HISTOLOGICAL AND HISTOCHEMICAL CHARACTERISTICS OF RAT MYOCARDIUM IN CADMIUM TOXICOSIS

Carcinogenic effects of cadmium on lungs, testicles and prostate are well known, so as cumulative and toxic effects on kidney, liver and bones; however, there have not been many published articles about the effects of cadmium on myocardium. The aim of this study was to estimate the morphological changes in rat myocardium chronically treated by cadmium. The study was carried out on male albino Wistar rats (n=30, age=35-37 days, body mass 120g +/- 10g). The animals were raised in controlled laboratory conditions and provided with standard laboratory rat food and tap water ad libitum. The rats were divided into two groups: ten animals composed the control group and did not undergo any treatment. The 20 experimental rats were exposed to 10mg of CdCl2 /L drinking water for 90 days. After 90 days, all animals were victimized and after the macroscopic inspection of the heart, myocardial tissue was routinely processed and embedded in paraffin. Sections 5 micrometers thick were stained by HE method and histochemical PAS-AB (pH 2, 5), Masson trichrome method for demonstrating collagen fibers and Toluidine blue for mast cells identification. Cross-striated banding pattern of cardiac cells was ruined. Noticeable atrophy and hydropic degeneration of subendocardial localized cardiac cells were found, with the focal presence of myocytolysis. Endothelial cell hyperplasia and edema of the intima were present on arteriolar type blood vessels causing the focal subocclusion. Fibrocytes, histiocytes and mast cells were numerous, perivascularly localized. Mast cells were polymorphic, larger than normal, oval and mostly degranulated. Instead of scanty endomysium, there is a noticeable interstitial fibrillar fibrosis with few fields of collagen in all myocardium layers between cardiac cells, which is particularly prominent around the larger blood vessels. Cadmium has pronounced vasculotropic properties causing morphological changes of cardiomyocytes, myocardial interstitial fibrillar collagen network and on the heart small blood vessels

The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events

AbstractOBJECTIVESThe impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events.BACKGROUNDAn embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined.METHODSThe relationship among the occurrence of major embolic events, echocardiographic vegetation size, endothelial cell activation, thrombin generation, fibrinolysis and APA was examined in 91 patients with definite infective endocarditis, including 26 patients with embolic events and 65 control subjects without embolic events.RESULTSOverall, 14.3% of patients exhibited elevated APA levels. Embolic events occurred more frequently in patients with elevated levels of APA than in patients without (61.5% vs. 23.1%; p = 0.008). Patients with elevated levels of APA showed higher levels of prothrombin-fragment F1+2 (p = 0.005), plasminogen-activator inhibitor 1 (p = 0.0002), von Willebrand factor (p = 0.002) and lower levels of activated protein C (p = 0.001) than patients with normal levels of APA. Thrombin generation and endothelial cell activation were both positively correlated with levels of APA. The occurrence of elevated APA levels was frequently associated with structural valve abnormalities (p = 0.01) and vegetations >1.3 cm (p = 0.002).CONCLUSIONSInfection-associated elevated APA levels in patients with infective endocarditis are related to endothelial cell activation, thrombin generation and impairment of fibrinolysis. This may contribute to the increased risk for major embolic events in these patients

Intramural haematoma of the thoracic aorta: who's to be alerted the cardiologist or the cardiac surgeon?

This review article is written so as to present the pathophysiology, the symptomatology and the ways of diagnosis and treatment of a rather rare aortic disease called Intra-Mural Haematoma (IMH). Intramural haematoma is a quite uncommon but potentially lethal aortic disease that can strike as a primary occurrence in hypertensive and atherosclerotic patients to whom there is spontaneous bleeding from vasa vasorum into the aortic wall (media) or less frequently, as the evolution of a penetrating atherosclerotic ulcer (PAU). IMH displays a typical of dissection progress, and could be considered as a precursor of classic aortic dissection. IMH enfeebles the aortic wall and may progress to either outward rupture of the aorta or inward disruption of the intima layer, which ultimately results in aortic dissection. Chest and back acute penetrating pain is the most commonly noticed symptom at patients with IMH. Apart from a transesophageal echocardiography (TEE), a tomographic imaging such as a chest computed tomography (CT), a magnetic resonance (MRI) and most lately a multy detector computed tomography (MDCT) can ensure a quick and accurate diagnosis of IMH. Similar to type A and B aortic dissection, surgery is indicated at patients with type-A IMH, as well as at patients with a persistent and/or recurrent pain. For any other patient (with type-B IMH without an incessant pain and/or without complications), medical treatment is suggested, as applied in the case of aortic dissection. The outcome of IMH in ascending aorta (type A) appears favourable after immediate (emergent or urgent) surgical intervention, but according to international bibliography patients with IMH of the descending aorta (type B) show similar mortality rates to those being subjected to conservative medical or surgical treatment. Endovascular surgery and stent-graft placement is currently indicated in type B IMH

Standardized endpoint definitions for transcatheter aortic valve implantation clinical trials: a consensus report from the Valve Academic Research Consortium†

To propose standardized consensus definitions for important clinical endpoints in transcatheter aortic valve implantation (TAVI), investigations in an effort to improve the quality of clinical research and to enable meaningful comparisons between clinical trials. To make these consensus definitions accessible to all stakeholders in TAVI clinical research through a peer reviewed publication, on behalf of the public health