Case report: Serious unexpected vascular events in two patients with lymphocytic variant hypereosinophilic syndrome.

Background: Lymphocytic-variant hypereosinophilic syndrome (L-HES) is a form of reactive hypereosinophilia, most commonly associated with interleukin-5 over-production by clonal, most commonly CD3-CD4+CD2hiCD5hiCD45RO+ T-cells. Patients often present with predominant cutaneous and soft-tissue manifestations, while cardiovascular involvement is uncommon. Methods: We reviewed the medical files of two L-HES patients followed in our center who developed serious vascular complications and performed a literature review for similar cases. Results: Patient 1, a 52-year-old female, presented with an ischemic stroke secondary to left middle cerebral artery dissection after 10 years of indolent L-HES. Blood eosinophilia was controlled with oral corticosteroids (OCS), but OCS-tapering attempts with hydroxyurea and pegylated interferon failed, prompting the introduction of mepolizumab with rapid normalization. Patient 2, a 62-year-old female, had been asymptomatic for 10 years without treatment when a NSTEMI occurred, due to coronary artery occlusion secondary to a large cauliflower-aneurysm of the proximal aorta and aneurysmal dilatation of several coronary arteries, requiring semi-urgent surgical management. Aortic wall staining for eosinophil major basic protein showed eosinophils in the adventitia. Blood eosinophilia was controlled with OCS. Conclusions: Patients with apparently clinically benign L-HES may develop arterial complications, consisting in dissection and/or aneurysm dilatation of medium-to-large vessels with serious consequences. The value of performing regular vascular imaging and monitoring during follow-up has yet to be determined.

Altered Left Ventricular Rat Gene Expression Induced by the Myosin Activator Omecamtiv Mecarbil.

To explore the impact of omecamtiv mecarbil (OM) on the gene expression profile in adult male rats. Fourteen male Wistar rats were randomly assigned to a single OM (1.2 mg/kg/h; n = 6) or placebo (n = 8) 30-min infusion. Echocardiography was performed before and after OM infusion. Seven days after infusion, rats were euthanized, and left ventricular (LV) tissues were removed for real-time quantitative polymerase chain reaction (RTq-PCR) experiments. After OM infusion, pro-apoptotic Bax-to-Bcl2 ratio was decreased, with increased Bcl2 and similar Bax gene expression. The gene expression of molecules regulating oxidative stress, including glutathione disulfide reductase (Gsr) and superoxide dismutases (Sod1/Sod2), remained unchanged, whereas the expression of antioxidant glutathione peroxidase (Gpx) increased. While LV gene expression of key energy sensors, peroxisome proliferator activator (Ppar) α and γ, AMP-activated protein kinase (Ampk), and carnitine palmitoyltransferase 1 (Cpt1) remained unchanged after OM infusion, and the expression of pyruvate dehydrogenase kinase 4 (Pdk4) increased. The LV expression of the major myocardial glucose transporter Glut1 decreased, with no changes in Glut4 expression, whereas the LV expression of oxidized low-density lipoprotein receptor 1 (Olr1) and arachidonate 15-lipoxygenase (Alox15) increased, with no changes in fatty acid transporter Cd36. An increased LV expression of angiotensin II receptors AT1 and AT2 was observed, with no changes in angiotensin I-converting enzyme expression. The Kalikrein-bradykinin system was upregulated with increased LV expression of kallikrein-related peptidases Klk8, Klk1c2, and Klk1c12 and bradykinin receptors B1 and B2 (Bdkrb1 and Bdkrb2), whereas the LV expression of inducible nitric oxide synthase 2 (Nos2) increased. LV expression in major molecular determinants involved in calcium-dependent myocardial contraction remained unchanged, except for an increased LV expression of calcium/calmodulin-dependent protein kinase II delta (Cacna1c) in response to OM. A single intravenous infusion of OM, in adult healthy rats, resulted in significant changes in the LV expression of genes regulating apoptosis, oxidative stress, metabolism, and cardiac contractility.

A novel metrics to predict right heart failure after left ventricular assist device implantation.

BACKGROUND: Right Heart Failure (RHF) is a severe complication that can occur after left ventricular assist device (LVAD) implantation, increasing early and late mortality. Although numerous RHF predictive scores have been developed, limited data exist on the external validation of these models. We therefore aimed at comparing existent risk score models and identifying predictors of severe RHF at our center. METHODS: In this retrospective, single-center analysis, clinical, biological and functional data were collected in patients implanted with a LVAD between 2011 and 2020. Early severe RHF was defined as the use of inotropes for ≥ 14 days, nitric oxide use for ≥ 48 h or unplanned right-sided circulatory support. Risk models were evaluated for the primary outcome of RHF or RVAD implantation by means of logistic regression and receiver operating characteristic curves. RESULTS: Among 92 patients implanted, 24 (26%) developed early severe RHF. The EUROMACS-RHF risk score performed the best in predicting RHF (C = 0.82-95% CI: 0.68-0.90), compared with the other scores (Michigan, CRITT). In addition, we developed a new model, based on four variables selected for the best reduced logistic model: the INTERMACS level, the number of inotropes used, the ratio of right atrial/pulmonary capillary wedge pressure and the ratio of right ventricle/left ventricle diameters by echocardiography. This model demonstrated significant discrimination of RHF (C = 0.9-95% CI: 0.76-0.96). CONCLUSION: Amongst available risk scores, EUROMACS-RHF performs best to predict the occurrence of RHF after LVAD implantation. Our model's performance compares well to the EUROMACS-RHF score, adding a more objective parameter to RV function evaluation.

Lung diffusion capacity correlates with pre-implant pulmonary hypertension and predicts outcome after LVAD implantation.

AIMS: Diffusing capacity of the lung for carbon monoxide (DLCO ) reduction is common in heart failure (HF) and is associated with a worse prognosis. Correlations between DLCO and pulmonary hypertension (PH) are unclear, and published data are conflicting; it has been shown that DLCO impairment may persist or even worsen after normalization of pulmonary pressures following left ventricle assist device (LVAD) implantation, maybe reflecting persistent pulmonary damage. We aimed to investigate the impact of pre-implant DLCO and central haemodynamics on outcome in patients with advanced HF implanted with a LVAD. METHODS AND RESULTS: We retrospectively analysed pre-implant and post-implant data from 42 patients implanted with a LVAD at our institution. Out of 42 patients, 35 had post-capillary PH before implantation, including 17 with combined post- and pre-capillary PH (Cpc-PH). Median DLCO was 59% (IQR 47-68%), and it inversely correlated with pulmonary vascular resistance (PVR) (P 0.037) and diastolic pulmonary gradient (DPG) (P 0.042). Compared with baseline, LVAD resulted in improvement in LV diameter (LVDd, P < 0.001), mitral regurgitation (P 0.022), and PH (mPAP 24 vs. 36 mmHg, P < 0.001; PAWP 12 vs. 23 mmHg, P 0.001; pulmonary artery compliance, CPA 3.1 vs. 1.9 mL/mmHg, P 0.021). Lower DLCO and Cpc-PH at baseline were associated with a better LV reverse remodelling post-implantation (P 0.027 for LVDd) but also with a smaller gain in CPA (P 0.049). CONCLUSIONS: Before LVAD implantation, DLCO impairment is associated with higher PVR and DPG, suggesting that it might be an expression of persistent pulmonary damage occurring in Cpc-PH. After LVAD implantation, both LV dimension and haemodynamics improve. Lower pre-implant DLCO is associated with better LV reverse remodelling.

Detection of soluble suppression of tumorigenicity 2 and N-terminal B-type natriuretic peptide in a rat model of aortic regurgitation: differential responses to omecamtiv mecarbil.

OBJECTIVES: Both N-terminal fragment of B-type natriuretic peptide (NT-proBNP) and soluble isoform of ST2 (sST2) have been identified as biomarkers of heart failure. We evaluated the plasma levels of NT-proBNP and sST2 in a rat model of severe aortic valve regurgitation (AR) and correlated these findings with echocardiographic measurements. We also examined the impact of omecamtiv mecarbil (OM) on these parameters. METHODS: The plasma levels of NT-proBNP and sST2 were measured in 18 rats both before and 2 months after surgical induction of AR, and at these same time points, in six rats assigned to a sham-procedure control group. Plasma biomarkers were then measured again after infusion of OM or placebo in rats with AR (n=8 and 10, respectively) and OM alone in the sham control rats (n=6). Echocardiographic measurements were collected before and 2 months after induction of AR. RESULTS: Our results revealed increased levels of plasma NT-proBNP (219 ± 34 pg/mL vs. 429 ± 374 pg/mL; p<0.001) in rats with AR at day 7 after infusion of placebo, whereas plasma levels of sST2 were higher in this cohort after infusion of either OM or placebo. We identified a significant positive correlation between plasma sST2 with posterior wall thickness in diastole (r=0.34, p<0.05) and total body weight (r=0.45, p<0.01) in rats with surgically induced AR. CONCLUSIONS: Because sST2 increased markedly, whereas NT-proBNP remained unchanged, when OM was administered, we hypothesize that sST2 has a distinct capability to detect deleterious effects of passive muscle tension, not reliably assessed by NT-proBNP, in the setting of AR.

Long-Term Outcome After Venoarterial Extracorporeal Membrane Oxygenation as Bridge to Left Ventricular Assist Device Preceding Heart Transplantation.

OBJECTIVES: To determine if venoarterial extracorporeal membrane oxygenation (VA ECMO) as a bridge to left ventricular assist device (LVAD) in heart transplant (HT) candidates (ie, double bridge to HT) was associated with increased morbidity and mortality when compared to LVAD bridging to HT (ie, single bridge to HT). DESIGN: A retrospective analysis of patients undergoing LVAD support from 2011 to 2020. A Kaplan-Meier survival curve and Cox-Mantel hazard ratios (HR) were calculated during LVAD support and after HT. Postoperative complications were collected. SETTING: University Hospital Erasme. PARTICIPANTS: HT candidates requiring LVAD. INTERVENTIONS: VA ECMO bridging to LVAD (ECMO-LVAD group [n = 24]) versus LVAD (LVAD group [n = 64]). MEASUREMENTS AND MAIN RESULTS: Eighty-eight patients underwent HeartWare LVAD (HVAD, Medtronic) placement. Survival to hospital discharge and during the entire study period were lower in the ECMO-LVAD group (66.7% v 92.2%; p = 0.0027, and 37.5% v 62.5%; p = 0.035, respectively). Overall HR of death was 2.46 (95% confidence interval [CI]: 1.13-5.37; p = 0.005) in the ECMO-LVAD group and remained elevated throughout their time on LVAD support (HR 3.24 [95% CI: 1.15-9.14]; p = 0.0036). However, in patients who underwent HT (n = 50), mortality was similar between groups (HR 1.33 [95% CI: 0.33-5.31]; p = 0.66). Postoperative complications were more frequent in the ECMO-LVAD group (infection = 83.3% v 51.6%, p = 0.007; renal replacement therapy = 45.8% v 9.4%, p = 0.0001; post-LVAD ECMO = 25.0% v 1.6%; p = 0.0003). CONCLUSIONS: VA ECMO as a bridge to LVAD support before HT was associated with increased morbidity and mortality during LVAD support. However, in patients who underwent HT, outcomes were similar regardless of VA ECMO bridging.

The myosin activator omecamtiv mecarbil improves wall stress in a rat model of chronic aortic regurgitation.

In patients with chronic aortic regurgitation (AR), excessive preload and afterload increase left ventricle wall stress, leading to left ventricular systolic dysfunction. Thus, the objective of the present study was to evaluate the effects of the myosin activator omecamtiv mecarbil (OM) on left ventricle wall stress in an experimental rat model of severe chronic AR. Forty adult male Wistar rats were randomized into two experimental groups: induction of AR (acute phase) by retrograde puncture (n = 34) or a sham intervention (n = 6). Rats that survived the acute phase (n = 18) were randomized into an OM group (n = 8) or a placebo group (n = 10). Equal volumes of OM (1.2 mg/kg/h) or placebo (0.9% NaCl) were continuously infused into the femoral vein over 30 min. OM significantly decreased end-systolic and end-diastolic and maximum wall stress in this experimental rat model of chronic severe AR (p < 0.001) and increased systolic performance assessed by fractional shortening and left ventricle end-systolic diameter; both p < 0.05). These effects were correlated with decreased indices of global cardiac function (cardiac output and stroke volume; p < 0.05) but were not inferior to baseline pump indices. Infusion with placebo did not affect global cardiac function but decreased end-systolic wall stress (p < 0.05) and increased systolic performance (all p < 0.001). In the sham-operated (control) group, OM decreased diastolic wall stress (p < 0.05). Based on these results, OM had a favorable effect on left ventricle wall stress in an experimental rat model of severe chronic AR.

Ability of a New Smartphone Pulse Pressure Variation and Cardiac Output Application to Predict Fluid Responsiveness in Patients Undergoing Cardiac Surgery.

BACKGROUND: Pulse pressure variation (PPV) can be used to predict fluid responsiveness in anesthetized patients receiving controlled mechanical ventilation but usually requires dedicated advanced monitoring. Capstesia (Galenic App, Vitoria-Gasteiz, Spain) is a novel smartphone application that calculates PPV and cardiac output (CO) from a picture of the invasive arterial pressure waveform obtained from any monitor screen. The primary objective was to compare the ability of PPV obtained using the Capstesia (PPVCAP) and PPV obtained using a pulse contour analysis monitor (PPVPC) to predict fluid responsiveness. A secondary objective was to assess the agreement and the trending of CO values obtained with the Capstesia (COCAP) against those obtained with the transpulmonary bolus thermodilution method (COTD). METHODS: We studied 57 mechanically ventilated patients (tidal volume 8 mL/kg, positive end-expiratory pressure 5 mm Hg, respiratory rate adjusted to keep end tidal carbon dioxide [32-36] mm Hg) undergoing elective coronary artery bypass grafting. COTD, COCAP, PPVCAP, and PPVPC were measured before and after infusion of 5 mL/kg of a colloid solution. Fluid responsiveness was defined as an increase in COTD of >10% from baseline. The ability of PPVCAP and PPVPC to predict fluid responsiveness was analyzed using the area under the receiver-operating characteristic curve (AUROC), the agreement between COCAP and COTD using a Bland-Altman analysis and the trending ability of COCAP compared to COTD after volume expansion using a 4-quadrant plot analysis. RESULTS: Twenty-eight patients were studied before surgical incision and 29 after sternal closure. There was no significant difference in the ability of PPVCAP and PPVPC to predict fluid responsiveness (AUROC 0.74 [95% CI, 0.60-0.84] vs 0.68 [0.54-0.80]; P = .30). A PPVCAP >8.6% predicted fluid responsiveness with a sensitivity of 73% (95% CI, 0.54-0.92) and a specificity of 74% (95% CI, 0.55-0.90), whereas a PPVPC >9.5% predicted fluid responsiveness with a sensitivity of 62% (95% CI, 0.42-0.88) and a specificity of 74% (95% CI, 0.48-0.90). When measured before surgery, PPV predicted fluid responsiveness (AUROC PPVCAP = 0.818 [P = .0001]; PPVPC = 0.794 [P = .0007]) but not when measured after surgery (AUROC PPVCAP = 0.645 [P = .19]; PPVPC = 0.552 [P = .63]). A Bland-Altman analysis of COCAP and COTD showed a mean bias of 0.3 L/min (limits of agreement: -2.8 to 3.3 L/min) and a percentage error of 60%. The concordance rate, corresponding to the proportion of CO values that changed in the same direction with the 2 methods, was poor (71%, 95% CI, 66-77). CONCLUSIONS: In patients undergoing cardiac surgery, PPVCAP and PPVPC both weakly predict fluid responsiveness. However, COCAP is not a good substitute for COTD and cannot be used to assess fluid responsiveness.

Proximal pressure reducing effect of wave reflection in the pulmonary circulation disappear in obstructive disease: insight from a rabbit model.

Locating the site of increased resistance within the vascular tree in pulmonary arterial hypertension could assist in both patient diagnosis and tailoring treatment. Wave intensity analysis (WIA) is a wave analysis method that may be capable of localizing the major site of reflection within a vascular system. We investigated the contribution of WIA to the analysis of the pulmonary circulation in a rabbit model with animals subjected to variable occlusive pulmonary disease. Animals were embolized with different sized microspheres for 6 wk ( n = 10) or underwent pulmonary artery (PA) ligation for 6 wk ( n = 3). These animals were compared with a control group ( n = 6) and acutely embolized animals ( n = 4). WIA was performed and compared with impedance-based methods to analyze wave reflections. The control group showed a relatively high extent of reflected waves (15.7 ± 10.6%); reflections had a net effect of pressure reduction during systole, suggesting an open-end reflector. The pattern of wave reflection was not different in the group with partial PA ligation (12.4 ± 4.1%). In the chronically embolized group, wave reflection was not observed (3.6 ± 1.5%). In the acute embolization group, wave reflection was more prominent (37.3 ± 12.6%), with the appearance of a novel wave increasing pressure, suggesting the appearance of a closed-end reflector. Wave reflections of an open-end type are present in the normal rabbit pulmonary circulation. However, the pattern and nature of reflections vary according to the extent of pulmonary vascular occlusion. NEW & NOTEWORTHY The study proposes an original framework of a complementary analysis of wave reflections in the time domain and in the frequency domain. The methodology was used in the pulmonary circulation with different forms of chronic obstructions. The results suggest that the pulmonary vascular tree generates a reflection pattern that could actually assist the heart during ejection, and chronic obstruction significantly modifies the pattern.

Effects of the cardiac myosin activator Omecamtiv-mecarbil on severe chronic aortic regurgitation in Wistar rats.

BACKGROUND: Aortic regurgitation (AR) is a valvular disease that can lead to systolic heart failure. Treatment options besides cardiac surgery are limited and consequently severe AR is associated with higher mortality and morbidity when not operated. In this investigation, we examined the effects of a novel cardiac myosin activator, Omecamtiv-mecarbil (OM), in rats with chronic severe AR. METHODS: AR was created by retrograde puncture of the aortic valve leaflets in 20 adults Wistar rats. 12 animals survived the acute AR phase and were randomized 2 months thereafter into OM (n = 7) or placebo groups (n = 5). Two rats underwent a sham operation and served as controls. Equal volumes of OM or placebo (NaCl 0.9%) were perfused in the femoral vein by continuous infusion (1.2 mg/kg/hour) during 30 min. Doppler-echocardiography was performed before and at the end of the infusion periods. RESULTS: OM increased indices of global cardiac function (cardiac output, stroke volume), and increased systolic performance (fractional shortening, ejection fraction, left ventricular end systolic diameter) (all p < 0.05). These effects concurred with decreases in indices of LV preload (left atrial size, left ventricular end diastolic diameter) as well in the aortic pre-ejection period / left ventricular ejection time ratio (all p < 0.05). The severity score of the regurgitant AR jet did not change. Placebo infusion did not affect these parameters. CONCLUSION: The cardiac myosin activator OM exerts favorable hemodynamic effects in rats with experimental chronic AR.

Measuring pulmonary arterial compliance: mission impossible? Insights from a novel in vivo continuous-flow based experimental model.

Arterial compliance (C) is related to the elasticity, size, and geometrical distribution of arteries. Compliance is a determinant of the load that impedes ventricular ejection. Measuring compliance is difficult, particularly in the pulmonary circulation in which resistive and compliant vessels overlap. Comparing different methods for quantification of compliance to a method that involves a continuous flow might help to identify the optimal method. Pulmonary arterial compliance was computed in six pigs based on the stroke volume to pulse pressure ratio, diastolic decay exponential fitting, area method, and the pulse pressure method (PPM). Compliance measurements were compared to those obtained under continuous flow conditions through a right ventricular bypass (Heartware Inc., Miami Lakes, FL, USA). Compliance was computed for various flows using diastolic decay exponential fitting after an abrupt interruption of the pump. Under the continuous flow conditions, resistance (R) was a decreasing function of the flow, and the fitting to P = e-t/RC yielded a pulmonary time constant (RC) of 2.06 s ( ± 0.48). Compliance was an increasing function of flow. Steady flow inter-method comparisons of compliance under pulsatile flow conditions showed large discrepancies and values (7.23 ± 4.47 mL/mmHg) which were lower than those obtained under continuous flow conditions (10.19 ± 1 0.31 mL/mmHg). Best agreement with steady flow measurements is obtained with the diastolic decay method. Resistance and compliance are both flow-dependent and are inversely related in the pulmonary circulation. The dynamic nature of the pulsatile flow may induce a non-uniformly distributed compliance, with an influence on the methods of measurement.

Chronic kidney disease as major determinant of the renal risk related to on-pump cardiac surgery: a single-center cohort study.

BACKGROUND: Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common complication and is associated with the poorest outcomes. Therefore, early prediction of CSA-AKI remains a major issue. Severity scores such as the STS score could estimate the risk of AKI preoperatively. The main objective of this study was to evaluate the risk factors of on-pump CSA-AKI and to assess the performance of the STS score in order to predict CSA-AKI. PATIENTS: We identified 252 patients with on-pump cardiac surgery, and the STS score was defined retrospectively. RESULTS: AKI occurred in 14.6% (n = 37/252) of patients and renal replacement therapy was required in 21.6% of AKI (n = 8/37). CSA-AKI was associated with 35.1% in-hospital mortality (vs. 1.4%) and nearly doubled length of stay (14.5 vs. 8.0 d). The risk of CSA-AKI was mainly determined by preoperative morbidities such as chronic kidney disease, peripheral vascular disease, and severe congestive heart failure. Long cardio-pulmonary bypass time was also a determinant. CSA-AKI + patients exhibited higher STS renal risk (5.6% vs. 2.0%; p < 0.0001), resulting in a good discrimination between AKI + and AKI - patients (area under curve [AUC] 0.80). Interestingly, a basal renal function ≤55 ml/min/1.73m2 was as good as the STS score to predict CSA-AKI (AUC 0.75; P 0.26). CONCLUSIONS: On-pump CSA-AKI was observed in nearly 15% of cases and was associated with poorer outcomes. Interestingly, the risk of CSA-AKI could be estimated preoperatively, thanks to the basal renal function, which exhibited an equal performance to the STS score.

The linear relationship between systolic pulmonary artery pressure and mean pulmonary artery pressure is maintained regardless of autonomic or rhythm disturbances.

BACKGROUND: In the pulmonary circulation, there is a linear relationship between systolic pulmonary arterial pressure (SPAP) and mean pulmonary arterial pressure (MPAP). The aim of this study was to determine the passive or active nature of this mechanism by exploring the relationship in patients with and without autonomic rhythm control of the heart and pulmonary circulation. METHODS: Pulmonary arterial pressure recordings from non-transplanted patients and patients with heart transplants or double lung transplants were retrospectively reviewed. The relationships between systolic, diastolic, and mean pulmonary arterial pressures were explored. RESULTS: A linear relationship was observed between the SPAP and MPAP, whether patients were paced (MPAP = 0.56 SPAP + 3.86 mmHg, r (2) = 0.889), treated with inotropes (MPAP = 0.55 SPAP + 5.52 mmHg, r (2) = 0.947) or pulmonary vasodilators (MPAP = 0.58 SPAP + 2.41 mmHg, r (2) = 0.927), were exercising (MPAP = 0.61 SPAP + 1.18 mmHg, r (2) = 0.967), had a heart transplant (MPAP = 0.66 SPAP +0.87 mmHg, r (2) = 0.849), a double lung transplant (MPAP = 0.7 SPAP +0.48 mmHg, r (2) = 0.915), or no intervention (MPAP = 0.59 SPAP +1.75 mmHg, r (2) = 0.937). CONCLUSION: We demonstrate that the linear relationship between SPAP and MPAP remains in several situations. Therefore, we conclude that the underlying mechanism is a passive consequence of the elastic properties of the cardiopulmonary unit.

How to cope with a temporarily aborted transplant program: solutions for a prolonged waiting period.

BACKGROUND: Due to budgetary restrictions our university heart transplant program came to a standstill to be gradually restarted early 2011. Consequently waiting-times for transplantation increased dramatically beyond the usual 10-15 months. We reviewed the clinical results of this peculiar transplant program over the past 4 years. METHODS: Since March 2011 until February 2015, 65 patients (age 48±23 years) were listed for heart transplantation. Eight patients (11%) of whom three in high emergency were transplanted without any form of mechanical assistance. Fifty-one patients required a left ventricular assist device (LVAD) Heartware (Heartware Inc., Miami Lakes, FL, USA) as a bridge-to-transplant due to terminal heart failure. Merely 5 listed patients remain without assistance. RESULTS: One patient without assistance and 11 LVAD patients (22%) died on the waiting-list. Meanwhile 10 LVAD patients were transplanted after a 2-year waiting time (770±717 days). Four transplanted patients died of early graft failure none after LVAD explantation. Survival at 1 and 3 years was respectively 78 (72%) and 83 (78%) for transplanted and assisted patients (log-rank P=0.056). Cox multivariable regression analysis identified crash-to-burn patients (P=0.002) and waiting-times over 2 years (P=0.044) as risk factors for early death, while age above 60 (P=0.008) and ischemic aetiology (P=0.029) and pulmonary hypertension (P=0.092) were risk factors for survival. CONCLUSIONS: In times of donor shortage mechanical assistance proves very effective as bridge-to-transplant in patients for whom candidacy follows the standard inclusion procedures. In our settings, a steep increase in LVAD implantation served to salvage patients for whom transplantation became jeopardized due to an ever increasing waiting-time. Circulatory LVAD support could be considered as primary therapy in the future.

Is there a place for intra-aortic balloon counterpulsation support in acute right ventricular failure by pressure-overload?

BACKGROUND: Most therapeutic strategies for acute right ventricular failure (RVF) by pressure-overload are directed to improve cardiac output and coronary perfusion pressure by vasopressive agents. The eventual role of intra-aortic balloon counterpulsation (IABP) support remains questionable. This study investigates the contribution of IABP for acute RVF by pressure-overload, in comparison with phenylephrine (PE) and norepinephrine (NOR). METHODS: Acute RVF is induced by fixed pulmonary artery constriction in 6 pigs, pursuing a 50% reduction of cardiac output. Assessment of the treatment interventions included biventricular PV-loop analysis, and continuous measurement of aortic and right coronary artery flow. RESULTS: Restoration of baseline cardiac output was only observed by administration of NOR (Baseline=3.82±1.52ml/min - RVF=2.03±0.59ml/min - IABP=2.45±0.62ml/min - PE=2.98±0.63ml/min - NOR=3.95±0.73ml/min, p<0.001). NOR had most effect on biventricular contractility (PRSW-slope-RV: IABP +24% - PE +59% - NOR +208%, p<0.001 and PRSW-slope-LV: IABP +36% - PE +53% - NOR +196%, p<0.001), heart rate acceleration (IABP +7% - PE +12% - NOR +51%, p<0.001), and RCA flow (IABP +31% - PE +58% - NOR +180%, p<0.001), concomitant to a higher increase of LV-to-RV pressure ratio (IABP: +7% versus -3%, PE: +36% versus +8%, NOR: +101% versus 42%). The hemodynamic contribution of IABP was limited, unless a modest improvement of LV compliance during PE and NOR infusion. CONCLUSION: In a model of acute pressure-overload RV failure, IABP appears to offer limited hemodynamic benefit. The administration of norepinephrine is most effective to correct systemic output and myocardial perfusion through adding an inotropic and chronotropic effect to systemic vasopression.

Patient-prosthesis mismatch in the mitral position affects midterm survival and functional status.

BACKGROUND: The definition and incidence of patient-prosthesis mismatch (PPM) in the mitral position are unclear. OBJECTIVES: To determine the impact of PPM on late survival and functional status after mitral valve replacement with a mechanical valve. METHODS: Between 1992 and 2005, 714 patients (mean [± SD] age 60±10 years) underwent valve replacement with either St Jude (St Jude Medical Inc, USA) (n=295) or Carbomedics (Sulzer Carbomedics Inc, USA) (n=419) valves. There were 52 concomitant procedures (50 tricuspid annuloplasties, 25 foramen oval closures and 20 radiofrequency mazes). The mean clinical follow-up period was 4.4±3.3 years. The severity of PPM was established with cut-off values for an indexed effective orifice area (EOAi) of lower than 1.2 cm(2)/m(2), lower than 1.3 cm(2)/m(2) and lower than 1.4 cm(2)/m(2). Parametric and nonparametric tests were used to determine predictors of outcome. RESULTS: The prevalence of PPM was 3.7%, 10.1% and 23.5% when considering values of lower than 1.2 cm(2)/m(2), lower than 1.3 cm(2)/m(2) and lower than 1.4 cm(2)/m(2), respectively. When considering functional improvement, patients with an EOAi of 1.4 cm(2)/m(2) or greater had a better outcome than those with an EOAi of lower than 1.4 cm(2)/m(2) (OR 1.98; P=0.03). When building a Cox-proportional hazard model, PPM with an EOAi of less than 1.3 cm(2)/m(2) was an independent predictive factor for midterm survival (HR 2.24, P=0.007). Other factors affecting survival were age (HR 1.039), preoperative New York Heart Association class (HR 1.96) and body surface area (HR 0.31). CONCLUSIONS: In a large cohort of patients undergoing mitral valve replacement with mechanical prostheses, PPM defined as an EOAi of lower than 1.3 cm(2)/m(2) significantly decreased midterm survival. This level of PPM was observed in 10.2% of patients. Patients with an EOAi of 1.4 cm(2)/m(2) or greater had greater improvement of their functional status.

Robotic-assisted surgical myotomy in a 27-year-old man with myocardial bridging of the left anterior descending coronary artery.

Myocardial bridging (MB) is a frequent condition usually considered benign but it may be associated with myocardial ischemia. When bridging is symptomatic, therapeutic options are numerous and in the absence of guidelines all options are conceivable. This is a case of a 27-year-old man who benefited from a new surgical approach: myotomy for MB of the left anterior descending coronary artery with the help of left robotic thoracoscopy.