Background: Patients with pulmonary hypertension develop intimal plaques in large pulmonary arteries. Objective: To test the hypothesis that the composition of such plaques differs depending on whether the aetiology of the disease is thromboembolic or hypertensive. Design: Chronic thromboembolic and plexogenic pulmonary hypertension (primary and secondary (Eisenmenger syndrome)) were investigated. These are spontaneous human models and were used to examine the independent role of thrombus and hypertension in plaque composition. Setting: A national tertiary referral centre for lung transplantation and pulmonary thromboendoarterectomy. Patients: Thirty nine patients with chronic thromboembolic pulmonary hypertension who had undergone thromboendoarterectomy (n = 32) or lung transplantation (n = 7), 28 with plexogenic diseases (nine primary and 19 Eisenmenger), and three with Eisenmenger syndrome complicated by thromboembolic events. Interventions: The lung and thromboendoarterectomy samples were sectioned, stained with Movat pentachrome, and immunostained with antibodies for fibrin, platelets, inflammatory cells, smooth muscle cells, and erythrocyte membrane glycophorin A. Main outcome measure: Composition of the plaques affecting large pulmonary arteries. Results: Two types of intimal lesion were distinguished in chronic thromboembolic pulmonary hypertension: fibrous plaques with angioneogenesis; and core-rich atherosclerotic plaques with pultaceous cores largely consisting of glycophorin immunoreactive material, with cholesterol clefts (61.5%), CD68 positive macrophages (84.6%), T lymphocytes (87%), and calcification (46.1%). The samples from the patients with Eisenmenger syndrome and thromboembolic complications had similar characteristics, whereas those from patients with uncomplicated primary pulmonary hypertension had core-free fibrous plaques, spotted with macrophages and T lymphocytes. Conclusions: Chronic thromboembolic pulmonary hypertension is associated with atherosclerotic plaques with glycophorin-rich pultaceous cores, and plexogenic pulmonary hypertension with fibrous plaques. Thromboembolic material thus plays a critical role in the formation of pultaceous cores, of which erythrocyte membrane derived glycophorin is a major component.
None of the variables considered was correlated with early death or functional nonsuccess. Neither preoperative severity of pulmonary hypertension nor degree of cardiac failure influenced the outcome of the operation. PTE leads to hemodynamic recovery even in very compromised patients.
CABG procedure in the presence of HM enhances LV recovery of function and has a favourable prognosis. Functional benefit of the left ventricle, however, appears to be time-limited, despite remarkable improvement in patient functional capacity. Advanced preoperative heart failure, minimal perioperative improvement of LVEF, and age account for a poor long-term prognosis.
Background-To allow performance of "stand-alone" mitral annuloplasty with minimal invasiveness, percutaneous techniques consisting of delivery into the coronary sinus (CS) of devices intended to shrink the mitral valve annulus have recently been tested in animal models. These techniques exploit the anatomic proximity of the CS and mitral valve annulus in ovine or dogs. Knowledge of a detailed anatomic relationship between the CS, coronary arteries, and mitral valve annulus in humans is essential to define the safety and efficacy of percutaneous techniques in clinical practice. We sought to determine the qualitative and quantitative anatomic relationships between CS and surrounding structures in human hearts. Methods and Results-The distance from the CS to the mitral valve annulus and the relationship between the CS and surrounding structures were studied in 61 excised cadaveric human hearts. Maximal distance from the CS to the mitral valve annulus was found to be up to 19 mm (mean, 9.7Ϯ3.2 mm). A diagonal or ramus branch, main circumflex artery, or its branches were located between anterior interventricular vein/CS and the mitral valve annulus in 16.4% and 63.9% of cases, respectively. Conclusions-Surgical anatomy suggests that in humans the CS is located behind the left atrial wall at a significant distance from the mitral valve annulus. Percutaneous mitral annuloplasty devices probably shrink the mitral valve annulus only by an indirect traction mediated by the left atrial wall; a theoretical risk of compressing coronary artery branches exists. Chronic studies are needed to address this problem and to determine long-term efficacy of such methods. (Circulation. 2006;114:377-380.)
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