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		<title>BMC Cardiovascular Disorders - Latest articles</title>
		<link>http://www.biomedcentral.com/bmccardiovascdisord/</link>
		<description>The latest articles from BMC Cardiovascular Disorders (ISSN 1471-2261) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/26"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/25"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/24"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/23"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/22"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/21"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/20"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/19"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2261/8/18"/>			    
            
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		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/26">
            
            <title>Pocket Doppler and vascular laboratory equipment yield comparable results for ankle brachial index measurement</title>
			<description>Background:
The ankle brachial index (ABI) is a well-established tool for screening and diagnosis of peripheral arterial disease (PAD). In this study we assessed the validity of ABI determination using a pocket Doppler device compared with automatic vascular laboratory measurement in patients suspected of PAD.
Methods:
Consecutive patients with symptoms of PAD referred for ABI measurement between December 2006 and August 2007 were included. Resting ABI was determined with a pocket Doppler, followed by ABI measurement with automatic vascular laboratory equipment, performed by an experienced vascular technician. The leg with the lowest ABI was used for analysis.
Results:
From 99 patients the mean resting ABI was 0.80 measured with the pocket Doppler and 0.85 measured with vascular laboratory equipment. A Bland-Altman plot demonstrated great correspondence between the two methods. The mean difference between the two methods was 0.05 (P&lt; .001). Multivariate linear regression analysis showed no dependency of the difference on either the average measured ABI or affected or unaffected leg.
Conclusions:
Since the small, albeit statistically significant, difference between the two methods is not clinically relevant, our study demonstrates that ABI measurements with pocket Doppler and vascular laboratory equipment yield comparable results and can replace each other. Results support the use of the pocket Doppler for screening of PAD, allowing initiation of cardiovascular risk factor management in primary care, provided that the equipment operator is experienced.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/26</link>
			
			 	<dc:creator>Saskia PA Nicolai, Lotte M Kruidenier, Ellen V Rouwet, Liliane Wetzels-Gulpers, Constantijn AM Rozeman, Martin H Prins and Joep AW Teijink</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:26</dc:source>
			<dc:date>2008-10-07</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-26</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>26</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-10-07</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/25">
            
            <title>The CHOICE (Choice of Health Options In prevention of Cardiovascular Events) replication trial: study protocol</title>
			<description>Background:
Although morbidity and mortality from coronary heart disease (CHD) are high, only a minority of acute coronary syndrome (ACS) survivors accesses an effective secondary prevention program. We aim to determine whether the previously proven CHOICE program can be replicated at multiple sites and whether ongoing reinforcement further improves risk factor modification.
Methods:
Participants eligible for but not accessing standard cardiac rehabilitation will be randomly allocated to either a previously tested 3-month CHOICE program or a 30-month CHOICE program (CHOICE-plus). Both groups will participate in individualised risk factor modules of differing duration that involve choice, goal setting and telephone follow-up for three months. CHOICE-plus will also receive additional face-to-face and telephone reinforcement between three and 30 months. At one site we will recruit a randomised control group, receiving conventional care. Primary outcomes are lipid levels, blood pressure, physical activity levels and smoking rates.  Secondary outcomes include readmission rates, death, the number of risk factors, other modifiable risk factors, quality of life and process evaluation measures over three years.DiscussionWe present the rationale and design of a multi-centre, replication study testing a modular approach for the secondary prevention of CHD following an ACS.
[Clinical Trial Registration Number, ACTRN12608000182392]</description>
			<link>http://www.biomedcentral.com/1471-2261/8/25</link>
			
			 	<dc:creator>Lis Neubeck, Julie Redfern, Tom Briffa, Adrian Bauman, David Hare and S B Freedman</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:25</dc:source>
			<dc:date>2008-10-06</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-25</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>25</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-10-06</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/24">
            
            <title>The effect of long-term homocysteine-lowering on carotid intima-media thickness and flow-mediated vasodilation in stroke patients: a randomized controlled trial and meta-analysis</title>
			<description>Background:
Experimental and epidemiological evidence suggests that homocysteine (tHcy) may be a causal risk factor for atherosclerosis. B-vitamin supplements reduce tHcy and improve endothelial function in short term trials, but the long-term effects of the treatment on vascular structure and function are unknown.
Methods:
We conducted a sub-study of VITATOPS, a randomised, double-blind, placebo-controlled intervention trial designed to test the efficacy of long term B-vitamin supplementation (folic acid 2 mg, vitamin B6 25 mg and vitamin B12 0.5 mg) in the prevention of vascular events in patients with a history of stroke. We measured carotid intima-medial thickness (CIMT) and flow-mediated dilation (FMD) at least two years after randomisation in 162 VITATOPS participants. We also conducted a systematic review and meta-analysis of studies designed to test the effect of B-vitamin treatment on CIMT and FMD.
Results:
After a mean treatment period of 3.9 &#177; 0.9 years, the vitamin-treated group had a significantly lower mean plasma homocysteine concentration than the placebo-treated group (7.9 &#956;mol/L, 95% CI 7.5 to 8.4 versus 11.8 &#956;mol/L, 95% CI 10.9 to 12.8, p &lt; 0.001). Post-treatment CIMT (0.84 &#177; 0.17 mm vitamins versus 0.83 &#177; 0.18 mm placebo, p = 0.74) and FMD (median of 4.0%, IQR 0.9 to 7.2 vitamins versus 3.0%, IQR 0.6 to 6.6 placebo, p = 0.48) did not differ significantly between groups. A meta-analysis of published randomised data, including those from the current study, suggested that B-vitamin supplements should reduce CIMT (-0.10 mm, 95% CI -0.20 to -0.01 mm) and increase FMD (1.4%, 95% CI 0.7 to 2.1%). However, the improvement in endothelial function associated with homocysteine-lowering treatment was significant in short-term studies but not in longer trials.
Conclusion:
Although short-term treatment with B-vitamins is associated with increased FMD, long-term homocysteine-lowering did not significantly improve FMD or CIMT in people with a history of stroke.Trial RegistrationClinical Trial Registration URL: http://www.actr.org.au/Trial Registration number: 12605000005651</description>
			<link>http://www.biomedcentral.com/1471-2261/8/24</link>
			
			 	<dc:creator>Kathleen Potter, Graeme J Hankey, Daniel J Green, John Eikelboom, Konrad Jamrozik and Leonard F Arnolda</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:24</dc:source>
			<dc:date>2008-09-20</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-24</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>24</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-20</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/23">
            
            <title>Passive tobacco exposure may impair symptomatic improvement in patients with chronic angina undergoing enhanced external counterpulsation</title>
			<description>Background:
The adverse effects of tobacco abuse on cardiovascular outcomes are well-known. However, the impact of passive smoke exposure on angina status and therapeutic response is less well-established. We examined the impact of second-hand smoke (SHS) exposure on symptomatic improvement in patients with chronic ischemic coronary disease undergoing enhanced external counterpulsation (EECP).
Methods:
This observational study included 1,026 non-smokers (108 exposed and 918 not-exposed to SHS) from the Second International EECP Patient Registry. We also assessed angina response in 363 current smokers. Patient demographics, symptomatic improvement and quality of life assessment were determined by self-report prior and after EECP treatment.
Results:
Non-smoking SHS subjects had a lower prevalence of prior revascularization (85% vs 90%), and had an increased prevalence of stroke (13% vs 7%) and prior smoking (72% vs 61%; all p &lt; 0.05) compared to non-smokers without SHS exposure. Despite comparable degrees of coronary disease, baseline angina class, medical regimens and side effects during EECP, fewer SHS non-smokers completed a full 35-hour treatment course (77% vs 85%, p = 0.020) compared to non-smokers without SHS. Compared to non-smokers without SHS, non-smoking SHS subjects had less angina relief after EECP (angina class decreased &#8805; 1 class: 68% vs 79%; p = 0.0082), both higher than that achieved in current smokers (66%). By multivariable logistic regression, SHS exposure was an independent predictor of failure to symptomatic improvement after EECP among non-smokers (OR 1.81, 95% confidence intervals 1.16&#8211;2.83).
Conclusion:
Non-smokers with SHS exposure had an attenuated improvement in anginal symptoms compared to those without SHS following EECP.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/23</link>
			
			 	<dc:creator>Stilianos Efstratiadis, Elizabeth D Kennard, Sheryl F Kelsey, Andrew D Michaels and the International EECP Patient Registry-2 Investigators</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:23</dc:source>
			<dc:date>2008-09-17</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-23</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>23</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-17</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/22">
            
            <title>Does interhospital transfer improve outcome of acute myocardial infarction? A propensity score analysis from the Cardiovascular Cooperative Project</title>
			<description>Background:
Many patients suffering acute myocardial infarction (AMI) are transferred from one hospital to another during their hospitalization. There is little information about the outcomes related to interhospital transfer. The purpose of this study was to compare processes and outcomes of AMI care among patients undergoing interhospital transfer with special attention to the impact on mortality in rural hospitals.
Methods:
National sample of Medicare patients in the Cooperative Cardiovascular Study (n = 184,295). Retrospective structured medical record review of AMI hospitalizations. Descriptive study using a retrospective propensity score analysis of clinical and administrative data for 184,295 Medicare patients admitted with clinically confirmed AMI to 4,765 hospitals between February 1994 and July 1995. Main outcome measure included: 30-day mortality, administration of aspirin, beta-blockers, ACE-inhibitors, and thrombolytic therapy.
Results:
Overall, 51,530 (28%) patients underwent interhospital transfer. Transferred patients were significantly younger, less critically ill, and had lower comorbidity than non-transferred patients. After propensity-matching, patients who underwent interhospital transfer had better quality of care anlower mortality than non-transferred patients. Patients cared for in a rural hospital had similar mortality as patients cared for in an urban hospital.
Conclusion:
Transferred patients were vastly different than non-transferred patients. However, even after a rigorous propensity-score analysis, transferred patients had lower mortality than non-transferred patients. Mortality was similar in rural and urban hospitals. Identifying patients who derive the greatest benefit from transfer may help physicians faced with the complex decision of whether to transfer a patient suffering an acute MI.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/22</link>
			
			 	<dc:creator>John M Westfall, Catarina I Kiefe, Norman W Weissman, Anthony Goudie, Robert M Centor, O Dale Williams and Jeroan J Allison</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:22</dc:source>
			<dc:date>2008-09-09</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-22</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>22</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-09</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/21">
            
            <title>Up-regulation of endothelin type B receptors in the human internal mammary artery in culture is dependent on protein kinase C and mitogen-activated kinase signaling pathways</title>
			<description>Background:
Up-regulation of vascular endothelin type B (ETB) receptors is implicated in the pathogenesis of cardiovascular disease. Culture of intact arteries has been shown to induce similar receptor alterations and has therefore been suggested as a suitable method for, ex vivo, in detail delineation of the regulation of endothelin receptors. We hypothesize that mitogen-activated kinases (MAPK) and protein kinase C (PKC) are involved in the regulation of endothelin ETB receptors in human internal mammary arteries.
Methods:
Human internal mammary arteries were obtained during coronary artery bypass graft surgery and were studied before and after 24 hours of organ culture, using in vitro pharmacology, real time PCR and Western blot techniques. Sarafotoxin 6c and endothelin-1 were used to examine the endothelin ETA and ETB receptor effects, respectively. The involvement of PKC and MAPK in the endothelin receptor regulation was examined by culture in the presence of antagonists.
Results:
The endohtelin-1-induced contraction (after endothelin ETB receptor desensitization) and the endothelin ETA receptor mRNA expression levels were not altered by culture. The sarafotoxin 6c contraction, endothelin ETB receptor protein and mRNA expression levels were increased after organ culture. This increase was antagonized by; (1) PKC inhibitors (10 &#956;M bisindolylmaleimide I and 10 &#956;M Ro-32-0432), and (2) inhibitors of the p38, extracellular signal related kinases 1 and 2 (ERK1/2) and C-jun terminal kinase (JNK) MAPK pathways (10 &#956;M SB203580, 10 &#956;M PD98059 and 10 &#956;M SP600125, respectively).
Conclusion:
In conclusion, PKC and MAPK seem to be involved in the up-regulation of endothelin ETB receptor expression in human internal mammary arteries. Inhibiting these intracellular signal transduction pathways may provide a future therapeutic target for hindering the development of vascular endothelin ETB receptor changes in cardiovascular disease.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/21</link>
			
			 	<dc:creator>David Nilsson, Lotta Gustafsson, Angelica Wackenfors, Bodil Gesslein, Lars Edvinsson, Per Paulsson, Richard Ingemansson and Malin Malmsj&#246;</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:21</dc:source>
			<dc:date>2008-09-08</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-21</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>21</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-08</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/20">
            
            <title>Prevalence of prehypertension and its relationship to risk factors for cardiovascular disease in Jamaica: Analysis from a cross-sectional survey</title>
			<description>Background:
Recent studies have documented an increased risk of cardiovascular disease (CVD) in persons with systolic blood pressures of 120&#8211;139 mmHg and/or diastolic blood pressures of 80&#8211;89 mmHg, classified as prehypertension in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. In this paper we estimate the prevalence of prehypertension in Jamaica and evaluate the relationship between prehypertension and other risk factors for CVD.
Methods:
The study used data from participants in the Jamaica Lifestyle Survey conducted from 2000&#8211;2001. A sample of 2012 persons, 15&#8211;74 years old, completed an interviewer administered questionnaire and had anthropometric and blood pressure measurements performed by trained observers using standardized procedures. Fasting glucose and total cholesterol were measured using a capillary blood sample. Analysis yielded crude, and sex-specific prevalence estimates for prehypertension and other CVD risk factors. Odds ratios for associations of prehypertension with CVD risk factors were obtained using logistic regression.
Results:
The prevalence of prehypertension among Jamaicans was 30% (95% confidence interval [CI] 27%&#8211;33%). Prehypertension was more common in males, 35% (CI 31%&#8211;39%), than females, 25% (CI 22%&#8211;28%). Almost 46% of participants were overweight; 19.7% were obese; 14.6% had hypercholesterolemia; 7.2% had diabetes mellitus and 17.8% smoked cigarettes. With the exception of cigarette smoking and low physical activity, all the CVD risk factors had significantly higher prevalence in the prehypertensive and hypertensive groups (p for trend &lt; 0.001) compared to the normotensive group. Odds of obesity, overweight, high cholesterol and increased waist circumference were significantly higher among younger prehypertensive participants (15&#8211;44 years-old) when compared to normotensive young participants, but not among those 45&#8211;74 years-old. Among men, being prehypertensive increased the odds of having >/=3 CVD risk factors versus no risk factors almost three-fold (odds ratio [OR] 2.8 [CI 1.1&#8211;7.2]) while among women the odds of >/=3 CVD risk factors was increased two-fold (OR 2.0 [CI 1.3&#8211;3.8])
Conclusion:
Prehypertension occurs in 30% of Jamaicans and is associated with increased prevalence of other CVD risk factors. Health-care providers should recognize the increased CVD risk of prehypertension and should seek to identify and treat modifiable risk factors in these persons.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/20</link>
			
			 	<dc:creator>Trevor S Ferguson, Novie OM Younger, Marshall K Tulloch-Reid, Marilyn B Lawrence Wright, Elizabeth M Ward, Deanna E Ashley and Rainford J Wilks</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:20</dc:source>
			<dc:date>2008-08-28</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-20</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>20</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-28</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/19">
            
            <title>Changes in clot lysis levels of reteplase and streptokinase following continuous wave ultrasound exposure, at ultrasound intensities following attenuation from the skull bone</title>
			<description>Background:
Ultrasound (US) has been used to enhance thrombolytic therapy in the treatment of stroke. Considerable attenuation of US intensity is however noted if US is applied over the temporal bone. The aim of this study was therefore to explore possible changes in the effect of thrombolytic drugs during low-intensity, high-frequency continuous-wave ultrasound (CW-US) exposure.
Methods:
Clots were made from fresh venous blood drawn from healthy volunteers. Each clot was made from 1.4 ml blood and left to coagulate for 1 hour in a plastic test-tube. The thrombolytic drugs used were, 3600 IU streptokinase (SK) or 0.25 U reteplase (r-PA), which were mixed in 160 ml 0.9% NaCl solution. Continuous-wave US exposure was applied at a frequency of 1 MHz and intensities ranging from 0.0125 to 1.2 W/cm2. For each thrombolytic drug (n = 2, SK and r-PA) and each intensity (n = 9) interventional clots (US-exposed, n = 6) were submerged in thrombolytic solution and exposed to CW-US while control clots (also submerged in thrombolytic solution, n = 6) were left unexposed to US.To evaluate the effect on clot lysis, the haemoglobin (Hb) released from each clot was measured every 20 min for 1 hour (20, 40 and 60 min). The Hb content (mg) released was estimated by spectrophotometry at 540 nm. The difference in effect on clot lysis was expressed as the difference in the amount of Hb released between pairs of US-exposed clots and control clots. Statistical analysis was performed using Wilcoxon's signed rank test.
Results:
Continuous-wave ultrasound significantly decreased the effects of SK at intensities of 0.9 and 1.2 W/cm2 at all times (P &lt; 0.05). Continuous-wave ultrasound significantly increased the effects of r-PA on clot lysis following 20 min exposure at 0.9 W/cm2 and at 1.2 W/cm2, following 40 min exposure at 0.3, 0.6, 0.9 and at 1.2 W/cm2, and following 60 min of exposure at 0.05 0.3, 0.6, 0.9 and at 1.2 W/cm2 (all P &lt; 0.05).
Conclusion:
Increasing intensities of CW-US exposure resulted in increased clot lysis of r-PA-treated blood clots, but decreased clot lysis of SK-treated clots.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/19</link>
			
			 	<dc:creator>Bjarne Madsen H&#228;rdig, Jonas Carlson and Anders Roijer</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:19</dc:source>
			<dc:date>2008-08-26</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-19</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>19</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/18">
            
            <title>Healthy Hearts &#8211; A community-based primary prevention programme to reduce coronary heart disease</title>
			<description>Background:
The ten year probability of cardiovascular events can be calculated, but many people are unaware of their risk and unclear how to reduce it. The aim of this study was to assess whether a community based intervention, for men and women aged between 45 and 64 years without pre-existing coronary heart disease, would reduce their Framingham scores when reassessed one year later.
Methods:
Individuals in the relevant age group from a defined geographical area were sent an invitation to attend for an assessment of their cardiovascular risk. Individuals with pre-existing cardiovascular disease or terminal illness were excluded. The invitation was in the form of a "Many Happy Returns" card with a number of self-screening questions including the question, "If you put the enclosed string around your waist, is it too short?" The card contained a red 80 cm piece of string in the case of women, or a green 90 cm piece of string in the case of men. At the assessment appointment, Framingham scores were calculated and a printout was given to each individual. Advice was provided for relevant risk factors identified using agreed guidelines. If appropriate, onward referral was also made to a GP, dietician, an exercise referral scheme, or to smoking cessation services, using a set of guidelines. Individuals were sent a second invitation one year later to return for re-assessment.Results and discussion2031 individuals were asked to self-assess their eligibility to participate, 596 individuals attended for assessment and 313 of these attended for follow-up one year later. The mean reduction in the Framingham risk score, was significantly lower at one year (0.876, 95% CI 0.211 to 1.541, p = 0.01). The mean 10-year risk of CHD at baseline was 13.14% (SD 9.18) and had fallen at follow-up to 12.34% (SD 8.71), a mean reduction of 6.7% of the initial 10-year Framingham risk. If sustained, the estimated NNT to prevent each year of CHD would be 1141 (95% CI 4739 to 649) individual appointments.
Conclusion:
This community intervention for primary prevention of CHD reduces Framingham risk scores at one year in those who engage with the programme.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/18</link>
			
			 	<dc:creator>Gill Richardson, Hugo C van Woerden, Lucy Morgan, Rhiannon Edwards, Monica Harries, Elaine Hancock, Susan Sroczynsk and Mererid Bowley</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:18</dc:source>
			<dc:date>2008-07-26</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-18</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>18</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
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		<item rdf:about="http://www.biomedcentral.com/1471-2261/8/17">
            
            <title>Gender differences in trends of acute myocardial infarction events: The Northern Sweden MONICA study 1985 &#8211; 2004</title>
			<description>Background:
The registration of non-fatal and fatal MI events initiated 1985 in the WHO MONICA project has been ongoing in northern Sweden since the end of the WHO project in 1995. The purpose of the present study was to analyze gender differences in first and recurrent events, case fatality and mortality in myocardial infarction (MI) in Northern Sweden during the 20-year period 1985 &#8211; 2004.
Methods:
Diagnosed MI events in subjects aged 25&#8211;64 years in the Counties of Norrbotten and V&#228;sterbotten were validated according to the MONICA protocol. The total number of events registered up to January 1, 2005 was 11,763: 9,387 in men and 2,376 in women.
Results:
The proportion of male/female events has decreased from 5.5:1 to 3:1. For males the reductions were 30% and 70% for first and recurrent MI, respectively, and for women 0% and 40% in the 55&#8211;64 year group. For both sexes a 50% reduction in 28-day case fatality was seen in the 25&#8211;64 year-group. Mortality was reduced by 69% and 45% in men and women, respectively.
Conclusion:
First and recurrent events of myocardial infarction was markedly reduced in men over the 20-year observation period, but for women the reduction was seen only for recurrent infarctions. Case fatality, on the other hand, was markedly reduced for both sexes. As a result of the positive effects on incidence and case fatality a substantial reduction was seen in total mortality, most pronounced for men.</description>
			<link>http://www.biomedcentral.com/1471-2261/8/17</link>
			
			 	<dc:creator>Dan Lundblad, Lars Holmgren, Jan-H&#229;kan Jansson, Ulf N&#228;slund and Mats Eliasson</dc:creator>
			
			<dc:source>BMC Cardiovascular Disorders 2008, 8:17</dc:source>
			<dc:date>2008-07-25</dc:date>
			<dc:identifier>doi:10.1186/1471-2261-8-17</dc:identifier>
			
			
							
					<prism:publicationName>BMC Cardiovascular Disorders</prism:publicationName>
					
			
							
					<prism:issn>1471-2261</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>17</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-25</prism:publicationDate>
					

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