Academic literature on the topic '3201 Cardiovascular medicine and haematology'

Background: Postoperative atrial fibrillation (PoAF) is the most common arrhythmic complication detected after coronary artery bypass grafting (CABG). It is associated with increased morbidity and mortality, especially in elderly patients. Mean platelet volume (MPV) shows the activation of platelets effective in the inflammatory and thrombotic process. The purpose of the present study was to investigate the relations between the preoperative MPV levels and development of PoAF in isolated CABG in elderly patients. Methods: A total of 103 elderly patients (aged ≥ 65 years), who underwent isolated CABG and were at preoperative sinus rhythm, were included in the study. Patients who did not have PoAF were identified as Group 1 (N = 74), and those with PoAF were identified as Group 2 (N = 29). Results: PoAF incidence was 28.2%. Preoperative MPV level was 8.41 ± 1.13 fL in Group 1, and 9.28 ± 1.00 fL in Group 2. The difference was statistically significant (P < .001). Multivariate logistic regression analysis revealed that age, preoperative hemoglobin, and preoperative MPV were independent predictive factors for PoAF development (OR [odds ratio]: 1.149, 95% CI [confidence interval]: 1.043-1.265, P = .005; OR: 1.334, 95% CI: 1.013-1.758, P = .040; OR: 2.103, 95% CI: 1.324-3.339, P = .002, respectively). The cut-off value for MPV as the predictor of PoAF development was found to be 8.43 (sensitivity: 82.8% and specificity: 55.4%). Conclusion: This study showed that MPV levels are associated with PoAF development in elderly patients, and other independent predictive factors include age and preoperative hemoglobin levels for POAF development.

We investigated the contribution of plasma folate deficiency to hyperhomocysteinaemia in selected patient groups. Based on our observations, we have determined a lower folate reference interval cut-off using homocysteine as a metabolic marker of folate deficiency. Four hundred and twenty-five consecutive plasma specimens from cardiology ( n=120), haematology ( n=190) and nephrology ( n=115) patients were analysed for homocysteine and plasma folate concentrations. Healthy volunteers were used as controls ( n=117). We observed elevated homocysteine values above our upper reference limit of 13 µmol/L in 20·1%, 28·4% and 74·8% of the cardiology, haematology and nephrology patients, respectively. All but 1·9% of the patients had plasma folate values greater than the lower reference interval limit (3·4 nmol/L) for our folate assay. The percentage of patients from cardiology and haematology clinics who were hyperhomocysteinaemic and had folate values > 15 nmol/L was 5·0% and 4·2% , respectively. In contrast, 58% of our nephrology patients with folate values > 15 nmol/L were hyperhomocysteinaemic. In all three groups, an inverse relationship was found between folate and homocysteine. The folate/homocysteine ratios in the patient groups were approximately one-third of the values observed in our control group. Folate deficiency appears to be the primary cause of hyperhomocysteinaemia in our cardiology and thrombosis patients. However, severe folate deficiency appears to be uncommon. The majority of our nephrology patients are hyperhomocysteinaemic without an apparent folate deficiency. We conclude that raising the lower reference interval cut-off for folate to 15 nmol/L would help to identify individuals at risk for hyperhomocysteinaemia in our non-uraemic patient population. Increasing folate supplementation to maintain a plasma concentration above 15 nmol/L in cardiac, thrombosis and renal patients would greatly reduce the occurrence of hyperhomocysteinaemia in these patients.

Transventricular mitral valve surgery combined with left ventricular restoration avoids atriotomy and provides a larger operative field. We describe a series of 5 patients in whom we performed transventricular mitral valve repair by various techniques, such as band annuloplasty, papillary muscle reattachment, chordal cutting, and edge-to-edge repair. The more acute forms of ischemic mitral regurgitation, as found in our patients, can coexist with post-myocardial infarction contained rupture or post-myocardial infarction ventricular septal rupture. Because these patients already have an indication for ventriculotomy, concomitant transventricular repair of the mitral valve can render a separate atriotomy unnecessary and thereby shorten the duration of cardiopulmonary bypass. Moreover, in patients with acute presentations, the absence of atrial dilation (this last associated with chronic cases) might make transventricular repair a better choice than the more difficult atrial approach.

In this COVID-19 crucial stage, cryptographic developments help to convey secret information inside the digital telemedicine frameworks. The novel corona virus had broken all configurations of our life. In the clinical medical sciences, patients are encouraged to select the remote based telemedicine services. Cardiac patients are especially defenseless to this COVID-19. Patients having Chronic Obstructive Pulmonary Diseases (COPDs) as co-morbidity are enthusiastically prescribed to remain protected at their remote isolations. Through such telecardiology, they might impart their basic data with various cardiovascular experts. This will diminish their odds of getting COVID-19 positive because of no actual developments outside homes. Patients experiencing such significant COPDs are to be analyzed and treated appropriately via cardiologists. Contemporary imperfections on patients' private data are an open challenge in such telecardiology. Electronic cardiac data are very much vulnerable in nature. Along these lines, it is exceptionally critical to force a high level security strategy in such COVID-19 telecardiology. In this paper, we have generated session key based on unsynchronized artificial neural networks and genetic algorithm. Two unsynchronized ANNs were considered to have two intermediate keys. These keys were genetically crossover to form the session key. Furthermore, that session key would e used in the secret share generation process. Entropy values observed with respect to the secret share were nearly closed to eight. Histogram, floating frequency, and autocorrelation, etc were generated by the proposed technique with well-distributed in shapes. The functional time in the form of encryption and decryption were evaluated in this paper for different secret shares. Patients' medical data are very much under severe risk of intrusion. Lastly, secret shares were transmitted through RSA. This framework acts against various security conducts in correspondence network particularly where online clinical exchanges have overflowed colossally in this COVID-19 period.

Many drugs affect lipid metabolism and have side effects which promote atherosclerosis. The prevalence of cancer-therapy-related cardiovascular (CV) disease is increasing due to development of new drugs and improved survival of patients: cardio-oncology is a new field of interest and research. Moreover, drugs used in transplanted patients frequently have metabolic implications. Increasingly, internists, lipidologists, and angiologists are being consulted by haematologists for side effects on metabolism (especially lipid metabolism) and arterial circulation caused by drugs used in haematology. The purpose of this article is to review the main drugs used in haematology with side effects on lipid metabolism and atherosclerosis, detailing their mechanisms of action and suggesting the most effective therapies.

AbstractThis guidance document was prepared on behalf of the International Council for Standardization in Haematology (ICSH), the aim of which is to provide hemostasis-related guidance documents for clinical laboratories. The current ICSH document was developed by an ad hoc committee, comprising an international collection of both clinical and laboratory experts. The purpose of this ICSH document is to provide laboratory guidance for (1) identifying hemostasis (coagulation) tests that have potential patient risk based on analysis, test result, and patient presentations, (2) critical result thresholds, (3) acceptable reporting and documenting mechanisms, and (4) developing laboratory policies. The basis for these recommendations was derived from published data, expert opinion, and good laboratory practice. The committee realizes that regional and local regulations, institutional stakeholders (e.g., physicians, laboratory personnel, hospital managers), and patient types (e.g., adults, pediatric, surgical) will be additional confounders for a given laboratory in generating a critical test list, critical value thresholds, and policy. Nevertheless, we expect this guidance document will be helpful as a framework for local practice.

Endothelial dysfunction is the initiating process in the development of atherosclerosis and cardiovascular disease (CVD) and is a significant predictor of future adverse cardiovascular events. Increasing evidence suggests a link between vascular function and the skeleton, an association that may be mediated by bone-derived proteins such as osteocalcin (OC). OC is an osteoblast-derived, vitamin K-dependent protein that primarily exists in two biological forms. Carboxylated osteocalcin (cOC) is involved in bone formation and undercarboxylated osteocalcin (ucOC) is suggested to be the bioactive form of the protein responsible for regulating energy metabolism and glucose homeostasis. As such, ucOC may be targeted as a therapeutic treatment for metabolic diseases such as diabetes. In humans, the association of OC with endothelial dysfunction and CVD is conflicting, with some suggesting that OC is associated with beneficial effects in the vasculature and others reporting adverse effects. Research in animals suggest that in vivo OC treatment improves vascular function. However, corresponding improvements in metabolic outcomes suggest that the improvements in vascular function may occur indirectly, due to improvements in energy metabolism. As such, the primary aim of this thesis is to investigate if ucOC has a direct biological effect on vascular function in normoglycaemic and hyperglycaemic environments in preclinical models and humans. This was examined in four studies. Study 1: Hyperglycaemia is a pathological condition that has a toxic effect on blood vessels and is a major risk factor for atherosclersosis and CVD. However, it is unclear whether the dysfunction caused by hyperglycaemia is blood vessel specific and whether the dysfunction is exacerbated by an atherogenic diet. It was important to identify which blood vessels developed dysfunction for subsequent studies to assess the vasoactive role of ucOC. Abdominal aorta, iliac and mesenteric arteries were dissected from male New Zealand White Rabbits following either a four week normal or atherogenic diet (n = 6 – 12 per group). The arteries were incubated ex vivo in normal or high glucose solutions (20 mM or 40 mM) for 2 h and isometric tension myography was used to determine endothelial-dependent vasodilation. The atherogenic diet reduced blood vessel relaxation, as measured by area under the curve (AUC), by 25% (p < 0.05) in the aorta, 17% (p = 0.06) in the iliac artery and 40% (p = 0.07) mesenteric artery. In the aorta of the atherogenic diet-fed rabbits the 20 mM glucose incubation altered EC50, thereby reducing the potency of acetylcholine (p < 0.05), and tended to reduce Emax and AUC in the normal diet-fed rabbits. Incubation of the iliac artery from atherogenic diet-fed rabbits in 40 mM glucose also altered EC50, reducing the potency of acetylcholine (p < 0.05). No dysfunction occurred in the mesentery with high glucose incubation following either the normal or atherogenic diet. High glucose-induced endothelial dysfunction appears to be blood vessel specific; the aorta may be the optimal artery to study potential therapeutic treatments of hyperglycaemia-induced endothelial dysfunction. Study 2: In Study 1, we established that acute high glucose incubations and an atherogenic diet cause endothelial dysfunction in rabbit aorta. As such, this study examined the biological effect of ucOC on blood vessel function in rabbit aorta ex vivo, as well as determining the effect of ucOC on markers of endothelial function in human cells in vitro. Isometric tension and immunohistochemistry techniques were used on the aorta of male New Zealand White Rabbits and human aortic endothelial cells (HAEC) were cultured to assess the effect of ucOC in normal and high glucose environments. Overall, ucOC, both 10 ng/ml and 30 ng/ml, did not significantly alter acetylcholine- induced blood vessel relaxation in rabbits (p > 0.05). The ucOC treatment did not cause any significant changes in the immunoreactivity of cellular signalling markers (endothelial nitric oxide synthase, protein kinase B, mammalian target of rapamycin and nitrotyrosine) in rabbit aorta (p > 0.05). In HAEC, ucOC did not attenuate endothelin 1, interleukin 6, vascular adhesion molecule 1, monocyte chemoattractant protein 1 or lactate dehydrogenase, all of which were increased in response to high glucose treatment (p > 0.05). In conclusion, the results of this study suggest that ucOC has no direct influence on endothelial function in rabbit aorta ex vivo or in human endothelial cells in vitro. Study 3: In this study we examined whether ucOC is related to blood pressure and vascular function in older adults and whether ucOC has a direct effect on endothelial function in the carotid artery of rabbits. To undertake the study, we used perfusion myography, which allows for the examination of whole vessel segments with pulsatile flow and pressure that mimics an endogenous environment. In older adults, ucOC, blood pressure, pulse wave velocity (PWV) and brachial artery flow mediated dilation (BAFMD) were measured (n = 38, 26 post-menopausal women and 12 men, mean age 73 ± 1 years). In male New Zealand White Rabbits, the vasoactivity of the carotid artery was assessed following a four week normal or atherogenic diet. An ucOC dose response curve (0.3 – 45 ng/ml) was administered following incubation of the arteries for 2 h in either normal or high glucose conditions. The concentration of ucOC was higher in normotensive older adults compared to those with stage 2 hypertension (34%, p < 0.05), particularly in women (43%, p < 0.01), but not men (p > 0.05). In all participants, higher ucOC was also associated with lower PWV (p < 0.05), but not BAFMD (p > 0.05). In rabbits, ucOC at any dose did not cause an alteration in the vasoactivity of the carotid artery, following either a normal or atherogenic diet (p > 0.05). In conclusion, ucOC is associated with vascular function in older adults, exclusively in post-menopausal women, but it has no direct effect on endothelial function in rabbit carotid arteries. Study 4: Vitamin K is a regulator of OC carboxylation, with higher vitamin K intake known to reduce circulating levels of ucOC. As ucOC was associated with vascular function in adults in Study 3, we tested the hypothesis that a suppression of ucOC following an increase in dietary vitamin K1 would exhibit a relative worsening of cardiometabolic risk factors. Men (n = 20) and women (n = 10) aged 62 ± 10 years participated in a randomised, controlled, crossover study. Participants were split into high and low responder subgroups following a four week high vitamin K1 diet (HK) of increased leafy green vegetables. High and low responders were defined based on the median percent reduction (30%) in ucOC following the HK diet. Blood pressure (resting and 24 h), arterial stiffness, plasma glucose and lipid concentrations, and serum OC forms were assessed. Following the HK diet, ucOC and ucOC/tOC were suppressed more (p < 0.01) in high responders (41% and 29% respectively) than in low responders (12% and 10% respectively). The reductions in ucOC and ucOC/tOC were not associated with changes in blood pressure, PWV, plasma glucose or lipid concentrations in the high responders (p > 0.05). The results from this study suggest that the suppression of ucOC via consumption of leafy green vegetables has no negative effects on cardiometabolic health, perhaps, in part, due to compensatory mechanisms, such as increased nitric oxide. General conclusions: Overall, the results of this thesis suggest that ucOC does not have a direct biological role in the regulation of endothelial function in rabbit arteries and human endothelial cells. In humans there is some association between ucOC and vascular function but the suppression of circulating ucOC does not influence vascular function or cardiovascular risk factors. As ucOC was not found to have a detrimental effect on vascular function, it may be targeted as a therapeutic treatment for metabolic diseases, such as T2DM, without a risk of adverse effects on the vasculature.

After menopause women experience an increased risk of developing cardiovascular disease, diabetes and osteoporosis. The work described in this thesis investigates the effects of exercise, hormonal therapy (HT) and rosiglitazone on cardiovascular risk variables, glucose and insulin levels and bone turnover markers. It was hypothesised that these interventions would independentiy improve parameters measured, whilst combined treatment would provide further benefit.

Central obesity, insulin resistance, atherogenic dyslipidemia and elevated blood pressure are the major components of metabolic syndrome. This complex disorder is considered to be a clinical challenge and an urgent public health issue. With the growing prevalence of obesity worldwide, effective strategies are needed to intervene in the development and progression of metabolic syndrome. Despite the short-term benefits of pharmaceutical treatment of obesity, current drug therapy is associated with adverse side effects, thus the use of complementary and alternative therapies has become increasingly popular among the general population as an alternative method for weight loss. Botanical extracts in combination with lifestyle modification may be effective agents for attenuating the development of metabolic syndrome as they often comprise of a vast range of bioactive compounds that have been associated with significant positive health outcomes with minimal side effects. However, the efficacy of many of these extracts and their chemical constituents have yet to be fully explored. The research presented in this thesis examines the effectiveness of two commonly used anti-obesity botanical extracts, namely Caralluma fimbriata and Citrus sinensis (Moro variety). The primary aim of this PhD project was to investigate the efficacy of C. fimbriata extract on the risk factors of metabolic syndrome in overweight and obese conditions.

Homocysteine was first suggested as a risk to CVD in 1969. Since then, elevated plasma homocysteine (derived from methionine) has remained a cardiovascular risk factor with no current treatment. Homocysteine is known to stimulate NADPH oxidase, and NADPH oxidase can be inhibited by stimulation of the Mas receptor (MasR) of the renin angiotensin system. Stimulation of MasR is known to reduce organ fibrosis through the production of NO. However, the role that MasR plays in homocysteine-induced vascular pathology, including endothelial dysfunction and organ fibrosis, is not known. The aim of this thesis is to determine if high methionine diet in MasR-/- mice will worsen cardiovascular pathology.

Excess plasma homocysteine (Hcy; hyperhomocysteinemia, HHcy) remains an independent risk factor for cardiovascular disease (CVD) and treatments remain elusive. The source of Hcy, methionine, is an essential amino acid acquired by ingestion of animal foods. Normal methionine metabolism effectively removes Hcy via recycling back into methionine or excretion via the kidney. However, in aberrant methionine metabolism, Hcy accumulates and causes damage to the vascular system by increasing oxidative stress; the exact mechanism of how this occurs is unknown. Importantly, the B vitamins B6, B9 and B12 are essential to proper methionine/Hcy metabolism and are often found in low levels in patients presenting with HHcy; this has provided a potentially viable treatment strategy in the clinical setting. Disappointingly, clinical trials administering B vitamins to reduce HHcy have been unsuccessful in reducing CVD and treatments continue to be sought. The NADPH oxidase (Nox) family of enzymes are expressed in a broad range of cell types throughout the body and are the primary source of superoxide (Nox1, Nox2) and hydrogen peroxide (Nox4) within the vasculature under both physiological and pathological conditions. Nox1, 2 and 4 are of primary interest in vascular disease, as there is evidence that Hcy can interfere with the proper function of Nox1, 2 and 4 signalling, potentially leading to an over-expression of pro-oxidants. Nox1, 2 and 4 have been implicated in vascular disease (endothelial dysfunction), hypertension, vascular inflammation, stroke, diabetes, and atherosclerosis, and putative inhibitors of these enzymes are now available. Additionally, nitric oxide (NO) is also measured as a marker of proper vascular function; indeed, the current gold standard of assessing NO availability is by indirectly measuring vascular responses to acetylcholine. Accordingly, a loss of NO bioavailability is linked to the development of many of the same vascular pathologies caused by HHcy and also potentially increased Nox1, 2, and 4 activity. Thus, this thesis examined if current putative Nox inhibitors could prevent vascular dysfunction caused by homocysteine (as indirectly measured by acetylcholine-mediated vasorelaxation). Using New Zealand white rabbits, C57BL/6 mice and a Nox2-/- (C57BL/6 background) mouse models, we observed that pharmacological intervention with single Nox1, 2 and 4 inhibitors reduced the effect of acetylcholine on vasorelaxation. In 1% methionine-fed Nox2-/- mice, we observed an improvement in function. We also assessed combinations of Nox1, 2 and 4 inhibitors and found that, although function was not restored to control levels, it was improved compared with single Nox inhibition. Due to these results, we performed a gp91ds-tat dose response in rabbit aorta. We found that in our models of vascular dysfunction, lower doses of gp91ds-tat significantly improved acetylcholine-mediated vasorelaxation. These results showed for the first time that in both pharmacological and diet-induced HHcy, high dose putative Nox inhibitors might not be effective. In conclusion, the observations made in this thesis highlight the important role that Hcy plays in the redox balance in the context of vascular function. Future work in this area should focus on low dose Nox inhibition in Hcy induced disease in in vivo models, in order to better determine which drug can be used to HHcy induced vascular damage.