Contractility In Patients Research Articles

Microvascular Endothelial Dysfunction and Enhanced Thromboxane and Endothelial Contractility in Patients with HIV

The prevalence of cardiovascular disease is increased with human immunodeficiency virus (HIV) infection, but the mechanism is unclear. We hypothesized that HIV increases microvascular reactive oxygen species, thereby impairing endothelial function and enhancing contractility. Subcutaneous microarterioles were isolated from gluteal skin biopsies in premenopausal, African American, HIV positive women receiving effective anti-retroviral therapy, but without cardiovascular risk factors except for increased body mass index (n=10) and healthy matched controls (n=10). The arterioles were mounted on myographs, preconstricted and relaxed with acetylcholine for: endothelium-dependent relaxation, endothelium-dependent relaxation factor (nitric oxide synthase-dependent relaxation), endothelium-dependent hyperpolarizing factor (potassium-channel dependent relaxation) and endothelium-independent relaxation (nitroprusside). Contractions were tested to endothelium-dependent contracting factor (acetylcholine contraction with blocked relaxation); phenylephrine, U-46,619 and endothelin-1. Plasma L-arginine and asymmetric dimethylarginine were measured by high performance capillary electrophoresis. The micro-arterioles from HIV positive women had significantly (% change in tension; P<0.05) reduced acetylcholine relaxation (-51 ± 6 vs. -78 ± 3%), endothelium-dependent relaxation factor (-28 ± 4 vs. -39 ± 3%), endothelium-dependent hyperpolarizing factor (-17 ± 4 vs. -37 ± 4%) and decreased nitric oxide activity (0.16 ± 0.03 vs. 0.70 ± 0.16 Δ unit) but unchanged nitroprusside relaxation. They had significantly enhanced endothelium-dependent contracting factor (+21 ± 6 vs. +7 ± 2%) and contractions to U-46,619 (+164 ± 10 vs. +117 ± 11%) and endothelin-1(+151 ± 12 vs. +97 ± 9%), but not to phenylephrine. There was enhanced reactive oxygen species with acetylcholine (0.11 ± 0.02 vs. 0.05 ± 0.01 Δ unit; P<0.05) and endothelin-1 (0.31 ± 0.06 vs. 0.10 ± 0.02 Δ unit; P<0.05). Plasma L-arginine: assymetric dimethyl arginine rates was reduced (173 ± 12 vs. 231 ± 6 μmol·μmol-1, P<0.05). Premenopausal HIV positive womenhad microvascular oxidative stress with severe endothelial dysfunction and reduced nitric oxide and arginine: assymetric dimethylarginine ratio but enhanced endothelial, thromboxane and endothelin contractions. These microvascular changes may herald later cardiovascular disease.

Recurrent orthostatic syncope due to left atrial and left ventricular collapse after a continuous-flow left ventricular assist device implantation

Left ventricular assist devices (LVADs) have become an established treatment for patients with advanced heart failure as a bridge to transplantation or for permanent support as an alternative to heart transplantation. Continuous-flow LVADs have been shown to improve outcomes, including survival, and reduce device failure compared with pulsatile devices. Although LVADs have been shown to be a good option for patients with end-stage heart failure, unanticipated complications may occur. We describe dynamic left atrial and left ventricular chamber collapse related to postural changes in a patient with a recent continuous-flow LVAD implantation.

Effect of levosimendan on pulmonary artery pressure in patients with pulmonary hypertension undergoing mitral valve replacement

Objective To investigate the effect of levosimendan on pulmonary artery pressure in patients with pulmonary hypertension undergoing mitral valve replacement.Methods Twenty-four ASA Ⅱ or Ⅲ and NY-HA class Ⅱ or Ⅲ patients,aged 35-60 yr,with mean pulmonary artery pressure (MPAP) ＞ 30 mm Hg,undergoing mitral valve replacement were randomly divided into 2 groups (n =12 each):control group (group C) and levosimendan group (group L).In group L,a loading dose of levosimendan 24 μg/kg was injected intravenously after aortic unclamping,followed by infusion of levosimendan at a rate of 0.2 μg· kg-1 · min-1 until 1 d after operation.Group C received the equal volume of normal saline.HR,MAP,MPAP,pulmonary capillary wedge pressure (PCWP),cardiac index (CI) were recorded at 5 min after induction (T0),at the end of CPB (T1) and at 1 h after operation (T2),and the pulmonary vascular resistance (PVR) and rate-pressure product (RPP) were calculated.The improvement in pulmonary hypertension was recorded.Results PCWP was significantly lower and CI higher at T1,2 in both groups,and HR was significantly higher at T1,2 and MPAP lower at T2 in group C,and MPAP and PVR were significantly lower at T1,2 in group L than at T0 (P ＜ 0.05).HR,MPAP and PVR were significantly lower and CI was significantly higher at T1,2,RPP was significantly lower at T2 and the improvement in pulmonary hypertension was higher in group L than in group C (P ＜ 0.05).Conclusion Levosimendan can improve pulmonary hypertension without increasing the myocardial oxygen consumption and with a significant increase in myocardial contractility in patients with pulmonary hypertension undergoing mitral valve replacement. Key words: Cardiotonic agents; Pyridazines; Heart valve prosthesis implantation; Mitral valve; Hypertension, pulmonary

Inhibition of uterine contractility with various tocolytics with and without progesterone: in vitro studies

Various tocolytics are used to suppress uterine contractility in patients in preterm labor. Progesterone (P4) is used in patients at high risk for preterm delivery. In this study, we evaluated the effects of various tocolytics with and without P4 to examine effects on uterine contractility. Uterine tissues (n = 280) from women undergoing cesarean at term were exposed in vitro to various agents (vehicle, magnesium sulfate [MgSO(4)], nifedipine, indomethacin, or pinacidil-all with and without P4). Contractility was measured before and after addition of the various agents. P4 alone at 10(-5) mol/L concentration has little effect to inhibit contractility (P ≥ .05). MgSO(4) (2-8 × 10(-3) mol/L) inhibits uterine contractility (P < .05) but there is no change when combined with P4 (P > .05). Nifedipine (10(-8) mol/L) and indomethacin (10(-5) mol/L) inhibit contractions alone (P < .05) and to a greater extent when combined with P4 (P < .05). P4 significantly (P < .05) reduced the effects of pinacidil (10(-6.5) mol/L). Combinations of P4 with nifedipine or indomethacin, but not MgSO(4), might be used to effectively suppress preterm labor.

Stress induced hypertensive response: should it be evaluated more carefully?

Various diagnostic methods have been used to evaluate hypertensive patients under physical and pharmacological stress. Several studies have shown that exercise hypertension has an independent, adverse impact on outcome; however, other prognostic studies have shown that exercise hypertension is a favorable prognostic indicator and associated with good outcome. Exercise hypertension may be encountered as a warning signal of hypertension at rest and future hypertensive left ventricular hypertrophy. The results of diagnostic stress tests support that hypertensive response to exercise is frequently associated with high rate-pressure product in hypertensives. In addition to the observations on high rate-pressure product and enhanced ventricular contractility in patients with hypertension, evaluation of myocardial contractility by Doppler tissue imaging has shown hyperdynamic myocardial function under pharmacological stress. These recent quantitative data in hypertensives suggest that hyperdynamic myocardial function and high rate-pressure product response to stress may be related to exaggerated hypertension, which may have more importance than that it has been already given in clinical practice.

Biventricular pacing in patients with Tetralogy of Fallot: Non-invasive epicardial mapping and clinical impact

IntroductionPatients who have undergone repair of Tetralogy of Fallot (TOF) often present with right bundle branch block. Cardiac resynchronization therapy (CRT) with right ventricular (RV) or biventricular (BiV) stimulation has been proposed as a modality to correct electrical abnormalities and improve cardiac contractility in patients with repaired TOF. We aimed to 1) compare ventricular electrical activation in adults with repaired TOF during RV versus BiV stimulation, using a non-invasive epicardial mapping system, and 2) examine the clinical mid-term effects of BiV resynchronization. Methods9 adults with repaired TOF were implanted with a CRT system and underwent 1) a non-invasive epicardial mapping (n=9) during sinus intrinsic rhythm, RV and BiV pacing 2) a clinical evaluation (n=7) before and after 6months CRT with assessment of NYHA class and exercise capacity. ResultsDuring intrinsic rhythm, non-invasive mapping demonstrated delayed activation of the right compared with the left ventricle in all patients, with the greatest activation delay noted near the infundibulum. However, we observed important differences among patients, in the severity of activation delays. Global activation time and an index of dyssynchrony were improved (p<0.05) during BiV pacing compared with RV pacing and spontaneous rhythm. BiV pacing increased (p<0.05) exercise tolerance and lowered the mean NYHA functional class at 6months of follow up. ConclusionPatients with corrected TOF present with different patterns of ventricular activation. RV stimulation modestly improved RV activation sequence and was associated with a delayed LV activation. Biventricular stimulation significantly decreased right and left ventricular dyssynchrony.

Extrasystolic stimulation with bi-ventricular pacing: an acute haemodynamic evaluation

Cardiac resynchronization therapy (CRT) by means of biventricular pacing (BiVP) is well established as a treatment for patients with heart failure (HF). Post-extrasystolic potentiation, (PESP) which involves a transient increase in myocardial contractility following a ventricular extrasystole, can be achieved using extrasystolic stimulation (ESS). On this basis, ESS has been proposed as a therapeutic. We assessed acute haemodynamic effects of ESS in the context of BiVP. Patients (n = 15, left ventricular ejection fraction < 40%, QRS ≥ 125 ms) with HF, received BiVP in combination with right ventricular (RV) ESS (single stimulus or pulse train). Left ventricular (LV) and peripheral arterial pressures were recorded and dP/dt was monitored. Addition of RV ESS to BiVP pacing led to a 21% increase in maximum (max) dP/dt (P < 0.001) and an 8.5 mm Hg increase in a systolic arterial pressure (P < 0.001). The modest fall in end-diastolic pressure (3.3 mmHg, P < 0.001) observed during ESS and BiVP was prevented by maintaining baseline sinus rate. Varying ESS modes or pacing outputs was not associated with differences in haemodynamic parameters. Biventricular pacing in combination with ESS, with maintenance of sinus rate, improves myocardial contractility in patients undergoing CRT.

Effects of the hypoxic test on left and right ventricular contractility in progressive systemic sclerosis with pulmonary arterial hypertension

The purpose of this investigation was to assess hypoxic test effects on left and right ventricular contractility in patients with progressive systemic sclerosis (PSS) and pulmonary arterial hypertension (PAH). Ten patients (mean age 48.8±13.2 years) who were diagnosed with PSS and PAH were included in the study. All the patients underwent left and right heart catheterization. Right ventricular (RV) contractility was measured according to the method of Ferlinz [1] and left ventricular (LV) contractility according to the method of Kennedy et al. [2] using indirect digital substraction angiography. The mean pulmonary artery pressures (\(\bar P\)PA) and oxygen saturation of the pulmonary artery (SaO2) were registered at each stage of graded hypoxic exposure 14%, 12%, and 10% of O2. Right atrial pressures (PRA,syst, PRA,diast,\(\bar P\)RA), right ventricular pressures (PRV,syst, PRV,diast,\(\bar P\)RV, PRV,end-diast), right and left ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI), cardiac index (CI), ejection fraction (EF), and heart rate (HR) were calculated before and after breathing a hypoxic mixture of 10% of O2 for 30 minutes. The hypoxic test induced significant elevation (p<0.05) of\(\bar P\)PA, PRA,syst, PRA,diast,\(\bar P\)RA, PRV,syst, PRV,end-diast, RV EDVI, LV, EDVI, CI, and HR, whereas, SaO2 decreased significantly after the hypoxic test. These findings suggest that patients with PSS and PAH are characterized by hyperreactivity of pulmonary artery to hypoxia and the preservation of compensatory mechanism of RV and LV contractility.

Relationship between intracardiac impedance and left ventricular contractility in patients undergoing cardiac resynchronization therapy

AimsCardiac resynchronization therapy (CRT) has dramatically improved the symptoms and prognosis of patients with heart failure in large randomized clinical trials. Optimization of device settings may maximize benefit on an individual basis, although the best method for this is not yet established. We evaluated the use of cardiogenic impedance measurements (derived from intracardiac impedance signals) in CRT device optimization, using invasive left ventricular (LV) dP/dtmax as the reference.Methods and resultsSeventeen patients underwent invasive haemodynamic assessment using a pressure wire placed in the LV cavity at the time of CRT device implantation. Intracardiac impedance measurements were made at different atrioventricular (AV) and interventricular (VV) delays and compared with LV dP/dtmax. We assessed the performance of patient-specific and generic impedance-based models in predicting acute haemodynamic response to CRT. In two patients, LV catheterization with the pressure wire was unsuccessful and in two patients LV lead delivery was unsuccessful; therefore, data were acquired for 13 out of 17 patients. Left ventricular dP/dtmax was 919 ± 182 mmHg/s at baseline and this increased acutely (by 24%) to 1121 ± 226 mmHg/s as a result of CRT. The patient-specific impedance-based model correctly predicted the optimal haemodynamic response (to within 5% points) for AV and VV delays in 90 and 92% of patients, respectively.ConclusionCardiogenic impedance measurements are capable of correctly identifying the maximum achievable LV dP/dtmax as measured by invasive haemodynamic assessment. This study suggests that cardiogenic impedance can potentially be used for CRT optimization and may have a role in ambulatory assessment of haemodynamics.

Attenuation of Stress-based Ventricular Contractility in Patients with Heart Failure and Normal Ejection Fraction

The maximal rate of change of pressure-normalised wall stress dσ*/dtmax has been proposed as cardiac index of left ventricular (LV) contractility. In this study, we assessed the capacity of dσ*/dtmax to diagnose heart failure with normal ejection fraction (HFNEF). One hundred healthy normal controls and 140 patients admitted with heart failure (100, HFREF and 40, HFNEF) underwent echocardiography for stress-based contractility dσ*/dtmax. Patients with signifi cant valvular heart disease were excluded. Tissue Doppler indices were also measured. dσ*/dtmax was 4.43 ± 1.27 s-1 in control subjects; reduced in HFNEF, 3.02 ± 0.98 s-1; and HFREF, 2.00 ± 0.67 s-1 (P <0.001). In comparison with age- and sex-matched groups (n = 26 each), we found similar trend on reduction of dσ*/dtmax (normal control; 3.91 ± 0.87 s-1; HFNEF, 2.90 ± 0.84 s-1; HFREF, 1.84 ± 0.59 s-1, P <0.001). On multivariate analysis, dσ*/dtmax was found to be the independent predictor of HFNEF and HFREF. The area under the curve of the receiver operating characteristics (ROC) in detecting HFNEF compared with normal controls (dσ*/dtmax>3.2 s-1) was 0.84 (P <0.0001), and in detecting HFREF compared with HFNEF (dσ*/dtmax>2.32 s-1) was 0.88 (P <0.0001). This data confi rms that dσ*/dtmax on echocardiography is a powerful independent predictor in patients with HFNEF. In a population with a high suspicion of HFNEF, dσ*/dtmax may significantly contribute to early diagnosis and hence be useful in the triage and management of HFNEF patients.

ASSESSMENT OF PERFORMANCE, SYSTOLIC FUNCTION AND CONTRACTILITY, AND THEIR CORRELATIONS WITH MYOCARDIAL DAMAGE MARKERS IN PATIENTS WITH SEVERE SEPSIS AND SEPTIC SHOCK

Abstract Category: 24. Myocardial Function/Heart Failure—Clinical Nonpharmacological TreatmentSession-Poster Board Number: 1054-4Authors: Sergio J. Baratta, Sr, Alejandro Hita, Demian Chejtman, Jorge Bilbao, Pablo Pratesi, Diego Bernardez, Sebastian Cosenza, Juan C. Escardo, Domingo Turri, Hospital Universitario Austral, Buenos Aires, Argentina Background: Several studies have assessed the role of the heart in sepsis, without focusing on performance, systolic function or contractility, nor their relation to markers of myocardial damage. Our objective was to assess performance indices of the left ventricle (LV), systolic function and contractility in patients (p) with a positive (> 0.1 ng/ml) or negative troponin T among a population of p with severe sepsis (SS) and septic shock (SSH).Methods: We analyzed 25 p, aged 45±13 years; 8 p had SS and 17 p had SSH. The following parameters were assessed in all p: a) ventricular performance: LV stroke work (SW), b) LV systolic function: ejection fraction (EF), c) LV contractility: EF adjusted by end-systolic stress (ESS), s tissue wave/ESS, midwall fractional shortening (MFS)/ESS, d) ventricular-arterial coupling index (V-A CI), and e) troponin T (TT). The population was divided into 2 groups: G1: TT+ (>0.1 ng/ml) and G2: TT- (≤0.1 ng/ml).Results: Patients with SSH were more frequently assigned to G1. Systolic function indices were more frequently abnormal in G1 compared to G2: EF (G1:45.8 % ±11.8 vs. G2:59.95 % ±9.92, p=0.013), as well as contractile status described by the EF/ESS ratio (G1:21.92±9.26 vs. G2:34.96±10.18, p=0.021), s wave/ESS (G1:2.58±1.38 vs. G2: 3.83±1.16, p=0.05), MFS/ESS (G1:6.78±4.33 vs. G2: 12.19±4.41, p=0.01). No differences were seen in performance, SW (G1:66.10 ± vs. G2:70.06±18.55, p=0.70) or V-A coupling: (G1:1.22±1.19 vs. G2:0.61±0.40, p=0.083).Conclusions: Patients with TT + are more frequent among the SSH group. The presence of this positive marker was associated to a greater impairment in systolic function and contractile status, with preserved ventricular-arterial coupling, thus reinforcing the concept of primary myocardial failure.

Resting global and regional left ventricular contractility in patients with heart failure and normal ejection fraction: insights from speckle-tracking echocardiography

ObejctiveTo compare left ventricular (LV) systolic performance and contractility in patients with heart failure and normal ejection fraction (HFNEF), compared with patients with heart failure and reduced ejection fraction (HFREF)...

N-terminal Pro brain natriuretic peptide is a reliable biomarker of reduced myocardial contractility in patients with lamin A/C gene mutations

BackgroundRecently, concerns have been raised about a possible lack of sensitivity of biomarkers to detect left ventricular (LV) dysfunction in patients with myopathies. We examined the ability of the N-terminal brain natriuretic peptide (NT-proBNP) to detect LV or right ventricular (RV) dysfunction in patients with lamin A/C (LMNA) gene mutations. MethodsWe prospectively measured plasma NT-proBNP in consecutive patients with documented LMNA mutations and age–sex matched controls. All patients underwent standard echocardiography implemented by pulsed tissue-Doppler echocardiography (TDE). ResultsTwenty-three patients were included (10 males, mean age 39.2±18.9years);10 had previous atrial arrhythmias, 8 had been implanted with cardioverter defibrillator for primary prevention of sudden death, 5 patients were of NYHA class II and 18 of NHYA class I. Sinus rhythm was recorded in all. NT-proBNP was increased in LMNA patients versus controls (123±229 versus 26±78pg/ml, p=0.0004); 7 patients had depressed LV and/or RV contractility. Patients with reduced LV or RV contractility had increased mean NT-proBNP (341±1032pg/ml versus 80±79pg/ml in patients with normal myocardial contractility, p=0.004). Receiver-operating-characteristics analysis shows that NT-proBNP reliably detected depressed contractility (area under the curve 0.889 [0.697–1.000]). Sensitivity and specificity were 88% and 83% respectively, applying manufacturer's recommended cut-off concentration of 125pg/ml. ConclusionNT-proBNP reliably detected the presence of reduced LV/RV contractility in LMNA patients.

RESTING GLOBAL AND REGIONAL LEFT VENTRICULAR CONTRACTILITY IN PATIENTS WITH HEART FAILURE AND NORMAL EJECTION FRACTION - INSIGHTS FROM SPECKLE-TRACKING ECHOCARDIOGRAPHY

Obejctive To compare left ventricular (LV) systolic performance and contractility in patients with heart failure and normal ejection fraction (HFNEF), compared with patients with heart failure and reduced ejection fraction (HFREF) and healthy subjects using newer echocardiographic techniques. Design A case–control trial. Setting University teaching hospital (tertiary referral centre). Patients Sixty healthy control subjects (53±10 years), 112 patients with HFNEF (74±12 years) and 175 patients with HFREF (67±13 years). Interventions All underwent standard two-dimensional, Doppler and speckle-tracking echocardiography. Main outcome measures Effective arterial (Ea) and LV end-systolic elastance (Ees), stress-corrected mid-wall shortening, preload recruitable stroke work, two-dimensional strain and torsion. Comparisons were adjusted for age, gender and body size. Results Besides diastolic dysfunction, patients with HFNEF had impaired load-independent ventricular contractility with a progressive decrease of the corrected Ees from controls (2.9±0.8 mm Hg/g) to HFNEF (2.2±0.9 mm Hg/g) followed by HFREF (0.8±0.3 mm Hg/g; all p 85% falling below their corresponding stress-corrected mean. Conclusions Impaired myocardial contractility is evident in many patients with HFNEF and this may contribute towards pathophysiology of HFNEF more than previously thought.

Right ventricular contractility as a measure of optimal interventricular pacing setting in cardiac resynchronization therapy

The aim of the present study was to assess whether right ventricular (RV) contractility can be used for optimization of the interventricular (VV) interval and to study the acute hemodynamic effect of different VV intervals on right and left ventricular (LV) contractility in patients referred for cardiac resynchronization therapy (CRT). Intracardiac LV and RV dP/dt were measured with a 0.014-in. sensor-tipped pressure guidewire during pacing at nine different VV intervals ranging from +80 ms (LV pre-excitation) to -80 ms (RV pre-excitation) in 26 patients who received a biventricular pacemaker. No correlation was found between the optimal VV intervals identified by maximum LV dP/dt and RV dP/dt, which were identical in only seven cases (27%). Only when testing slightly broader intervals (+/-20 ms) was there a statistically significant correlation (P= 0.037) between the optimized VV intervals. In the majority of patients (58%) either LV or RV pre-excitation was superior to simultaneous pacing according to LV dP/dt(max) measurements. RV dP/dt(max) failed to identify the optimal VV interval when compared with LV dP/dt(max) and can therefore not be recommended for VV optimization in CRT patients.

Continuous assessment of cardiac function during rotary blood pump support: A contractility index derived from pump flow

The clinical application of rotary blood pumps (RBPs) for bridge-to-recovery and destination therapy has focused interest on the remaining contractile function of the heart and its course. This study reports a method to determine contractility that uses readily measured variables of the RBP. The proposed index (I(Q)) is defined as the slope of a linear regression between the maximum derivative of the pump flow and its peak-to-peak value. I(Q) was compared with the maximal derivative of ventricular pressure (dP/dt(max)) vs end-diastolic volume (EDV) and the pre-load-recruitable stroke work. All indices were evaluated using computer simulations and animal experiments. For in vivo studies, a MicroMed-DeBakey ventricular assist device (VAD) was implanted in 7 healthy sheep. Ventricular contractility was examined under normal conditions and after pharmacologic intervention. For the computer simulation, variations of ventricular contractility, ventricular pre-load and after-load, and pump speeds were studied. In vivo and computer simulations showed the I(Q) index to be sensitive to changes of cardiac contractility, similar to other classic indices. For reduced cardiac contractility, it decreased to 9.3 +/- 3.9 (s(-1)) vs 15.3 +/- 4.0 (s(-1)) in the control condition (in vivo experiments). The I(Q) index was only marginally influenced by pre-load and after-load changes: a variation of 7.0% +/- 8.9% and 1.3% +/- 7.1%, respectively, was observed in computer simulations. The I(Q) index, which can be derived from pump data only, is a useful parameter for continuous monitoring of the cardiac contractility in patients with RBP support.

Can we use the end systolic volume index to monitor intrinsic right ventricular function after repair of tetralogy of Fallot?

After tetralogy of Fallot (ToF) repair the right ventricle (RV) is commonly exposed to abnormal volume load resulting from pulmonary regurgitation (PR) leading to progressive RV dilatation. The objective of this study was to assess the relationship between RV volumes, especially the end systolic volume index (ESVi), and RV contractility in patients after ToF repair and significant PR and to determine whether RV dilatation reflects intrinsic RV dysfunction in these patients. Twenty-nine ToF patients were studied 11.6 (range: 1.9-30.1) years after repair with the pressure-volume conductance system. The patient cohort was divided into two groups according to the median ESVi (group 1: ESVi<34.7 ml/m(2)(×1.18), n = 14; group 2: ESVi ≥ 34.7 ml/m(2)(×1.18), n = 15). The slope of the end systolic pressure-volume relationship (end systolic elastance, Ees) was higher in group 1 compared to group 2 both at baseline and during dobutamine infusion (0.87 ± 0.36 vs. 0.46 ± 0.28 mm Hg/ml and 1.50 ± 0.77 vs. 0.92 ± 0.37 mm Hg/ml; P<0.005 and P = 0.02, respectively). Overall, Ees at baseline correlated significantly with ESVi and also with the end diastolic volume index (r = -0.64, and P<0.001 for both). Receiver operating characteristic curve analysis revealed that ESVi was superior to RV ejection fraction (EF) in predicting an Ees in the lowest quartile of the study group (area under curve ESVi vs. EF: 0.84 (0.64-0.95) vs. 0.68 (0.47-0.85); P = 0.015). ESVi is a valid estimate of intrinsic RV function in repaired ToF patients with residual PR and in this respect seems superior to EF. These data underscore the importance of serial ventricular volume assessment in the follow-up of these patients.

Spatio‐temporal analysis reveals aberrant linkage among sequential propagating pressure wave sequences in patients with symptomatically defined obstructed defecation

Available evidence implicates abnormal colonic contractility in patients suffering from constipation. Traditional analysis of colonic manometry focuses on the frequency, extent and amplitude of propagating sequences (PS). We tested the hypotheses that the spatio-temporal linkage among sequential PSs exists throughout the healthy human colon and is disrupted during constipation. In eight patients with severe constipation and eight healthy volunteers, we recorded colonic pressures from 16 regions (caecum-rectum) for 24 h. Sequential PSs were regionally linked if the two PSs originated from different colonic regions but the segments of colon traversed by each PS overlapped. In order to determine whether this linkage occurred by chance, a computer program was used to randomly rearrange all PSs in time. Data were re-analysed to compare regional linkage between randomly re-ordered PSs (expected) and the natural distribution of PSs (observed). In controls the observed regional linkage (82.5 +/- 9.0%) was significantly greater than the expected value (60.5 +/- 4.3%; P = 0.0001). In patients the observed and expected regional linkage did not differ. The (observed - expected) delta value of regional linkage in controls was significantly greater than in patients (21.7 +/- 8.5%vs-2.3 +/- 7.0%; P = 0.01). Regional linkage among sequential PSs in the healthy colon appears to be a real phenomenon and this linkage is lost in patients with constipation. Regional linkage may be important for normal colonic transit and loss of linkage might have pathophysiological relevance to and provide a useful biomarker of severe constipation.

Alterations in left ventricular function assessed by two-dimensional speckle tracking echocardiography and the clinical utility of cardiac troponin I in survivors of high-voltage electrical injury

There has been limited study regarding the effects of high-voltage electrical injury on left ventricular (LV) function, as well as the clinical utility of using cardiac troponin I (cTnI) to assess such injuries. We investigated changes in LV function by using two-dimensional speckle tracking imaging, and we also studied the clinical utility of cTnI for predicting myocardial damage in survivors of high-voltage electrical injury. Prospective clinical study. Burn care unit and echocardiography laboratory of a university hospital. Twenty male patients surviving a high-voltage electrical injury. From July 2006 to October 2007, 20 patients suffering from high-voltage electrical injury were prospectively evaluated. A serial echocardiogram was obtained from each patient on hospital days 1, 3, and 7. Serum cTnI levels were drawn at baseline and every 6 hours for the first 24 hours. All parameters of the study patients were compared with age-, sex-, and body mass index-matched healthy controls. On the day of admission and during follow-up, there were no significant differences in LV dimension, stroke volume index, LV fractional shortening, LV ejection fraction, or peak systolic strain as compared with the controls. In contrast to the peak systolic strain, the peak systolic strain rate was significantly increased at baseline and during follow-up for the patient group. There were no significant differences in LV systolic function parameters between the two groups according to the level of cTnI. The current study demonstrates that LV dysfunction after high-voltage electrical injury is uncommon, and that the serum cTnI level does not seem to be a useful diagnostic test for predicting impairment of LV contractility in patients who did not experience cardiac arrest or fatal arrhythmia.

Levosimendan does not improve survival time in a rat model of verapamil toxicity

Calcium channel blocker (CCB) toxicity, in particular that induced by verapamil and diltiazem, presents clinical challenges with no true antidote. Levosimendan, a calcium sensitizer, improves cardiac contractility in patients with heart failure. We tested the hypothesis that calcium channel sensitization will prolong survival in a rat model of severe verapamil poisoning. This was a blinded, randomized, controlled animal study. Wistar rats (mean weight, 371 +/- 50 g) were used. Verapamil (2.5 mg/ml) was infused at a rate of 37.5 mg/kg per hour. Bolus doses of levosimendan (5 microg/mL) were given at 0 min (12 microg/kg) and 5 min (18 microg/kg); saline control was of equal volume. The rats were intubated and maintained under general anesthesia with isoflurane. Electrocardiographic activity and core temperature were monitored during the poisoning and treatment phases. Each rat underwent femoral vein cannulation and was then randomized, in blinded fashion, to receive either levosimendan or an equal volume of saline at 0 and 5 minutes. Death, defined as 1 minute of asystole, was used as the primary endpoint. Rats treated with levosimendan died before the control group (7.37 +/- 0.7 min [n=7] vs. 16.4 +/- 4.2 [n=7] [ p=.053]). All animals experienced bradycardia prior to asystole. Although levosimendan has the ability to sensitize and enhance binding of troponin C to Ca2+, this study did not show an improvement in survival time in the setting of verapamil toxicity. This may be attributed to levosimendan's inhibition of phosphodiesterase, which possibly exacerbated the CCB-induced hypotension. In this rat model, levosimendan as a solitary antidotal treatment for verapamil toxicity was not beneficial.