Aim
Haemodynamic normalisation is the ultimate goal of pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH). However, whether normalisation of haemodynamics ...translates into normalisation of exercise capacity is unknown. The incidence, determinants and clinical implications of exercise intolerance after PEA are unknown. We performed a prospective analysis to determine the incidence of exercise intolerance after PEA, assess the relationship between exercise capacity and (resting) haemodynamics and search for preoperative predictors of exercise intolerance after PEA.
Methods
According to clinical protocol all patients underwent cardiopulmonary exercise testing (CPET), right heart catheterisation and cardiac magnetic resonance (CMR) imaging before and 6 months after PEA. Exercise intolerance was defined as a peak oxygen consumption (
V
′
O
2
) <80% predicted. CPET parameters were judged to determine the cause of exercise limitation. Relationships were analysed between exercise intolerance and resting haemodynamics and CMR-derived right ventricular function. Potential preoperative predictors of exercise intolerance were analysed using logistic regression analysis.
Results
68 patients were included in the final analysis. 45 (66%) patients had exercise intolerance 6 months after PEA; in 20 patients this was primarily caused by a cardiovascular limitation. The incidence of residual pulmonary hypertension was significantly higher in patients with persistent exercise intolerance (p=0.001). However, 27 out of 45 patients with persistent exercise intolerance had no residual pulmonary hypertension. In the multivariate analysis, preoperative transfer factor of the lung for carbon monoxide (
T
LCO
) was the only predictor of exercise intolerance after PEA.
Conclusions
The majority of CTEPH patients have exercise intolerance after PEA, often despite normalisation of resting haemodynamics. Not all exercise intolerance after PEA is explained by the presence of residual pulmonary hypertension, and lower preoperative
T
LCO
was a strong predictor of exercise intolerance 6 months after PEA.
The pathophysiology of chronic thromboembolic pulmonary hypertension (CTEPH) is not fully understood. Poor-quality anticoagulation may contribute to a higher risk of CTEPH after acute pulmonary ...embolism (PE), partly explaining the transition from acute PE to CTEPH. We assessed the association between the time in therapeutic range (TTR) of vitamin-K antagonist (VKA) treatment and incidence of CTEPH after a PE diagnosis.
Case-control study in which the time spent in, under and above therapeutic range was calculated in 44 PE patients who were subsequently diagnosed with CTEPH (cases). Controls comprised 150 consecutive PE patients in whom echocardiograms two years later did not show pulmonary hypertension. All patients were treated with VKA for at least 6 months after the PE diagnosis. Time in (TTR), under and above range were calculated. Mean differences between cases and controls were estimated by linear regression.
Mean TTR during the initial 6-month treatment period was 72% in cases versus 78% in controls (mean difference -6%, 95%CI -12 to -0.1), mainly explained by more time above the therapeutic range in the cases. Mean difference of time under range was 0% (95%CI -6 to 7) and 2% (95CI% -3 to 7) during the first 3 and 6 months, respectively. In a multivariable model, adjusted odds ratios (ORs) for CTEPH were around unity considering different thresholds for 'poor anticoagulation', i.e. TTR <50%, <60% and <70%.
Subtherapeutic initial anticoagulation was not more prevalent among PE patients diagnosed with CTEPH than in those who did not develop CTEPH.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Background Endovascular repair has become a viable alternative for aortic pathological features, including those located within the aortic arch. We investigated the anatomic suitability for branched ...thoracic endovascular repair in patients previously treated with conventional open surgery for aortic arch pathological features. Methods and Results Patients who underwent open surgery for aortic arch pathological features at our institution between 2000 and 2018 were included. Anatomic suitability was determined by strict compliance with the anatomic criteria within manufacturers' instructions for use for each of the following branched thoracic stent grafts: Relay Plus Double-Branched (Terumo-Aortic), TAG Thoracic Branch Endoprosthesis (W.L. Gore & Associates), Zenith Arch Branched Device (Cook-Medical), and Nexus Stent Graft System (Endospan Ltd/Jotec GmbH). Computed tomography angiography images were analyzed with outer luminal line measurements. A total of 377 patients (mean age, 64±14 years; 64% men) were identified, 153 of whom had suitable computed tomography angiography images for measurements. In total, 59 patients (15.6% of the total cohort and 38.6% of the measured cohort) were eligible for endovascular repair using at least one of the devices. Device suitability was 30.9% for thoracic aneurysms, 4.6% for type A dissections, 62.5% for type B dissections, and 28.6% for other pathological features. Conclusions The anatomic suitability for endovascular repair of all aortic arch pathological features was modest. The highest suitability rates were observed for thoracic aneurysms and for type B dissections, of which repair included part of the aortic arch. We suggest endovascular repair of arch pathological features should be reserved for high-volume centers with experience in endovascular arch repair.
According to computed tomography-pulmonary angiography, CTEPH was classified as either proximal (level I/II disease: lesions starting in the main or lobar arteries) or distal (level III-IV disease: ...lesions starting in the segmental and subsegmental) (3) for each side separately. ...Zc may be a relevant additional component of afterload that was not accounted for in the current or any prior studies on load in CTEPH, which all focus on PVR and compliance. ...RV function in CTEPH may be critically dependent on proximal vascular properties and wave propagations, which are not reflected in the three-component windkessel. ...although patients with proximal and distal CTEPH present with similar resistance and compliance, we observed important differences in cardiac function.
Tyrosine kinase inhibitors (TKI) are known to be highly effective in the treatment of various cancers with kinase-domain mutations such as chronic myelogenous leukemia. However, they have important ...side effects such as increased vascular permeability and pulmonary hypertension. In patients undergoing pulmonary endarterectomy with deep hypothermic circulatory arrest, these side effects may exacerbate postoperative complications such as reperfusion edema and persistent pulmonary hypertension. We report on a simple modification of the perfusion strategy to increase intravascular oncotic pressure by retrograde autologous priming and the addition of packed cells and albumin in a patient treated with a TKI.
Objective
Little is known about the prevalence and degree of deformation of surgically implanted aortic biological valve prostheses (bio-sAVRs). We assessed bio-sAVR deformation using ...multidetector-row computed tomography (MDCT).
Methods
Three imaging databases were searched for patients with MDCT performed after bio-sAVR implantation. Minimal and maximal valve ring diameters were obtained in systole and/or diastole, depending on the acquired cardiac phase(s). The eccentricity index (EI) was calculated as a measure of deformation as (1 − (minimal diameter/maximal diameter)) × 100%. EI of < 5% was considered none or trivial deformation, 5–10% mild deformation, and > 10% non-circular. Indications for MDCT and implanted valve type were retrieved.
Results
One hundred fifty-two scans of bio-sAVRs were included. One hundred seventeen measurements were performed in systole and 35 in diastole. None or trivial deformation (EI < 5%) was seen in 67/152 (44%) of patients. Mild deformation (EI 5–10%) was seen in 59/152 (39%) and non-circularity was found in 26/152 (17%) of cases. Overall, median EI was 5.5% (IQR 3.4–7.8). In 77 patients, both systolic and diastolic measurements were performed from the same scan. For these scans, the median EI was 6.5% (IQR 3.4–10.2) in systole and 5.1% (IQR3.1–7.6) in diastole, with a significant difference between both groups (
p
= 0.006).
Conclusions
Surgically implanted aortic biological valve prostheses show mild deformation in 39% of cases and were considered non-circular in 17% of studied valves.
Key Points
• Deformation of surgically implanted aortic valve bioprostheses (bio-sAVRs) can be adequately assessed using MDCT.
• Bio-sAVRs show at least mild deformation (eccentricity index > 5%) in 56% of studied cases and were considered non-circular (eccentricity index > 10%) in 17% of studied valves.
• The higher deformity rate found in bio-sAVRs with (suspected) valve pathology could suggest that geometric deformity may play a role in leaflet malformation and thrombus formation similar to that of transcatheter heart valves.
Background Pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension improves resting hemodynamics and right ventricular (RV) function. Because exercise tolerance frequently ...remains impaired, RV function may not have completely normalized after PEA. Therefore, we performed a detailed invasive hemodynamic study to investigate the effect of PEA on RV function during exercise. Methods and Results In this prospective study, all consenting patients with chronic thromboembolic pulmonary hypertension eligible for surgery and able to perform cycle ergometry underwent cardiac magnetic resonance imaging, a maximal cardiopulmonary exercise test, and a submaximal invasive cardiopulmonary exercise test before and 6 months after PEA. Hemodynamic assessment and analysis of RV pressure curves using the single-beat method was used to determine load-independent RV contractility (end systolic elastance), RV afterload (arterial elastance), RV-arterial coupling (end systolic elastance-arterial elastance), and stroke volume both at rest and during exercise. RV rest-to-exercise responses were compared before and after PEA using 2-way repeated-measures analysis of variance with Bonferroni post hoc correction. A total of 19 patients with chronic thromboembolic pulmonary hypertension completed the entire study protocol. Resting hemodynamics improved significantly after PEA. The RV exertional stroke volume response improved 6 months after PEA (79±32 at rest versus 102±28 mL during exercise;
<0.01). Although RV afterload (arterial elastance) increased during exercise, RV contractility (end systolic elastance) did not change during exercise either before (0.43 0.32-0.58 mm Hg/mL versus 0.45 0.22-0.65 mm Hg/mL;
=0.6) or after PEA (0.32 0.23-0.40 mm Hg/mL versus 0.28 0.19-0.44 mm Hg/mL;
=0.7). In addition, mean pulmonary artery pressure-cardiac output and end systolic elastance-arterial elastance slopes remained unchanged after PEA. Conclusions The exertional RV stroke volume response improves significantly after PEA for chronic thromboembolic pulmonary hypertension despite a persistently abnormal afterload and absence of an RV contractile reserve. This may suggest that at mildly elevated pulmonary pressures, stroke volume is less dependent on RV contractility and afterload and is primarily determined by venous return and conduit function.
Introduction:
Pulmonary endarterectomy requires cardiopulmonary bypass and deep hypothermic circulatory arrest, which may prolong the activated clotting time. We investigated whether activated ...clotting time–guided anticoagulation under these circumstances suppresses hemostatic activation.
Methods:
Individual heparin sensitivity was determined by the heparin dose–response test, and anticoagulation was monitored by the activated clotting time and heparin concentration. Perioperative hemostasis was evaluated by thromboelastometry, platelet aggregation, and several plasma coagulation markers.
Results:
Eighteen patients were included in this study. During cooling, tube-based activated clotting time increased from 719 (95% confidence interval = 566-872 seconds) to 1,273 (95% confidence interval = 1,136-1,410 seconds; p < 0.01) and the cartridge-based activated clotting time increased from 693 (95% confidence interval = 590-796 seconds) to 883 (95% confidence interval = 806-960 seconds; p < 0.01), while thrombin–antithrombin showed an eightfold increase. The heparin concentration showed a slightly declining trend during cardiopulmonary bypass. After protamine administration (protamine-to-heparin bolus ratio of 0.82 (0.71-0.90)), more than half of the patients showed an intrinsically activated coagulation test and intrinsically activated coagulation test without heparin effect clotting time >240 seconds. Platelet aggregation through activation of the P2Y12 (adenosine diphosphate test) and thrombin receptor (thrombin receptor activating peptide-6 test) decreased (both −33%) and PF4 levels almost doubled (from 48 (95% confidence interval = 42-53 ng/mL) to 77 (95% confidence interval = 71-82 ng/mL); p < 0.01) between weaning from cardiopulmonary bypass and 3 minutes after protamine administration.
Conclusion:
This study shows a wide variation in individual heparin sensitivity in patients undergoing pulmonary endarterectomy with deep hypothermic circulatory arrest. Although activated clotting time–guided anticoagulation management may underestimate the level of anticoagulation and consequently result in a less profound inhibition of hemostatic activation, this study lacked power to detect adverse outcomes.
For evaluation of prosthetic heart valve obstruction echocardiography and fluoroscopy provide primarily functional information but may not unequivocally establish the cause of dysfunction. Our ...objective was to evaluate whether multidetector-row computed tomographic (MDCT) imaging could detect the morphologic substrate for such functional abnormalities. Thirteen patients with 15 prosthetic valves, in whom prosthetic valve obstruction was suspected from echocardiography or fluoroscopy but no sufficient cause could be found, underwent electrocardiographically gated multidetector-row computed tomography. MDCT data were retrospectively reconstructed at every 10% of the electrocardiographic interval and analyzed using multiplanar reformatting in anatomically adapted planes. MDCT images were evaluated for morphologic prosthetic and periprosthetic abnormalities. Results could be compared to intraoperative findings or autopsy in 7 patients. Multidetector-row computed tomography disclosed a morphologic substrate for obstruction in 8 of 13 patients. MDCT findings compatible with obstruction were confirmed at surgery or autopsy in 6 patients. In a seventh patient, incomplete leaflet closure found with multidetector-row computed tomography was confirmed at surgery. The most commonly identified causes for obstruction were subprosthetic tissue (6 patients) and abnormal anatomic orientation (3 patients). Despite an indication for surgery, 2 patients were not operated on due to recurrent bacteremias and prohibitive co-morbidity. Multidetector-row computed tomography detected leaflet motion restriction in 7 patients compared to 4 by fluoroscopy. Confirmation of leaflet restriction was available in 5 patients. Multidetector-row computed tomography missed a periprosthetic leak. In conclusion, this initial experience demonstrates that multidetector-row computed tomography can identify causes of prosthetic valve obstruction that constitute indications for surgery but are missed at echocardiography or fluoroscopy.
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