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 1,639 records · Page 91Linked to original sources
PubMed1979

Impaired maximal rate of left ventricular relaxation in patients with coronary artery disease and left ventricular dysfunction.

It has been suggested that the rate of left ventricular (LV) relaxation is related to the inotropic state, end-systolic fiber length and peak LV pressure, but little information is available regarding the rate of LV relaxation in patients with coronary artery disease (CAD) and LV dysfunction. To assess the rate of LV relaxation we obtained high-fidelity LV pressure measurements with manometer-tip catheters in 39 patients. The signal was analyzed by a digital computer to yield the maximal rate of pressure rise (pos dP/dt) and the maximal rate of pressure fall (neg dP/dt). Selective coronary arteriography and biplane LV angiography with determination of LV volumes, ejection fraction (EF) and percent abnormally contracting segments (ACS) when present, were performed in all patients. In 10 patients with normal LV function (EF greater than 0.50, no asynergy) mean neg dP/dt (2074 +/- 121 mm Hg/sec) was significantly (p less than 0.01) greater than in 29 patients with CAD and LV dysfunction (1695 +/- 66 mm Hg/sec). In nine patients with LV dysfunction and EF less than 0.35, mean neg dP/dt was reduced to 1405 +/- 107 mm Hg/sec, significantly (p less than 0.01) lower than in patients with normal LV function. Neg dP/dt correlated well with pos dP/dt (r = 0.75), with EF (r = 0.74), and with ACS (r = -0.74), and less well with LV end-systolic volume (r = 0.67). There was very poor correlation between neg dP/dt and peak LV pressure (r = 0.30). These data suggest that the rate of LV relaxation, as assessed by neg dP/dt, is impaired in patients with CAD and LV dysfunction, and the extent of impairment is related to the severity of the dysfunction as determined hemodynamically by pos dP/dt, and angiographically by EF and ACS. In these patients the maximal rate of LV relaxation is inversely related to LV end-systolic volume, and is not related to peak LV pressure.

Adult↗
PubMed2000

Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock.

BACKGROUND: Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock. METHODS: Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography. RESULTS: Increased plasma concentrations of cTnI (>/=0.4 microgram/L) and cTnT (>/=0.1 microgram/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated (r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction (P <0.0001). CONCLUSIONS: These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.

Adolescent↗
PubMed2000

Psychosocial factors as predictors of functional status at 1 year in patients with left ventricular dysfunction.

Chronic heart failure patients often experience significant functional impairments. A better understanding of the biopsychosocial correlates of functional status may lead to interventions that improve quality of life in this population. Social isolation, mood disturbance, low socioeconomic status, and non-White ethnicity were evaluated as possible correlates of impaired functional status in 2,992 U.S. patients with left ventricular ejection fractions (LVEFs) </= 35%. Even after controlling for age and clinical characteristics, all of the psychosocial variables examined were significant predictors of risk for experiencing severe limitations in intermediate and social activities of daily living at 1 year, with adjusted odds ratios in the 1.5-2.0 range. The ability of psychosocial characteristics to predict future functional status was also independent of baseline functional status, comorbid medical conditions, and deterioration in heart failure signs and symptoms over the intervening year. These results suggest that psychosocial factors influence patient functional status even in the later phases of cardiac disease.

Activities of Daily Living↗
PubMed2003

New-onset QT prolongation and torsades de pointes accompanied by left ventricular dysfunction secondary to acute pancreatitis.

A 70-year-old woman presented with acute pancreatitis and new-onset QT prolongation with subsequent torsades de pointes. Coronary catheterization was performed and was unremarkable. After persistent QT prolongation, despite temporary atrial pacing, a permanent dual chamber cardioverter defibrillator was implanted. In addition to the QT prolongation, significant depression in the left ventricular function was noted. Both resolved once the pancreatitis abated.

Acute Disease↗
PubMed2000

Bradycardia and the role of beta-blockade in the amelioration of left ventricular dysfunction.

BACKGROUND: It is clear that beta-blockers are effective for treatment of congestive heart failure, but their mechanism of action remains controversial. Hypothesized mechanisms include normalization of beta-receptor function and myocardial protection from the effects of catecholamines, possibly by the institution of bradycardia. We hypothesized that beta-blockade-induced bradycardia was an important mechanism by which these agents were effective for correction of LV dysfunction. METHODS AND RESULTS: In 2 groups of dogs with mitral regurgitation and LV dysfunction, beta-blockers were instituted. In 1 group that received beta-blockers and pacing (group beta+P), a pacemaker prevented the natural bradycardia that beta-blockers cause. In both groups, substantial LV dysfunction developed. Before beta-blockade, the end-systolic stiffness constant decreased from 3. 5+/-0.1 to 2.7+/-0.2 (P<0.01) at 3 months in group beta+P. A similar reduction occurred in the group that eventually received only beta-blockers (group betaB). In group betaB, end-systolic stiffness improved after 3 months of beta-blockade from 2.9+/-0.2 to 3.5+/-0.4 and was not different from baseline. However, in group beta+P, end-systolic stiffness failed to improve (2.7+/-0.2) after 3 months of mitral regurgitation, and was 2.9+/-0.2 at the end of the studies. The contractile function of cardiocytes isolated from the ventricles at the end of the studies confirmed these in vivo estimates of contractility. CONCLUSIONS: We conclude that institution of bradycardia is a major mechanism by which beta-blockers are effective for restoration of contractile function in a model of LV dysfunction.

Adrenergic beta-Antagonists↗
PubMed1994

Reduced peak aerobic capacity in asymptomatic left ventricular systolic dysfunction. A substudy of the studies of left ventricular dysfunction (SOLVD). SOLVD Investigator. Studies of Left Ventricular Dysfunction.

BACKGROUND: Peak oxygen consumption is reduced in patients with symptomatic congestive heart failure, but functional capacity of patients with asymptomatic left ventricular systolic dysfunction has not been assessed by measurement of peak oxygen consumption attained during graded exercise testing. METHODS AND RESULTS: Peak oxygen consumption, that is, aerobic capacity (VO2, mL/kg per minute), was determined during graded treadmill exercise using the modified Naughton protocol in 40 patients with left ventricular systolic dysfunction (mean ejection fraction ranging from 14% to 35%; mean, 29%) who, while not receiving any cardiac medications, were totally asymptomatic, and in 41 age-matched normal subjects. Peak exercise duration and VO2 were significantly lower in patients with asymptomatic left ventricular systolic dysfunction than in normal subjects (948 +/- 273 versus 1239 +/- 372 seconds, P < .001, and 22.1 +/- 5.9 versus 29.8 +/- 7.7 mL/kg per minute, respectively, P < .001), while asymptomatic patients and normal subjects reached similar respiratory equivalents (1.14 +/- 0.11 versus 1.11 +/- 0.11 [NS]) and level of perceived exertion, using the modified Borg scale (7.4 +/- 2.6 versus 8.1 +/- 1.5 [NS]). Heart rate, systemic blood pressure, and oxygen pulse response to peak exercise were significantly lower in asymptomatic patients than in normal subjects. CONCLUSIONS: Although patients with left ventricular systolic dysfunction can be totally asymptomatic in their daily activities, they have experienced a substantial reduction in peak aerobic capacity when compared with normal subjects of similar age.

Aged↗
PubMed2001

Ventricular dysfunction after cardioplegic arrest is improved after myocardial gene transfer of a beta-adrenergic receptor kinase inhibitor.

BACKGROUND: Acute cardiac contractile dysfunction is common after cardiopulmonary bypass (CPB). A potential molecular mechanism is enhanced beta-adrenergic receptor kinase (betaARK1) activity, because beta-adrenergic receptor (betaAR) signaling is altered in cardiomyocytes after cardioplegia. Therefore, we examined whether adenovirus-mediated intracoronary delivery of a betaARK1 inhibitor (Adv-betaARKct) could prevent post-CPB dysfunction. METHODS AND RESULTS: Rabbits were randomized to receive 5x10(11) total viral particles of Adv-betaARKct or PBS. After 5 days, hearts were arrested with University of Wisconsin solution, excised, and stored at 4 degrees C for 15 minutes or 4 hours before reperfusion on a Langendorff apparatus. Left ventricular (LV) function measured by end-diastolic pressure response to preload augmentation, contractility (LV dP/dt(max)), and relaxation (LV dP/dt(min)) was assessed by use of increasing doses of isoproterenol and compared with a control group of nonarrested hearts acutely perfused on the Langendorff apparatus. In the PBS-treated hearts, LV function decreased in a temporal manner and was significantly impaired compared with control hearts after 4 hours of cardioplegic arrest. LV function in Adv-betaARKct-treated hearts, however, was significantly enhanced compared with PBS treatment and was similar to control nonarrested hearts even after 4 hours of cardioplegia. Biochemically, several aspects of betaAR signaling were dysfunctional in PBS-treated hearts, whereas they were normalized in betaARKct-overexpressing hearts. CONCLUSIONS: Myocardial gene transfer of Adv-betaARKct stabilizes betaAR signaling and prevents LV dysfunction induced by prolonged cardioplegic arrest. Thus, betaARK1 inhibition may represent a novel target in limiting depressed ventricular function after CPB.

Adenoviridae↗