Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Systolic 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 325 records · Page 18Linked to original sources
PubMed1996

Effects of aging on neuroendocrine activation in subjects and patients in the presence and absence of heart failure with left ventricular systolic dysfunction.

The neuroendocrine profile and echocardiographic features of 40 patients (81 +/- 1 years, means +/- standard error) with heart failure and impaired left ventricular systolic function were compared with those of an age-matched group of healthy subjects, 20 younger patients with heart failure (aged 58 +/- 1 years) and 15 younger healthy subjects. Normal elderly subjects had a neuroendocrine profile similar to that of healthy younger subjects apart from elevated plasma norepinephrine (958 +/- 84 vs 302 +/- 118 pg/ml; p< 0.001) and atrial natriuretic peptide ( 40 +/- 6 vs 28 +/- 5 pg/ml; p<0.05). Despite a similar severity of heart failure, elderly patients had smaller ventricular dimensions (left ventricular internal dimension in diastole 51 +/- 2 vs 69 +/- 3 mm;p<0.0001 and greater impairment of ventricular compliance using Doppler indexes. Plasma norepinephrine was higher (1,191 +/- 80 vs 620 +/- 67 ppg/ml; p<0.01), and plasma atrial natriuretic peptide, plasma active renin, and angiotensin II were lower in elderly patients than in the younger patients with heart failure. As functional capacity declines with age, elderly patients may have less severe cardiac dysfunction for any given level of functional impairment, and this may account for most of the differences in neuroendocrine activity with age. Age appears to be an important determinant of plasma norepinephrine and may be a confounding factor in interpreting the prognostic significance of this hormone.

Aged↗
PubMed2006

Role of regional mechanical dyssynchrony as a determinant of functional mitral regurgitation in patients with left ventricular systolic dysfunction.

OBJECTIVE: To assess regional mechanical dyssynchrony as a determinant of the degree of functional mitral regurgitation (FMR). SETTING: Tertiary cardiology clinic. PATIENTS: 74 consecutive patients with left ventricular (LV) dysfunction (ejection fraction < 40%, mean 32.2 (SD 7.3)%) were evaluated. METHODS: Effective regurgitant orifice (ERO) area, indices of mitral deformation (systolic valvular tenting, mitral annular contraction) and of global LV function and remodelling (ejection fraction, end systolic volume, sphericity index) and local remodelling (papillary-fibrosa distance, regional wall motion score index), and tissue Doppler-derived dyssynchrony index (DI) (regional DI, defined as the standard deviation of time to peak myocardial systolic contraction of eight LV segments supporting the papillary muscles attachment) were measured. RESULTS: All the assessed variables correlated significantly with ERO. By multivariate analysis, systolic valvular tenting was the strongest independent predictor of ERO (R(2) = 0.77, p = 0.0001), with a minor influence of papillary-fibrosa distance (R(2) = 0.77, p = 0.01) and regional DI (R(2) = 0.77, p = 0.03). Local LV remodelling (regional wall motion score index: R(2) = 0.58, p = 0.001; papillary-fibrosa distance: R(2) = 0.58, p = 0.002) and global remodelling indices (sphericity index: R(2) = 0.58, p = 0.003) were the main determinants of systolic valvular tenting, whereas regional DI did not enter into the model. Regional DI was an independent predictor of ERO (R(2) = 0.56, p = 0.005) in patients with non-ischaemic LV dysfunction but not in patients with ischaemic LV dysfunction when these groups were analysed separately. CONCLUSIONS: The degree of FMR is associated mainly with mitral deformation indices. The regional dyssynchrony also has an independent association with ERO but with a minor influence; however, it is not a determinant of FMR in patients with ischaemic LV dysfunction.

Cardiac Output↗
PubMed2002

Contribution of exercise-induced mitral regurgitation to exercise stroke volume and exercise capacity in patients with left ventricular systolic dysfunction.

BACKGROUND: Functional mitral regurgitation (MR) is common in patients with heart failure and left ventricular (LV) dysfunction, and its severity may vary over time, depending primarily on the loading conditions. Because dynamic changes in the severity of functional MR may affect forward stroke volume, we hypothesized that exercise-induced changes in MR severity influence the stroke volume response of patients with LV dysfunction to exercise, and hence their exercise capacity. METHODS AND RESULTS: Heart failure patients (n=25; mean age 53+/-12 years) with LV dysfunction underwent dynamic bicycle exercise at steady-state levels of 30%, 60%, and 90% of predetermined peak VO2. During each exercise level, right heart pressures, cardiac output, VO2, and MR severity were measured simultaneously. During exercise, MR severity, as evaluated by the ratio of MR jet over left atrium area, increased from 15+/-8% to 33+/-15%. Peak VO2, exercise-induced changes in stroke volume, and those in capillary wedge pressure correlated with the changes in MR (r=-0.55, -0.87, and 0.62, respectively, P<0.01). The changes in MR severity also correlated with those in end-diastolic (r=-0.75, P<0.01) and end-systolic (r=-0.72, P<0.01) sphericity indexes and those in the coaptation distance (r=0.86, P<0.01). CONCLUSIONS: Our data indicate that in patients with LV dysfunction, exercise-induced changes in MR severity limit the stroke volume adaptation during exercise and therefore contribute to limitation of exercise capacity.

Adult↗
PubMed2004

Relationship of systolic dysfunction to area at risk and infarction size after ischemia-reperfusion in mice.

Whereas the extent of wall-motion abnormality (WMA) correlates well with the area at risk (AAR) and infarction size in murine models of nonreperfused myocardial infarction, this relationship is less clear in the setting of ischemia-reperfusion injury. Echocardiography was performed in mice at baseline, after left anterior descending coronary artery ligation (30 minutes) followed by reperfusion (24 hours), and after religation of the left anterior descending coronary artery. The extent of WMA before and after religation was compared with the initial infarction size measured by triphenyltetrazolium chloride and the AAR measured by fluorescent microspheres, respectively. Echocardiography showed left ventricular dilation and dysfunction after ischemia and reperfusion. WMA after religation correlated well with AAR (r2 = 0.70, P <.0001). The correlation between WMA and infarction size was incomplete (r2 = 0.59, P <.0002) in part because of underestimation of nontransmural infarcts. Echocardiography can reliably assess AAR after ischemia-reperfusion in mice; however, it does not allow for precise quantification of the small areas of necrosis that often occur in this setting.

Animals↗
PubMed2004

[Comparison of eprosartan and captopril in left ventricular systolic dysfunction: relation of efficacy to myocardial viability].

Patients with left ventricular ejection fraction below 45% (mean 39+/-3.7%) were randomized either to captopril (n=33) or eprosartan after miocardial infarction (n=33) on days 3-7 of myocardial infarction. All patients were subjected to echocardiography and 40 to perfusion myocardial scintigraphy with (99m)TC-Technetril. Myocardial viability was defined as presence of perfusion reserve in dysfunctional segments during test with nitroglycerin. Dysfunctional myocardium was found to be viable in 62.5% of patients. Fifty six patients completed 3 months follow up and were restudied. By the time of the second study 28 patients continued captopril (37.5-150 mg, average dose 72+/-34.2 mg/day) and 28 - eprosartan (300-600 mg, average dose 471+/-151 mg/day). Captopril was stopped or its dose corrected in 28% of patients. In eprosartan group there were no side effects which required withdrawal of the drug. Similar increases of ejection fraction occurred on both groups (from 38+/-2.1 to 49+/-6.7%, p<0.001 and from 39+/-4 to 51+/-6.5%, p<0.001, in eprosartan and captopril groups, respectively). Magnitude of left ventricular ejection fraction change did not depend on the presence of viable myocardium. However in both treatment groups improvement of myocardial perfusion and decrease of left atrial dimensions were found only in patients with viable myocardium at initial study.

Acrylates↗
PubMed2005

Prevalence of echocardiographically detected ventricular asynchrony in patients with left ventricular systolic dysfunction.

OBJECTIVES: QRS complex width is not an accurate marker of cardiac asynchrony. Our aims were to determine the prevalence of cardiac asynchrony by Doppler echocardiography for patients with left ventricular (LV) dysfunction and to evaluate whether QRS width is a reliable method for detecting asynchrony. METHODS: In all, 316 consecutive patients with a LV ejection fraction less than 40% from 13 hospitals comprised the study group. Interventricular asynchrony was defined by the interventricular mechanical delay. Intraventricular asynchrony was evaluated using the calculation of the septal-to-posterior wall motion delay, the difference between time from Q wave to LV ejection end, and time from Q wave to the end of the systolic wave of the most delayed basal segment by Doppler tissue imaging, the SD of the time from the Q wave to the end of the systolic wave of 4 basal segments, and the maximum difference in the time from the Q wave to the end of the systolic wave of all 4 basal segments. RESULTS: Mean age was 62.14 +/- 13.5 years (234 men; 74.1%). Interventricular asynchrony was present in 50 (26.2%) patients in the narrow QRS group and in 57 (55.3%) patients in the prolonged QRS group (P < .001). Intraventricular asynchrony was present in 40 (20.8%) to 136 (72.8%) patients in the narrow QRS group and in 27 (26.2%) to 82 (79.6%) in the prolonged QRS group, depending on the method used. CONCLUSIONS: Cardiac asynchrony is highly prevalent for patients with LV dysfunction but there is a very poor agreement among the different methods used to detect it. Interventricular asynchrony is more prevalent for patients with prolonged QRS but intraventricular asynchrony is irrespective of the QRS duration. Further studies are needed to evaluate which method is the best to detect cardiac resynchronization therapy responders.

Adult↗
PubMed2005

Combined use of amino terminal-pro-brain natriuretic peptide levels and QRS duration to predict left ventricular systolic dysfunction in patients with dyspnea.

The combination of elevated amino-terminal pro-brain natriuretic peptide levels and wide QRS duration was highly sensitive and specific for the prediction of impaired left ventricular systolic function among a group of patients presenting with dyspnea to the emergency department. This strategy can be used to predict depressed function and target more formal evaluation with echocardiography in patients with dyspnea.

Age Factors↗
PubMed2004

Mortality and morbidity reduction with Candesartan in patients with chronic heart failure and left ventricular systolic dysfunction: results of the CHARM low-left ventricular ejection fraction trials.

BACKGROUND: Patients with symptomatic chronic heart failure (CHF) and reduced left ventricular ejection fraction (LVEF) have a high risk of death and hospitalization for CHF deterioration despite therapies with angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, and even an aldosterone antagonist. To determine whether the angiotensin-receptor blocker (ARB) candesartan decreases cardiovascular mortality, morbidity, and all-cause mortality in patients with CHF and depressed LVEF, a prespecified analysis of the combined Candesartan in Heart Failure Assessment of Reduction in Mortality and morbidity (CHARM) low LVEF trials was performed. CHARM is a randomized, double-blind, placebo-controlled, multicenter, international trial program. METHODS AND RESULTS: New York Heart Association (NYHA) class II through IV CHF patients with an LVEF of < or =40% were randomized to candesartan or placebo in 2 complementary parallel trials (CHARM-Alternative, for patients who cannot tolerate ACE inhibitors, and CHARM-Added, for patients who were receiving ACE inhibitors). Mortality and morbidity were determined in 4576 low LVEF patients (2289 candesartan and 2287 placebo), titrated as tolerated to a target dose of 32 mg once daily, and observed for 2 to 4 years (median, 40 months). The primary outcome (time to first event by intention to treat) was cardiovascular death or CHF hospitalization for each trial, with all-cause mortality a secondary end point in the pooled analysis of the low LVEF trials. Of the patients in the candesartan group, 817 (35.7%) experienced cardiovascular death or a CHF hospitalization as compared with 944 (41.3%) in the placebo group (HR 0.82; 95% CI 0.74 to 0.90; P<0.001) with reduced risk for both cardiovascular deaths (521 [22.8%] versus 599 [26.2%]; HR 0.84 [95% CI 0.75 to 0.95]; P=0.005) and CHF hospitalizations (516 [22.5%] versus 642 [28.1%]; HR 0.76 [95% CI 0.68 to 0.85]; P<0.001). It is important to note that all-cause mortality also was significantly reduced by candesartan (642 [28.0%] versus 708 [31.0%]; HR 0.88 [95% CI 0.79 to 0.98]; P=0.018). No significant heterogeneity for the beneficial effects of candesartan was found across prespecified and subsequently identified subgroups including treatment with ACE inhibitors, beta-blockers, an aldosterone antagonist, or their combinations. The study drug was discontinued because of adverse effects by 23.1% of patients in the candesartan group and 18.8% in the placebo group; the reasons included increased creatinine (7.1% versus 3.5%), hypotension (4.2% versus 2.1%), and hyperkalemia (2.8% versus 0.5%), respectively (all P<0.001). CONCLUSIONS: Candesartan significantly reduces all-cause mortality, cardiovascular death, and heart failure hospitalizations in patients with CHF and LVEF < or =40% when added to standard therapies including ACE inhibitors, beta-blockers, and an aldosterone antagonist. Routine monitoring of blood pressure, serum creatinine, and serum potassium is warranted.

Aged↗
PubMed2003

Contrast-enhanced Doppler hemodynamics for noninvasive assessment of patients with chronic heart failure and left ventricular systolic dysfunction.

We sought to evaluate whether contrast-enhanced Doppler echocardiography can improve the noninvasive estimation of hemodynamic variables in left ventricular (LV) dysfunction. Right-heart catheterization and Doppler echocardiography were simultaneously performed in 45 patients with LV dysfunction (ejection fraction: 29 +/- 7%) in sinus rhythm. Noninvasive variables were estimated as follows: cardiac output by pulsed Doppler of LV outflow tract; pulmonary capillary wedge pressure by a regression equation including mitral and pulmonary venous flow variables; pulmonary artery mean pressure from the calculated systolic and diastolic pulmonary artery pressures; and pulmonary vascular resistance from the previous measurements according to hemodynamic definition. Contrast enhancement increased the feasibility of pulmonary capillary wedge pressure estimation from 60% to 100%; of pulmonary artery mean pressure from 42% to 91%; and of pulmonary vascular resistance from 42% to 91%. Strong correlations between invasive and noninvasive hemodynamic variables were found: r = 0.90, standard error of the estimate (SEE) 0.45 L/min for cardiac output; r = 0.90, SEE 3.1 mm Hg for pulmonary capillary wedge pressure; r = 0.93, SEE 3.7 mm Hg for pulmonary artery mean pressure; and r = 0.85 SEE 1.0 Wood units for pulmonary vascular resistance. Weaker correlations for PAMP (r = 0.82, SEE 5.6 mm Hg) and PVR (r = 0.66, SEE 1.7 Wood units) were apparent prior to contrast enhancement. When patients were separated according to PVR threshold values, the contrast allowed the correct placement of 88% of patients, whereas only 57% were correctly assigned without it. The contrast increased accuracy and reduced interobserver variability in the evaluation of hemodynamic variables. The contrast-enhanced study is capable of increasing the value of noninvasive hemodynamic assessment in LV dysfunction.

Adult↗
PubMed1994

Prevalence of left ventricular systolic dysfunction in Duchenne muscular dystrophy: an echocardiographic study.

The prevalence and hemodynamic consequences of regional wall motion abnormalities (RWMA) were evaluated in 84 advanced-stage Duchenne muscular dystrophy (DMD) patients who underwent echocardiographic and systolic time interval (STI) examination. A satisfactory echocardiogram was obtained in 72 patients who were divided into two groups: group I (33 patients) had normal wall motion or minor changes, and group II (39 patients) had akinetic and/or dyskinetic areas. In group II, 15 patients had ventricular dilation; 8 of the 15 had a history of cardiac failure and 4 died during the study. Wall motion index (WMI), end-diastolic volume (EDV), and STI values increased significantly from group I to group II. In the whole group, a strong correlation was found between WMI and STI ratios. This study demonstrates a high prevalence of RWMA and supports the viewpoint that RWMA, consequences of the myopathic process, result in progressive left ventricular dilation, heart failure, and cardiac death.

Adolescent↗
PubMed1993

Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction.

Previous investigators have hypothesized that myocardial "stunning" may result either from a primary impairment in excitation or from electromechanical dissociation. Thrombolytic therapy and angioplasty have increased the importance of understanding the electrophysiologic effects of brief ischemia followed by reperfusion. We investigated the electrophysiologic properties of mechanically dysfunctional stunned myocardium in 18 dogs anesthetized with pentobarbital (30 mg/kg, intravenously administered). After thoracotomy, the proximal anterior descending coronary artery was occluded for 15 minutes, which was followed by 20 minutes of reperfusion. At baseline, peak ischemia, and 20 minutes of reperfusion, local electrogram durations, activation times, and refractory periods were measured from 12 standardized sites within the ischemic and border zones. Echocardiographic percentage of systolic wall thickening confirmed normal preischemic and markedly reduced postischemic function in the investigated region. Despite the marked electrophysiologic abnormalities observed in the ischemic zone during ischemia, mean electrogram duration, calculated conduction velocity, and mean effective refractory period after 20 minutes of reperfusion had returned almost to baseline values 39.2 +/- 11.5 msec versus 37.2 +/- 12.1 msec, 0.65 +/- 0.15 m/sec versus 0.68 +/- 0.15 m/sec, and 134 +/- 14 msec versus 131 +/- 8 msec, respectively. Corresponding mean values within the ischemic border zone were similarly close to baseline values after reperfusion. There was no significant difference in local heterogeneity (coefficient of variation) within the ischemic or border zone after reperfusion versus baseline values. Although the postischemic electrophysiologic status returned to normal, systolic thinning and dyskinesis persisted in the region of measurement. The contractile dysfunction that results from reperfusion-induced injury can thus occur in the setting of apparent excitation-contraction uncoupling.

Analysis of Variance↗
PubMed2004

[Clinical outcome and reversibility of systolic dysfunction in patients with dilated cardiomyopathy due to hypertension and chronic heart failure].

INTRODUCTION AND OBJECTIVES: There is little information on the clinical and functional course of patients with heart failure secondary to dilated cardiomyopathy due to hypertension. The objectives of our study were to assess the clinical and functional course of these patients, and to identify possible predictors of prognosis. PATIENTS AND METHOD: We evaluated a series of 49 patients with this condition diagnosed in our hospital from 1994 to 2003. Mean age was 63(11) years, and 40% were women. Left ventricular ejection fraction was 30.1(4.8)%. Follow-up was 45(23) months (median, 41 months). RESULTS: Four-year survival was 0.84, the 4-year rate of hospitalization due to heart failure was 0.12, and likelihood of readmission-free survival was 0.80 at 4 years. Left ventricular ejection fraction increased from 30.1(4.8)% to 57.6(13.5)% (P< .001). An unfavorable clinical and functional outcome at 4 years (death, readmission for heart failure or persistence of dilated cardiomyopathy) was recorded in only in 40% of the patients. Multivariate analysis with the Cox model showed appropriate control of blood pressure to be the only independent predictor of a favorable clinical outcome (absence of death or readmission for heart failure) (hazard ratio = 4.58; 95% CI, 1.32-9.83; P=.032). CONCLUSIONS: The course of patients with severe dilated cardiomyopathy due to hypertension was favorable in 60% of cases. Adequate control of blood pressure was the only independent predictor of a favorable clinical outcome.

Cardiomyopathy, Dilated↗
PubMed2004

Elucidating the B bump on the mitral valve M-mode echogram in patients with severe left ventricular systolic dysfunction.

BACKGROUND: The B bump on mitral valve M-mode echogram is predictive of significant elevation of left ventricular end-diastolic pressure (LVEDP). However, its pathophysiologic mechanism remains unclear. METHODS: We investigated, by means of Doppler echocardiography, the hemodynamic events that take place at late diastole in left atrium (LA) and left ventricle (LV). The study group consisted of 10 consecutive and strictly selected patients with severe dilated LV dysfunction. The noninvasive validated index used for definition of high LVEDP was the difference between the durations of atrial reverse (AR) wave in pulmonary venous flow (PVF) and atrial (A) wave in mitral flow (MF). Peak velocities of PVF and MF were measured. The time interval from ECG P wave to the end of B bump (P-B) and from P wave to the end of AR (P-AR) were measured and correlated. Mitral diastolic regurgitation (DR) was searched with M-mode color Doppler. RESULTS: All patients presented with restrictive diastolic signs on MF and PVF. The mean value of AR time minus A time was 61+/-12 ms. There was a strong linear correlation between P-B and P-AR (r=0.94, p<0.001). Only five patients had DR. No patient had LV inflow during B bump. CONCLUSIONS: (1) Mitral B bump is essentially a late diastolic phenomenon in which the leaflets keep a semi-open position without LV inflow effectiveness. (2) The resultant LA pressure which prolongates the duration of AR wave beyond A wave, analogously work over mitral leaflets, pushing them toward LV generating the bump. (3) DR is caused by LVEDP higher than LA pressure and coexists with B bump without a cause-effect relationship.

Adolescent↗