The Experts below are selected from a list of 8928 Experts worldwide ranked by ideXlab platform

Patrick Segers - One of the best experts on this subject based on the ideXlab platform.

  • noninvasive evaluation of left ventricular Afterload part 2 arterial pressure flow and pressure volume relations in humans
    Hypertension, 2010
    Co-Authors: Julio A Chirinos, Patrick Segers
    Abstract:

    The mechanical load imposed by the systemic circulation to the left ventricle is an important determinant of normal and abnormal cardiovascular function. Left ventricular Afterload is determined by complex time-varying phenomena, which affect pressure and flow patterns generated by the pumping ventricle. Left ventricular Afterload is best described in terms of pressure-flow relations, allowing for quantification of various components of load using simplified biomechanical models of the circulation, with great potential for mechanistic understanding of the role of central hemodynamics in cardiovascular disease and the effects of therapeutic interventions. In the second part of this tutorial, we review analytic methods used to characterize left ventricular Afterload, including analyses of central arterial pressure-flow relations and windkessel modeling (pressure-volume relations). Conceptual descriptions of various models and methods are emphasized over mathematical ones. Our review is aimed at helping researchers and clinicians obtain and interpret results from analyses of left ventricular Afterload in clinical and epidemiological settings.

  • noninvasive evaluation of left ventricular Afterload part 1 pressure and flow measurements and basic principles of wave conduction and reflection
    Hypertension, 2010
    Co-Authors: Julio A Chirinos, Patrick Segers
    Abstract:

    The mechanical load imposed by the systemic circulation to the left ventricle is an important determinant of normal and abnormal cardiovascular function. Left ventricular Afterload is determined by complex time-varying phenomena, which affect pressure and flow patterns generated by the pumping ventricle and cannot be expressed as a single numeric measure or described in terms of pressure alone. Left ventricular Afterload is best described in terms of pressure-flow relations. High-fidelity arterial applanation tonometry can be used to record time-resolved central pressure noninvasively, whereas contemporary noninvasive imaging techniques, such as Doppler echocardiography and phase-contrast MRI, allow for accurate assessments of aortic flow. Central pressure and flow can be analyzed using simplified biomechanical models to characterize various components of Afterload, with great potential for mechanistic understanding of the role of central hemodynamics in cardiovascular disease and the effects of therapeutic interventions. In the first part of this tutorial, we review noninvasive techniques for central pressure and flow measurements and basic concepts of wave conduction and reflection as they relate to the interpretation of central pressure-flow relations. Conceptual descriptions of various models and methods are emphasized over mathematical ones. Our review is aimed at helping researchers and clinicians apply and interpret results obtained from analyses of left ventricular Afterload in clinical and epidemiological settings.

Adelino F Leitemoreira - One of the best experts on this subject based on the ideXlab platform.

  • load as an acute determinant of end diastolic pressure volume relation
    American Journal of Physiology-heart and Circulatory Physiology, 2001
    Co-Authors: Adelino F Leitemoreira, Jorge Correiapinto
    Abstract:

    Leite-Moreira, Adelino F., and Jorge Correia-Pinto. Load as an acute determinant of end-diastolic pressurevolume relation. Am J Physiol Heart Circ Physiol 280: H51‐H59, 2001.—Afterload-induced changes in myocardial relaxation are a mechanism for diastolic dysfunction when Afterload is elevated beyond certain limits. The present study investigated the effects of acute Afterload and preload changes on the position of the end-diastolic (ED) pressurevolume (P-V) relation. Beat-to-beat Afterload elevations were induced in seven open-chest rabbits by gradually occluding the ascending aorta to increase peak left ventricular pressure (LVP) from baseline to isovolumetric level. Afterload elevations were performed at three ED LVP: 2.0 6 0.2 (low), 5.7 6 0.2 (mid), and 9.6 6 0.6 (high) mmHg. Preload was altered with caval occlusions and/or intravenous dextran. Afterload elevations induced an upward shift of the diastolic P-V relation, which became more important as Afterload and/or preload increased. For instance, maximal Afterload elevations shifted this relation upward 2.2 6 0.5, 5.1 6 0.8, and 12.1 6 1.7 mmHg at low, mid, and high preload, respectively. These effects were partially due to changes in relaxation rate and time available to relax. In conclusion, load is an acute determinant of the ED P-V relation, which, therefore, does not provide a load-independent assessment of diastolic function. Afterload; diastole; heart failure; myocardial relaxation; preload

  • Afterload induced changes in myocardial relaxation a mechanism for diastolic dysfunction
    Cardiovascular Research, 1999
    Co-Authors: Adelino F Leitemoreira, Jorge Correiapinto, Thierry C Gillebert
    Abstract:

    Background: Diastolic left ventricular (LV) dysfunction manifests as an upward shift of the diastolic pressure–volume relation. One of the possible causes of diastolic LV dysfunction is incomplete myocardial relaxation. It is well known that high Afterload slows myocardial relaxation. This contribution investigated to what extent Afterload elevation could also affect LV filling pressures including end-diastolic LV pressure (LVP). Methods: Selective, beat-to-beat elevations of Afterload were induced in anaesthetised open-chest rabbits ( n =9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat. This was performed with physiological heart rate and blood pressure. Results: These interventions increased systolic LVP from 90±3 mm Hg at baseline to 103±4, 123±5, 139±5 and 154±6 mm Hg. The last intervention was a total aortic occlusion inducing a first beat isovolumetric contraction. Smaller Afterload elevations decreased τ (accelerated LVP fall) and did not elevate diastolic pressure-internal diameter relation (P-ID). Larger Afterload elevations increased τ (decelerated LVP fall), induced an upward shift of the diastolic P-ID and increased end-diastolic LVP. Effects of Afterload on end-diastolic LVP were correlated with effects on τ ( r =0.89; P <0.01). Incomplete relaxation or load-dependent residual active state appeared to be the mechanism for this diastolic dysfunction. Similar findings were made retrospectively in dogs instrumented with circumferential segment length gauges ( n =16). Conclusions: Diastolic LV dysfunction was induced by elevated Afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.

Jorge Correiapinto - One of the best experts on this subject based on the ideXlab platform.

  • load as an acute determinant of end diastolic pressure volume relation
    American Journal of Physiology-heart and Circulatory Physiology, 2001
    Co-Authors: Adelino F Leitemoreira, Jorge Correiapinto
    Abstract:

    Leite-Moreira, Adelino F., and Jorge Correia-Pinto. Load as an acute determinant of end-diastolic pressurevolume relation. Am J Physiol Heart Circ Physiol 280: H51‐H59, 2001.—Afterload-induced changes in myocardial relaxation are a mechanism for diastolic dysfunction when Afterload is elevated beyond certain limits. The present study investigated the effects of acute Afterload and preload changes on the position of the end-diastolic (ED) pressurevolume (P-V) relation. Beat-to-beat Afterload elevations were induced in seven open-chest rabbits by gradually occluding the ascending aorta to increase peak left ventricular pressure (LVP) from baseline to isovolumetric level. Afterload elevations were performed at three ED LVP: 2.0 6 0.2 (low), 5.7 6 0.2 (mid), and 9.6 6 0.6 (high) mmHg. Preload was altered with caval occlusions and/or intravenous dextran. Afterload elevations induced an upward shift of the diastolic P-V relation, which became more important as Afterload and/or preload increased. For instance, maximal Afterload elevations shifted this relation upward 2.2 6 0.5, 5.1 6 0.8, and 12.1 6 1.7 mmHg at low, mid, and high preload, respectively. These effects were partially due to changes in relaxation rate and time available to relax. In conclusion, load is an acute determinant of the ED P-V relation, which, therefore, does not provide a load-independent assessment of diastolic function. Afterload; diastole; heart failure; myocardial relaxation; preload

  • Afterload induced changes in myocardial relaxation a mechanism for diastolic dysfunction
    Cardiovascular Research, 1999
    Co-Authors: Adelino F Leitemoreira, Jorge Correiapinto, Thierry C Gillebert
    Abstract:

    Background: Diastolic left ventricular (LV) dysfunction manifests as an upward shift of the diastolic pressure–volume relation. One of the possible causes of diastolic LV dysfunction is incomplete myocardial relaxation. It is well known that high Afterload slows myocardial relaxation. This contribution investigated to what extent Afterload elevation could also affect LV filling pressures including end-diastolic LV pressure (LVP). Methods: Selective, beat-to-beat elevations of Afterload were induced in anaesthetised open-chest rabbits ( n =9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat. This was performed with physiological heart rate and blood pressure. Results: These interventions increased systolic LVP from 90±3 mm Hg at baseline to 103±4, 123±5, 139±5 and 154±6 mm Hg. The last intervention was a total aortic occlusion inducing a first beat isovolumetric contraction. Smaller Afterload elevations decreased τ (accelerated LVP fall) and did not elevate diastolic pressure-internal diameter relation (P-ID). Larger Afterload elevations increased τ (decelerated LVP fall), induced an upward shift of the diastolic P-ID and increased end-diastolic LVP. Effects of Afterload on end-diastolic LVP were correlated with effects on τ ( r =0.89; P <0.01). Incomplete relaxation or load-dependent residual active state appeared to be the mechanism for this diastolic dysfunction. Similar findings were made retrospectively in dogs instrumented with circumferential segment length gauges ( n =16). Conclusions: Diastolic LV dysfunction was induced by elevated Afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.

Kazuaki Negishi - One of the best experts on this subject based on the ideXlab platform.

  • sex differences in left ventricular Afterload and diastolic function are independent from the aortic size
    PLOS ONE, 2019
    Co-Authors: Hidemi Sorimachi, Masaru Obokata, Koji Kurosawa, Kuniko Yoshida, Takashi Noguchi, Minoru Naka, Shoichi Tange, Masahiko Kurabayashi, Kazuaki Negishi
    Abstract:

    Background Women have a greater risk of heart failure with preserved ejection fraction (HFPEF) than men do, yet the basis for this disparity remains unclear. Greater arterial stiffness and Afterload causes left ventricular (LV) diastolic dysfunction, a central mechanism of HFPEF. Because of smaller body habitus, previous reports have used body surface area as a surrogate of the size of the aorta. We performed a comprehensive hemodynamic evaluation of elderly patients with preserved EF and evaluated sex differences in the associations between LV function and Afterload, before and after adjusting for the aortic sizes. Methods and results Four hundred and forty-three patients (mean age: 73 years, 169 women) who underwent clinically indicated echocardiography and computed tomography (CT) were identified. Linear regression analyses were performed to assess the independent contributions of sex to and its interaction with LV function before and after adjusting for CT-derived aortic length and volume. Although blood pressures were similar between the sexes, women had greater arterial elastance, lower arterial compliance, and greater LV ejection fraction (all p<0.001). Sex differences were detected in the associations between LV Afterload and relaxation (mitral e′) as well as in the left atrial (LA) emptying fraction, but not in LA size. These differences remained significant after adjusting for the aortic length and volume. Sensitivity analyses in an age-matched subgroup (n = 324; 162 of each sex) confirmed the robustness of these sex disparities in LV diastolic function and Afterload. Conclusion Women had worse LV relaxation than men did against the same degree of Afterload, before and even after adjusting for the aortic sizes.

Burkhard Lachmann - One of the best experts on this subject based on the ideXlab platform.

  • the effect of open lung ventilation on right ventricular and left ventricular function in lung lavaged pigs
    Critical Care, 2006
    Co-Authors: Dinis Reis Miranda, Burkhard Lachmann, Ad J.j.c. Bogers, Jack J Haitsma, Lennart Klompe, Filippo Cademartiri, Alessandro Palumbo, Johanna J M Takkenberg, Diederik Gommers
    Abstract:

    Introduction Ventilation according to the open lung concept (OLC) consists of recruitment maneuvers, followed by low tidal volume and high positive end-expiratory pressure, aiming at minimizing atelectasis. The minimization of atelectasis reduces the right ventricular (RV) Afterload, but the increased intrathoracic pressures used by OLC ventilation could increase the RV Afterload. We hypothesize that when atelectasis is minimized by OLC ventilation, cardiac function is not affected despite the higher mean airway pressure.

  • the open lung concept effects on right ventricular Afterload after cardiac surgery
    BJA: British Journal of Anaesthesia, 2004
    Co-Authors: Reis D Miranda, Ad J.j.c. Bogers, Diederik Gommers, Ard Struijs, Han Meeder, Ronald M Schepp, Wim C J Hop, Jan Klein, Burkhard Lachmann
    Abstract:

    Background. The open lung concept (OLC) is a method of ventilation intended to maintain end-expiratory lung volume by increased airway pressure. Since this could increase right ventricular Afterload, we studied the effect of this method on right ventricular Afterload in patients after cardiac surgery. Methods. We studied 24 stable patients after coronary artery surgery and/or valve surgery with cardiopulmonary bypass. Patients were randomly assigned to OLC or conventional mechanical ventilation (CMV). In the OLC group, recruitment manoeuvres were applied until P a 2 / F 2 was greater than 50 kPa (reflecting an open lung). This value was maintained by sufficient positive airway pressure. In the CMV group, volume-controlled ventilation was used with a PEEP of 5 cm H2O. Cardiac index, right ventricular preload, contractility and Afterload were measured with a pulmonary artery thermodilution catheter during the 3-h observation period. Blood gases were monitored continuously. Results. To achieve P a 2 / F 2 > 50 kPa, 5.3 (3) (mean, sd ) recruitment attempts were performed with a peak pressure of 45.5 (2) cm H2O. To keep the lung open, PEEP of 17.0 (3) cm H2O was required. Compared with baseline, pulmonary vascular resistance and right ventricular ejection fraction did not change significantly during the observation period in either group. Conclusion. No evidence was found that ventilation according to the OLC affects right ventricular Afterload.