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Byline: Unal. Ozturk, Onder. Ozturk Background: Acute stroke is an important cause of morbidity and mortality. Myocardial injury is an important complication of acute cerebrovascular events. Neurogenic stress cardiomyopathy (NSC) [...]

Purpose Shortness of breath (SOB) is a common symptom referral for dobutamine stress echocardiography (DSE). Patients with SOB and a normal DSE have worse long-term outcome than the general population. This suggests multiple aetiologies are involved. The purpose of this study was to assess the prevalence and clinical significance of undiagnosed COPD amongst patients referred for a DSE with SOB. Methods We prospectively studied 114 patients referred for DSE with SOB without prior evidence of lung disease (mean age 64.9 ± 18.5 years, 60 male). Respiratory function testing using spirometry was performed on all patients on the day of their DSE. The study end-points were cardiac events and total mortality. Results Respiratory function testing and DSE was performed in all patients and COPD was highly prevalent (n = 93). Multivariate Cox regression analysis was used to estimate the effect of dyspnoea on non-fatal cardiac events (NFCE) and all-cause mortality. Over a mean follow-up of 4.5 ± 2.6 years, the composite end-point of NFCE and all-cause mortality occurred in 62.7% and 16.7% patients, respectively. COPD (HR 1.27; 95% CI 1.17-1.93), previous myocardial infarction (HR 1.84; 95% CI 1.06-3.2), myocardial ischaemia (HR 2.56; 95% CI 1.48-4.43), peak wall motion score index (HR 4.66; 95% CI 2.26-9.6), and mitral E/E' (HR 1.21; 95% CI 1.1-1.33) were significantly associated with a NFCE. Myocardial ischaemia (HR 4.43; 95% CI 1.24-15.81) was the only independent predictor of all-cause mortality. Conclusion Undiagnosed COPD is highly prevalent and independently associated with worse outcome amongst patients with SOB referred for DSE. Symptom presentation is therefore an important consideration when interpreting DSE results., Author(s): Jamie M. O'Driscoll [sup.1] [sup.2], Dimitrios Giannoglou [sup.1], Ibrahim Bashar [sup.1], Konstantina Kipourou [sup.1], Emanuela Alati [sup.1], Brendan Madden [sup.3], Anna Marciniak [sup.1], Rajan Sharma [sup.1] Author Affiliations: (1) [...]

Purpose Mortality in circulatory shock is high. Enhanced resolution of shock may improve outcomes. We aim to determine whether adding hemodynamic monitoring with continual transesophageal echocardiography (hTEE) to usual care accelerates resolution of hemodynamic instability. Methods 550 patients with circulatory shock were randomly assigned to four groups stratified using hTEE (hTEE vs usual care) and assessment frequency (minimum every 4 h vs 8 h). Primary outcome was time to resolution of hemodynamic instability, analyzed as intention-to-treat (ITT) analysis at day 6 and in a predefined secondary analysis at days 3 and 28. Results Of 550 randomized patients, 271 with hTEE and 274 patients with usual care were eligible and included in the ITT analysis. Time to resolution of hemodynamic instability did not differ within the first 6 days [hTEE vs usual care adjusted sub-hazard ratio (SHR) 1.20, 95% confidence interval (CI) 0.98-1.46, p = 0.067]. Time to resolution of hemodynamic instability during the 72 h of hTEE monitoring was shorter in patients with TEE (hTEE vs usual care SHR 1.26, 95% CI 1.02-1.55, p = 0.034). Assessment frequency had no influence. Time to resolution of clinical signs of hypoperfusion, duration of organ support, length of stay and mortality in the intensive care unit and hospital, and mortality at 28 days did not differ between groups. Conclusions In critically ill patients with shock, hTEE monitoring or hemodynamic assessment frequency did not influence resolution of hemodynamic instability or mortality within the first 6 days. Trial registration and statistical analysis plan ClinicalTrials.gov Identifier: NCT02048566., Author(s): Tobias M. Merz [sup.1], Luca Cioccari [sup.1], Pascal M. Frey [sup.2], Andreas Bloch [sup.1], David Berger [sup.1], Bjoern Zante [sup.1], Stephan M. Jakob [sup.1], Jukka Takala [sup.1] Author Affiliations: [...]

Purpose To assess the feasibility, image quality, diagnostic accuracy, therapeutic impact and tolerance of diagnostic and hemodynamic assessment using a novel miniaturized multiplane transesophageal echocardiography (TEE) probe in ventilated ICU patients with cardiopulmonary compromise. Study design Prospective, descriptive, single-center study. Methods Fifty-seven ventilated patients with acute circulatory or respiratory failure were assessed, using a miniaturized multiplane TEE probe and a standard TEE probe used as reference, randomly by two independent experienced operators. Measurements of hemodynamic parameters were independently performed off-line by a third expert. Diagnostic groups of acute circulatory failure (n = 5) and of acute respiratory failure (n = 3) were distinguished. Hemodynamic monitoring was performed in 9 patients using the miniaturized TEE probe. TEE tolerance and therapeutic impact were reported. Results The miniaturized TEE probe was easier to insert than the standard TEE probe. Despite lower imaging quality of the miniaturized TEE probe, the two probes had excellent diagnostic agreement in patients with acute circulatory failure (Kappa: 0.95; 95 % CI: 0.85-1) and with acute respiratory failure (Kappa: 1; 95 % CI: 1.0-1.0). Accordingly, therapeutic strategies derived from both TEE examinations were concordant (Kappa: 0.82; 95 % CI: 0.66-0.97). The concordance between quantitative hemodynamic parameters obtained with both TEE probes was also excellent. No relevant complication secondary to TEE probes insertion occurred. Conclusions Hemodynamic assessment of ventilated ICU patients with cardiopulmonary compromise using a miniaturized multiplane TEE probe appears feasible, well-tolerated, and relevant in terms of diagnostic information and potential therapeutic impact. Further larger-scale studies are needed to confirm these preliminary results., Author(s): Emmanuelle Begot [sup.1] [sup.2] [sup.3], François Dalmay [sup.4], Caroline Etchecopar [sup.3], Marc Clavel [sup.1] [sup.3], Nicolas Pichon [sup.1] [sup.3], Bruno Francois [sup.1] [sup.3], Roberto Lang [sup.5], Philippe Vignon [sup.1] [...]

Most elderly persons with heart failure have a preserved left ventricular (LV) ejection fraction (HFPEF). The pathophysiology of this disorder is not well understood, and there are conflicting data regarding the role of decreased LV distensibility. To assess LV distensibility over a range of preload conditions while minimizing the large, confounding changes in contractility, afterload, and heart rate characteristic of exercise, we measured LV end-diastolic volume (EDV), stroke volume (SV), and cardiac output (CO) using two-dimensional echocardiography in 48 elderly (mean age, 69 yr) HFPEF patients and 25 healthy age-matched controls during quiet supine rest, 45[degrees] head-up tilt (HUT), and 45[degrees] head-down tilt (HDT). As a result, when compared with controls, HFPEF patients had reduced percent changes in EDV (-7 [+ or -] 2 vs. -17 [+ or -] 2%; P = 0.003), SV (-7 [+ or -] 3 vs. -27 [+ or -] 2%; P = 0.003), and CO (-6 [+ or -] 4 vs. -34 [+ or -] 4%; P = 0.001) during the transition from supine to HUT. HFPEF also had reduced percent changes in EDV (8 [+ or -] 2 vs. 15 [+ or -] 2%; P = 0.02), SV (11 [+ or -] 3 vs. 21 [+ or -] 3%; P = 0.002), and CO (1 [+ or -] 4 vs. 12 [+ or -] 4%; P = 0.04) during the transition from HUT to HDT. In conclusion, HFNEF patients have reduced LV distensibility in response to postural change, resulting in blunted EDV, SV, and CO. This provides further support for the hypothesis that a blunted Frank-Starling mechanism may contribute to the pathophysiology of HFPEF. tilt test; aging doi: 10.1152/ajpheart.00332.2010.

Left ventricular (LV) active relaxation begins before aortic valve closure and is largely completed during isovolumic relaxation (IVR), before mitral valve opening. During IVR, despite closed mitral and aortic valves, indirect assessments of LV volume have suggested volume increases during this period. The aim of this study is to measure LV volume throughout IVR and to determine the sources of any volume changes. For 10 healthy individuals (26.0 [+ or -] 3.8 yr), magnetic resonance imaging was used to measure time courses of LV volume, principal myocardial strains (circumferential, longitudinal, radial), and LV twist. Mitral leaflet motion was observed using echocardiography. During IVR, LV volume measurements showed an apparent increase of 4.6 [+ or -] 1.5 ml (5.0 [+ or -] 2.0% of the early filling volume change), the LV untwisted by 4.5 [+ or -] 1.9[degrees] (36.6 [+ or -] 18.0% of peak systolic twist), and changes in circumferential, longitudinal, and radial strains were +0.87 [+ or -] 0.64%, +0.93 [+ or -] 0.57%, and - 1.46 [+ or -] 1.66% (4.2 [+ or -] 3.3%, 5.9 [+ or -] 3.3%, and 5.3 [+ or -] 7.5% of peak systolic strains), respectively. The apparent changes in volume correlated (P < 0.01) with changes in circumferential, longitudinal, and radial strains (r = 0.86, 0.69, and -0.37, respectively) and untwisting (r = 0.83). The closed mitral valve leaflets were observed to descend into the LV throughout IVR in all subjects in apical four- and three-chamber and parasternal long-axis views by 6.0 [+ or -] 3.3, 5.1 [+ or -] 2.4, and 2.1 [+ or -] 5.0 mm, respectively. In conclusion, LV relaxation during IVR is associated with changes in principal strains and untwisting, which are all correlated with an apparent increase in LV volume. Since closed mitral and aortic valves ensure true isovolumic conditions, the apparent volume change likely reflects expansion of the LV myocardium and the inward bowing of the closed mitral leaflets toward the LV interior. diastolic function; active relaxation; mitral valve leaflets doi: 10.1152/ajpheart.00131.2010.

Various studies have been conducted to evaluate the role of antiretroviral therapy in the onset of cardiovascular risk among HIV-1-infected patients, while fewer data are available regarding antiretroviral-naive patients. Our objective was to evaluate the cardiovascular risk among naive subjects examining traditional risk factors, immunovirologic parameters, assessing the Framingham risk score (FRS), and detecting the presence of subclinical carotid lesions by means of color Doppler ultrasonography. One hundred seventy-two antiretroviral-naive patients underwent color Doppler ultrasonography. An intima-media thickness (IMT) greater than 0.9 mm and/or atherosclerotic plaques were considered pathologic findings. Demographic, immunovirologic data, and risk factors for cardiovascular disease were collected. The 10-year probability of acute coronary events was assessed by the FRS. The statistical analysis was performed using t test and [chi square], Fisher's test, and conditional multiple logistic. Thirty-six patients (20.9%) had lesions at ultrasonographic investigation. The presence of lesions was significantly related to male gender (p = 0.005), age (p = 0.003), sedentary life (p = 0.05), Centers for Disease Control and Prevention (CDC) group C or [CD4.sup.+] less than 150 cells/[mm.sup.3] and viral load (VL) > 100,000 copies per milliliter (p = 0.04). The presence of subclinical carotid lesions showed a highly significant direct association with the estimated FRS (p < 0.002). The presence of subclinical atheromasic lesion results was also high among antiretroviral-naive patients. FRS is highly predictive of the lesions, but also an advanced stage of disease plays a significant role. Our data support the hypothesis that HIV infection per se is a risk factor for atherosclerosis. We recommend an ultrasonographic assessment both among patients with FRS 6% or more and among those in advanced stage of disease. DOI: 10.1089/apc.2009.0102

Two-dimensional (2-D) speckle tracking echocardiography (STE) accurately quantifies circumferential strain (Scare) and radial strain ([S.sub.rad]) in humans and in large and small animals. This study was performed to assess sensitivity of [S.sub.circ] and [S.sub.rad] to left ventricular (LV) dysfunction in mouse models. We performed 2-D and M-mode echocardiography 1) in 6 mice during superficial and profound isoflurane anesthesia, 2) serially in 12 mice to monitor the development of heart failure induced by transverse aortic constriction (TAC) and in 8 corresponding control mice, and 3) in 26 mice with varying degrees of TAC-induced heart failure and 12 corresponding control mice immediately before euthanasia. Fractional shortening (FS) and LV mass were measured from standard M-mode tracings, whereas [S.sub.circ] and [S.sub.rad] were derived by STE. Percent fibrosis and myocyte diameters were assessed from whole heart cross-sectional specimens stained by Masson trichrome. Profound isoflurane anesthesia decreased [S.sub.circ] (P = 0.027) but not [S.sub.rad] (P > 0.05). Mice subjected to TAC showed an immediate and sustained decrease in FS (P = 0.035), [S.sub.circ] (P = 0.016), and [S.sub.rad] (P = 0.012). [S.sub.circ] showed better correlation with FS (r = 0.56 and P < 0.0001) and LV mass (r = 0.42 and P = 0.0003) than [S.sub.rad] (r = 0.54 and P < 0.0001 for FS and r = 0.37 and P = 0.014 for LV mass, respectively). Percent fibrosis correlated better with Scare (r = 0.46 and P = 0.004) than with [S.sub.rad] (r = -0.32 and P = 0.05), whereas myocyte diameter showed similar correlation with both strains (r = 0.45 and r = -0.44, respectively, and P = 0.006 for both). STE correctly identifies LV dysfunction and histological changes in mice and can be used for the serial assessment of cardiac remodeling in murine models. transverse aortic constriction; systolic strain; systolic function

Serotonergic drugs, such as pergolide, have been associated with the development of cardiac valvular myxoid thickening and regurgitation in humans and more recently in rats. These effects are potentially mediated by the 5-hydroxytryptamine [(5-HT).sub.2B] receptor ([5-HT.sub.2B]R). Therefore, we sought to determine whether cyproheptadine, a [5-HT.sub.2B]R antagonist, might prevent toxic valvulopathy in an animal model of pergolide-induced valvular heart disease. For this purpose, 50 male Wistar rats received daily intraperitoneal injections of pergolide (0.5 mg/kg, n = 14), pergofide (0.5 mg/kg) combined with cyproheptadine (10 mg/kg, n = 12), cyprobeptadine (10 mg/kg, n = 12), or no injections (control, n = 12) for 20 wk. Echocardiography was performed blindly at baseline and at 10 and 20 wk followed by pathology. At baseline, no differences between groups were found with echocardiography. At 20 wk, aortic regurgitation was present in all pergolide-treated animals, whereas it was less frequently observed in the other groups (P < 0.0001). For the other valves, this difference was less pronounced. On histopathology, not only aortic but also mitral valves were thicker, myxoid, and exhibited more [5-HT.sub.2B]R-positive cells in pergolide-treated animals compared with the other groups. Moreover, regurgitant aortic and mitral valves were thicker than nonregurgitant aortic and mitral valves. In conclusion, we found that cyproheptadine prevented pergolide-induced valvulopathy in rats, which was associated with a reduced number of [5-HT.sub.2B]R-positive valvular cells. This may have important clinical implications for the prevention of serotonergic drug-induced valvular heart disease. drugs; echocardiography; pathology; valves

During a whole body heat stress, stroke volume is either maintained or slightly elevated despite reduced ventricular filling pressures and central blood volume, suggestive of improved cardiac diastolic and/or systolic function. Heat stress improves cardiac systolic and diastolic function in patients with congestive heart failure, although it remains unknown whether similar responses occur in healthy individuals, which is the hypothesis to be tested. Nine male volunteers underwent a whole body heat stress. Echocardiographic indexes of diastolic and systolic function were performed following a supine resting period, and again following an increase in internal temperature of ~ 1.0[degrees]C via passive heat stress. Despite previous reports of heat stress-induced decreases in ventricular filling pressures and central blood volume, no changes in indexes of diastolic function were identified during heating [i.e., unchanged early diastolic mitral annular tissue velocity (E'), mitral inflow during the early diastolic phase (E), the E/E' ratio, and isovolumetric relaxation time]. Heat stress increased late diastolic septal (P = 0.03) and lateral (P = 0.0l) mitral annular tissue velocities (A'), mitral inflow velocity during atrial contraction (P < 0.001), and the relative contribution of atrial contraction to left ventricular filling during diastole (P = 0.01), all indicative of improved atrial systolic function. Furthermore, indexes of ventricular systolic function were increased by heat stress [i.e., increased septal (P = 0.001) and lateral (P = 0.01) mitral annular systolic velocities and isovolumic acceleration at the septal (P = 0.03) and lateral (P < 0.001) mitral annulus]. These data are suggestive of improved atrial and ventricular systolic function by the heat stress. Together these data support previous findings, which used the less precise measure of ejection fraction, that heat stress improves indexes of systolic function, while diastolic function is maintained. cardiac systolic function; stroke volume

Byline: Sergio L. Zanotti-Cavazzoni (1,2), Massimiliano Guglielmi (1), Joseph E. Parrillo (1), Tracy Walker (1), R. Phillip Dellinger (1), Steven M. Hollenberg (1) Keywords: Sepsis; Hemodynamics; Echocardiography; Fluid resuscitation; Animal model Abstract: Rationale Current murine models of sepsis do not account for the effects of aggressive fluid resuscitation on hemodynamics and mortality. Objectives Evaluate the impact of fluid resuscitation regimens on cardiovascular performance and survival in a murine model of sepsis. Methods Mice (n = 90) were made septic by cecal ligation and puncture (CLP), and received antibiotics plus Low, Intermediate, or High fluid resuscitation regimens. Stroke volume (SV), cardiac output (CO), and fractional shortening (FS) were measured by echocardiography at predefined time points. Measurements and main results Baseline echocardiographic measurements were similar in all groups. After CLP, SV and CO decreased early in all groups High: 57.2 +- 9.2 to 23.9 +- 7.2 AuL, and 26.8 +- 4.9 to 13.1 +- 5.8 ml/min Intermediate: 52.1 +- 7.0 to 21.5 +- 6.6 AuL, and 24.9 +- 4.1 to 11.9 +- 3.9 ml/min Low: 54.0 +- 7.0 to 20.3 +- 5.6 AuL, and 25.8 +- 4.0 to 11.3 +- 3.9 ml/min (P < 0.05 for all vs. baseline). With resuscitation there was a dose-dependent improvement in SV and CO (P < 0.05). At 24 h SV and CO were 44.0 +- 13.8 AuL and 20.7 +- 8.5 ml/min in the High group, 39.8 +- 12.3 AuL and 16.7 +- 6.5 ml/min in the Intermediate group, and 30.1 +- 12.4 AuL and 14.0 +- 7.2 ml/min in the Low group. Survival was improved in the High fluid group (75%) compared to the Intermediate (58%) and the Low (35%) resuscitation groups (P < 0.05). Conclusions In this model, as in human sepsis, the intensity of fluid resuscitation modulates hemodynamic response and mortality. Incorporation of early and aggressive fluid resuscitation can significantly enhances the clinical relevance of murine models of sepsis. Author Affiliation: (1) Divisions of Cardiovascular Disease and Critical Care Medicine, Cooper University Hospital, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Camden, NJ, USA (2) Division of Critical Care Medicine, Cooper University Hospital, Dorrance 360, Once Cooper Plaza, Camden, NJ, 08103, USA Article History: Registration Date: 25/11/2008 Received Date: 24/04/2008 Accepted Date: 10/11/2008 Online Date: 09/12/2008 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00134-008-1360-9) contains supplementary material, which is available to authorized users.

The study explores the association between exercise capacity and left ventricular diastolic function parameters as assessed by echocardiography and determines if these associations are modified by sex or advancing age. Findings indicate abnormalities of left ventricular diastolic function are independently associated with exercise capacity.

Histone deacetylase (HDAC) inhibitors show remarkable therapeutic potential for a variety of disorders, including cancer, neurological disease, and cardiac hypertrophy. However, the specific HDAC isoforms that mediate their actions are unclear, as are the physiological and pathological functions of individual HDACs in vivo. To explore the role of Hdac3 in the heart, we generated mice with a conditional Hdac3 null allele. Although global deletion of Hdac3 resulted in lethality by E9.5, mice with a cardiac-specific deletion of Hdac3 survived until 3-4 months of age. At this time, they showed massive cardiac hypertrophy and upregulation of genes associated with fatty acid uptake, fatty acid oxidation, and electron transport/oxidative phosphorylation accompanied by fatty acid--induced myocardial lipid accumulation and elevated triglyceride levels. These abnormalities in cardiac metabolism can be attributed to excessive activity of the nuclear receptor PPAR[alpha]. The phenotype associated with cardiac-specific Hdac3 gene deletion differs from that of all other Hdac gene mutations. These findings reveal a unique role for Hdac3 in maintenance of cardiac function and regulation of myocardial energy metabolism., Introduction Heart failure is a complex disorder that arises from multiple pathological insults including myocardial infarction, hypertension, and coronary artery disease. Initially, these insults are followed by an increase in [...]

Byline: Antoine Vieillard-Baron (1), Michel Slama (2,3), Bernard Cholley (4), Gerard Janvier (5), Philippe Vignon (6) Keywords: Echocardiography; Monitoring; Hemodynamic; Cardiac function; Educational program Abstract: Background Over recent decades, echocardiography has become a pivotal diagnostic tool for the assessment of patients with hemodynamic compromise in general intensive care units (ICUs). In addition to its imaging capability, echocardiography provides a detailed cardiovascular assessment, based on the combination of real-time two-dimensional evaluation of cardiac structure and function and hemodynamic information provided by Doppler measurement of blood flow velocity. However, despite its ease of use, portability and accuracy, the diffusion of echocardiography among ICUs has been limited by various factors. Discussion We discuss here the main reasons for the slow acceptance by the critical care community of echocardiography as a first-line diagnostic tool for the evaluation of hemodynamically unstable patients. One of these reasons is probably the absence, in most countries, of a training program in echocardiography specifically dedicated to intensivists. We report recent French experience in the organization of specific echocardiographic certification aimed at intensivists and anesthesiologists. We strongly believe that a broader use of echocardiography would be beneficial in terms of diagnostic capability and patient management. Therefore, we would like to involve colleagues from other countries and the European Society of Intensive Care Medicine in defining the objectives of echocardiography training for intensivists and in organizing postgraduate courses and training programs aimed at developing the use of echocardiography in ICUs. This would allow the current 'evolution' in mentalities to become a true 'revolution' in our daily practice. Author Affiliation: (1) Intensive Care Unit, Hopital Ambroise Pare, Assistance Publique -- Hopitaux de Paris, 9, avenue Charles de Gaulle, 92104, Boulogne Cedex, France (2) Medical Intensive Care Unit, South Hospital, Avenue Rene Laennec, 80054, Cedex 1, Amiens, France (3) INSERM ERI 12, Amiens, France (4) Department of Anesthesiology, Lariboisiere Hospital, Assistance Publique -- Hopitaux de Paris, 2, rue Ambroise Pare, 75010, Paris, France (5) Department of Anesthesiology, Pellegrin Hospital, 1, place Amelie Raba-Leon, 33076, Bordeaux, France (6) Medical--Surgical Intensive Care Unit, Dupuytren Hospital, 2, avenue Martin Luther King, 87042, Limoges, France Article History: Registration Date: 12/10/2007 Received Date: 25/04/2007 Accepted Date: 09/09/2007 Online Date: 09/11/2007 Article note: From the 'ECHO-in-ICU group' This article is discussed in the editorial available at: http://dx.doi.org/10.1007/s00134-007-0924-4.

Hypertension is a major risk factor for developing cardiac hypertrophy and heart failure. Previous studies show that hypertrophied and failing hearts display alterations in excitation-contraction (E-C) coupling, However, it is unclear whether remodeling of the E-C coupling system occurs before or after heart disease development. We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. Here we tested this hypothesis by utilizing the progressive development of hypertensive heart disease in the spontaneously hypertensive rat (SHR) to identify a window period when SHR had just developed hypertension but had not yet developed hypertrophy. We found the following major changes in cardiac E-C coupling during this window period. 1) Using echocardiography and hemodynamics measurements, we found a decrease of left ventricular ejection fraction and cardiac output after the onset of hypertension. 2) Studies in isolated ventricular myocytes showed that myocardial contraction was also enhanced at the same time. 3) The action potential became prolonged. 4) The E-C coupling gain was increased. 5) The systolic [Ca.sup.2+] transient was augmented. These data show that profound changes in E-C coupling already occur at the onset of hypertension and precede hypertrophy development. Prolonged action potential and increased E-C coupling gain synergistically increase the [Ca.sup.2+] transient. Functionally, augmented [Ca.sup.2+] transient causes enhancement of myocardial contraction that can partially compensate for the greater workload to maintain cardiac output. The increased [Ca.sup.2+] signaling cascade as a molecular mechanism linking hypertension to cardiac hypertrophy development is also discussed. heart failure; action potential; L-type [Ca.sup.2+] channel; ryanodine receptor

Byline: Philippe Vignon (1,2), Anthony Dugard (1,2), Julie Abraham (1), Dominique Belcour (1), Guillaume Gondran (1), Frederic Pepino (1), Benoit Marin (4), Bruno Francois (1,2), Herve Gastinne (1,3) Keywords: Transthoracic echocardiography; Two-dimensional echocardiography; Curriculum; Intensive care Abstract: Objective We sought to evaluate the efficacy of a limited training dedicated to residents without knowledge in ultrasound for performing goal-oriented echocardiography in ICU patients. Design Prospective pilot observational study. Setting Medical-surgical ICU of a teaching hospital. Patients 61 consecutive adult ICU patients (SAPSa-II score: 38a-+-a-17 46 ventilated patients) requiring a transthoracic echocardiography were studied. Interventions After a curriculum including a 3-h training course and 5a-h of hands-on training, one of four noncardiologist residents and an intensivist experienced in ultrasound subsequently performed hand-held echocardiography (HHE), independently and in random order. Assessable 'rule in, rule out' clinical questions were purposely limited to easily identifiable conditions by the sole use of two-dimensional imaging. Measurements and results When compared with residents, the experienced intensivist performed shorter examinations (4a-+-a-1 vs. 11a-+-a-4a-min: pa- Conclusions Limited training of noncardiologist ICU residents without previous knowledge in ultrasound appears feasible and efficient to address simple clinical questions using point-of-care echography. Influence of the learning curve on diagnostic accuracy and potential therapeutic impact remain to be determined. Author Affiliation: (1) Medical-Surgical Intensive Care Unit, CHU Dupuytren, 2 Ave. Martin Luther King, 87042, Limoges Cedex, France (2) Centre de Recherche Clinique, CHU Limoges, Limoges, France (3) University of Limoges, Limoges, France (4) Unit of Clinical Research and Biostatistics, Dupuytren Teaching Hospital, 2 Ave. Martin Luther King, 87042, Limoges Cedex, France Article History: Registration Date: 22/05/2007 Received Date: 13/03/2007 Accepted Date: 16/05/2007 Online Date: 16/06/2007

Chronic obstructive pulmonary disease (COPD) may lead to pulmonary hypertension (PH) and reduced function of the right ventricle (RV). However, COPD patients may also develop left ventricular (LV) diastolic dysfunction. We hypothesized that alveolar hypoxia induces LV diastolic dysfunction and changes in proteins governing [Ca.sup.2+] removal from cytosol during diastole. Mice exposed to 10% oxygen for 1, 2, or 4 wk were compared with controls. Cardiac hemodynamics were assessed with Doppler echocardiography and a microtransducer catheter under general anesthesia. The pulmonary artery blood flow acceleration time was shorter and RV pressure was higher after 4 wk of hypoxia compared with controls (both P < 0.05). In the RV and LV, 4 wk of hypoxia induced a prolongation of the time constant of isovolumic pressure decay (51% RV, 43% LV) and a reduction in the maximum rate of decline in pressure compared with control (42% RV, 42% LV, all P < 0.05), indicating impaired relaxation and diastolic dysfunction. Alveolar hypoxia induced a 38%, 47%, and 27% reduction in Ser16-phosphorylated phospholamban (PLB) in the RV after 1, 2, and 4 wk of hypoxia, respectively, and at the same time points, Ser16-phosphorylated PLB in the LV was downregulated by 32%, 34%, and 25% (all P < 0.05). The amounts of PLB and sarco(endo)plasmic reticulum [Ca.sup.2+] ATPase (SERCA2a) were not changed. In conclusion, chronic alveolar hypoxia induces hypophosphorylation of PLB at Ser16, which might be a mechanism for impaired relaxation and diastolic dysfunction in both the RV and LV. diastole; calcium; echocardiography doi:10.1152/ajpheart.00862.2005