Prophylactic veno-arterial extracorporeal membrane oxygenation in patients undergoing high-risk percutaneous coronary intervention.

PURPOSE: Complex high-risk percutaneous coronary intervention (PCI) is challenging and frequently accompanied by haemodynamic instability. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) can provide cardiopulmonary support in high-risk PCI. However, the outcome is unclear. METHODS: A two-centre, retrospective study was performed of all patients undergoing high-risk PCI and receiving VA-ECMO for cardiopulmonary support. RESULTS: A total of 14 patients (92% male, median age 69 (53-83) years), of whom 50% had previous coronary artery disease in the form of a coronary artery bypass graft (36%) and a PCI (14%) underwent high-risk PCI and received VA-ECMO support. The main target lesion was a left main coronary artery in 78%, a left anterior descending artery in 14%, a right coronary artery in 7%, and 71% underwent multi-vessel PCI in addition to main target vessel PCI. The median SYNTAX score was 27.2 (8-42.5) and in 64% (9/14) there was a chronic total occlusion. Left ventricular function was mildly impaired in 7% (1/14), moderately impaired in 14% (2/14) and severely impaired in 64% (9/14). Cannulation was femoral-femoral in all patients. Median ECMO run was 2.57 h (1-4). Survival was 93% (13/14). One patient died during hospitalisation due to refractory cardiac failure. All other patients survived to discharge. Complications occurred in 14% (2/14), with one patient developing a transient ischaemic attack post-ECMO and one patient developing a thrombus in the femoral vein used for ECMO cannulation. CONCLUSION: VA-ECMO in high-risk PCI is feasible with a good outcome. It can be successfully used for cardiopulmonary support in selected patients.

Safety and efficacy of balloon pulmonary angioplasty in chronic thromboembolic pulmonary hypertension in the Netherlands.

BACKGROUND: Balloon pulmonary angioplasty (BPA) is an emerging treatment in patients with chronic thromboembolic pulmonary hypertension (CTEPH) and chronic thromboembolic disease (CTED). We describe the first safety and efficacy results of BPA in the Netherlands. METHODS: We selected all consecutive patients with inoperable CTEPH and CTED accepted for BPA treatment who had a six-month follow-up in the St. Antonius Hospital in Nieuwegein and the Amsterdam University Medical Center (UMC) in Amsterdam. Functional class (FC), N­terminal pro-brain natriuretic peptide (NT-proBNP), 6­minute walking test distance (6MWD) and right-sided heart catheterisation were performed at baseline and six months after last BPA. Complications for each BPA procedure were noted. RESULTS: A hundred and seventy-two BPA procedures were performed in 38 patients (61% female, mean age 65 ± 15 years). Significant improvements six months after BPA treatment were observed for functional class (63% FC I/II to 90% FC I/II, p = 0.014), mean pulmonary artery pressure (-8.9 mm Hg, p = 0.0001), pulmonary vascular resistance (-2.8 Woods Units (WU), p = 0.0001), right atrial pressure (-2.0 mm Hg, p = 0.006), stroke volume index (+5.7 ml/m2, p = 0.009) and 6MWD (+48m, p = 0.007). Non-severe complications occurred in 20 (12%) procedures. CONCLUSIONS: BPA performed in a CTEPH expert centre is an effective and safe treatment in patients with inoperable CTEPH.

Healthcare utilization in chronic thromboembolic pulmonary hypertension after acute pulmonary embolism.

Essentials Diagnostic delay of chronic thromboembolic pulmonary hypertension (CTEPH) is long. We explored healthcare utilisation of patients diagnosed with CTEPH after pulmonary embolism. A large number of physicians were consulted and test results were not always interpreted correctly. Better education and higher awareness of CTEPH may lead to faster diagnosis. SUMMARY: Background The median diagnostic delay of chronic thromboembolic pulmonary hypertension (CTEPH) is 14 months, which may affect prognosis. We aimed to explore the healthcare utilization of patients diagnosed with CTEPH after acute pulmonary embolism (PE), and to identify the causes of diagnostic delay. Methods We collected all data on patient symptoms, medical specialist referrals and ordered diagnostic tests to reconstruct the clinical pathways of 40 patients referred to the VU University Medical Center Amsterdam (VUMC, the Netherlands) for CTEPH treatment. Diagnostic delay was defined as the time between first symptom onset and referral to the VUMC. Correlations of patient-specific characteristics and diagnostic delay were evaluated. Results Patients consulted four (median) different physicians for a median of 13 (interquartile range [IQR] 10-18) consultations before the correct diagnosis was made. The median diagnostic delay was 21 months (IQR 12-49 months). Echocardiographic results suggestive of CTEPH were not always followed by an adequate work-up; most patients were not subjected to ventilation/perfusion scanning. Prior cardiopulmonary comorbidity and recurrent venous thromboembolism were predictors of a longer delay. Conclusion Healthcare utilization in patients before their final CTEPH diagnosis was far from optimal, contributing to a considerable diagnostic delay. Better education and higher awareness of CTEPH among PE caretakers may lead to faster diagnosis.

[Chronic thromboembolic pulmonary hypertension: recognition, diagnosis and treatment]. / Chronische trombo-embolische pulmonale hypertensie.

- Chronic thromboembolic pulmonary hypertension (CTEPH), characterised by pulmonary hypertension and persistent perfusion defects despite adequate anticoagulation, causes significant morbidity and mortality.- Persistent dyspnoea after acute pulmonary embolism is frequent and an indication for additional diagnostics. Only a minority of these patients develop CTEPH.- Echocardiography and perfusion scintigraphy are the cornerstone of diagnostics when suspecting CTEPH. Right-heart catheterisation and pulmonary angiography should confirm the diagnosis.- The diagnostic phase is preferably carried out in an expert centre in order to optimise the diagnosis and choose the optimal treatment for each individual patient.- Treatment of patients with CTEPH is a multidisciplinary team effort.- Pulmonary endarterectomy is the only potentially curative treatment; perioperative mortality is less than 5% in experienced centres. Inoperable patients can be treated with medication that specifically targets pulmonary arterial hypertension, but a survival benefit has not yet been shown for this medication.- Balloon pulmonary angioplasty has recently become available in the Netherlands as a treatment option, but the exact role of this new technique in the treatment of patients with CTEPH still needs to be investigated.

HNK-1 expression patterns in the embryonic rat heart distinguish between sinuatrial tissues and atrial myocardium.

HNK-1 expression was studied by immunohistochemistry in serial sections of embryonic and fetal rat hearts from 11.5 to 16.5 embryonic days. Graphic reconstructions were made to obtain detailed 3D information on the localization of immunoreactive tissues. The antibody used appeared to stain most parts of the venous sinus and the sinuatrial transitional zone as well as the atrioventricular transitional zone, but the patterns varied through the different developmental stages. At 11.5 days, positive myocardium was found in the right atrium and on top of the ventricular septal primordium. At 13.5 days, the left venous valve and the posterior atrial wall containing the orifice of the pulmonary vein were immunoreactive, and so were the right venous valve, the septum spurium and the superior, right-lateral and inferior parts of the atrioventricular canal. From the latter, immunoreactivity continued onto the crest of the ventricular septum. At 15.5 days, HNK-1 positivity in the two venous valves had become continuous, whereas the right-lateral part of the atrioventricular canal had lost its positivity, thus making the positive areas in the superior and inferior parts of this canal discontinuous. From the venous valves immunoreaction continued into the venous sinus septum but this area remained discontinuous with the inferior part of the atrioventricular canal. It is concluded that the entirety of venous sinus and sinuatrial transitional zone expresses the HNK-1 antigen and that the orifice of the pulmonary vein belongs to this complex, rather than to the embryonic atrium proper, which is HNK-1 negative. Extrapolation of these data to the adult human atrium leads to the conclusion hat most "atrial septal structures" are of sinuatrial origin, leaving the flap valve of the oval fossa (atrial septum primum) as the only really atrial structure. It is suggested that the atrioventricular node is derived from the inferior portion of the atrioventricular canal, and that two expansions of sinuatrial tissue form the substrate for anterior and posterior atrionodal inputs which in the literature have been described as internodal tracts.

Platelet-activating factor antagonism: a new concept in the management of regional myocardial ischemia-reperfusion injury.

Reperfusion therapies for treatment of myocardial infarction successfully reduce patient mortality; however, regional myocardial ischemia-reperfusion (RMIR) causes its own expression of cardiovascular dysfunction, including myocardial depression, hemodynamic instability, and dysrhythmias, which have increased patient mortality within the first 24 h after starting reperfusion therapy. Current evidence suggests that the release of oxygen-derived reactive substances and subsequent inflammatory mediators during ischemia-reperfusion contribute toward this injury. Platelet-activating factor (PAF), a mediator released during RMIR, has been emphasized by many investigators as playing a central role in causing RMIR injury. Similar cardiovascular dysfunctions that occur during RMIR, including myocardial depression, hemodynamic instability, and dysrhythmias, occur after administration of PAF and are ameliorated with PAF antagonists. Further, PAF antagonists have been shown to be cardioprotective and improve survival when administered before onset of reperfusion. A variety of phospholipid analogues, naturally derived compounds, and synthetic compounds have been developed that form the different classes of PAF antagonists, each with unique antagonizing properties. Several of these compounds have successfully passed safety and efficacy testing in humans; however, to date, no clinical trials have investigated the protective effects of PAF antagonists against RMIR injury. A current theory in the pathogenesis of RMIR injury considers the ischemic and necrotic portion of the myocardium and regional dysfunction due to tissue necrosis to be solely responsible for global cardiac dysfunction leading to hemodynamic instability and death. Evidence now suggests, however, that the global dysfunction is also due to the effect of inflammatory mediators such as PAF, thromboxanes, leukotrienes, and endothelins that are released during RMIR and are distributed throughout the heart on reperfusion. Antagonizing a central inflammatory mediator such as PAF, as adjunct treatment with currently used reperfusion therapies, improves cardiovascular function and survival in animals and should be introduced into clinical trials to investigate if similar protective effects can be provided in humans.