Clinical anatomy of the spatial structure of the right ventricular outflow tract.

BACKGROUND: The right ventricular outflow tract (RVOT) is located above the supraventricular crest and reaches the level of the pulmonary valve. Detailed knowledge of the RVOT spatial structure and its morphology is extremely important for cardiac invasive therapeutic procedures. OBJECTIVES: To examine the spatial structure of the RVOT using virtual models of the right ventricle (RV) interior obtained post mortem. MATERIAL AND METHODS: The study was carried out using 40 adult hearts from both sexes fixed in formalin. Donors had a negative history of cardiovascular diseases. Silicone models of the interior of the RV were made and then subjected to a digital modelling procedure using the photogrammetry technique. For each 3D model of the RV, the RVOT was extracted and measurements were performed. RESULTS: Statistical analysis demonstrated that the dimensions of the transverse (p < 0.001) and sagittal (p = 0.002) axis at the level of the upper and lower border of the RVOT differed significantly. There was also a significant difference between the right and left height of the RVOT (p = 0.009). A clear correlation was found between the volume of the RVOT and the volume of the entire RV (r = 0.718, p < 0.001). CONCLUSIONS: The obtained 3D models of the RVOT can help standardize the data related to RVOT architecture. Furthermore, they can extend knowledge about the RVOT in the field of cardiology and improve the procedures in cardiac surgery.

Cardiovascular and Respiratory Toxicity of Protamine Sulfate in Zebrafish and Rodent Models.

Protamine sulfate (PS) is the only available option to reverse the anticoagulant activity of unfractionated heparin (UFH), however it can cause cardiovascular and respiratory complications. We explored the toxicity of PS and its complexes with UFH in zebrafish, rats, and mice. The involvement of nitric oxide (NO) in the above effects was investigated. Concentration-dependent lethality, morphological defects, and decrease in heart rate (HR) were observed in zebrafish larvae. PS affected HR, blood pressure, respiratory rate, peak exhaled CO2, and blood oxygen saturation in rats. We observed hypotension, increase of HR, perfusion of paw vessels, and enhanced respiratory disturbances with increases doses of PS. We found no effects of PS on human hERG channels or signs of heart damage in mice. The hypotension in rats and bradycardia in zebrafish were partially attenuated by the inhibitor of endothelial NO synthase. The disturbances in cardiovascular and respiratory parameters were reduced or delayed when PS was administered together with UFH. The cardiorespiratory toxicity of PS seems to be charge-dependent and involves enhanced release of NO. PS administered at appropriate doses and ratios with UFH should not cause permanent damage of heart tissue, although careful monitoring of cardiorespiratory parameters is necessary.

Individual variability of vascularization of the anterior papillary muscle within the right ventricle of human heart.

BACKGROUND: To date there is scarce published evidence reporting the dual blood supply reaching anterior papillary muscle (APM), which descends from both major coronary arteries. Such a vascular configuration can prevent the dysfunction of right ventricular entire valvular system in case of the occlusion of proximal part of either right coronary artery (RCA) or left coronary artery (LCA). The aim of our study was to determine the vascular pattern of APM blood supply which originates from two main coronary arteries, in the context of the APM and septomarginal trabecula (SMT) topography. METHODS: The study was carried out using tissue obtained from 36 human hearts. The material was divided into four morphological types of SMT/APM arrangement. Vascularization and blood supply pattern of papillary muscle was investigated following the analysis of multiple tissue cross sections. The origin of APM arterial supply was traced back to both main coronary arteries. Cross-sectional area of the arteries was estimated at the base of APM and compared within mixed male-female population, aged 18-76. RESULTS: We noted that as much as 78% of entire APM material had a blood supply vasculature originating from both LCA and RCA branches. In contrast, 22% of cases APM was supplied by a single coronary artery, while in each case it proved to be LCA. We have never found APM arterial supply provided exclusively by RCA. In case of double AMP blood supply an average of total cross-section area of the arteries branching from LCA, was noted to be in excess of two and a half times bigger in type III and more than two times bigger in type IV, as compared with the arteries originating from RCA. CONCLUSIONS: Our research confirm the possibility of double blood supply which vascularizes APM, but the finding does not necessarily apply in all cases. However, APM seems to be predominantly vascularized by arteries deriving from LCA, regardless of their morphological type.

The structure of the vascular system of the septomarginal trabecula in the heart of an adult.

BACKGROUND: In cardiology, the paths of the arteries penetrating the septomarginal trabecula (SMT) are especially important. They provide blood supply to the apparatus of the right atrioventricular orifice and often form anastomoses with the system of the right coronary artery. Despite this, only a few publications discuss the morphological aspect of the septomarginal trabecula, and available histological analyses seldom deal with its blood supply. OBJECTIVES: The aim of this study was to analyze the vessel structure of the septomarginal trabecula in terms of the variability of the area of the cross-section of the lumen and the muscular layer of the artery. MATERIAL AND METHODS: The study was carried out on the material of 50 human hearts from adults of both sexes. The material was divided into 4 morphological types. Histological examinations were conducted by means of classic staining methods. RESULTS: At the initial cross-section of the septomarginal trabecula, the area of the cross-section increased to half of the length of the trabecula, and then it started to decrease. This is connected with the thickening of the inner muscular layer of the artery, which proportionally takes up more area of the cross-section of the whole artery of the SMT. The total area of the cross-section of all vessels in both types examined was also the largest in the middle part of the SMT. Furthermore, the results of this study confirm the presence of a connection between both systems of coronary arteries. CONCLUSIONS: As the septomarginal trabecula passes through the lumen of the right ventricle, its arteries become exposed to the influence of the factors which may evoke a biological response from the walls of this vessel, causing the thickening of the muscular layer and, as a result, of the section of the whole artery, in particular its middle part.

Promising effects of xanthine oxidase inhibition by allopurinol on autonomic heart regulation estimated by heart rate variability (HRV) analysis in rats exposed to hypoxia and hyperoxia.

BACKGROUND: It has long been suggested that reactive oxygen species (ROS) play a role in oxygen sensing via peripheral chemoreceptors, which would imply their involvement in chemoreflex activation and autonomic regulation of heart rate. We hypothesize that antioxidant affect neurogenic cardiovascular regulation through activation of chemoreflex which results in increased control of sympathetic mechanism regulating heart rhythm. Activity of xanthine oxidase (XO), which is among the major endogenous sources of ROS in the rat has been shown to increase during hypoxia promote oxidative stress. However, the mechanism of how XO inhibition affects neurogenic regulation of heart rhythm is still unclear. AIM: The study aimed to evaluate effects of allopurinol-driven inhibition of XO on autonomic heart regulation in rats exposed to hypoxia followed by hyperoxia, using heart rate variability (HRV) analysis. MATERIAL AND METHODS: 16 conscious male Wistar rats (350 g): control-untreated (N = 8) and pretreated with Allopurinol-XO inhibitor (5 mg/kg, followed by 50 mg/kg), administered intraperitoneally (N = 8), were exposed to controlled hypobaric hypoxia (1h) in order to activate chemoreflex. The treatment was followed by 1h hyperoxia (chemoreflex suppression). Time-series of 1024 RR-intervals were extracted from 4kHz ECG recording for heart rate variability (HRV) analysis in order to calculate the following time-domain parameters: mean RR interval (RRi), SDNN (standard deviation of all normal NN intervals), rMSSD (square root of the mean of the squares of differences between adjacent NN intervals), frequency-domain parameters (FFT method): TSP (total spectral power) as well as low and high frequency band powers (LF and HF). At the end of experiment we used rat plasma to evaluate enzymatic activity of XO and markers of oxidative stress: protein carbonyl group and 8-isoprostane concentrations. Enzymatic activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were measures in erythrocyte lysates. RESULTS: Allopurinol reduced oxidative stress which was the result of hypoxia/hyperoxia, as shown by decreased 8-isoprostane plasma concentration. XO inhibition did not markedly influence HRV parameters in standard normoxia. However, during hypoxia, as well as hyperoxia, allopurinol administration resulted in a significant increase of autonomic control upon the heart as shown by increased SDNN and TSP, with an increased vagal contribution (increased rMSSD and HF), whereas sympathovagal indexes (LF/HF, SDNN/rMSSD) remained unchanged. CONCLUSIONS: Observed regulatory effects of XO inhibition did not confirm preliminary hypothesis which suggested that an antioxidant such as allopurinol might activate chemoreflex resulting in augmented sympathetic discharge to the heart. The HRV regulatory profile of XO inhibition observed during hypoxia as well as post-hypoxic hyperoxia corresponds to reported reduced risk of sudden cardiovascular events. Therefore our data provide a new argument for therapeutical use of allopurinol in hypoxic conditions.