			Home About us Contact

LV Contractility (lv + contractility)

Distribution by Scientific Domains

Medical Sciences	60%
Life Sciences	40%

Selected Abstracts

Validation of a New Noninvasive Device for the Monitoring of Peak Endocardial Acceleration in Pigs: Implications for Optimization of Pacing Site and Configuration

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008
PIERRE BORDACHAR M.D.
Introduction: The peak of endocardial acceleration (PEA) is an index of myocardial contractility. We aimed to (1) demonstrate that the PEA measured by the noninvasive cutaneous precordial application of an accelerometer sensor is related to left ventricular (LV) dP/dt max and (2) assess the usefulness of PEA monitoring during graded ischemia and during different configurations of sequential biventricular pacing. Methods and Results: Measurements of invasive LV dP/dt max were compared with measurements of transcutaneous PEA in seven pigs at baseline and during acute drug infusions; increased heart rate; right, left, biventricular and sequential biventricular pacing before and after graded ischemia induced by the constriction of the left anterior descending coronary artery. A consistent PEA signal was obtained in all animals. PEA changes were highly related to LV dP/dt max changes (r= 0.93; P < 0.001). The changes of LV contractility induced by the different pacing configurations were detected by PEA analysis in the absence of ischemia (r= 0.94; P < 0.001) and in the presence of ischemic LV dysfunction (r= 0.91; P < 0.001). Conclusion: Noninvasive PEA measurement allows monitoring of left ventricular contractility and may be a useful tool to detect global effect of ventricular ischemia and to optimize the choice of both pacing site and pacing configuration. [source]

Prolonged strenuous exercise alters the cardiovascular response to dobutamine stimulation in male athletes

THE JOURNAL OF PHYSIOLOGY, Issue 1 2005
Robert C. Welsh
Prolonged strenuous exercise has been associated with transient impairment in left ventricular (LV) systolic and diastolic function that has been termed ,cardiac fatigue'. It has been postulated that cardiac ,-adrenoreceptor desensitization may play a central role; however, data are limited. Accordingly, we assessed the cardiovascular response to progressive dobutamine stimulation after prolonged strenuous exercise (2 km swim, 90 km bike, 21 km run). Nine experienced male athletes were studied: PRE (2,3 days before), POST (after) and REC (1,2 days later). The cardiovascular response to progressive continuous dobutamine stimulation (0, 5, 20, and 40 ,g kg,1 min,1) was assessed, including heart rate (HR), systolic blood pressure (SBP), LV cavity areas (two-dimensional echocardiography) and contractility (end-systolic elastance, SBP/end-systolic cavity area (ESCA)). POST there was limited evidence of myocardial necrosis (measured by troponin I), while catecholamines were elevated. HR was higher POST (mean ±s.d.; PRE, 58 ± 9; POST, 79 ± 9; REC, 57 ± 7 beats min,1; P < 0.05), while SBP was lower (PRE, 127 ± 15; POST, 116 ± 9; REC, 121 ± 12 mmHg; P < 0.05). A blunted HR, SBP and LV contractility (SBP/ESCA; PRE 29 ± 6 versus POST 20 ± 6 mmHg cm,2; P < 0.05) response to dobutamine was demonstrated POST, with values returning towards baseline in REC. Following prolonged strenuous exercise, the chronotropic and inotropic response to dobutamine stimulation is blunted. This study supports the hypothesis that beta-receptor downregulation and/or desensitization may play a major role in prolonged-strenuous-exercise-mediated cardiac fatigue. [source]

Coenzyme Q10 improves contractility of dysfunctional myocardium in chronic heart failure

BIOFACTORS, Issue 1-4 2005
Romualdo Belardinelli
Abstract Background: There is evidence that plasma CoQ10 levels decrease in patients with advanced chronic heart failure (CHF). Objective: To investigate whether oral CoQ10 supplementation could improve cardiocirculatory efficiency in patients with CHF. Methods: We studied 21 patients in NYHA class II and III (18M, 3W, mean age 59 ±9 years) with stable CHF secondary to ischemic heart disease (ejection fraction 37 ± 7%), using a double-blind, placebo-controlled cross-over design. Patients were assigned to oral CoQ10 (100 mg tid) and to placebo for 4 weeks, respectively. Results: CoQ10 supplementation resulted in a threefold increase in plasma CoQ10 level (P<0.0001 vs placebo). Systolic wall thickening score index (SWTI) was improved both at rest and peak dobutamine stress echo after CoQ10 supplementation (+12.1 and 15.6%, respectively, P<0.05 vs placebo). Left ventricular ejection fraction improved significantly also at peak dobutamine (15% from study entry P<0.0001) in relation to a decrease in LV end-systolic volume index (from 57 ± 7 mL/m2 to 45 mL/m2, P<0.001). Improvement in the contractile response was more evident among initially akinetic (+33%) and hypokinetic (+25%) segments than dyskinetic ones (+6%). Improvement in SWTI was correlated with changes in plasma CoQ10 levels (r=,0.52, P<0.005). Peak VO2 was also improved after CoQ10 as compared with placebo (+13%, <0.005). No side effects were reported with CoQ10. Conclusions: Oral CoQ10 improves LV contractility in CHF without any side effects. This improvement is associated with an enhanced functional capacity. [source]

Cardioprotective Effects of Angiotensin II Type 1 Receptor Blockade with Olmesartan on Reperfusion Injury in a Rat Myocardial Ischemia-Reperfusion Model

CARDIOVASCULAR THERAPEUTICS, Issue 1 2010
Wangde Dai
We determined the effects of olmesartan on infarct size and cardiac function in a rat ischemia/reperfusion model. Rats underwent 30 min of left coronary artery (CA) occlusion followed by 2 h of reperfusion. In protocol 1, the rats received (by i.v.) 1 mL of vehicle at 10 min after CA occlusion (Group 1, n = 15); olmesartan (0.3 mg/kg) at 10 min after CA occlusion (Group 2, n = 15); 1 mL of vehicle at 5 min before CA reperfusion (Group 3, n = 15); or olmesartan (0.3 mg/kg) 5 min before CA reperfusion (Group 4, n = 15). In protocol 2, the rats received (by i.v.) 1 mL of vehicle at 5 min before CA reperfusion (Group 5, n = 21); or olmesartan (3 mg/kg) at 5 min before CA reperfusion (Group 6, n = 21). Systemic hemodynamics, left ventricular (LV) function, LV ischemic risk zone, no-reflow zone, and infarct size were determined. In protocol 1, olmesartan (0.3 mg/kg) did not affect blood pressure (BP), heart rate, LV ± dp/dt or LV fractional shortening during the experimental procedure, and did not alter no-reflow or infarct size. In protocol 2, olmesartan (3 mg/kg) significantly reduced infarct size to 21.7 ± 4.1% from 34.3 ± 4.1% of risk zone in the vehicle group (P= 0.035), but did not alter the no-reflow size. Prior to CA reperfusion, olmesartan (3 mg/kg) significantly reduced mean BP by 22% and LV ±dp/dt, but did not affect heart rate. At 2 h after reperfusion, olmesartan significantly decreased heart rate by 21%, mean BP by 14%, and significantly increased LV fractional shortening from 54.1 ± 1.4% to 61.3 ± 1.6% (P= 0.0018). Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects. [source]

Cardiovascular changes induced by cold water immersion during hyperbaric hyperoxic exposure

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2007
Alain Boussuges
Summary The present study was designed to assess the cardiac changes induced by cold water immersion compared with dry conditions during a prolonged hyperbaric and hyperoxic exposure (ambient pressure between 1·6 and 3 ATA and PiO2 between 1·2 and 2·8 ATA). Ten healthy volunteers were studied during a 6 h compression in a hyperbaric chamber with immersion up to the neck in cold water while wearing wet suits. Results were compared with measurements obtained in dry conditions. Echocardiography and Doppler examinations were performed after 15 min and 5 h. Stroke volume, left atrial and left ventricular (LV) diameters remained unchanged during immersion, whereas they significantly fell during the dry session. As an index of LV contractility, percentage fractional shortening remained unchanged, in contrast to a decrease during dry experiment. Heart rate (HR) significantly decreased after 5 h, although it had not changed during the dry session. The changes in the total arterial compliance were similar during the immersed and dry sessions, with a significant decrease after 5 h. In immersed and dry conditions, cardiac output was unchanged after 15 min but decreased by almost 20% after 5 h. This decrease was related to a decrease in HR during immersion and to a decrease in stroke volume in dry conditions. The hydrostatic pressure exerted by water immersion on the systemic vessels could explain these differences. Indeed, the redistribution of blood volume towards the compliant thoracic bed may conceal a part of hypovolaemia that developed in the course of the session. [source]