Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ventricular dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,315 records · Page 73Linked to original sources
PubMed2003

Correlates of subclinical left ventricular dysfunction in ESRD.

BACKGROUND: Abnormalities of the left ventricle are common in patients with end-stage renal disease (ESRD) both before and after the start of renal replacement therapy. The purpose of this study is to identify possible causes of subclinical left ventricular (LV) dysfunction in patients with ESRD. In particular, we sought to determine whether the presence of ESRD was itself associated with dysfunction independent of LV hypertrophy and coronary artery disease. METHODS: Assessment of cardiovascular risk factors and dialysis adequacy was completed in 145 unselected patients with ESRD who were recruited from the renal dialysis unit and compared with age- and sex-matched controls. Among the 68 patients with ESRD who had undergone a dobutamine stress echocardiogram with normal findings, regional cardiac function was quantified by myocardial Doppler velocity, LV volumes and mass were measured using three-dimensional echocardiography, and vascular function was assessed using brachial artery reactivity (BAR). RESULTS: LV diastolic velocity was impaired in patients with ESRD, but there was no significant difference in systolic velocity compared with control patients of similar age. Age, diabetes mellitus, hypertension, and LV mass were independent predictors of diastolic velocity (model R2 = 0.45; P < 0.001), whereas age and risk factor number were predictors of systolic velocity (model R2 = 0.19; P = 0.002). Increasing risk factor number had no significant relationship with LV mass or volume. There was no detected association between BAR and incremental risk factors (P = 0.51). CONCLUSION: Subclinical LV dysfunction occurs in patients with ESRD, but is evidenced as abnormal myocardial diastolic, rather than systolic, function. Correlates of abnormal function are age, diabetes mellitus, hypertension, and LV mass, rather than ESRD alone, dialysis adequacy, or abnormal endothelial function.

Adult↗
PubMed1995

Exercise-induced left ventricular dysfunction in alcoholic and non-alcoholic cirrhosis.

BACKGROUND/AIMS: Autonomic and cardiac dysfunction have been reported in patients with cirrhosis. We studied left ventricular and autonomic function in 20 patients with both alcoholic and non-alcoholic cirrhosis. METHODS: Autonomic function was assessed by a standard battery of cardiovascular reflex tests. Supine exercise radionuclide ventriculography was used to assess the cardiac response to exercise. RESULTS: Exercise capacity was reduced in all patients in association with marked chronotropic incompetence (peak heart rates 120.5 +/- 6 bpm). Unlike normal subjects there was no increase in left ventricular ejection fraction on exercise. Stroke volume increased by 23 +/- 6%, mediated by an increase in end-diastolic.volume of > 20%. Cardiac output was subnormal at maximal exercise, increasing by only 96 +/- 14% and 97 +/- 11% in alcoholic and non-alcoholic groups respectively. The majority (83%) of our patients had autonomic reflex abnormalities. CONCLUSIONS: Patients with cirrhosis of alcohol and non-alcohol related aetiologies have significantly impaired cardiovascular responses to exercise, which are similar to those of a denervated heart. This may have important clinical implications for the ability of these patients to withstand cardiovascular stress.

Autonomic Nervous System↗
PubMed2000

Aortic valve replacement in patients with aortic stenosis and severe left ventricular dysfunction.

BACKGROUND: The outcome of aortic valve replacement for severe aortic stenosis is worse in patients with impaired left ventricular function. Such dysfunction in aortic stenosis may be reversible if caused by afterload mismatch, but not if it is caused by superimposed myocardial infarction. METHODS: From our echocardiography database, 55 patients with severe aortic stenosis (valve area < or =0.75 cm2) and ejection fractions of 30% or lower who subsequently underwent aortic valve replacement were included. The operative mortality and clinical follow-up were detailed. RESULTS: There were 10 perioperative deaths (operative mortality, 18%). Twenty (36%) of the 55 patients had a prior myocardial infarction. In the 35 patients without prior myocardial infarction, there was only 1 death (3%). In contrast, 9 of 20 patients with prior myocardial infarction died (mortality rate, 45%; P< or =.001). The factors significantly associated with perioperative death on univariate analysis (functional class, mean aortic gradient, and prior myocardial infarction) were entered into a model for stepwise logistic regression. This multivariate analysis showed that only prior myocardial infarction was independently associated with perioperative death (odds ratio, 14.9; 95% confidence interval, 2.4-92.1; P = .004). CONCLUSIONS: The risk of aortic valve replacement in patients with severe aortic stenosis and severely reduced left ventricular systolic function is extremely high if the patients have had a prior myocardial infarction. This information should be factored into the risk-benefit analysis that is done preoperatively for these patients, and it may preclude operation for some.

Aged↗
PubMed1995

Effects of growth hormone in rats with postinfarction left ventricular dysfunction.

Growth hormone may affect cardiac function. In rats, chronic hypersecretion of growth hormone leads to increased maximum isometric contractile force of the left ventricular papillary muscle in vitro. In humans, administration of growth hormone can increase myocardial contractility. However, cardiac effects of growth hormone in heart failure or cardiac dysfunction have not been studied to date. The current study was to evaluate the cardiac effects of growth hormone in conscious rats with postinfarction left ventricular dysfunction and sham controls. Ligation of the left coronary artery or sham operation was performed, then 4 weeks after surgery, recombinant human growth hormone (2 mg/kg/day, SC) or vehicle was administered for 15 days. Catheters were implanted 13 days after treatment with growth hormone or vehicle. Hemodynamic parameters were measured in conscious rats 2 days after catheterization. In vehicle-treated rats, left ventricular systolic pressure, maximum dP/dt, and arterial pressure were significantly decreased and left ventricular end-diastolic pressure was significantly increased in the ligation group compared with sham controls. Growth hormone treatment increased left ventricular systolic pressure (p < 0.05) and dP/dt (p < 0.05) and reduced left ventricular end-diastolic pressure (p < 0.05), significantly in the ligated rats. In sham rats, growth hormone tended to decrease arterial pressure but did not alter ventricular contractility. Neither ligation nor growth hormone significantly altered heart rate and right atrial pressure. These results suggest that growth hormone treatment may improve cardiac function by increasing myocardial contractility in cardiac dysfunction or heart failure.

Analysis of Variance↗
PubMed2006

Reduction of N terminal-pro-brain (B-type) natriuretic peptide levels with exercise-based cardiac rehabilitation in patients with left ventricular dysfunction after myocardial infarction.

INTRODUCTION: N-terminal-pro-brain (B-type) natriuretic peptide (NT-pro-BNP) is a peptide hormone released from ventricles in response to myocyte stretch. The aim of the study was to investigate the influence of exercise training on plasma NT-pro-BNP to verify if this parameter could be used as a biological marker of left ventricular remodelling in myocardial infarction patients undergoing an exercise training programme. METHODS: Forty-four patients after myocardial infarction were enrolled into a cardiac rehabilitation programme, and were randomized in two groups of 22 patients each. Group A patients followed a 3-month exercise training programme, while group B patients received only routine recommendations. All patients underwent NT-pro-BNP assay, and cardiopulmonary exercise test before hospital discharge and after 3 months. RESULTS: In Group A, exercise training reduced NT-pro-BNP levels (from 1498+/-438 to 470+/-375 pg/ml, P=0.0026), increased maximal (VO2peak+4.3+/-2.9 ml/kg per min, P<0.001; Powermax+38+/-7, P<0.001) exercise parameters and work efficiency (Powermax/VO2peak+1.3+/-0.4 Power/ml per kg per min, P<0.001); there was also an inverse correlation between changes in NT-pro-BNP levels and in VO2peak (r=-0.72, P<0.001), E-wave (r=-0.51, P<0.001) and E/A ratio (r=0.59, P<0.001). In group B, at 3 months, no changes were observed in NT-pro-BNP levels, exercise and echocardiographic parameters. CONCLUSION: Three months exercise training in patients with moderate left ventricular systolic dysfunction after myocardial infarction induced a reduction in NT-pro-BNP levels, an improvement of exercise capacity and early left ventricular diastolic filling, without negative left ventricular remodelling. Whether the reduction of NT-pro-BNP levels could be useful as a surrogate marker of favourable left ventricular remodelling at a later follow-up remains to be further explored.

Biomarkers↗
PubMed1998

Pulmonary and systemic responses to exogenous endothelin-1 in patients with left ventricular dysfunction.

Plasma levels of immunoreactive endothelin-1 (ET-1) are elevated in chronic heart failure (CHF) and have been reported to correlate closely with pulmonary hemodynamic measurements. We investigated the effects of exogenous ET-1 on the pulmonary vasculature in patients with left ventricular systolic dysfunction (LVD), with or without overt heart failure. ET-1 was infused at 1, 5, and 15 pmol/min into a distal pulmonary artery of 10 patients with LVD. Hemodynamics were measured by a thermodilution catheter and arterial line. Intravascular Doppler and local pulmonary angiography were used to assess local pulmonary blood flow in the first four patients. Systemic hemodynamic changes occurred with ET-1 infusion in a dose-dependent fashion. Mean arterial pressure (100 +/- 8-107 +/- 11 mm Hg; p < 0.01) and systemic vascular resistance (1,699 +/- 375-2,033 +/- 427 dynes/s/cm-5; p < 0.001) rose, whereas the cardiac index fell from 2.43 +/- 0.53 to 2.20 +/- 0.491/min/m2 (p < 0.002). However, mean pulmonary artery pressure (21 +/- 7 mm Hg) and pulmonary vascular resistance (151 +/- 43-147 +/- 43 dynes/s/cm-5) did not change. Exogenous ET-1, when infused into patients with LVD, causes systemic but not pulmonary vasoconstriction.

Aged↗
PubMed1996

Increased left ventricular dysfunction in elderly patients despite successful thrombolysis: the GUSTO-I angiographic experience.

OBJECTIVE: This study sought to determine whether the recovery of regional and global left ventricular function is reduced in elderly patients despite successful thrombolytic therapy for acute myocardial infarction. Comparisons were made between elderly (> or = 75 years old, n = 47) and adult (< 75 years old, n = 434) patients enrolled in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) angiographic trial who underwent catheterization at 90 min and 5 to 7 days after thrombolysis and who had an open infarct-related artery with Thrombolysis in Myocardial Infarction (TIMI) grade 2 to 3 flow at both times. BACKGROUND: The morbidity and mortality of acute myocardial infarction is increased in elderly patients, presumably because of multiple adverse coexistent baseline variables. However, functional recovery after thrombolysis has not been characterized in the elderly. METHODS: Ejection fraction, end-systolic volume index, infarct and noninfarct zone contractile function (SD/chord) and infarct extent (number of chords) were determined. RESULTS: At 90 min, elderly patients with an open infarct-related artery had decreased infarct zone contractile function (-2.8 +/- 0.2 vs. -2.3 +/- 0.1 SD/chord in adults, p < or = 0.05) and a greater extent of injury (26.0 +/- 2.6 vs. 20.7 +/- 0.8 chords in adults, p < or = 0.05). At 5- to 7-day follow-up ventriculography, ejection fraction was reduced, and end-systolic volume index was significantly increased in elderly patients compared with adults. The severity of regional wall motion dysfunction in the infarct zone was also greater in the elderly than in adults at 5- to 7-day follow-up (-2.6 +/- 0.2 vs. -1.9 +/- 0.1 SD/chord, respectively, p < or = 0.005). Non-infarct zone contractile function at 90-min ventriculography was similar in both groups. Despite a patent infarct-related artery at 90-min, the 30-day mortality rate in the elderly remained elevated (17.8%) compared with that of adults (4%) (p < or = 0.0001). Elderly patients were predominantly female and had a higher prevalence of hypertension, multivessel coronary disease, previous infarction, anterior infarctions and later time to treatment (between 3 and 6 h) than adults. However, age > or = 75 years remained an independent determinant by multivariable regression analysis of 1-week postinfarction end-systolic volume index, regional left ventricular dysfunction (p = 0.02 and p < or = 0.008, respectively) and 30-day mortality (p < or = 0.0001). CONCLUSIONS: Elderly patients had increased damage in the infarct zone and had persistently increased mortality despite sustained infarct-related artery patency after successful thrombolysis. Although the causes are probably multifactorial, a more rapid progression of ischemic injury or a blunted postreperfusion recovery appears to contribute to the poorer outcomes in elderly patients.

Adult↗
PubMed1995

Nitric oxide inhibits the positive inotropic response to beta-adrenergic stimulation in humans with left ventricular dysfunction.

BACKGROUND: Nitric oxide (NO) attenuates the contractile response to beta-adrenergic stimulation in cultured cardiac myocytes in vitro and in myocardium in vivo. We tested the hypothesis that NO synthesized in the heart inhibits the positive inotropic response to beta-adrenergic stimulation in humans with left ventricular (LV) dysfunction. METHODS AND RESULTS: Patients with various degrees of LV dysfunction and free from epicardial coronary artery disease were instrumented with an infusion catheter in the left main coronary artery and a high-fidelity micromanometer-tipped catheter in the LV. Measurements included LV pressure, aortic pressure, heart rate, and LV peak +dP/dt. In eight subjects, dobutamine was infused via the left main coronary artery (25 or 50 micrograms/min) before and concurrent with intracoronary infusion of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 20 mumol/min for 10 minutes). In six other subjects, dobutamine was infused (6, 10, or 15 micrograms.kg-1.min-1) via a peripheral vein. Intracoronary (n = 8) dobutamine infusions increased LV peak +dP/dt by an average of 33 +/- 3%. The intracoronary infusion of L-NMMA had no effect on baseline LV peak +dP/dt, LV systolic or end-diastolic pressures, aortic pressure, or heart rate. The intracoronary infusion of L-NMMA, concurrent with a second infusion of dobutamine, potentiated the +dP/dt response to dobutamine by 30 +/- 10% (P < .04 versus dobutamine alone). The intracoronary infusion of L-NMMA likewise potentiated the +dP/dt response to the peripheral infusion of dobutamine by 37 +/- 18%. CONCLUSIONS: Nitric oxide produced in the heart attenuates the positive inotropic response to beta-adrenergic stimulation in humans with LV dysfunction. NO may contribute to beta-adrenergic hyporesponsiveness in patients with LV dysfunction.

Adrenergic beta-Agonists↗
PubMed2004

Prognostic value of endocardial electromechanical mapping in patients with left ventricular dysfunction undergoing percutaneous coronary intervention.

Endocardial electromechanical mapping (EEM) has been proposed as a method for myocardial viability assessment. However, the impact of EEM data on clinical outcome has not been studied before. We sought to assess the prognostic value of EEM in patients with left ventricular (LV) dysfunction undergoing percutaneous coronary intervention (PCI). Seventy-five patients with coronary artery disease and LV dysfunction (angiographic LV ejection fraction [EF] 49 +/- 15%) underwent LV EEM for myocardial viability assessment before coronary revascularization. EEM parameters included mean unipolar electrographic amplitude, mean local shortening, LV volumes, LVEF, number of regions with electrographic amplitudes <7.5 mV, number of electromechanical mismatch, and match regions. Cardiac death, nonfatal myocardial infarction, nonfatal stroke, and acute heart failure requiring hospitalization were defined as clinical events. During a follow-up of 3.6 +/- 1.8 years, 20 clinical events occurred. Event-free survival after coronary revascularization was significantly better in patients with a mean unipolar electrographic amplitude of >/=9.5 mV than in patients with a mean unipolar electrographic amplitude of <9.5 mV (88% vs 57%; p <0.005). Cox regression analysis revealed angiographic LVEF, mean electrographic amplitude, number of regions with electrographic amplitudes <7.5 mV, number of electromechanical match regions, and EEM EF as univariate predictors of clinical events. In a multivariate analysis, angiographic LVEF <40% (hazard ratio 4.78, p <0.005) and mean electrographic amplitude <9.5 mV (hazard ratio 2.92, p <0.05) were independent predictors of clinical events. Thus, EEM provides prognostic information in patients with LV dysfunction undergoing coronary revascularization.

Aged↗
PubMed1985

Ischemia at rest is independent of the extent of ventricular dysfunction and arrhythmias in patients with coronary artery disease.

To assess the relation between myocardial ischemia, ventricular arrhythmias (VA), and left ventricular (LV) dysfunction, we evaluated 74 patients with coronary artery disease (CAD) using radionuclide angiography (to determine the resting ejection fraction [EF]), resting thallium-201 scintigraphy (to ascertain the extent of resting ischemia), and 24-hour Holter monitoring (to assess VA). Thirty patients had resting ischemia, 26 had resting EF less than 30%, and 27 had repetitive VA. Patients with and without ischemia had similar EFs (36 +/- 14 vs 38 +/- 14, p = NS). Further, patients with and without repetitive forms of VA had a similar number of resting ischemic segments (1.1 +/- 1.7 vs 1.1 +/- 2.2, p = NS). Patients with EFs less than 30 had more VA than patients with EFs greater than or equal to 30 (Holter class 4.3 +/- 2.3 vs 3.0 +/- 1.8, p less than 0.01) but a similar extent of ischemia (1.4 +/- 2.2 vs 1.0 +/- 1.7, p = NS). Thus, while patients with lower EFs have more repetitive forms of VA, ischemia at rest is independent of VA and EF. These data suggest that prognostic stratification of patients with CAD for intervention studies should include a separate consideration of ischemia.

Arrhythmias, Cardiac↗
PubMed2006

Prediction of subclinical left ventricular dysfunction with strain rate imaging in patients with mild to moderate rheumatic mitral stenosis.

BACKGROUND: Left ventricular (LV) long-axis function evaluated by Doppler tissue echocardiography-derived strain rate (SR) imaging has been shown to be a useful index of LV systolic function; however, it has not been evaluated in patients with mitral stenosis (MS). We examined the LV long-axis function of patients with pure MS and normal global systolic function as assessed by LV ejection fraction. METHOD: In all, 30 patients (22 women; 45 +/- 9 years) with mild to moderate MS (mitral valve area = 1.5 +/- 0.3 cm2) and 28 healthy volunteers (20 women; 44 +/- 10 years) were evaluated by both conventional and Doppler tissue echocardiography. Two-dimensional Doppler tissue echocardiography was performed in the apical 4-chamber view in the septal and lateral wall on the mitral annular level. Peak systolic myocardial SR and end-systolic strain data were measured for both segments. RESULTS: Peak systolic SR (1.2 +/- 0.4% vs 1.8 +/- 0.39%, P < .001) and end-systolic strain (10 +/- 5 vs 25 +/- 6 s(-1), P < .001) were both significantly lower in patients with MS than in control subjects. CONCLUSIONS: Patients with MS had significantly impaired long-axis function evaluated by Doppler tissue echocardiography-derived SR imaging despite normal global systolic function.

Adult↗
PubMed2001

Long axis electromechanics during dobutamine stress in patients with coronary artery disease and left ventricular dysfunction.

OBJECTIVE: To dissociate the effect of inotropy from activation change during dobutamine stress on left ventricular long axis function in patients with coronary artery disease (CAD). METHODS: 25 patients with CAD and normal left ventricular cavity size and 30 with cavity dilatation-18 with normal activation (DCM-NA) and 12 with left bundle branch block (DCM-LBBB)-were compared with 20 controls. 12 lead ECG and septal long axis echograms were assessed at rest and peak dobutamine stress. Amplitude, shortening and lengthening velocities, postejection shortening, Q wave to onset of shortening (Q-OS), and A2 to onset of lengthening (A2-OL) were measured. Inotropy was evaluated from peak aortic acceleration. RESULTS: In controls, amplitude, shortening and lengthening velocities, and peak aortic acceleration increased with stress; QRS, Q-OS, and A2-OL shortened (all p < 0.001); and contraction remained coordinate. In the group of patients with CAD and normal left ventricular cavity size, shortening velocity and peak aortic acceleration increased with stress (p < 0.005). However, amplitude and lengthening velocity did not change, QRS, Q-OS, and A2-OL lengthened (p < 0.01), and incoordination appeared. Results were similar in the group with DCM-NA. In the DCM-LBBB group, shortening velocity and peak aortic acceleration increased modestly with stress (p < 0.01) but amplitude, lengthening velocity, QRS, Q-OS, A2-OL, and incoordination remained unchanged. Overall, change in shortening velocity correlated with that in peak aortic acceleration (r(2) = 0.71), in amplitude with that in lengthening velocity (r(2) = 0.74), and in QRS with both Q-OS (r(2) = 0.69) and A2-OL (r(2) = 0.63). CONCLUSION: The normal long axis response to dobutamine reflects both inotropy and rapid activation. In CAD, inotropy is preserved with development of ischaemia but the normal increase in amplitude is lost and prolonged activation delays the time course of shortening, causing pronounced incoordination. Overall, shortening rate uniformly reflects inotropy while lengthening rate depends mainly on systolic amplitude rather than primary diastolic involvement, even with overt ischaemia.

Cardiotonic Agents↗
PubMed2001

Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy.

Cell death has been questioned as a mechanism of ventricular failure. In this report, we tested the hypothesis that apoptotic death of myocytes, endothelial cells, and fibroblasts is implicated in the development of the dilated myopathy induced by ventricular pacing. Accumulation of reactive oxygen products such as nitrotyrosine, potentiation of the oxidative stress response by p66(shc) expression, formation of p53 fragments, release of cytochrome c, and caspase activation were examined to establish whether these events were coupled with apoptotic cell death in the paced dog heart. Myocyte, endothelial cell, and fibroblast apoptosis was detected before indices of severe impairment of cardiac function became apparent. Cell death increased with the duration of pacing, and myocyte death exceeded endothelial cell and fibroblast death throughout. Nitrotyrosine formation and p66(shc) levels progressively increased with pacing and were associated with cell apoptosis. Similarly, p50 (DeltaN) fragments augmented paralleling the degree of cell death in the failing heart. Moreover, cytochrome c release and activation of caspase-9 and -3 increased from 1 to 4 weeks of pacing. In conclusion, cardiac cell death precedes ventricular decompensation and correlates with the time-dependent deterioration of function in this model. Oxidative stress may be critical for activation of apoptosis in the overloaded heart.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Left ventricular aneurysmectomy in advanced left ventricular dysfunction.

Despite widespread application in clinical practice and extensive laboratory investigations, many basic issues regarding left ventricular aneurysmectomy remain to be resolved. Analysis of clinical data from the authors' three centers and application of powerful modern imaging techniques provide important information to resolve these issues.

Aged↗
PubMed2003

Screening for left ventricular dysfunction using a hand-carried cardiac ultrasound device.

BACKGROUND: The hand-carried cardiac ultrasound (HCU) device is a recently introduced imaging device, which may be potentially useful in the primary care setting. AIM: To test the screening potential of a HCU for the detection of left ventricular (LV) dysfunction by evaluating LV ejection fraction (LVEF) and inferior vena cava (IVC) collapse. Standard echocardiographic system (SE) and plasma brain natriuretic peptide (BNP) measurements were used as a reference. METHODS: Eighty-eight consecutive patients (56 male, aged 59+/-12 years) with suspected LV dysfunction were enrolled in the study. The HCU-LVEF was visually estimated and the SE-LVEF was derived by the Simpson's biplane method. A LVEF <40% represented LV dysfunction. An IVC collapse of <50% and BNP levels > or =15 pmol/l were considered abnormal. The correlation of HCU-LVEF, HCU-IVC and BNP to the SE-LVEF and SE-IVC was analysed independently using 2x2 tables. RESULTS: Six patients were excluded because of poor echo images. 19/82 patients had LV dysfunction. The HCU and BNP could identify 17 and 18 out of these 19 patients, respectively. The agreement for LVEF and IVC collapse between SE and HCU was 96% for both parameters. The sensitivity of IVC collapse, HCU-LVEF and BNP in identifying patients with LV dysfunction was 26, 89 and 94%, respectively. CONCLUSION: A HCU device can reliably be used as a screening tool for LV dysfunction.

Echocardiography↗
PubMed2003

Echocardiographic prediction of left ventricular dysfunction after mitral valve repair for mitral regurgitation as an indicator to decide the optimal timing of repair.

OBJECTIVES: This study sought to determine whether echocardiography before mitral valve repair (MVR) for mitral regurgitation (MR) was predictive of postoperative left ventricular (LV) dysfunction and useful for deciding the optimal timing of repair. BACKGROUND: Some reports have shown that the preoperative echocardiographic data of left ventricular ejection fraction (LVEF) and left ventricular end-systolic diameter (LVDs) were good predictors of postoperative LV dysfunction. However, few reports were based on long-term follow-up data of large numbers of patients who underwent MVR in the last decade. METHODS: A total of 274 patients with moderate or severe MR underwent MVR between October 1, 1991, and September 30, 2000. Among them, 171 patients who had both an operation for isolated MR due to degenerative pathology and a postoperative echocardiogram were studied. Postoperative echocardiograms were performed 3.9 +/- 2.4 years after the operation. The LVEF decreased from 66 +/- 10% before surgery to 63 +/- 11% after surgery (p < 0.0001). On univariate analysis, preoperative LVEF and LVDs correlated with postoperative LVEF (r = 0.41 and r = -0.39, respectively). Overall, postoperative LV dysfunction (defined as LVEF <50%) was not frequent (12%). However, the incidence of postoperative LV dysfunction was high in patients with preoperative LVEF <55% (38%) or LVDs > or =40 mm (23%). CONCLUSIONS: In patients with MR, the echocardiographic data of LVEF and LVDs were good predictors of postoperative LV dysfunction. When a decrease in LVEF or an increase in LVDs is detected, MVR should be considered to preserve postoperative LV function.

Adult↗
PubMed1998

Overexpression of alpha1B-adrenergic receptor induces left ventricular dysfunction in the absence of hypertrophy.

The stimulation of cardiac alpha1-adrenergic receptors (AR) modulates the heart's inotropic response and plays a role in the induction of cardiomyocyte hypertrophy. We have analyzed transgenic mouse lines overexpressing a wild-type alpha1B-AR specifically in the heart. Basal level systolic and diastolic left ventricular (LV) contractile function was depressed both in the anesthetized closed-chest mouse and the perfused working-heart preparation. Intrinsic LV function was further characterized under controlled preload and afterload conditions using the perfusion model. Contractile parameters were restored by chronic treatment with the alpha-AR antagonist prazosin. In ventricular function curves, the load-dependent force increases (length-tension effects) remained intact, although the transgenic curve was shifted to lower levels. The basal level contractile deficits were paralleled by a decrease in calcium transients in isolated LV cardiomyocytes. LV function comparable to controls was restored by isoproterenol stimulation. The physiological changes occurred in the absence of cardiomyocyte hypertrophy. This transgenic model will be useful for studying the potential role of alpha1-AR in cardiac contractility and hypertrophy.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2001

Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: prognostic utility and prediction of benefit from carvedilol in chronic ischemic left ventricular dysfunction. Australia-New Zealand Heart Failure Group.

OBJECTIVES: We sought to assess plasma concentrations of the amino (N)-terminal portion of pro-brain natriuretic peptide (N-BNP) and adrenomedullin for prediction of adverse outcomes and responses to treatment in 297 patients with ischemic left ventricular (LV) dysfunction who were randomly assigned to receive carvedilol or placebo. BACKGROUND: Although neurohormonal status has known prognostic significance in heart failure, the predictive power of either N-BNP or adrenomedullin in chronic ischemic LV dysfunction has not been previously reported. METHODS: Plasma N-BNP and adrenomedullin were measured in 297 patients with chronic ischemic (LV) dysfunction before randomization to carvedilol or placebo, added to established treatment with a converting enzyme inhibitor and loop diuretic (with or without digoxin). The patients' clinical outcomes, induding mortality and heart failure events, were recorded for 18 months. RESULTS: Above-median N-BNP and adrenomedullin levels conferred increased risks (all p < 0.001) of mortality (risk ratios [95% confidence intervals]: 4.67 [2-10.9] and 3.92 [1.76-8.7], respectively) and hospital admission with heart failure (4.7 [2.2-10.3] and 2.4 [1.3-4.5], respectively). Both of these predicted death or heart failure independent of age, New York Heart Association functional class, LV ejection fraction, previous myocardial infarction or previous admission with heart failure. Carvedilol reduced the risk of death or heart failure in patients with above-median levels of N-BNP or adrenomedullin, or both, to rates not significantly different from those observed in patients with levels below the median value. CONCLUSIONS: In patients with established ischemic LV dysfunction, plasma N-BNP and adrenomedullin are independent predictors of mortality and heart failure. Carvedilol reduced mortality and heart failure in patients with higher pre-treatment plasma N-BNP and adrenomedullin.

Adrenergic beta-Antagonists↗