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PubMed1978

Effects of oxyfedrine on left ventricular function in patients several months after myocardial infarction.

Left ventricular (LV) function was investigated by left heart catheterization at rest and during exercise in 15 men 3--5 months after acute myocardial infarction. The effect of 8 mg oxyfedrine i.v. in 10 patients was compared to placebo in 5. The administration of oxyfedrine led to a significant decrease of LV end-diastolic pressure; an increase of LV dp/dt max, heart rate, LV ejection fraction and LV stroke work; and a shift of LV function curve indicating its improvement. These results give evidence for a positive inotropic effect of this drug which could have therapeutic implications in patients with impaired LV function after myocardial infarction.

Adult↗

PubMed1998

Effect of increased coronary venous pressure on left ventricular function in sheep.

We studied the effect of increased coronary venous pressure (Pcv) on left ventricular (LV) function in nine anesthetized open-chested sheep. Pcv was increased by inflating a balloon in the coronary sinus. LV function was estimated by measuring maximum rate of change in LV pressure (dP/dt max) and LV end-diastolic pressure (LVEDP). Left anterior descending (LAD) coronary artery blood flow was measured with an electromagnetic flow probe. A control group (n=6) was studied similarly except that Pcv was not elevated. After completion of the experiment, LV wet/dry weight ratios were measured to estimate LV myocardial water content. The balloon inflation increased Pcv from 8.6+/-1.1 to 23.8+/-1.7 mmHg (mean+/-SEM), which decreased dP/dt max from 1611+/-236 at baseline to 1041+/-210 after 120 min of increased Pcv (P < 0.05). The dP/dt max in the control group did not change significantly. Heart rate, LAD flow, LVEDP, and aortic pressures were similar in two groups but the LV water content was significantly higher (P < 0.05) in the experimental group (76.2+/-1.0 vs. 79.1+/-0.5%). These data suggest that acute increases in Pcv result in LV dysfunction and that coronary vascular congestion and myocardial edema may, at least in part, be responsible for this finding.

Animals↗

PubMed1987

Potential mechanisms of improved left ventricular function with enoximone in severe congestive heart failure.

Enoximone, a phosphodiesterase inhibitor, is a potent inotropic vasodilator agent that causes a marked improvement in systemic hemodynamics in patients with severe chronic congestive heart failure. Cardiac index, stroke volume index and stroke work index increase, and there is a significant decrease in pulmonary capillary wedge pressure. Left ventricular dP/dt increases, despite a decrease in arterial pressure and systemic vascular resistance and without any significant change in heart rate, indicating a positive inotropic effect. A marked decrease in systemic vascular resistance indicates that decreased left ventricular outflow resistance resulting from peripheral vasodilation also contributes to improvement in left ventricular function. In some patients, left ventricular end-diastolic volume increases despite a marked decrease in pulmonary capillary wedge pressure, suggesting an improvement in apparent left ventricular compliance, which may also be contributory to improved left ventricular function.

Cardiotonic Agents↗

PubMed1990

[Noninvasive evaluation of left ventricular function using new systolic time intervals obtained from continuous-wave Doppler echocardiography].

Left ventricular function was evaluated using parameters derived from the flow velocity waveforms at the ascending aorta as obtained at the suprasternal notch by continuous-wave Doppler echocardiography in 39 patients; 12 with chest pain but without coronary stenosis, eight with angina pectoris; and 19 with myocardial infarction. Peak flow velocity and the time interval from the beginning of the Q wave of lead II of the ECG to peak flow velocity (Q-V peak) correlated with specific invasive hemodynamic parameters, such as max dp/dt and (max dp/dt)/IP (IP: total left ventricular pressure at the same instant) during isometric contraction of the left ventricle measured with a catheter tip manometer, and left ventricular ejection fraction (LVEF) obtained by bi-plane cineangiography (using the area-length method). There was no correlation between the peak flow velocity and the invasive hemodynamic parameters. However, significant negative correlations were observed between the Q-V peak time and max dp/dt, with r = 0.40 (p less than 0.05), and between the Q-V peak time and (max dp/dt)/IP with r = -0.61 (p less than 0.01). A negative correlation was obtained between the Q-V peak time and LVEF (r = -0.75, p less than 0.01). The regression equation was LVEF = -0.67 x (Q-V peak) + 176. To compare the effectiveness for predicting LVEF between the Q-V peak and the established systolic time intervals as PEP and PEP/ET, these time intervals were measured from flow velocity waveforms invasively obtained with a catheter-type electromagnetic flowmeter inserted into the ascending aorta in 14 patients selected from the original subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2001

[Aortic stenosis with low transvalvular pressure gradients and impaired left ventricular function. Dobutamine stress echocardiography helps in therapy planning].

BACKGROUND: Aortic valve replacement is recommended in case of symptomatic severe aortic stenosis. This decision is difficult for patients with low-gradient aortic stenosis and severely impaired left ventricular function because of high perioperative mortality in this group. Although aortic valve replacement is usually justified if severe aortic stenosis is proved, patients with primary myocardial dysfunction and subsequent reduced aortic valve opening do not benefit from aortic valve replacement. Distinguishing these two groups of patients is necessary but not possible with echocardiography at rest. Positive inotropic stimulation with dobutamine stress echocardiography enables a more reliable graduation of aortic stenosis under these circumstances. CASE REPORT: We report on a symptomatic 58-year-old man with aortic stenosis and severely impaired left ventricular function. Using echocardiography at rest, there was a severely reduced aortic valve area of 0.6 cm2 and a mean pressure gradient of 24 mm Hg. Determined by cardiac catheterization, the peak-to-peak gradient was 20 mm Hg and the aortic valve area calculated by the Gorlin formula was 0.6 cm2. After positive inotropic stimulation using dobutamine stress echocardiography, the aortic valve area increased to 1.5 cm2 indicating an only moderate aortic stenosis. Thus aortic valve replacement was not performed and myocardial failure was medically treated. After 1.5 years of follow-up, the patient is in good condition and without complaints.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1989

Effect of nifedipine on left ventricular function during exercise in patients with stable effort angina. Relation of its efficacy to the severity of coronary artery disease.

To evaluate whether the effect of nifedipine on left ventricular function relates to the severity of coronary artery disease (CAD) or not, supine graded ergometer exercise testing was performed before and after sublingual administration of 10 mg nifedipine in 24 patients with stable effort angina. To minimize the effect of nifedipine on myocardial oxygen consumption, exercise before and after nifedipine was discontinued at the same target rate pressure product. Percent (%) left ventricular ejection fraction (EF) [EF during exercise/EF at rest.100] was measured before and after nifedipine by radionuclide angiocardiography. The angiographic degree of CAD was defined by Gensini's CAD scoring as follows: severe CAD: greater than or equal to 50, moderate: less than 50 greater than 20 and mild: less than or equal to 20. After nifedipine, left ventricular function (%EF) was improved in all 6 patients with mild CAD, but was worsened in all 9 patients with severe CAD. Maximal ST segment depression during exercise was improved in 5 of 6 patients with mild CAD, while improvement was induced in 5 of 9 patients with moderate CAD and in 3 of 9 patients with severe CAD. Jeopardy of coronary collateral vessels may have an influence on the effect of nifedipine. It is suggested that the effect of nifedipine on left ventricular function is influenced by the severity of CAD when most of its effect on myocardial oxygen consumption is eliminated.

Adult↗

PubMed2006

[Assessment of global left ventricular function with multi-slice spiral computed tomography].

OBJECTIVE: To investigate the value of multi-slice spiral computed tomography (MSCT) in the determination of global left ventricular function. METHODS: Twenty-nine patients with confirmed or suspected coronary heart diseases were imaged with a contrast-enhanced retrospective electrocardiogram (ECG) -gated technique on a 64-slice spiral CT scanner. The data sets were reconstructed at both end-diastolic and end-systolic phases in order to measure left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular stroke volume (LVSV), and left ventricular ejection fraction (LVEF). The results were compared with corresponding values obtained from conventional left ventriculography (LVG). RESULTS: LVEDV, LVESV, LVSV, and LVEF obtained with 64-slice spiral CT were significantly correlated with the LVG data (r = 0. 887-0.956, P < 0.001). According to the Bland-Altman approach, the mean differences for LVEDV, LVESV, LVSV, and LVEF were -2.3 ml, 4.1 ml, -6.4 ml, and - 3.5%, respectively. The limits of agreement for LVEDV, LVESV, LVSV, and LVEF were -27.2-22.4 ml, -10.2-18.4 ml, -26.4-13.6 ml, and -9.8%-3.0%, respectively. CONCLUSION: MSCT has clinically acceptable agreement with LVG for the quantification of global left ventricular function.

Adult↗

PubMed1983

The importance of the mitral apparatus in left ventricular function after correction of mitral regurgitation.

This study evaluates the possible role of the mitral apparatus in left ventricular function after correction of chronic mitral regurgitation. Seventeen patients underwent complete preoperative and early postoperative heart catheterization. Six patients underwent conventional mitral valve replacement (group 1), six mitral valve replacement with preservation of chordae tendineae and papillary muscles (group 2), and five mitral valvuloplasty (group 3). There was no statistically significant difference among the three groups for any hemodynamic parameter as compared before surgery by analysis of variance. After correction of mitral regurgitation the increase in cardiac index was similar for all three groups. Left ventricular end-diastolic volume did not decrease significantly in group 1 (p = NS), but it did in groups 2 and 3 (p less than .005 for both). Left ventricular end-systolic volume increased in group 1 (p less than .025) and decreased in groups 2 and 3 (p less than .01 and .005, respectively). Ejection fraction decreased in group 1 (p less than .005) and did not change in groups 2 or 3 (p = NS). Left ventricular end-diastolic pressure increased in group 1 (p less than .005) and decreased in groups 2 and 3 (p less than .01 for both). These findings suggest that continuity between mitral anulus and left ventricular wall through leaflets, chordae tendineae, and papillary muscles plays a role in left ventricular function after correction of the chronic mitral regurgitation.

Adult↗

PubMed1997

Effects of commonly used adrenergic agonists on left ventricular function and systemic vascular resistance in young piglets.

This study compared the effects of high-dose infusions of various adrenergic agonists on cardiovascular function in piglets. We hypothesized that agonists would have different effects on systolic, diastolic, and vascular functions. Nine anesthetized 3-week-old piglets underwent cardiac catheterization. Manometric and conductance catheters measured pressures and volumes. Data were acquired at rest and during infusions of epinephrine, norepinephrine, dopamine, dobutamine, isoproterenol, and phenylephrine. End-systolic elastance, preload-recruitable stroke work, cardiac output, the maximum and minimum derivatives of left ventricular pressure, the relaxation constant tau, peak filling rate, and end-diastolic stiffness were obtained. Contractile efficiency and the cardiac output/pressure-volume area ratio were calculated. Regression was used for analysis of variance; p < 0.05 was considered significant. All agonists increased indexes of contractility. beta-Adrenergic agonists enhanced relaxation. Isoproterenol and dopamine increased efficiency. No drug changed diastolic stiffness. Therefore both alpha-adrenergic and beta-adrenergic agonists have inotropic effects in the 3-week-old piglet. Some beneficial effects of beta-agonists on cardiac output may be due to enhancement of relaxation and to afterload reduction. Various agents exert different effects on the cardiovascular system, and these differences may be clinically important.

Adrenergic Agonists↗

PubMed2002

A six-month trial of valacyclovir in the Epstein-Barr virus subset of chronic fatigue syndrome: improvement in left ventricular function.

This study was designed to determine safety and efficacy of a 6-month trial of valacyclovir in single-virus Epstein-Barr virus (EBV) persistent infection. Phase I of this study used four specific criteria to define a subset of patients with chronic fatigue syndrome (CFS). In the second phase, myocardial dynamics were measured by MUGA rest/stress radionuclide ventriculographic (RVG) examinations pre- and posttreatment with valacyclovir. In phase I, a trial was performed in 19 consecutive CFS patients with the following diagnostic conditions: patients met criteria for diagnosis of CFS; they had had CFS for less than 1 year. They demonstrated repetitively abnormal oscillating T waves (ischemic or flat) at 24-h Holter monitoring; and they had elevated serum IgM antibody titers to EBV viral capsid antigen and/or total diffuse early antigen as measured by the enzyme-linked immunosorbent assay method. The treatment group comprised 10 CFS patients with no serum antibodies to human cytomegalovirus, but the control group (nine CFS patients) had, additionally, high titers of serum antibodies (IgG) to conformational structural antigens of human cytomegalovirus. Both the parallel treatment and control CFS groups received valacyclovir 1.0-1.5 gm q.6.h. for 6 months. This valacyclovir dose achieved serum acyclovir C(max) of > 7 microm and high antiviral activity versus EBV (IC(50) of 4.4-13.3 m). In phase II, six additional CFS patients met the same four criteria as the 19 CFS patients in phase I. They had, however, been ill for a mean of 55.8 months. Thus, 25 CFS patients comprise this study. The studies were carried out at a single outpatient practice in Birmingham, MI, U.S.A. Before initiating valacyclovir, and after 6 months of treatment, clinical and laboratory observations were made. The CFS Energy Index point score (Table I) was used to record each CFS patient's functional capacity at baseline and after 1, 3 and 6 months of valacyclovir. Energy Index point scores, as well as EBV and human cytomegalovirus serum antibody titers were assessed. In the second phase, left ventricular dynamics were repeated after 6 months of treatment with valacyclovir. We concluded that the 16 CFS patients (included in both phases of this study) with EBV-persistent infection (EBV single-virus subset) are improved after 6 months of continuous pharmacokinetic dosing with valacyclovir. Nine CFS patients with EBV/human cytomegalovirus co-infection did not benefit from 6 months of similar treatment. Valacyclovir is not an effective anti-human cytomegalovirus antiviral drug. Unimproved CFS patients with co-infections EBV and human cytomegalovirus may require combined treatment with valacyclovir and another drug more active against human cytomegalovirus. This preliminary trial, with a small number of patients, may be critical to an appropriately designed larger, double-blind, placebo-controlled trial.

Acyclovir↗

PubMed1989

[Correlation between Selvester's QRS score and left ventricular function at rest and during effort in patients who survived myocardial infarction].

This study was carried out in order to determine if there is any correlation between QRS score and left ventricular function at rest and during exercise after single myocardial infarction. Selvester's QRS scoring system to determine infarct size by observing Q and R standard 12-lead ECG was independently applied by three cardiologists. Left ventricular function was determined using the resting angiographic LVEF, the pulmonary wedge pressure in supine position and during exercise. The total work performed and the heart rate and systolic blood pressure percentage increase (delta) were also considered. Forty-eight male pts (mean age 52.3 +/- 8.7) were studied within 2 months after acute myocardial infarction. The site of the myocardial infarction was anterior in 13, inferior in 20, inferior plus posterior in 15. There were poor correlations between QRS score and left ventricular ejection fraction (r = -0.44) and pulmonary wedge pressure in supine position and during exercise, total work performed, delta heart rate and delta systolic blood pressure. There was no significant difference in mean QRS score between pts with abnormal (greater than 12 mmHg) and normal resting pulmonary wedge pressure in supine position (10.8 +/- 8.4 vs 7.3 +/- 5.8) or between pts with abnormal (greater than 20 mmHg) and normal exertional pulmonary wedge pressure (10.5 +/- 8.4 vs 7.4 +/- 5.7). In conclusion, the QRS score, obtained up to 30 days following an acute myocardial infarction, is not useful in determining left ventricular function at rest or during exercise.

Blood Pressure↗

PubMed2001

Six months of recombinant human GH therapy in patients with ischemic cardiac failure does not influence left ventricular function and mass.

Beneficial effects of recombinant human GH on cardiac function have been reported in humans with GH deficiency and in patients with idiopathic dilated cardiomyopathy. No randomized controlled trial has been performed on the effects of recombinant human GH on cardiac function in patients with ischemic cardiac failure. We therefore randomly assigned 22 patients with ischemic cardiac failure (left ventricular ejection fraction, <40%; 19 men and 3 women; mean age, 64 yr) to receive 6 months of unblinded therapy with recombinant human GH (2.0 IU/d) or no treatment. Primary end points were left ventricular ejection fraction and left ventricular mass. Left ventricular end-diastolic volume, left ventricular end-systolic volume, and myocardial perfusion, both at rest and during exercise, were assessed as well. Cardiac imaging techniques were electrocardiographically gated single photon emission computer tomography and magnetic resonance imaging. In addition, biochemical and biometric measurements were performed. Nineteen patients completed the study (10 controls and 9 GH-treated subjects). IGF-I and IGF-binding protein-3 increased significantly after recombinant human GH treatment (+24% and +58%, respectively) compared with control values (-14% and +5%; P < 0.05). Left ventricular ejection fraction, left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular mass, and myocardial perfusion were not influenced by recombinant human GH therapy. We conclude that 6 months of recombinant human GH treatment in patients with ischemic cardiac failure had no beneficial effect on left ventricular function and mass.

Aged↗

PubMed1991

Different effects of acute intravenous administration of k-strophanthidin and prenalterol on the diastolic phase of left ventricular function in patients with coronary arterial disease.

In 21 patients with coronary arterial disease, and with maintained (or mildly depressed) systolic function, we studied the effects of two well-known inotropic agents, namely prenalterol and k-strophanthidin, on the diastolic phase. Selected variables of both systolic and diastolic function were assessed at controlled heart rate by cardiac catheterization and left ventriculography before and after acute intravenous administration of the beta 1 agonist prenalterol (35 micrograms/kg for 3 min) and of k-strophanthidin (0.008 mg/kg for 5-10 min). Ten patients received prenalterol, and 11 patients were injected with k-strophanthidin. Administration of prenalterol induced a remarkable diminution of end-systolic volume index (mean values from 41.8 +/- 11.9 to 32.2 +/- 10.4), while k-strophanthidin showed only a tendency towards a decrease (mean values from 43.4 +/- 13.2 to 40.7 +/- 15.1). After k-strophanthidin, we did not observe any significant changes in the peaks of maximal rate in volumetric increase during filling phase whereas, after prenalterol, a noteworthy increase of the first peak was accompanied by a significant decrease of the second peak. The lowest and end filling left ventricular pressures were decreased by prenalterol (mean values from -0.8 +/- 0.1 to -2 +/- 0.5 and from 10.6 +/- 4.6 to 4.1 +/- 1.1 respectively), whereas k-strophanthidin increased left ventricular end diastolic pressure (mean values from 11.6 +/- 4.3 to 17.1 +/- 9.1). Prenalterol induced a relevant increase of ejection fraction (mean values from 0.52 +/- 0.1 to 0.61 +/- 0.008), whereas k-strophanthidin produced only a nearly significant (P less than 0.06) mild increase (mean values from 0.51 +/- 0.06 to 0.54 +/- 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

The effects of gonadectomy on left ventricular function and cardiac contractile proteins in male and female rats.

To examine the influence of the sex hormones on mechanical properties and biochemistry of the adult heart, we studied left ventricular function and cardiac contractile proteins in hearts from 20-week-old male and female rats that had been gonadectomized at 18 days of age, compared with hearts from sham-operated animals. Testosterone and estradiol were not detectable in serum from male and female gonadectomized rats, respectively. The male rats had lower body and heart weights than male sham operated rats, whereas these values were higher in female gonadectomized than in female sham-operated rats. Left ventricular function was studied in a working heart apparatus at similar heart rate and at controlled levels of aortic diastolic pressure and left atrial pressure. At moderate left atrial pressure, end-diastolic pressure and volume per gram dry left ventricle were the same in all groups, but at high left atrial pressure, end-diastolic pressure, and volume per gram dry left ventricle were lower in male and female gonadectomized than in the respective sham-operated rats. Further increases in left atrial pressure were associated with mechanical alternans in male and female gonadectomized rats. Significantly (P less than 0.05) lower values for cardiac output, peak systolic pressure, ejection fraction, and myocardial oxygen consumption occurred in male gonadectomized compared with sham-operated rats at moderate and high left atrial pressure at higher levels of aortic diastolic pressure. Decreases in these values for female gonadectomized compared with sham-operated rats occurred only at high left atrial pressure. A significant downward shift in the mean force-velocity relationship was observed in all gonadectomized rats at both moderate and high left atrial pressure. In a follow-up study, when end-diastolic pressure was kept the same at both moderate and high left atrial pressure in female sham-operated and gonadectomized rats by reducing heart rate, decreases in contractile function in gonadectomized rats were observed at all preloads. Ca++-myosin ATPase activity was significantly reduced by 34% in male and by 19% in female gonadectomized rats when compared to respective sham-operated control hearts. These alterations in myosin ATPase activity were associated with a reduction in the V1 myosin isoenzyme and an increase in the V3 isoenzyme. Thus, left ventricular filling and left ventricular function were impaired in hearts of gonadectomized rats. Alterations in function were associated with depressed cardiac myosin ATPase activity in male and female gonadectomized rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1979

Left ventricular function before and following surgical treatment of mitral valve disease.

Nineteen patients with mitral valve disease were studied before and a mean 11 months +/- 9 months following valve replacement or reconstruction, which resulted in good postoperative valve function. Biplane left ventricular angiography and pressures were utilized to determine end-diastolic volume/M. (EDV), end-systolic volume/M. (ESV), ejection fraction (EF), left ventricular mass/M. (LVM), and stroke work/M. (SW). There were 19 patients--six with mitral stenosis (MS), six with mitral stenosis and regurgitation (MS + MR), and seven with mitral regurgitation (MR). Those with MS and MS + MR preoperatively had no significant change in left ventricular end-diastolic pressure (LVEDP), EDV, ESV, LVM, or EF following surgery. Patients with MR had a significant reduction in LVEDP, EDV, SV, and SW. More importantly, the EF fell in four of these seven patients and LVM did not decrease following surgery. It is concluded that surgical treatment for MS and MS + MR had little effect on left ventricular performance. Following surgical treatment for MR, reduction in EDV is not associated with reduction in LVM, and frequently left ventricular performance deteriorates as judged by the EF.

Angiocardiography↗

PubMed1985

Left ventricular function after myocardial infarction: clinical and angiographic correlations.

There is a paucity of information correlating the angiographic findings immediately after myocardial infarction with the clinical status before infarction. Therefore, the coronary anatomy, collateral circulation and quantitative left ventricular function were studied in 39 patients who underwent angiography within 3 weeks of a first transmural myocardial infarction. In all patients, the vessel supplying the infarct was totally occluded at the time of angiography. Patients without angina before infarction (Group I) had fewer coronary obstructions than did patients with a long history of angina before infarction (Group II) (1.5 +/- 0.5 versus 2.5 +/- 0.5, respectively, p less than 0.001) but worse overall and regional left ventricular function. These paradoxical differences between Groups I and II were evident in patients with anterior as well as inferior infarction. Patients in Group I had significantly lower collateral scores than did patients in Group II (0.6 +/- 0.8 versus 1.9 +/- 0.9, respectively, p less than 0.0001) and 13 of 22 patients in Group I had no collateral vessels compared with only 1 of 17 in Group II (p less than 0.001). Partial preservation of anterior wall function in Group II patients with anterior infarction was related both to the presence of collateral vessels and to the more distal obstruction of the left anterior descending coronary artery in these patients as compared with patients with anterior infarction in Group I. In contrast, in patients with inferior wall infarction, no relation could be found between the presence of collateral vessels and regional left ventricular function, although only two patients in this series with inferior infarction did not have collateral vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed2005

Autologous skeletal myoblast transplantation improved hemodynamics and left ventricular function in chronic heart failure dogs.

BACKGROUND: Previous studies have suggested that autologous skeletal myoblast transplantation (ASMT) improves left ventricular (LV) function in small animals after myocardial infarction. We tested the effects of ASMT on hemodynamics, LV function and remodeling in coronary microembolization-induced chronic heart failure (CHF) in conscious dogs. METHODS: Nineteen dogs were continuously instrumented with LV pressure sensors and mid-myocardial sonomicrometry crystals for dP/dt(max) and LV volume determination. Each dog underwent baseline assessment in a conscious state. CHF (20% to 30% reduction in dP/dt(max) and LV end-diastolic pressure >16 mm Hg) was created by daily coronary microembolizations via a continuously implanted coronary catheter. Skeletal muscle biopsy was performed and myoblasts were isolated and expanded. Then 2.7 x 10(8) to 8.3 x 10(8) myoblasts were injected into the infarcted region of 11 dogs after establishment of CHF. Saline injection (sham) was performed in 8 control dogs. Animals were evaluated every 2 weeks for up to 10 weeks. Global ejection fraction was determined by echocardiography. The end-systolic pressure-end-systolic volume relationship (ESPVR) was analyzed by the Sonomicrometic system. RESULTS: Compared with saline injection, ASMT significantly increased dP/dt(max) (105 +/- 9% vs 97 +/- 7%, values were expressed as percentage change from baseline CHF, p = 0.013) and ejection fraction (46 +/- 3% vs 40 +/- 2%, p = 0.034) at 10 weeks after myoblast transplantation. There was a significant leftward and upward shift of the ESPVR back toward normal at 10 weeks after myoblast transplantation (p = 0.034). Three animals labeled with BrdU myoblasts showed no histologic evidence of viable engraftment. CONCLUSIONS: ASMT provided mild improvements in hemodynamics and LV function and reduced LV remodeling in conscious dogs with CHF.

Animals↗

PubMed2001

Effects of tribromoethanol anesthesia on echocardiographic assessment of left ventricular function in mice.

BACKGROUND AND PURPOSE: Pentobarbital and ketamine-xylazine anesthesia in mice result in markedly decreased left ventricular fractional shortening and cardiac output. However, to the authors' knowledge, the effect of short-acting, alcohol-based anesthesia on these parameters is unknown. METHODS: Fifteen mice (FVB/N, C57Bl/6J, A/J, n = 5 each) underwent high-resolution (15 MHz) 2-dimensional-directed M-mode echocardiography before and after undergoing 2.5% tribromoethanol anesthesia (0.01 ml/g of body weight). RESULTS: Tribromoethanol anesthesia resulted in significant heart rate slowing (29%) and left ventricular enlargement (20%), and a more modest (12%) reduction in left ventricular fractional shortening. Cardiac output was unchanged. The differences in left ventricular function between conscious and tribromoethanol studies were similar for each of the three strains of mice. CONCLUSIONS: Tribromoethanol anesthesia induced only modest effects on M-mode estimates of basal cardiac function and did not influence cardiac output. The effects to tribromoethanol anesthesia were similar among three commonly used mice strains.

Anesthesia↗