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At least 811 records · Page 45Linked to original sources
PubMed2003

Isolated bundle branch block and left ventricular dysfunction.

BACKGROUND: Population studies have identified the presence of bundle branch block (BBB) as a risk factor for increased mortality in patients with known cardiac disease. It is unknown how chronic ventricular dyssynchrony resulting solely from conduction delay affects ventricular function. METHODS AND RESULTS: Subjects were retrospectively identified from the University of California, San Francisco, electrocardiogram database with QRS prolongation. Subjects who had no evidence of heart disease and had baseline and serial studies evaluating ongoing risk of coronary artery disease status and left ventricular function were followed over time. Documentation of a minimum of 2 serial evaluations of cardiac status were present in a total of 51/176 (20%) subjects with isolated BBB who constitute the study population. After a mean follow-up of 52 +/- 45 months-adjusting for differences due to age, sex, the presence of hypertension, hyperlipidemia, and diabetes mellitus-left ventricular ejection fraction diminished by -7.3 +/- 12% per year in the isolated left BBB cohort versus -1.9 +/- 4% in isolated right BBB cohort and -1.1 +/- 3% reduction in the isolated nonspecific intraventricular conduction delay cohort (P =.019). CONCLUSIONS: Left bundle branch block itself may be a cause of ventricular dysfunction.

Aged↗
PubMedDate not supplied

Relationship of extent and nature of dysfunctional myocardium to brain natriuretic peptide in patients with ischemic left ventricular dysfunction.

We studied the relationship between brain natriuretic peptide (BNP) levels and viable myocardium and ischemic myocardium, regional scar and regional contractile function. Fifty-nine patients underwent dobutamine echocardiography and magnetic resonance imaging and resting BNP levels were determined. By magnetic resonance imaging, total extent of dysfunctional myocardium correlated strongest with BNP (r = 0.60, p < 0.0001). The extent of scar, viability and ischemia also correlated. At dobutamine echocardiography, a composite of dysfunctional and ischemic myocardium was the strongest correlate of BNP (r = 0.48, p < 0.0001), with less strong correlations by global parameters. The extent of dysfunctional myocardium, rather than its nature determines BNP levels.

Adult↗
PubMed1998

Protectant activity of hexarelin or growth hormone against postischemic ventricular dysfunction in hearts from aged rats.

The ability of hexarelin, a recently synthesized hexapeptide with a strong growth hormone (GH)-releasing activity, or of GH itself to display a protectant activity against postischemic ventricular dysfunction in senescent hearts was studied in 24-month-old male rats. Heart preparations from control (saline-treated) senescent rats, subjected to moderate ischemia, showed at reperfusion: (a) a low recovery of postischemic left ventricular developed pressure (LVDP; 37% of the preischemic values; from 90 +/- 5.7 to 33.5 +/- 3.8 mm Hg; p < 0.01; n = 10) coupled to a substantial increase in coronary perfusion pressure (CPP; 71% over baseline; from 68.3 +/- 5.2 to 116.8 +/- 4.6 mm Hg; p < 0.01; n = 10); (b) a marked increase of creatine kinase (CK) released in the perfusates (6.6-fold increase over preischemic values; from 45 +/- 4 to 298 +/- 25 mU/min/g wet tissue; p < 0.001; n = 10). In vivo administration of hexarelin (80 microg/kg, b.i.d., s.c.) for 21 days resulted in a striking heart protection against reperfusion stunning. In fact, the recovery of LVDP at reperfusion was almost complete (90% of the preischemic values; from 93 +/- 5.8 to 83.7 +/- 5.9 mm Hg; p > 0.05; n = 9), and the increase in coronary resistance was minimal (from 67 +/- 5.8 to 79.7 +/- 6.9 mm Hg; p > 0.05; n = 9). Furthermore, the concentration of CK in the perfusates was increased only twofold (from 45.8 +/- 5.5 to 90 +/- 7.2 mU/min/g wet tissue; p < 0.05; n = 9), with a gradual return toward basal values at the end of reperfusion. The protectant activity of hexarelin was divorced from any detectable alteration of the somatotropic function, as assessed by pituitary GH messenger RNA (mRNA) and plasma insulin-like growth factor I levels. In vivo administration of GH (400 microg/kg b.i.d., s.c.) for the same time lapse resulted in only a partial protectant activity: 55% of LVDP recovery (from 91.5 +/- 6.2 to 50 +/- 3.5 mm Hg; p < 0.01; n = 6); 65% increase of coronary resistance (from 68 +/- 4.3 to 112.2 +/- 5.2 mm Hg; p < 0.01; n = 6); 5.3-fold increase of CK concentrations in heart perfusates on reperfusion (from 43.8 +/- 3.8 to 232 +/- 16 mU/min/g wet tissue; p < 0.001; n = 6). Evaluation of the rate of release of 6-keto-prostaglandin F1alpha (PGF1alpha), the stable metabolite of prostacyclin, in heart perfusates, and assessment of the vasopressor activity of angiotensin II on the coronary vasculature, did not show any change in these parameters among the three experimental groups. Collectively these data indicate that hexarelin displays a strong heart-protectant activity against myocardial stunning in senescent rats. The protection afforded by the peptide is likely due to a direct cardiotropic action and is far greater than that of GH. Neither compound appears able to interfere with the endothelium-dependent relaxant mechanism.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

A systematic review: effect of angiotensin converting enzyme inhibition on left ventricular volumes and ejection fraction in patients with a myocardial infarction and in patients with left ventricular dysfunction.

BACKGROUND AND AIM: To summarize and quantify results of echocardiographic studies examining the effect of angiotensin converting enzyme (ACE) inhibition on left ventricular remodelling in patients with acute myocardial infarction (MI) and in patients with left ventricular systolic dysfunction (LVSD). METHODS: Systematic review of the literature and meta-analysis of eligible studies providing data on end-diastolic and end-systolic volumes and left ventricular ejection fraction (LVEF) were performed. RESULTS: Data from 16 eligible studies were meta-analysed. The results of studies including patients with MI and preserved LVEF (>45%) showed no significant benefit of ACE inhibition. Results of studies/subgroups with mean LVEF < or =45% demonstrated significant differences in diastolic and systolic volumes of 3.0 (0.1, 6.0) ml and 2.25 (0.04, 4.4) ml in short-term (4-14 weeks) follow-up in favour of ACE inhibitor, p=0.041 and p=0.046 respectively. In the long-term (6-12 months) follow-up, the differences in diastolic and systolic volumes were 4.2 (0.98, 7.4) ml and 3.3 (0.9, 5.8) ml in favour of ACE inhibitor, p=0.01 and p=0.007 respectively. LVEF improved in both short and long-term follow-up, p=0.034 and p=0.021, respectively. CONCLUSION: Chronic use of ACE inhibition has a small but sustained and beneficial effect on remodelling in patients with myocardial infarction and patients with chronic left ventricular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Prognostic value of iodine-123-metaiodobenzylguanidine imaging and cardiac natriuretic peptide levels in patients with left ventricular dysfunction resulting from cardiomyopathy.

This study assessed the prognostic value of Iodine-123-metaiodobenzylguanidine (MIBG) imaging and of the plasma level of cardiac natriuretic peptides in patients with left ventricular dysfunction resulting from cardiomyopathy. Predictors of cardiac death or hospitalization related to progressive heart failure were examined in 171 patients with chronic heart failure (96 patients with idiopathic cardiomyopathy and 75 patients with ischemic cardiomyopathy). All patients underwent MIBG imaging at rest and other hemodynamic studies. During a mean (+/-SD) follow-up period of 27+/-11 months, 11 patients died from heart failure and 16 required hospitalization. High MIBG washout was an independent predictor of cardiac death (relative risk [RR] = 1.158, p<0.0001) whereas the plasma level of brain natriuretic peptide (BNP: relative risk [RR] = 1.005, p<0.0001) and high MIBG washout (relative risk [RR] = 1.094, p<0.0001) were predictors of progressive heart failure (ie, combined cardiac death and hospitalization). Accelerated myocardial adrenergic nerve activity as assessed by MIBG imaging and the plasma levels of BNP are powerful predictors of the patient's prognosis.

3-Iodobenzylguanidine↗
PubMedDate not supplied

Severe left ventricular dysfunction and arrhythmias as complications of gram-positive sepsis: rapid recovery in children.

Severe left ventricular dilatation and dysfunction in children may be associated with poor outcome in as many as 45% of cases. The prognosis for children with poor left ventricular function or arrhythmias associated with septic shock may be better, however, this has been inadequately studied. We report the favorable outcome of three children who presented with Gram-positive sepsis and significant cardiovascular compromise-two with severely dilated, poorly contractile left ventricle, and one with mild left ventricular dysfunction and incessant, malignant, and rapid atrial and ventricular arrhythmias. Our experience with these patients shows that complete and rapid resolution of these complications may be achieved with aggressive therapy.

Adolescent↗
PubMed2005

Right ventricular dysfunction and pulmonary obstruction index at helical CT: prediction of clinical outcome during 3-month follow-up in patients with acute pulmonary embolism.

PURPOSE: To retrospectively quantify right ventricular dysfunction (RVD) and the pulmonary artery obstruction index at helical computed tomography (CT) on the basis of various criteria proposed in the literature and to assess the predictive value of these CT parameters for mortality within 3 months after the initial diagnosis of pulmonary embolism (PE). MATERIALS AND METHODS: Institutional review board approval was obtained, and informed consent was not required for retrospective study. In 120 consecutive patients (55 men, 65 women; mean age +/- standard deviation, 59 years +/- 18) with proved PE, two readers assessed the extent of RVD by quantifying the ratio of the right ventricle to left ventricle short-axis diameters (RV/LV) and the pulmonary artery to ascending aorta diameters, the shape of the interventricular septum, and the extent of obstruction to the pulmonary artery circulation on helical CT images, which were blinded for clinical outcome in consensus reading. Regression analysis was used to correlate these parameters with patient outcome. RESULTS: CT signs of RVD (RV/LV ratio, >1.0) were seen in 69 patients (57.5%). During follow-up, seven patients died of PE. Both the RV/LV ratio and the obstruction index were shown to be significant risk factors for mortality within 3 months (P = .04 and .01, respectively). No such relationship was found for the ratio of the pulmonary artery to ascending aorta diameters (P = .66) or for the shape of the interventricular septum (P = .20). The positive predictive value for PE-related mortality with an RV/LV ratio greater than 1.0 was 10.1% (95% confidence interval [CI]: 2.9%, 17.4%). The negative predictive value for an uneventful outcome with an RV/LV ratio of 1.0 or less was 100% (95% CI: 94.3%, 100%). There was a 11.2-fold increased risk of dying of PE for patients with an obstruction index of 40% or higher (95% CI: 1.3, 93.6). CONCLUSION: Markers of RVD and pulmonary vascular obstruction, assessed with helical CT at baseline, help predict mortality during follow-up.

Acute Disease↗
PubMed2005

Selective down-regulation of sub-endocardial ryanodine receptor expression in a rabbit model of left ventricular dysfunction.

Defective sarcoplasmic reticulum (SR) Ca2+ handling is evident in cardiomyopathy and may be mediated by selective dysregulation of SR Ca2+ handling proteins. To assess whether regulation of SR Ca2+ release may vary regionally within the normal and diseased heart, left ventricular transmural expression and activity of the ryanodine receptor (RyR2) was studied in a rabbit coronary artery ligation model of left ventricular dysfunction (LVD). Tissue/cells were isolated from both the sub-endocardial and subepicardial layers of the left ventricular free wall from sham-operated and coronary artery ligated rabbit hearts. Three independent methods were used to study alterations in RyR2 mRNA (real-time quantitative PCR (RT-PCR)) and protein expression (quantitative immunoblotting and [3H] ryanodine binding). These biochemical data were compared with functional measurements of fractional SR Ca2+ release from both of these regions. Data from RT-PCR revealed lower RyR2 mRNA levels in the sub-endocardium compared with subepicardium in both experimental groups with the reduction being significantly lower in the sub-endocardium from the LVD group. Quantitative analysis of RyR2 protein levels revealed the same expression patterns. Calsequestrin mRNA and protein levels showed no significant changes. This study demonstrates a lower expression level of RyR2 in the sub-endocardium of the left ventricle of rabbit hearts and is the first to show a further specific reduction in LVD. There is a corresponding decrease in fractional SR Ca2+ release in cells isolated from the sub-endocardium of hearts from the LVD group, relating these selective biochemical alterations to changes in function.

Animals↗
PubMed1992

[Effect of denopamine on residual left ventricular dysfunction after complete revascularization].

Denopamine (15 mg/day) was administered to 20 patients with residual left ventricular dysfunction after successful percutaneous transluminal coronary angioplasty (75% or more diameter stenosis). Echocardiography was performed before and 6 months after denopamine administration to analyze the left ventricular function. There were significant decreases in both end-diastolic and end-systolic dimensions from 58 +/- 8.3 to 54 +/- 8.4 mm (p = 0.001), and from 44 +/- 10.1 to 40 +/- 10.3 mm (p = 0.005)), respectively, while % fractional shortening remained nearly constant (from 25 +/- 8.3 to 27 +/- 9.6%). Thus, denopamine improved the left ventricular function by decreasing left ventricular size while maintaining wall contractility.

Adrenergic beta-Agonists↗
PubMed2005

Managed care patients with heart failure: spectrum of ventricular dysfunction and predictors of medication utilization.

BACKGROUND: Heart failure (HF) is a common clinical syndrome resulting in high morbidity and mortality. We examined the spectrum of ventricular dysfunction, and investigated the predictors of angiotensin-converting enzyme (ACE) inhibitor, beta-blocker, and spironolactone prescription in 1613 managed care patients with HF. METHODS AND RESULTS: The diagnosis of HF was made by a HF discharge diagnosis or at least 3 physician encounters with a HF diagnosis during 2000. Logistic regression was used to identify predictors of medication prescription. Preserved systolic function was documented in 37%, moderate-severe systolic dysfunction in 31%, mild systolic in 14%, and 18% had inadequate documentation. The mean age was 69 years, 58% were women, 24% African American, and 60% were Medicare patients. Patients without HF type documented were the least aggressively treated. Coronary artery disease, hypertension, and diabetes predicted increased utilization of ACE inhibitor and beta-blocker therapies. History of nephropathy was associated with less ACE inhibitor prescription. Advancing age predicted less utilization of beta-blockers and spironolactone. Neither ethnicity nor gender influenced medication prescription. CONCLUSION: Preserved left ventricular function was common. Documentation of significant systolic dysfunction was associated with improved quality of care. Interventions to encourage documentation of HF type and further study of HF with preserved systolic function are warranted.

Adrenergic beta-Antagonists↗
PubMed1984

The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction.

We examined the relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality after the occurrence of myocardial infarction in 766 patients who enrolled in a nine-hospital study and underwent two special tests. Frequency and repetitiveness of ventricular premature depolarizations (VPDs) were determined by computer analysis of predischarge 24 hr electrocardiographic recordings. The left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography and dichotomized at its optimal value of 30%. Frequency of VPDs was divided into three categories: (1) less than one per hour, (2) one to 2.9 per hour, and (3) three or more per hour. Repetitiveness of VPDs was also divided into three categories: (1) no repetitive VPDs, (2) paired VPDs, and (3) VPD runs. These variables were related, one at a time and jointly, to total mortality and to deaths caused by arrhythmias. The hazard ratios for dying in the higher or highest risk stratum vs the lower or lowest stratum for each variable (adjusted for the effects of the others) were: LVEF below 30%, 3.5; VPD runs, 1.9; and VPD frequency of three or more per hour, 2.0. There were no significant interactions among the three variables with respect to effects on the risk of mortality. There was a suggestion of an interaction between each risk variable and time after infarction. LVEF below 30% was a better predictor of early mortality (less than 6 months) and the presence of ventricular arrhythmias was a better predictor of late mortality (after 6 months).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1997

Fish consumption, n-3 fatty acids in cell membranes, and heart rate variability in survivors of myocardial infarction with left ventricular dysfunction.

To elucidate a possible antiarrhythmic effect of long-chained n-3 polyunsaturated fatty acids, heart rate variability was assessed in 52 patients with a previous myocardial infarction and left ventricular dysfunction. The content of n-3 polyunsaturated fatty acids in platelets was closely associated with the patient's fish-consuming habits, and a significant positive correlation was observed between the n-3 fatty acid docosahexaenoic acid and heart rate variability.

Aged↗
PubMed2004

Effect of aldosterone blockade in patients with systolic left ventricular dysfunction: implications of the RALES and EPHESUS studies.

Aldosterone blockade has been shown to be effective in reducing total mortality as well as hospitalization for heart failure in patients with systolic left ventricular dysfunction (SLVD) due to chronic heart failure and in patients with SLVD post acute myocardial infarction. The evidence for the effectiveness of aldosterone blockade in chronic heart failure comes from the randomized aldactone evaluation study (RALES) while that for patients post infarction from the eplerenone post acute myocardial infarction efficacy and survival study (EPHESUS). These studies suggest that mineralocorticoid receptor activation remains important despite the use of an angiotensin converting enzyme-inhibitor/angiotensin receptor blocking (ARB) agent and a beta blocker. Increasing evidence suggest that aldosterone blockade has important effects not only on the kidney but on ventricular remodeling, myocardial fibrosis, autonomic balance, fibrinolysis, oxidative stress, and activation of the NF-kappaB and AP-1 signaling pathways. The results of these studies in patients with SLVD has important implications not only for patients with chronic heart failure and post infarction but also for the therapy of patients with essential hypertension and other cardiovascular diseases.

Aldosterone↗
PubMedDate not supplied

Left ventricular dysfunction and heart failure. Mechanistic and therapeutic distinctions.

Dysfunction of the left ventricle may result from a variety of insults, all of which may initiate a self-perpetuating process of ventricular remodeling which may progress to end-stage heart disease. Symptoms of heart failure may or may not co-exist with this ventricular remodeling. Treatment and prevention of these two largely distinct entities differ. Symptoms may respond to diuretics, vasodilators and digoxin. Progressive ventricular remodeling may be slowed by angiotensin converting enzyme inhibitors, hydralazine + isosorbide dinitrate and beta blockers. Prevention of symptomatic heart failure is dependent on early recognition of ventricular dysfunction and aggressive treatment to slow its progression. Development of more effective and targeted therapies will be dependent on expanded insight into the cellular and molecular mechanisms contributing to the remodeling process.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Landmark study: the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction Study (CAPRICORN).

The benefit of beta-blockers for secondary prevention of death and reinfarction after myocardial infarction (MI) has been conclusively demonstrated in randomized clinical trials. Before the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction Study (CAPRICORN)-a multicenter, multinational, double-blind, randomized, placebo-controlled trial that enrolled 1,959 patients who had an acute MI and a left ventricular ejection fraction of <==0.40-it was not known whether beta-blockers confer additional benefit when used in the context of modern post-MI management (eg, fibrinolytic therapy and primary percutaneous transluminal coronary angioplasty, aspirin, and angiotensin-converting enzyme inhibitors). Patients in CAPRICORN were treated with a maximum dose of 25 mg bid and observed until 633 validated primary end points had occurred. Because the overall mortality was lower than had been predicted, a co-primary end point was adopted that included the original primary end point (all-cause mortality) plus the first of the prespecified secondary end points (all-cause mortality or cardiovascular hospitalizations). A significant 23% reduction in the original primary end point of all-cause mortality was observed. A total of 340 (35%) patients died or had a cardiovascular hospitalization in the carvedilol group versus 367 (37%) in the placebo group. Therefore, the revised primary end point of all-cause mortality or cardiovascular hospitalization was reduced by 8%, which was not statistically significant. Significant reductions in cardiovascular mortality, nonfatal MI, and the combination of all-cause mortality or nonfatal MI were observed. Although statistical significance for the revised primary end point was not reached, CAPRICORN has an important role in guiding future use of beta-blockers in the early post-MI period.

Adrenergic beta-Antagonists↗
PubMed1988

Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction.

In a randomised, double-blind trial 60 patients with left ventricular dysfunction (ejection fraction less than 45%) but without clinical evidence of heart failure 1 week after Q wave myocardial infarction were given captopril 25 mg thrice a day, frusemide 40 mg daily, or placebo. Left ventricular volumes were measured at baseline and at 1, 3, 6, 9, and 12 months with cross-sectional echocardiography and Simpson's rule analysis of standardised apical views. The captopril group showed no significant change in left ventricular end-diastolic volume index but left ventricular end-systolic volume index was significantly reduced and stroke volume index and ejection fraction were significantly increased from 1 month on. In contrast, the frusemide and placebo groups showed significant increases in ventricular volumes, with stroke volume index unchanged and ejection fraction slightly reduced. The changes in the captopril group were significantly different from those in the other groups.

Adult↗
PubMed1995

Improvement in exercise-induced left ventricular dysfunction by infusion of alpha-human atrial natriuretic peptide in coronary artery disease.

The effects of recombinant alpha-human atrial natriuretic peptide (alpha-hANP) infusion an acute left ventricular dysfunction provoked by exercise were examined in 14 men with coronary artery disease. Patients performed symptom-limited, graded exercise on a supine bicycle ergometer. Plasma alpha-hANP and guanosine 3',5'-monophosphate (cyclic GMP) concentrations as well as hemodynamic variables were measured at rest, during and after exercise. In 14 patients whose pulmonary artery wedge pressure was > 20 mm Hg at peak exercise, the same exercise protocol was repeated at 30 minutes after starting intravenous alpha-hANP infusion (0.05 microgram.kg-1.min-1). In 8 of these patients, a Webster thermodilution catheter was advanced into the coronary sinus for measurement of coronary sinus blood flow. From the control exercise test, plasma alpha-hANP concentration increased from 86 +/- 20 pg/ml at rest to 188 +/- 32 pg/ml at peak exercise (p < 0.001), and plasma cyclic GMP concentration increased from 4.8 +/- 1.9 pmol/ml at rest to 7.2 +/- 2.9 pmol/ml at peak exercise (p < 0.001). Both plasma alpha-hANP and cyclic GMP concentrations showed a significant positive correlation with pulmonary artery wedge pressure during control exercise. With alpha-hANP infusion, systolic and diastolic pulmonary artery pressures and pulmonary artery wedge pressure were significantly decreased at all time points during exercise testing. Heart rate was increased and systolic blood pressure was significantly decreased at rest and at 3 minutes of exercise. Diastolic blood pressure, systemic vascular resistance, and pulmonary vascular resistance were significantly decreased at rest.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗