antagonist or ACE inhibitor reduced cardiac hypertrophy without any deterioration of left ventricular function in both essential hypertension and isolated systolic hypertension.

Aged↗
PubMed2006

Beta-adrenergic receptor desensitization in man: insight into post-exercise attenuation of cardiac function.

Desensitization of the beta-adrenoreceptors (beta-AR) may contribute to a post-exercise reduction in left ventricular (LV) function. However, attenuation of the chronotropic and inotropic responses to a beta-AR agonist may depend upon alterations in parasympathetic tone. Furthermore, changes in cardiac output and LV diastolic function in response to a beta-AR agonist, pre- to post-prolonged exercise, remain unclear. Seven trained males (mean+/-s.d., age 27+/-6 years) performed 4 h of ergometer rowing. Peak heart rate (HR) and LV systolic and diastolic functional responses to incremental isoproterenol (isoprenaline) infusion (2, 4 and 6 microg kg min-1) were assessed after vagal blockade (glycopyrrolate, 1.2 mg). LV systolic function was assessed by the pressure/volume ratio (systolic blood pressure/end systolic volume) and , whilst diastolic function was evaluated as peak early and late transmitral filling velocities. Following exercise, the pressure/volume ratio decreased by 25% (P<0.05), whereas was unchanged (P>0.05). The early/late filling ratio was reduced by 36% after exercise, due to an elevation in late LV filling (P<0.01). The increase in HR response to isoproterenol infusion was blunted post-exercise at both 4 and 6 microg kg min-1 (127+/-7 and 132+/-6 beats min-1) compared with pre-exercise (138+/-8 and 141+/-12 beats min-1, P<0.05). Additionally, the pressure/volume ratio and were blunted post-exercise in response to isoproterenol (P<0.05). In contrast, diastolic function was similar before and after exercise during isoproterenol infusion (P>0.05). Desensitization of the beta-AR contributes to an attenuated left ventricular systolic but not diastolic function following prolonged exercise.

Adrenergic beta-Agonists↗
PubMed1982

Effects of antiarrhythmic agents on cardiac function.

Many, if not most antiarrhythmic drugs, even with differing pharmacologic properties, are capable of myocardial depression. That this has not occurred commonly with most drugs currently available may reflect several factors. These may include depression of myocardial function which is not clinically overt or which is masked by preexisting cardiac decompensation, limitation of dosages because of the difficulty in accurately determining a therapeutic endpoint, and the lack of physician awareness of the effects of these drugs on myocardial performance. However, as techniques for monitoring and quantifying arrhythmia permit more aggressive drug therapy, and as more drugs become available for clinical use, the incidence of clinically overt myocardial depression from anti-arrhythmic therapy will undoubtedly rise. Hopefully, awareness of the hemodynamic effects of these drugs and applications of new technology permitting accurate, noninvasive assessment of left ventricular function will identify and hence limit the occurrence of toxic hemodynamic effects, as well as permit the usage of maximum dosages of antiarrhythmic drugs when warranted by clinical circumstances.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Monitoring of cardiac function in patients with a left ventricle assist device.

In complex therapy of acute or chronic cardiac failure, the use of valve-free centrifugal pumps or artificial heart ventricles takes place. In these cases, simultaneous monitoring of cardiac and pump performance is very important. In this study, an ultrasound dilution method based on the registration of two dilution curves after intravenous injection of isotonic and hypertonic sodium solution was developed. Comparison of total cardiac output (TCO), which included pump and heart output measured by thermodilution and ultrasound (TCOus) dilution, yielded TCOus = 1.11TCOth - 0.54 (n = 13).

Cardiac Output↗
PubMed2006

In vivo and in vitro models to test the hypothesis of particle-induced effects on cardiac function and arrhythmias.

Exposure to ultrafine particles (UFPs) by inhalation increases the number and severity of cardiac events. The specific mechanism(s) of action are unknown. This study was designed to examine whether UFPs could exert a direct effect on the cardiovascular system without dependence upon lung-mediated responses. The direct effects of UFPs were determined in normal rats (infused intravenously with UFPs), and in the isolated Langendorff perfused rat heart. UFPs from either ambient air (UFAAs) or diesel engine exhaust (UFDGs) were studied. Infusion of UFDGs prepared in our laboratory caused ventricular premature beats (VPBs) in 2 of 3 rats in vivo. Ejection fraction increased slightly (approximately 4.5%) in rats receiving UFPAA and was unchanged in the UFDG and saline groups in vivo. In the isolated rat heart, perfused according to Langendorff, UFDGs caused a marked increase in left-ventricular end-diastolic pressure (LVEDP; from 12.0 +/- 4.6 mmHg to 24.8 +/- 11.2 mmHg, p < 0.05) after 30 min of exposure. UFPs isolated from industrial diesel particulate matter (UFIDs), obtained from the National Institute of Standards and Technology, caused a significant decrease in left-ventricular systolic pressure (LVSP; from 85.7 +/- 4.0 mmHg to 37.9 +/- 20.3 mmHg, p < 0.05) and +/- dP/dt (from 2,365 +/- 158 mmHg/s to 1,188 +/- 858 mmHg/s, p < 0.05) at 30 min after the start of infusion. This effect was absent when the soluble fraction (containing no particles) isolated from the UFIDs was studied. These findings indicate that UFPs can have direct effects on the cardiovascular system that are independent of effects of particles on the lungs.

Air Pollutants↗
PubMed1982

[Abnormal findings of cardiac function in patients with systemic lupus erythematosus (author's transl)].

To find out the rate of cardiac involvement among patients with systemic lupus erythematosus (SLE), 34 patients with SLE were examined by ECG, x-ray of the chest, body plethysmography, one- and two-dimensional echocardiography In addition, in 23 patients with SLE a microcatheterization of the right heart side was undertaken with measuring of the mean pulmonary artery pressure and cardiac index during exercise. Echocardiography revealed moderate abnormal findings in 62% of the patients. In particular, there was a thickening of the interventricular septum (31%), an enlargement of the right ventricle (23%), a diminution of the left ventricular fractional shortening (16%), an augmentation of the left atrium (10%) and of the left ventricle (6%). A small pericardial effusion was observed in 6% and a thickening of the left ventricular posterior wall in 3%. At micro-catheterization in 19 out of 23 patients with SLE, there was an increase of the mean pulmonary artery pressure up to abnormal values. In 5 patients, mean pulmonary pressure rose over 40 mm Hg. Most of the patients also showed an increase of the arterial pressure up to pathological values. Furthermore, most of the patients finished exercise because of muscular insufficiency or dyspnoea. Only 4 of 23 patients with SLE reached 90% of the age-corresponding maximal heart rate. The results indicate that with about 80% of all patients with SLE the cardiac capacity is reduced. In about 20% of the patients with SLE, this diminution of cardiac capacity is severe, and the necessity of medical treatment has to be discussed.

Adolescent↗
PubMed1998

Phospholamban: protein structure, mechanism of action, and role in cardiac function.

A comprehensive discussion is presented of advances in understanding the structure and function of phospholamban (PLB), the principal regulator of the Ca2+-ATPase of cardiac sarcoplasmic reticulum. Extensive historical studies are reviewed to provide perspective on recent developments. Phospholamban gene structure, expression, and regulation are presented in addition to in vitro and in vivo studies of PLB protein structure and activity. Applications of breakthrough experimental technologies in identifying PLB structure-function relationships and in defining its interaction with the Ca2+-ATPase are also highlighted. The current leading viewpoint of PLB's mechanism of action emerges from a critical examination of alternative hypotheses and the most recent experimental evidence. The potential physiological relevance of PLB function in human heart failure is also covered. The interest in PLB across diverse biochemical disciplines portends its continued intense scrutiny and its potential exploitation as a therapeutic target.

Animals↗
PubMed2003

Molecular mechanisms in endothelial regulation of cardiac function.

Endothelium is now recognized as a massive, regionally specific, multifunctional organ. Given its strategic anatomic location between the circulating blood components and the vascular smooth muscle or the cardiac muscle, it is a biologically significant interface whose dysfunction can be a critical factor in various pathological conditions. Two types of endothelial cells are recognized in the heart, the endocardial endothelial (EE) cells and the microvascular endothelial cells (MVE). Both produce common autacoids and share similar roles in signal transduction induced by neurotransmitters, hormones or mechanical stimuli. They are however two distinct cell populations with dissimilar embryological origin, cytoskeletal organization, receptor mediated functions and electrophysiological properties. Both the MVE and EE are modulators of cardiac performance. Myocardial contraction may be modulated by cardioactive agents such as nitric oxide, prostanoids, endothelin, natriuretic peptides, angiotensin II, kinins, reactive oxygen species and adenyl purines released from the cardiac endothelium. Two mechanisms have been proposed for the signal transduction from EE to the underlying myocytes: stimulus-secretion-contraction coupling and blood-heart barrier. Nitric oxide, bradykinin and myofilament desensitizing agent are probably important in short-term regulation of myocardial functions. Endothelin and Angiotensin II are probably involved in long-term regulation. Besides its sensory function and paracrine modulation of myocardial performance, EE as a blood-heart barrier could be of significance for the ionic homeostasis of the cardiac interstitium. In cardiac diseases, the damage to EE or MVE leading to failure of the endothelial cells to perform its regulatory and modulator functions may have serious consequences. A better understanding of the endothelial signaling pathways in cardiac physiology and pathophysiology may lead to the development of novel therapeutic strategies.

Animals↗
PubMed1991

Assessment of cardiac function by M-mode echocardiography in selenium-deficient phenylketonuric children.

Selenium (Se) deficiency is associated with cardiac and skeletal muscle dysfunction. Twenty well children aged 2-16 years (10 male) attending the Phenylketonuria (PKU) Clinic at the Royal Children's Hospital, Brisbane, had low Se levels (mean 0.29 +/- 0.02 s.e.m. mumol/L; normal range 0.56-1.16 mumol/L). Their myocardial function was assessed at rest and after exercise provocation by M-mode echocardiography in order to exclude occult left ventricular dysfunction. At rest, fractional shortening (FS) was normal (mean 38.1 +/- 1.1 s.e.m. %, n = 20). After exercise, FS increased significantly (P less than 0.001) from 37.6 +/- 1.4% to 44.3 +/- 1.2%, n = 12). This was associated with a significant rise (P less than 0.001) in heart rate (HR) from 77.3 +/- 3.1 beats/min to 125.8 +/- 5.2 beats/min (n = 12). The normal resting FS and normal increase in FS and HR with exercise is evidence against significant cardiac impairment in this group of Se-deficient children.

Adolescent↗
PubMed1995

Effects of sedation with detomidine hydrochloride on echocardiographic measurements of cardiac dimensions and indices of cardiac function in horses.

Twenty-six horses were sedated with detomidine hydrochloride (Domosedan, SmithKline Beecham Animal Health, Tadworth, Surrey, UK) at a dose of 10 micrograms/kg bwt, administered i.v. Echocardiograms were recorded before and after sedation, measurements of cardiac dimensions were made and functional indices were calculated. The pre- and post sedation values were compared. No significant change was detected following sedation in the ejection time (ET), left ventricular dimension, left atrial diameter at the sinotubular junction at end-systole or end-diastole or at the sinus of Valsalva at end-diastole. Sedation was found to result in a statistically significant increase in end-systolic left ventricular diameter and internal area and aortic diameter measured at the sinus of Valsalva. Left ventricular free-wall thickness and interventricular septal thickness at end-systole, fractional shortening, fractional area change and heart rate were significantly reduced following sedation. A significant increase in pre-ejection period (PEP), duration of electromechanical systole (EMS) and PEP/ET (ejection time) was detected.

Animals↗
PubMed1972

Mechanography: a non-invasive technique for the evaluation of cardiac function in children.

Experience in the pediatric age group with mechanography, an indirect method of cardiovascular investigation, is described with emphasis on the recording technique and on the analysis of the tracings. A few examples are presented with comments on the morphological aspects and the time characteristics of the pulse curves, showing how much information about cardiac disease and especially myocardial function in children may be obtained.

Adolescent↗
PubMed2000

Left ventricular function, cardiac dysrhythmias, atrial activation, and volumes in nondipper hypertensive individuals with left ventricular hypertrophy.

BACKGROUND: Arrhythmic patterns and left ventricular geometric adaptations to pressure overload were investigated in 76 patients with untreated borderline-to-moderate sustained essential hypertension studied by 2-dimensional and M-mode echocardiography, 12-lead, Holter, and signal-averaged electrocardiography, and ambulatory blood pressure monitoring. METHODS AND RESULTS: Sixty-two age- and sex-matched normal adults were chosen for data comparison. Hypertrophic hypertensive patients were subdivided into 2 subgroups: 44 patients with nocturnal blood pressure reduction (dippers) and 32 patients without it (nondippers). Common afterload and diastolic function indexes were found to be lower in combined nondipper and dipper groups, but only fractional shortening decreased in nondippers. The number of premature atrial and ventricular contractions per hour was high in dippers and nondippers, with no statistically significant differences between them; atrial and ventricular complex dysrhythmias were similar. Signal-averaged electrocardiography showed a prolonged P-wave duration in dipper and nondipper patients with high atrial volumes but no late ventricular potentials and no difference in quantitative P-wave analysis. Left atrial volumes, P-wave duration, and premature atrial contractions were found to be positively linked to left ventricular hypertrophy. In nondipper patients a linear correlation was observed between left atrial volume and P-wave duration, although supraventricular ectopic activity was connected to left atrial volume enlargement both in dipper and nondipper patients. CONCLUSIONS: These data suggest that the nondipper pattern is not linked to a worse arrhythmogenic substrate; only atrial volume increase may be related to significant supraventricular activity and prolonged atrial activation in nondipper patients, but late ventricular potentials are uncommon in hypertrophic hypertensive patients.

Arrhythmias, Cardiac↗
PubMed1984

[Assessment of cardiac function by left heart catheterization: an analysis of left ventricular pressure-volume (length) loops].

The mechanical property of the cardiac muscle has been classically analyzed in two ways; shortening of muscle fiber, and the development of tension within the muscle. In the ejecting ventricle, left ventricular (LV) function can be analyzed by the analogous two-dimensional framework of pressure-volume loops, which are provided by plotting the instantaneous volume against corresponding LV pressure. The integral pressure with respect to volume allows to assess a total external ventricular work during ejection. The diastolic pressure-volume relations reflect a chamber stiffness of the ventricle. Force-velocity relations also provide an useful conceptual framework for understanding how the ventricle contracts under given afterload, with modification of preload. In the presence of coronary artery disease, the regional nature of left ventricular contractile function should be defined as well as the global ventricular function as described above, because the latter is determined by the complex interaction of dysfunction of the ischemic myocardium and of compensatory augmentation of shortening of the normally perfused myocardium. We utilized a computer technique to analyze the local wall motion of the ischemic heart by cineventriculography. The boundaries of serial ventricular images are automatically traced and superimposed using the external reference system. Radial grids are drawn from the center of gravity of the end-diastolic image. Measurement of length of each radial grid throughout cardiac cycle provides the analysis of movement of the ventricle at a particular point on the circumference. Using phasic pressure obtained simultaneously with opacification as the common parameter, segmental pressure-length loops are constructed simultaneously at various segments. The loops are similar over the entire circumference in the normal heart, being rectangular in morphology and with synchronous behavior during contraction and relaxation. However, the marked distortion of pressure-length loops with clockwise rotation or figure of eight inscription is observed in the ischemic segments. Systolic work of the ischemic segment diminishes dramatically, and the loops exhibit varying degrees of inclination. The control segment loops also show an inclination to the opposite direction of the ischemic loops. These differences are presumably related to the local redistribution of the myocardial tension during systole in the ischemic ventricle. Thus, the method described should be of particular value in assessing the regional myocardial function in the ischemic ventricle and effects of various interventions which modify ischemia.

Cardiac Catheterization↗
PubMedDate not supplied

Exercise and posture-related changes of atrial natriuretic factor and cardiac function in diabetes.

To study whether the release of atrial natriuretic factor (ANF) was altered in diabetic cardiac autonomic neuropathy (CAN), we determined plasma ANF concentrations during exercise and changes of posture in three groups of age- and sex-matched subjects (9 healthy subjects, 7 diabetic patients with CAN, and 7 diabetic patients without CAN). During exercise, plasma ANF concentrations rose threefold (P less than .001), and this increase was similar in the three groups. However, heart-rate response to exercise was impaired in the two groups of diabetic patients (P less than .004 vs. healthy subjects) but was more severely impaired in patients with CAN (P less than .03 vs. patients without CAN). In healthy subjects and patients without CAN, the increases of ANF during exercise correlated significantly with those of heart rate, systolic blood pressure, and rate-pressure product (P less than .01). In patients with CAN, the correlation was found exclusively with heart rate (P less than .01). An increase of ventricular ejection fraction occurred in all groups (P less than .001) but without showing statistical differences between groups. After 30 min of standing, a similar postural drop of plasma ANF concentrations (P less than .002) was observed in all subjects, reflecting preserved sympathetic control of vessels. In conclusion, exercise induces an increase of plasma ANF in diabetic patients with CAN. This increase, occurring similarly to healthy subjects, indicates that autonomic activation plays a minor role in ANF release during exercise. Impaired heart-rate response to exercise in patients without CAN suggests early damage of autonomic function, undetected by conventional rest tests.

Adult↗
PubMed1997

Doxorubicin-induced acute changes in cytotoxic aldehydes, antioxidant status and cardiac function in the rat.

Doxorubicin (DOX)-induced cardiotoxicity is thought to be caused by free radical-mediated mechanisms. An in vivo rat model was developed to investigate the DOX-induced cascade of early biochemical changes focusing on the central role of the aldehydic lipid peroxidation products. Antioxidant status was evaluated by glutathione measurements. Creatine Kinase (CK) activity was measured as an index of cardiac injury. Development of functional abnormalities were documented by echocardiography. The results showed that aldehydes in rat plasma and heart tissues increased significantly following DOX treatment. The changes occurred early, peaked around 2 h after DOX administration, and the levels declined or returned to baseline value within 8-24 h. Toxic aldehyde levels including malondialdehyde, hexanal and 4-hydroxy-non-2-enal also increased. Acyloin levels, metabolic products of aldehydes, increased early and then decreased in plasma, and there was a significant decrease in heart tissues after DOX treatment. GSH levels decreased early, then increased by 24 h, while GSSG levels decreased initially, then increased after DOX treatment, suggesting early depletion of GSH and a later rebound phenomenon. CK levels were elevated after treatment. The functional abnormalities were documented by stress echocardiography in some rats although the changes were not consistent at such an early stage following treatment. Our data confirmed the involvement of free radicals, and suggested that the cytotoxic aldehydes play a central role in initiating the steps that lead to functional impairment of the myocardium following DOX administration. Scavengers and the metabolic removal of some of the aldehydes also play a role in protecting the myocardium against injury.

Aldehydes↗
PubMed2000

Significance of brain natriuretic peptide measurement as a diagnostic indicator of cardiac function.

Brain natriuretic peptide (BNP) is increased in patients with heart failure due to myocardial infarction and cardiac hypertrophy, in proportion to the severity of left ventricular dysfunction. The aims of this study were to clarify the clinical features of BNP and to determine the diagnostic value of BNP for mass screening. The subjects were 818 office workers (565 males and 253 females; mean age 47 +/- 12 years) who participated in a 1996 routine health check at Kansai University All individuals were examined for blood pressure, serological findings, ECG and plasma BNP level. Thirty-three males underwent 2-D echocardiography. Plasma BNP levels were measured using IRMA (immunoradiometric assay). The results were as follows: (1) BNP levels in females were higher than those in males for healthy subjects (N = 551), in each age group from 20 to 60 years. (2) BNP levels increased with age. (3) There were significant correlations between BNP level and systolic blood pressure and creatinine level. (4) There were significant differences in BNP level between the hypertensive groups with and without hypertensive ECG changes and the age-matched healthy control group. (5) Marked correlations were observed between BNP level and left ventricular wall thickness, fractional shortening, deceleration time and peak early filling velocity. (6) A BNP cut-off-point of 25 pg/ml was best for detecting LV diastolic dysfunction and LV hypertrophy. Measurement of BNP is useful for detecting asymptomatic heart failure in the general population, and is a clinical marker useful in preventing symptomatic heart failure.

Adult↗