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PubMed1994

A controlled trial of the effects of esmolol on cardiac function.

We have examined the effects of two different bolus doses of esmolol hydrochloride (Brevibloc) on haemodynamic variables in a placebo-controlled, double-blind, randomized trial. Sixty healthy adult patients undergoing minor orthopaedic surgery were given a standardized general anaesthetic using a laryngeal mask airway. Heart rate (HR), mean arterial pressure (MAP), stroke volume (SV) and cardiac output (Q) were measured (the latter two by Doppler ultrasonography) every 1 min for 5 min after injection of either placebo or esmolol 100 mg or 200 mg. HR, MAP, SV and Q decreased significantly (P < 0.05) for both esmolol groups compared with placebo and, except for MAP, esmolol 200 mg had a greater effect than esmolol 100 mg (P < 0.05). Depression was maximal at 2 min after which recovery was observed but was still incomplete at 5 min.

Adolescent↗
PubMed1991

Cardiac function in massively obese patients and the effect of weight loss.

Massively obese patients are at increased risk for heart disease. Blood volume and capillary flow are increased to supply the excess body mass, and there is a concomitant increase in preload and, often, afterload. The heart compensates for the expanded blood volume by increasing stroke volume and cardiac work to provide increased cardiac output. The result is left ventricular dilatation followed by eccentric left ventricular hypertrophy. Cardiac compensatory reserve is limited, leading, at times, to overt congestive failure. After reduction of the excess body fat, most of the cardiovascular derangements appear to reverse. The authors review the effect of massive obesity on the heart and the cardiovascular consequences of weight reduction.

Heart↗
PubMed1989

Plasma oxalate concentration, oxalate clearance and cardiac function in patients receiving haemodialysis.

Pre-dialysis plasma oxalate concentration was measured in a cross-sectional study of 75 patients receiving maintenance haemodialysis. The aims of this study were to enable formulation of hypotheses regarding the determinants of plasma oxalate concentration and to allow preliminary examination of the possibility that hyperoxalaemia confers an increased risk of cardiac and vascular disease even in the absence of primary hyperoxaluria. Plasma oxalate concentration ranged between 7 and 76 mumol/l, mean (SD) 34.6 (18.1) mumol/l (normal range less than 0.8-2.0 mumol/l). Significant correlations were found between plasma oxalate concentration and plasma creatinine, duration of dialysis, current dose of ascorbic acid, and serum phosphate, and each of these variables retained significance on multiple linear regression. Oxalate clearance across a 1 m2 hollow-fibre Cuprophan dialyser, at 500 ml/min dialysate flow and blood flow between 175 and 225 ml/min, was measured 1 h after commencement of dialysis (n = 19). Mean (SD) clearance was 96.5 (27.0) ml/min. No significant association was found between self-reported maximum walking distance or the occurrence of symptoms of cardiac failure and plasma oxalate concentration. No relationship was found between plasma oxalate concentration and electrocardiographic conduction disturbances (n = 8) 'major' ST/T wave changes (n = 22), 'minor' ST/T wave changes (n = 49). Plasma oxalate was significantly greater in patients with radiologically detectable calcification of medium-sized arteries than in those without calcification, but duration of dialysis was also significantly longer in these patients. Routine haemodialysis results in marked hyperoxalaemia, which may be exacerbated by ascorbate supplementation. Oxalate clearance is similar to that of other small molecules such as creatinine and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Systolic time intervals and their derivatives for evaluation of cardiac function.

Systolic time intervals provide a noninvasive indication of global left ventricular performance, are relatively sensitive, and are easily obtained from an M-mode echocardiogram. This paper defines systolic time intervals (preejection period, left ventricular ejection time, and total electromechanical systole) and their derivatives (preejection period/left ventricular ejection time and velocity of circumferential fiber shortening). Their utility and weaknesses, as well as the effects of heart rate, loading conditions, cardiac contractility, and drug therapies on systolic time intervals are discussed. Normal values for systolic time intervals for the dog and cat are provided.

Animals↗
PubMed2003

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation.

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1-10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After beta-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without beta-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after beta-blockade. We conclude that a burst of 15-30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.

Adrenergic Uptake Inhibitors↗
PubMed1989

The pharmacodynamic and pharmacokinetic interaction between single doses of flecainide acetate and verapamil: effects on cardiac function and drug clearance.

Flecainide and verapamil are antiarrhythmic agents that may be used in combination. We have examined their pharmacodynamic interaction by M-mode echocardiography and electrocardiography in eight normal male volunteers (24 +/- 1.8 years of age). Flecainide decreased the left ventricular ejection fraction (LVEF) (-4.4 +/- 1.2%, p less than 0.008), but verapamil did not. Neither drug affected cardiac output or vascular resistance. Both drugs increased the PR interval (12 +/- 4 msec, p less than 0.01 for flecainide; 12 +/- 5, p less than 0.04 for verapamil). Flecainide, but not verapamil, increased the QTc interval (23 +/- 8 msec, p less than 0.02). Both drugs also increased the systolic time interval ratio (PEPc/LVETc) (0.074 +/- 0.012, p less than 0.0004 for flecainide; 0.029 +/- 0.008, p less than 0.007 for verapamil). The combination of flecainide and verapamil had additive effects on myocardial contractility and on atrioventricular conduction. Verapamil slightly decreased the plasma clearance of flecainide (7.78 +/- 0.60 ml/kg/min for flecainide alone, 7.34 +/- 0.48 ml/kg/min for flecainide and verapamil together, p less than 0.05). On the other hand, flecainide had no effect on the plasma clearance of verapamil, which suggests that there was little interaction between the two drugs on their pharmacokinetic parameters.

Administration, Oral↗
PubMed2003

Vanadate improves cardiac function and myocardial energy metabolism in diabetic rat hearts.

Vanadium mimicking the metabolic effects of insulin is known to decrease serum glucose levels and to influence glucose metabolism in diabetes mellitus. However, it is unclear whether vanadium ameliorates the metabolic disorder in diabetic hearts causing myocardial dysfunction. The purpose of this study was to assess the effects of vanadium on cardiac performance and energy metabolism in diabetic rat hearts. Four groups of Wistar rats were studied: untreated control rats (group C, n = 8). vanadate-treated rats (group V, n = 10), untreated diabetic rats (group DM, n = 9) induced by streptozotocin. and vanadate-treated diabetic rats (group DMV, n = 8). Vanadate-treated rats drank a 1.5 mM sodium orthovanadate (Na3VO4) solution during a 4 week diabetic condition. Hearts were perfused with Krebs-Henseleit buffer after the diabetic duration. After the maximum left ventricular dP/dt and cardiac efficiency were calculated, the myocardial contents of ATP and creatine phosphate (P-Cr) and myocardial energy metabolism were assessed by cytosolic phosphorylation potential. Peak positive and negative dP/dt, and cardiac efficiency decreased significantly in group DM compared with group C, while there were no significant differences between groups C and DMV. The myocardial contents of ATP (micromol/g wet heart) and P-Cr (micromol/g wet heart), and cytosolic phosphorylation potential (M(-1)) increased from 2.72 +/- 0.46. 1.45 +/- 0.58. and 3,530 +/- 1,220 in group DM to 3.88 +/- 0.76, 3.81 +/- 1.36, and 11,200 +/- 2,400 in group DMV, respectively. It is concluded that vanadium restored the production of high energy phosphates in the myocardium and improved myocardial dysfunction by regulating metabolic processes in diabetic rat hearts.

Animals↗
PubMed1986

Left intraventricular pressure-impedance diagrams (DPZ) to assess cardiac function. Part II: determination of end-systolic loci.

UNLABELLED: By means of tetrapolar intraventricular impedancimetric measurements and by modifying the aortic impedance with a brief volume unit step afterload increase, with a balloon catheter, we obtained the geometric locus of the end-systolic pressure-admittance points (PES-YES) from the beat to beat pressure-impedance diagram (DPZ), usually three or four beats after inflation. Six experiments in five anesthetized mongrel dogs (average weight 21.6 kg, SD 2.5) were carried out under control conditions and after a slow infusion (4 micrograms/kg/min) of epinephrine to change the myocardial inotropic state. In control, the PES-YES points fell in all cases on a straight line (average correlation 0.968, SD 0.033). After epinephrine, linearity was still good in four experiments (average correlation 0.938, SD 0.059). All animals showed displacements of the regression lines after epinephrine with respect to control. However, the direction of the shifts was not always consistent: three dogs yielded an upward-leftward shift; one showed a crossing point between the two regression lines with an increase in slope after epinephrine; in the remaining two experiments (same dog in different days), the post-epinephrine regression lines of the pressure-admittance end-systolic points were displaced downwards and rightwards. Five out of the six experiments increased the slopes of the lines after infusion of epinephrine. IN CONCLUSION: the method supplied the end-systolic point locus obtained from simple cardiac catheterization and this locus was altered by inotropic intervention.

Animals↗
PubMed1984

A microcomputer-based package for determination of regional and global cardiac function and coronary hemodynamics.

A multichannel data acquisition package for reduction of systemic and coronary hemodynamic data that utilizes a personal microcomputer is described. The system provides a printout of heart rate, maximal rate of left ventricular pressure development (+dP/dt), maximal rate of ventricular relaxation (-dP/dt), absolute and normalized myocardial segment lengths, the degree of shortening of the segment over the cardiac cycle, systolic, diastolic, and mean coronary blood flow velocities, left ventricular systolic and end diastolic pressures, and systolic, diastolic, and mean aortic blood pressure from six channels of input data. Obtained values are precisely linked to the cardiac cycle. To illustrate the output of this system, data obtained by reading strip-chart records are compared to microcomputer-derived values in conscious, instrumented dogs.

Animals↗
PubMed1984

Changes in cardiac function after effective treatment of hypertensive emergencies with i.v. clonidine.

Clonidine administration by i.v. infusion in 12 patients with hypertension emergencies (diastolic blood pressure over 130 mmHg) resulted in the normalization of blood pressure (BP) in all patients. Lowering of BP was associated with a reduction in total and lower limb vascular resistance. Heart rate showed a slight and brief decrease. Cardiac performance (determined by radionuclide angiocardiography) was improved as indicated by the significant increase of ejection fraction and decrease of both end-diastolic and end-systolic volumes. The dosage of clonidine was progressively increased until a normal BP (mean BP less than or equal to 105 mmHg) was obtained. In all patients a normal BP was achieved and in none was an initial hypertension effect observed. The total mean dose required for control of BP was 382.5 +/- 98.3 micrograms, administered over a mean period of 26.5 +/- 4.6 min. Side-effects, represented by dry mouth and drowsiness, were well tolerated and of short duration. It is concluded that clonidine is an effective and safe alternative in the treatment of hypertensive emergencies.

Adult↗
PubMed2001

Segmental cardiac function computed from ECG-gated SPECT images through solution of equations of continuity for fluids.

Segmental contractions were quantified from images of electrocardiographic-gated single-photon emission computed tomography. Counts were integrated in 64 angles about the centre on short-axis images and projected onto a cylindrical screen. Changes in the projected count were shown to obey the equation of continuity for two-dimensional fluids (the Poisson equation). Displacements of each pixel point were calculated from the velocity field to quantify the amount of dislocation. Changes in the configuration of the pixel points were projected back on the cardiac wall, and finally segmental contractions were evaluated as a percentage reduction of the area. Computer simulations were performed for numerical models of circumferential and long-axial contractions, uneven eccentric contractions and rotations. These models were blurred with a three-dimensional Gaussian function. The results obtained using this method (quantification of segmental function by solving the Poisson equation (QSFP)) were compared with the wall-thickening method (WTM) and the maximum-count method. Both QSFP and WTM yielded good agreement with predicted values for circumferential and long-axial contractions. Only QSFP gave satisfactory results for uneven eccentric contractions, and rotation models. QSFP should provide a useful tool for in vivo quantification of contraction tangential to the cardiac wall by eliminating errors due to displacements.

Aged↗
PubMed2003

Disruption of type 5 adenylyl cyclase gene preserves cardiac function against pressure overload.

The sympathetic nervous system is designed to respond to stress. Adenylyl cyclase (AC) is the keystone of sympathetic transmission, yet its role in response to acute overload in the heart or in the pathogenesis of heart failure is controversial. We examined the effects of pressure overload, induced by thoracic aortic banding, in mice in which type 5 AC, a major cardiac AC isoform, was disrupted (AC5-/-). Left ventricular weight/tibial length ratio (LVW/TL) was not different between the WT and AC5-/- at baseline and increased progressively and similarly in both groups at 1 and 3 wk after aortic banding. However, LV ejection fraction (LVEF) fell in WT at 3 wk after banding (from 70 +/- 2.8 to 57 +/- 3.9%, P < 0.05), and this decrease was associated with LV dilatation, indicating incipient cardiac failure. In contrast, AC5-/- mice did not exhibit a fall in LVEF from 74 +/- 2.2%. The number of apoptotic myocytes was similar at baseline, but it increased roughly 4-fold in WT at both 1 and 3 wk after banding, and significantly less, P < 0.05, in AC5-/-. Importantly, the increase in apoptosis occurred before the decline in LVEF in WT. The protective mechanism seems to involve Bcl-2, which was up-regulated significantly more in AC5-/- mice with pressure overload. Our findings suggest that limiting type 5 AC plays a protective role in response to pressure overload and the development of heart failure, potentially through limiting the incidence of myocardial apoptosis.

Adenylyl Cyclases↗
PubMed2000

Reduced cytosolic Ca(2+) loading and improved cardiac function after cardioplegic cold storage of guinea pig isolated hearts.

BACKGROUND: Hypothermia is cardioprotective, but it causes Ca(2+) loading and reduced function on rewarming. The aim was to associate changes in cytosolic Ca(2+) with function in intact hearts before, during, and after cold storage with or without cardioplegia (CP). METHODS AND RESULTS: Guinea pig hearts were initially perfused at 37 degrees C with Krebs-Ringer's (KR) solution (in mmol/L: Ca(2+) 2.5, K(+) 5, Mg(2+) 2.4). One group was perfused with CP solution (Ca(2+) 2.5, K(+) 18, Mg(2+) 7.2) during cooling and storage at 3 degrees C for 4 hours; another was perfused with KR. LV pressure (LVP), dP/dt, O(2) consumption, and cardiac efficiency were monitored. Cytosolic phasic [Ca(2+)] was calculated from indo 1 fluorescence signals obtained at the LV free wall. Cooling with KR increased diastolic and phasic [Ca(2+)], whereas cooling with CP suppressed phasic [Ca(2+)] and reduced the rise in diastolic [Ca(2+)]. Reperfusion with warm KR increased phasic [Ca(2+)] 86% more after CP at 20 minutes and did not increase diastolic [Ca(2+)] at 60 minutes, compared with a 20% increase in phasic [Ca(2+)] after KR. During early and later reperfusion after CP, there was a 126% and 50% better return of LVP than after KR; during later reperfusion, O(2) consumption was 23% higher and cardiac efficiency was 38% higher after CP than after KR. CONCLUSIONS: CP decreases the rise in cardiac diastolic [Ca(2+)] observed during cold storage in KR. Decreased diastolic [Ca(2+)] and increased systolic [Ca(2+)] after CP improves function on reperfusion because of reduced Ca(2+) loading during and immediately after cold CP storage.

Animals↗
PubMed2006

Sex-specific characteristics of cardiac function, geometry, and mass in young adult elite athletes.

PURPOSE: To study young adult elite athletes with age- and sex-matched sedentary controls to assess sex-specific differences for left ventricular (LV) and right ventricular (RV) volumes and mass as well as for LV contraction and relaxation. MATERIALS AND METHODS: A total of 23 male athletes (mean age 25 +/- 4 years, training 22 +/- 7 hours/week in rowing, swimming, or triathlon) and 20 female athletes (mean age 24 +/- 4 years, training 19 +/- 5 hours/week in rowing, swimming, or triathlon) and age- and sex-matched sedentary controls (21 male/17 female) underwent cardiovascular magnetic resonance (CMR) imaging (1.5 Tesla). Cardiac phase contrast imaging using a black-blood k-space segmented gradient echo sequence was used for analysis of cardiac contraction and relaxation and steady-state free-precession cine images were acquired for determination of cardiac volumes and mass. RESULTS: Male and female athletes showed similar increases in LV and RV volume and mass indices when compared to controls (ranging between 15% and 42%). No sex-specific differences in training effect on LV and RV volumes, mass indices, and ejection fractions, as well as LV to RV ratios of these volume and mass indices (parameters of balanced LV and RV dilatation and hypertrophy) were observed (all P for interaction >0.05). Similarly, no sex-specific differences in training effect on cardiac contraction and relaxation were found (all P for interaction >0.05). CONCLUSION: Young adult elite athletes do not show sex-specific adaptive structural and functional changes to exercise training in accordance with the benign nature of the hypertrophy associated with athlete's heart.

Adult↗
PubMed1991

The interplay of ischemic and hypertensive pathophysiology on cardiac function.

Many patients with systemic hypertension also have concomitant angina pectoris. Hypertension is a risk factor for the development of coronary artery disease as well as an aggravating factor once symptomatic ischemic heart disease develops. It would be prudent to use one agent that reduced the elevated blood pressure and relieved anginal symptoms while providing no negative affects on hemodynamics or other cardiac risk factors. beta-Adrenergic blockers (traditional agents and newer compounds with ancillary properties) and calcium-entry blockers have been shown to be effective as monotherapies in patients with angina. They also have the ability to induce left ventricular hypertrophy regression. There is some evidence that some of these therapies may arrest the development of arteriosclerosis and may have an inhibitory effect on platelet aggregation. What remains controversial is the optimal amount of blood pressure reduction in patients with hypertension coexistent with angina, or whether one specific agent or drug class would have an overall advantage in reducing the risk of morbidity or mortality.

Adrenergic beta-Antagonists↗