«What is the role of surgery in thromboembolic pulmonary hypertension? Pulmonary endarterectomy»

Carlos Porras, Hans-Joachim Schäfers

Cardiocore 2013; 48:65-8.

Chronic thromboembolic pulmonary hypertension (CTEPH) is an infrequent sequela of acute pulmonary embolism that develops in 1 to 4% of individuals, in whom thrombus material is not dissolved but organized into scar tissue. Remodeling of previously unaffected pulmonary arteries ensues, the patients develop progressive pulmonary hypertension (PH) and right heart failure. The diagnosis can be confirmed by ventilation/perfusion scanning and CT. Pulmonary angiography will give additional information, in particular with respect to central extension of scar. The administration of pulmonary vasodilators is of limited value in CTEPH. On the other hand, this disease can be treated causatively by pulmonary endarterectomy (PEA).

The operation requires a a high degree of precision. The chest is opened via a median sternotomy and the patient cooled to a nasopharyngeal temperature of 20°C. The central pulmonary arteries are opened, and a closed endarterectomy of the involved pulmonary arterial bed is performed. Postoperative intensive care involves careful management to avoid complications related to residual PH.

With careful patient selection the hospital mortality is less than 5% in patients with preoperative heart failure class III NYHA. The hemodynamic and clinical results are impressive. Pulmonary vascular resistance is markedly reduced within the first 48 hours, and a further reduction if often seen in the subsequent weeks. The patients are drastically improved in their exercise ability; in the majority of patients the hemodynamic and clinical improvement persists beyond 5 years postoperatively.

«Identification of Reference Genes for Quantitative RT-PCR in Ascending Aortic Aneurysms»

Dominic Henn, Doris Bandner-Risch, Hilja Perttunen, Wolfram Schmied, Carlos Porras, Francisco Ceballos, Noela Rodriguez-Losada, Hans-Joachim Schäfers

PLoS One. 2013;8(1):e54132. doi: 10.1371/journal.pone.0054132. Epub 2013 Jan 11.

Hypertension and congenital aortic valve malformations are frequent causes of ascending aortic aneurysms. The molecular mechanisms of aneurysm formation under these circumstances are not well understood. Reference genes for gene activity studies in aortic tissue that are not influenced by aortic valve morphology and its hemodynamic consequences, aortic dilatation, hypertension, or antihypertensive medication are not available so far. This study determines genes in ascending aortic tissue that are independent of these parameters.

Tissue specimens from dilated and undilated ascending aortas were obtained from 60 patients (age ≤70 years) with different morphologies of the aortic valve (tricuspid undilated n = 24, dilated n = 11; bicuspid undilated n = 6, dilated n = 15; unicuspid dilated n = 4). Of the studied individuals, 36 had hypertension, and 31 received ACE inhibitors or AT1 receptor antagonists. The specimens were obtained intraoperatively from the wall of the ascending aorta. We analyzed the expression levels of 32 candidate reference genes by quantitative RT-PCR (RT-qPCR). Differential expression levels were assessed by parametric statistics. The expression analysis of these 32 genes by RT-qPCR showed that EIF2B1, ELF1, and PPIA remained constant in their expression levels in the different specimen groups, thus being insensitive to aortic valve morphology, aortic dilatation, hypertension, and medication with ACE inhibitors or AT1 receptor antagonists. Unlike many other commonly used reference genes, the genes EIF2B1, ELF1, and PPIA are neither confounded by aortic comorbidities nor by antihypertensive medication and therefore are most suitable for gene expression analysis of ascending aortic tissue.