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At least 109 records · Page 6Linked to original sources
PubMed2006

Macrophage colony-stimulating factor treatment after myocardial infarction attenuates left ventricular dysfunction by accelerating infarct repair.

OBJECTIVES: We aimed to determine the effects of macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) treatment on both the repair process and ventricular function after myocardial infarction (MI). BACKGROUND: The M-CSF and G-CSF have multiple potential effects on cells involved in wound repair. METHODS: Myocardial infarction was induced by 45- or 90-min coronary occlusion and reperfusion in rats with or without subsequent injection of M-CSF (10(6) IU/kg/day) or G-CSF (50 microg/kg/day) for five days. We examined histology and messenger ribonucleic acid (mRNA), and assessed left ventricular function in situ using a conductance catheter. RESULTS: Five days after MI, M-CSF increased the number of ED-1-positive cells, mRNA levels of transforming growth factor-beta-1, collagen I and III, and collagen fibers within the infarct. Fourteen days after MI, induced by 45-min ischemia, left ventricular end-systolic elastance (Ees) was reduced (1,191 +/- 87 mm Hg/ml vs. 1,812 +/- 150 mm Hg/ml) and both isovolumic relaxation time constant (tau) (11.9 +/- 0.9 ms vs. 8.5 +/- 0.4 ms) and left ventricular end-diastolic volume (LVEDV) (0.225 +/- 0.014 ml vs. 0.172 +/- 0.011 ml) increased versus sham-operated rats. These alterations after MI were attenuated by M-CSF (Ees = 1,650 +/- 146, tau = 9.7 +/- 0.7, LVEDV = 0.199 +/- 0.012) but not by G-CSF. This beneficial effect of M-CSF on Ees was also detected in hearts with MI induced by 90-min ischemia. Furthermore, M-CSF increased collagen content within infarcts and reduced the proportion of thin collagen fibers 14 days after MI. The Ees significantly correlated with infarct collagen content. Nevertheless, neither M-CSF nor G-CSF modified infarct size. CONCLUSIONS: The M-CSF treatment attenuates deterioration of left ventricular function after MI by accelerating infarct repair.

Animals↗
PubMed1991

[Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction].

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.

Adolescent↗
PubMed2000

Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction.

Patients with congestive heart failure or left ventricular dysfunction (LVD) have a high incidence of ventricular tachyarrhythmias and sudden cardiac death. In addition to structural, metabolic and neuroendocrine changes, mechanoelectrical feedback may play a role in arrhythmogenesis in heart failure. Three groups of rabbits (n = 10 for each) were studied: chronic coronary ligation with ejection fraction (EF) > or = 0.45 or < 0.45, and sham-operated controls. Ventricular fibrillation (VF) thresholds were measured at LV pressures of 0 and 40 mm Hg during modified Langendorff perfusion. Intervals between local activations during VF (VFI) were used as an index of refractoriness. Global dispersion was expressed as coefficient of variation of VFI; local dispersion by maximum difference in VFI between adjacent sites. Median VF threshold was lower at 0 mm Hg in the lower EF group compared to controls (30 vs. 67.5 mA, P<0.05). VF threshold in control hearts was lower at 40 mm Hg than at 0 mm Hg (P<0.01), but there was no further reduction in threshold in LVD hearts at 40 mm Hg. Global dispersion of VFI did not differ significantly between groups. Local dispersion of VFI in the lower EF group was greater than in controls at 0 mm Hg in the infarct border zone (P<0.05). At 40 mm Hg, local dispersion of VFI in zones bordering and remote from the infarct were greater in both LVD groups than in controls (P<0.05). Local inhomogeneity of refractoriness is more marked in the infarct border zone, but latent abnormalities are evident in normal myocardium of rabbits with left ventricular dysfunction and are revealed by left ventricular distension.

Animals↗
PubMed1997

Determinants of the pulmonary artery pressure rise in left ventricular dysfunction.

Pulmonary artery hypertension in patients with left ventricular dysfunction is related to poor outcome but the role of cardiac functional abnormalities in the genesis of pulmonary hypertension remains unknown. The aim of this prospective study was to identify the determinants of pulmonary hypertension in 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%). Systolic pulmonary artery pressure was measured by continuous wave Doppler. Left ventricular systolic and diastolic function, severity of functional mitral regurgitation, cardiac output, and left atrial volume were assessed using Doppler echocardiography. In patients with left ventricular dysfunction, systolic pulmonary artery pressure was increased (51 +/- 14 mmHg, range 23 to 87 mmHg). Mitral deceleration time (r = -0.61; p = 0.0001) and mitral effective regurgitant orifice (r = 0.50; p = 0.0001) were the strongest parameters related to systolic pulmonary artery pressure. Multivariate analysis identified these two variables as the strongest predictors of systolic pulmonary artery pressure in association with the mitral E/A ratio (p = 0.006) and age (p = 0.005). In conclusion, pulmonary hypertension is common and variable in patients with left ventricular dysfunction. It is closely related to diastolic dysfunction and severity of functional mitral regurgitation but not independently to the degree of left ventricular systolic dysfunction. These findings underline the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.

Blood Pressure↗
PubMed1999

Comparison of candesartan, enalapril, and their combination in congestive heart failure: randomized evaluation of strategies for left ventricular dysfunction (RESOLVD) pilot study. The RESOLVD Pilot Study Investigators.

BACKGROUND: We investigated the effects of candesartan (an angiotensin II antagonist) alone, enalapril alone, and their combination on exercise tolerance, ventricular function, quality of life (QOL), neurohormone levels, and tolerability in congestive heart failure (CHF). METHODS AND RESULTS: Seven hundred sixty-eight patients in New York Heart Association functional class (NYHA-FC) II to IV with ejection fraction (EF) <0.40 and a 6-minute walk distance (6MWD) <500 m received either candesartan (4, 8, or 16 mg), candesartan (4 or 8 mg) plus 20 mg of enalapril, or 20 mg of enalapril for 43 weeks. There were no differences among groups with regard to 6MWD, NYHA-FC, or QOL. EF increased (P=NS) more with candesartan-plus-enalapril therapy (0.025+/-0.004) than with candesartan alone (0.015+/-0.004) or enalapril alone(0.015+/-0.005). End-diastolic (EDV) and end-systolic (ESV) volumes increased less with combination therapy (EDV 8+/-4 mL; ESV 1+/-4 mL; P<0.01) than with candesartan alone (EDV 27+/-4 mL; ESV 18+/-3 mL) or enalapril alone (EDV 23+/-7 mL; ESV 14+/-6 mL). Blood pressure decreased with combination therapy (6+/-1/4+/-1 mm Hg) compared with candesartan or enalapril alone (P<0.05). Aldosterone decreased (P<0.05) with combination therapy (23.2+/-5.3 pg/mL) at 17 but not 43 weeks compared with candesartan (0.7+/-7.8 pg/mL) or enalapril (-0.8+/-11. 3 pg/mL). Brain natriuretic peptide decreased with combination therapy (5.8+/-2.7 pmol/L; P<0.01) compared with candesartan (4. 4+/-3.8 pmol/L) and enalapril alone (4.0+/-5.0 pmol/L). CONCLUSIONS: Candesartan alone was as effective, safe, and tolerable as enalapril. The combination of candesartan and enalapril was more beneficial for preventing left ventricular remodeling than either candesartan or enalapril alone.

Aged↗
PubMed1998

Right and left ventricular dysfunction in patients with severe pulmonary disease.

OBJECTIVE: To determine the prevalence of right and left ventricular dysfunction in a prescreened population of patients with severe pulmonary disease, and to analyze the relationship between right and left ventricular function. DESIGN: Retrospective record review of 434 patients with severe pulmonary disease. PATIENTS: Patients with end-stage pulmonary disease, including alpha1-antitrypsin deficiency emphysema, COPD, cystic fibrosis (CF), idiopathic pulmonary fibrosis, and pulmonary hypertension (primary and Eisenmenger's syndrome), who were evaluated for lung transplantation between January 1993 and December 1995. MEASUREMENTS: Pulmonary function tests, arterial blood gases, radionuclide ventriculography, two-dimensional transthoracic echocardiography, pulmonary hemodynamics, coronary angiography. RESULTS: Right ventricular dysfunction (right ventricular ejection fraction [RVEF] <45%) was present in 267 patients (66%), but the prevalence was highest (94%) in patients with pulmonary vascular disease. Among the patients with airway or parenchymal lung disease, the prevalence ranged from 59% in COPD to 66% in CF. In contrast, left ventricular dysfunction (left ventricular ejection fraction [LVEF] <45%) was present in only 6.4%, but it, too, was most common in the group with pulmonary hypertension (19.6%). In the groups with parenchymal or airway disease, the prevalence was 3.6%, and there was no statistical difference among the four diagnoses (alpha1-antitrypsin deficiency emphysema; COPD; CF; idiopathic pulmonary fibrosis). LVEF showed a significant correlation with RVEF (r=0.44; p<0.05), and left ventricular dysfunction was associated with the presence of moderate-to-severe tricuspid regurgitation but not with coronary artery disease. In a subset of patients with both right and left ventricular dysfunction who subsequently underwent lung transplantation, RVEF and LVEF increased pari passu after transplantation. CONCLUSION: The prevalence of right ventricular dysfunction is high in patients with end-stage pulmonary disease, but the prevalence of left ventricular dysfunction is relatively low. Left ventricular dysfunction appears to be related to right ventricular dysfunction, perhaps through ventricular interdependence.

Adult↗
PubMed2005

Post-systolic shortening during dobutamine stress echocardiography predicts cardiac survival in patients with severe left ventricular dysfunction.

BACKGROUND: Patients with severe left ventricular dysfunction and myocardial viability by dobutamine stress echocardiography (DSE) or F18-fluorodeoxyglucose-single-photon emission computed tomography (FDG-SPECT), experience improved survival after coronary revascularization. Pulsed wave-tissue Doppler imaging (PW-TDI)-derived ejection phase shortening (EPS) and post-systolic shortening (PSS) velocities may help to quantify DSE. We assessed these variables in a prospective long-term follow-up. METHODS: Eighty patients (58 men, mean age 63+/-9 years) with left ventricular dysfunction (radionuclide ventriculography mean ejection fraction, 34+/-11%) underwent both DSE and FDG-SPECT for myocardial viability. Viable myocardium was improvement from rest to low dose or worsening of wall motion at peak DSE and normal perfusion, mildly reduced perfusion with FDG uptake or severely reduced or absent perfusion with increased FDG uptake (mismatch) at FDG-SPECT. EPS, PSS velocities and EPS/PSS ratio during DSE were analysed using a six-segment model. Coronary revascularization bypass grafting was performed in 62 patients. All patients completed a long-term (9-year) follow-up for cardiac death. RESULTS: The segmental prevalence of severe dyssynergy was 77%. On a patient basis myocardial viability was detected by EPS/PSS ratio (31%), FDG-SPECT (34%) and DSE (26%). A significant improvement of Kaplan-Meier survival was predicted in viable compared with nonviable revascularized patients (P < 0.01). Both EPS/PSS ratio and FDG-SPECT, compared to DSE alone, tended to allocate more accurately univariate prediction of death-free outcome (odds ratio, 2.5 and 2.7 compared with 2.1). CONCLUSIONS: TDI adds objective variables to DSE, helping to recognize viable myocardium and optimize prediction of death-free outcome in long-term follow-up, with favorable comparison with nuclear techniques.

Cardiomyopathies↗
PubMedDate not supplied

Decreased and abnormal left ventricular filling in acute heart failure: role of pericardial constraint and its mechanism.

Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.

Acute Disease↗
PubMed2000

Left ventricular dysfunction and cytoprotection.

With the projections of increasing aging of the population, heart failure is expected to become a major health problem for most Western societies. Therefore, the study of the pathophysiological mechanisms involved in heart failure should be one of the main priorities of cardiovascular research. A substantial amount of knowledge has been gathered in the recent years on the mechanisms involved in the development of heart failure. One such mechanism is the development of myocyte's apoptosis. This apoptotic mechanism is responsible for a substantial decrease in the number of cardiac myocytes, and therefore for the worsening of heart failure. This apoptotic mechanism can be triggered by a number of mechanisms such as the adrenergic stimulation, the angiotensin II production, changes in calcium homeostasis, and changes in cellular metabolism. At least in theory, the development of therapies (such as beta blockers, ACE inhibitors, calcium channel blockers and trimetazidine) that can inhibit these mechanisms can have a cytoprotective role and therefore reduce the development of heart failure. Because of its main role in the production of energy for the cell, the mitochondrion is one of the mainframes of cell viability. If the mitochondrial function is decreased the myocyte will be in jeopardy. Therefore, drugs that can prevent mitochondrial dysfunction will obviously have a cytoprotective role in heart failure.

Cytoprotection↗