991 resultados para heart valve prostheses


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BACKGROUND: Half of the patients with end-stage heart failure suffer from persistent atrial fibrillation (AF). Atrial kick (AK) accounts for 10-15% of the ejection fraction. A device restoring AK should significantly improve cardiac output (CO) and possibly delay ventricular assist device (VAD) implantation. This study has been designed to assess the mechanical effects of a motorless pump on the right chambers of the heart in an animal model. METHODS: Atripump is a dome-shaped biometal actuator electrically driven by a pacemaker-like control unit. In eight sheep, the device was sutured onto the right atrium (RA). AF was simulated with rapid atrial pacing. RA ejection fraction (EF) was assessed with intracardiac ultrasound (ICUS) in baseline, AF and assisted-AF status. In two animals, the pump was left in place for 4 weeks and then explanted. Histology examination was carried out. The mean values for single measurement per animal with +/-SD were analysed. RESULTS: The contraction rate of the device was 60 per min. RA EF was 41% in baseline, 7% in AF and 21% in assisted-AF conditions. CO was 7+/-0.5 l min(-1) in baseline, 6.2+/-0.5 l min(-1) in AF and 6.7+/-0.5 l min(-1) in assisted-AF status (p<0.01). Histology of the atrium in the chronic group showed chronic tissue inflammation and no sign of tissue necrosis. CONCLUSIONS: The artificial muscle restores the AK and improves CO. In patients with end-stage cardiac failure and permanent AF, if implanted on both sides, it would improve CO and possibly delay or even avoid complex surgical treatment such as VAD implantation.

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Lymphatic valves are essential for efficient lymphatic transport, but the mechanisms of early lymphatic-valve morphogenesis and the role of biomechanical forces are not well understood. We found that the transcription factors PROX1 and FOXC2, highly expressed from the onset of valve formation, mediate segregation of lymphatic-valve-forming cells and cell mechanosensory responses to shear stress in vitro. Mechanistically, PROX1, FOXC2, and flow coordinately control expression of the gap junction protein connexin37 and activation of calcineurin/NFAT signaling. Connexin37 and calcineurin are required for the assembly and delimitation of lymphatic valve territory during development and for its postnatal maintenance. We propose a model in which regionally increased levels/activation states of transcription factors cooperate with mechanotransduction to induce a discrete cell-signaling pattern and morphogenetic event, such as formation of lymphatic valves. Our results also provide molecular insights into the role of endothelial cell identity in the regulation of vascular mechanotransduction.

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ABSTRACT: BACKGROUND: Chest pain raises concern for the possibility of coronary heart disease. Scoring methods have been developed to identify coronary heart disease in emergency settings, but not in primary care. METHODS: Data were collected from a multicenter Swiss clinical cohort study including 672 consecutive patients with chest pain, who had visited one of 59 family practitioners' offices. Using delayed diagnosis we derived a prediction rule to rule out coronary heart disease by means of a logistic regression model. Known cardiovascular risk factors, pain characteristics, and physical signs associated with coronary heart disease were explored to develop a clinical score. Patients diagnosed with angina or acute myocardial infarction within the year following their initial visit comprised the coronary heart disease group. RESULTS: The coronary heart disease score was derived from eight variables: age, gender, duration of chest pain from 1 to 60 minutes, substernal chest pain location, pain increases with exertion, absence of tenderness point at palpation, cardiovascular risks factors, and personal history of cardiovascular disease. Area under the receiver operating characteristics curve was of 0.95 with a 95% confidence interval of 0.92; 0.97. From this score, 413 patients were considered as low risk for values of percentile 5 of the coronary heart disease patients. Internal validity was confirmed by bootstrapping. External validation using data from a German cohort (Marburg, n = 774) revealed a receiver operating characteristics curve of 0.75 (95% confidence interval, 0.72; 0.81) with a sensitivity of 85.6% and a specificity of 47.2%. CONCLUSIONS: This score, based only on history and physical examination, is a complementary tool for ruling out coronary heart disease in primary care patients complaining of chest pain.

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A massive and homogeneous amount of amastigote-like forms was detected in the stomodeal valve (SV) and the thoracic mid-gut (TMG) of Leishmania major-infected Phlebotomus papatasi, which received a second blood meal 13 to 21 days post-infection on healthy anaesthetized hamsters. After re-feeding, the infected sand flies were dissected out to examine the morphology of the parasite in SV, TMG and the abdominal mid-gut (AMG). Different promastigote forms were seen in the infected flies. Among these included typical promastigotes (nectomonads and haptomonads), paramastigotes, metacyclic promastigotes and, in some samples, the here-reported amastigote-like forms. The Leishmania amastigote-like forms were detected in the SV of sand flies with 14, 18 and 21 days of infection as well as in the TMG at 13 and 18 days post-infection. However, the amastigote-like forms were not detected in the AMG. Factors such as the acidic pH predominating the TMG and the SV, as well as the temperature of the ingested blood, among others, are suggested as contributing to the transformation of the typical promastigotes into the amastigote-like forms. The significance of this finding is discussed and the possible biological advantage for transmission of Leishmania is considered.

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14.10.2014 International Working Group Report on the Optimal All-Island Hospital Service for Cardiology and Cardiac Surgery for Congenital Heart Disease in the Republic of Ireland and Northern Ireland. The International Working Group (IWG) visited Belfast and Dublin from April 7- April 11, 2014.  The IWG consisted of Dr. John Mayer, Dr. Adrian Moran, Dr. John Sinclair, and Dr. Patricia Hickey. Download the report here. View the Joint Policy Statement by the Minister of Health and Social Services and Public Safety Northern Ireland, Jim Wells and the Minister of Health in the Republic of Ireland, Leo Varadkar on the report here.

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To download an Application Form, Guidance Notes and other information, please visit the website www.nichsa.com or contact Caoimhe Devlin, Research Assistant by email: cdevlin@nichsa.com or phone: 02890 266714 / 02890 320184 ext 248.

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This project will work with men aged 50 and upwards on a range of health issues including physical health, healthy lifestyle, mental health etc. Other organisations will be brought into talk to the men during the sessions. The project aims to improve the health of the men and encourage them to make healthier choices.

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The project will develop a relationship with the pharmacist in Bessbrook and Kilkeel. 3 sessions will be held in each area allowing time for 1-1 support for clients and carers.

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To assess the role of arginine vasopressin (AVP) in congestive heart failure (CHF), 10 patients with CHF refractory to conventional treatment were studied before and 60 minutes after intravenous administration of 5 micrograms/kg of d(CH2)5Tyr(Me)AVP, a specific antagonist of AVP at the vascular receptor level. Heart rate, systemic arterial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac index by thermodilution and cutaneous blood flow by laser-Doppler technique were measured. In 9 patients with no significant hemodynamic and cutaneous blood flow response to the AVP antagonist, baseline values (mean +/- standard deviation) were: heart rate, 77 +/- 14 beats/min; systemic arterial pressure, 120/79 +/- 18/8 mm Hg; pulmonary arterial pressure, 42/21 +/- 12/8 mm Hg; pulmonary capillary wedge pressure, 19 +/- 7 mm Hg; cardiac index, 2.2 +/- 0.6 liters/min/m2; plasma AVP, 2.3 +/- 0.8 pg/ml; and plasma osmolality, 284 +/- 14 mosm/kg H2O. The tenth patient had the most severe CHF. His plasma AVP level was 55 pg/ml and plasma osmolality was 290 mosm/kg. He responded to the AVP antagonist with a decrease in systemic arterial pressure from 115/61 to 79/41 mm Hg, in pulmonary arterial pressure from 58/31 to 33/13 mm Hg and in pulmonary capillary wedge pressure from 28 to 15 mm Hg. Simultaneously, cardiac index increased from 1.1 to 2.2 liters/min/m2 and heart rate from 113 to 120 beats/min; cutaneous blood flow increased 5-fold.(ABSTRACT TRUNCATED AT 250 WORDS)

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This poster highlights that alcohol increases your risk of heart attack.

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On World Heart Day, 29 September 2011, the Public Health Agency is urging all smokers to stop smoking and reduce their risk of developing heart disease (cardiovascular disease - CVD) or suffering a stroke or a heart attack.Heart disease is one of the leading causes of death and illness in the UK. Research shows that smoking is one of the main contributors of the disease, causing around 25,000 deaths a year in the UK. Cigarette smokers are two times more likely than non-smokers to suffer a heart attack.The majority of people who suffer a heart attack before the age of 50 are smokers. Cigarette smoke causes heart disease by:· reducing oxygen to the heart;· increasing blood pressure and heart rate;· increasing blood clotting;· damaging cells that line coronary arteries and other blood vessels, causing narrowing of the arteries.From the moment smoke reaches your lungs, your heart is forced to work harder. Your pulse quickens, forcing your heart to beat an extra 10 to 25 times per minute, as many as 36,000 additional times per day. Because of the irritating effect of nicotine and other components of tobacco smoke, your heartbeat is more likely to be irregular. This can contribute to cardiac arrhythmia and many other serious coronary conditions, such as heart attack.For smokers who already suffer from heart problems, quitting will dramatically help. Many heart patients notice an almost immediate improvement when they stop smoking. Often, they need less medication and can cope better with physical exertion.Gerry Bleakney, Head of Health and Social Wellbeing Improvement, PHA, said: "Smoking is one of the major causes of cardiovascular disease and smokers are almost twice as likely to have a heart attackas someone who has never smoked. One in every two long-term smokers will die prematurely from smoking-related diseases, many suffer very poor health before they die. However one year after successfully quitting smoking, an individual will have reduced their risk of having a heart attack to half that of a person continuing to smoke."Across Northern Ireland, there are over 600 support services for people who wish to stop smoking, based in GP surgeries, community pharmacies, hospitals, community centres and workplaces. I would encourage everyone who is thinking about quitting to log on to our Want 2 Stop website: www.want2stop.info and order a 'Quit Kit' free of charge alternatively contact the Smokers' Helpline on 0808 812 8008."

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The number of deaths from coronary heart disease in Northern Ireland has dropped significantly, according to recent figures. However, the Public Health Agency is urging everyone to take steps to protect their heart and reduce their chances of developing the disease during National Heart Month (February).Despite the number of deaths dropping significantly in recent years, coronary heart disease is still the number one killer across the country. Over 2,200 people died in Northern Ireland from coronary heart disease in 2010 compared to just over 2,300 people in 2009 - an overall reduction of 100 province-wide. The latest figure reveals the positive downward trend is continuing - in 2008, there were 2,410 deaths, 2,493 in 2007 and 2,554 in 2006, while in 1979 there were nearly 5,000 deaths. Throughout National Heart Month in February, the PHA is calling for people to follow a number of steps in a bid to reduce their chances of developing the disease.Smoking is a major risk factor and, the more cigarettes you smoke, the higher the risk, according to Dr Christine McMaster, Consultant in Public Health Medicine, with responsibility for cardiovascular disease in the PHA."The reduction in smoking over the past number of years through public education, stop smoking programmes and smoke free legislation has had a major impact on reducing deaths from heart disease. However, 24% of the population in Northern Ireland still smoke, putting them at risk of developing the disease."People who suffer from high blood pressure also run an increased risk of developing coronary heart disease. High blood pressure is a silent, but treatable condition. In order to minimise the risk, I would urge everyone over the age of 45 to have their blood pressure measured every five years by their GP," said Dr McMaster.Simple lifestyle changes will also reduce the risk of heart disease, including eating at least five servings of fruit and vegetables a day, avoiding saturated fats, limiting alcohol intake and taking at least 30 minutes of exercise a day, five days a week.Dr McMaster described the reduction in deaths from coronary heart disease over the past few years as "a big success story". "It shows that people can take very positive steps to reduce their risk of heart disease by getting their blood pressure checked and adopting a healthier lifestyle; in particular by not smoking," he added. "The message is clear during National Heart Month - you only have one heart and you can take steps to keep it healthy."

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High-dose dobutamine magnetic resonance stress testing has been shown to be superior to dobutamine stress echocardiography for diagnosis of coronary artery disease (CAD). We determined the feasibility of quantitative myocardial tagging during low- and high-dose dobutamine stress and tested the ability of global systolic and diastolic quantitative parameters to identify patients with significant CAD. Twenty-five patients suspected of having significant CAD were examined with a standard high-dose dobutamine/atropine stress magnetic resonance protocol (1.5-T scanner, Philips). All patients underwent invasive coronary angiography as the standard of reference for the presence (n = 13) or absence (n = 12) of significant CAD. During low-dose dobutamine stress, systolic (circumferential shortening, systolic rotation, and systolic rotation velocity) and diastolic (velocity of circumferential lengthening and diastolic rotation velocity) parameters changed significantly in patients without CAD (all P < 0.05 vs. rest) but not in patients with CAD. Identification of patients without and with CAD during low-dose stress was possible using the diastolic parameter of "time to peak untwist." At high-dose stress, none of the global systolic or diastolic parameters showed the potential to identify the presence of significant CAD. With myocardial tagging, a quantitative analysis of systolic and diastolic function was feasible during low- and high-dose dobutamine stress. In our study, the diastolic parameter of time to peak untwist as assessed during low-dose dobutamine stress was the most promising global parameter for identification of patients with significant CAD. Thus quantitative myocardial tagging may become a tool that reduces the need for high-dose dobutamine stress.

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In Chagas disease serious cardiac dysfunction can appear. We specifically studied the cardiac function by evaluating: ventricle contractile force and norepinephrine response, affinity and density of beta-adrenergic receptors, dynamic properties of myocardial membranes, and electrocardiography. Albino swiss mice (n = 250) were infected with 55 trypomastigotes, Tulahuen strain and studied at 35, 75, and 180 days post-infection, that correspond to the acute, indeterminate, and chronic phase respectively. Cardiac beta-adrenergic receptors' affinity, myocardial contractility, and norepinephrine response progressively decreased from the acute to the chronic phase of the disease (p < 0.01). The density (expressed as fmol/mg.prot) of the receptors was similar to non-infected mice (71.96 ± 0.36) in both the acute (78.24 ± 1.67) and indeterminate phases (77.28 ± 0.91), but lower in the chronic disease (53.32 ± 0.71). Electrocardiographic abnormalities began in the acute phase and were found in 65% of the infected-mice during the indeterminate and chronic phases. Membrane contents of triglycerides, cholesterol, and anisotropy were similar in all groups. A quadratic correlation between the affinity to beta-adrenergic receptors and cardiac contractile force was obtained. In conclusion the changes in cardiac beta-adrenergic receptors suggests a correlation between the modified beta-adrenergic receptors affinity and the cardiac contractile force.