Monthly Archives: January 2009

Periodontal disease – another cardiovascular risk factor to consider?

Br J Cardiol 2009;16:11–12 Leave a comment
Click any image to enlarge
Authors:

General practitioners (GPs) have become used to asking their patients fairly detailed questions about the traditional risk factors, such as smoking habits, and measuring blood pressure, cholesterol and glucose to allow cardiovascular risk to be calculated. However, few would dream of including an oral examination within an assessment of global cardiovascular risk. Oral health has been viewed as the domain of dentists and has not troubled physicians when considering the prevention and management of cardiovascular disease.

However, this may be set to change. There is a growing tide of interest, swelled by a burgeoning literature, in the possible links between periodontal infection and a number of chronic diseases and conditions – including cardiovascular diseases and certain cancers.1-7

Review of the contemporary literature reveals evidence from large epidemiological datasets and meta-analyses of small-scale longitudinal studies and periodontal intervention studies, which shows that after adjustment for variables known to increase cardiovascular risk, there remains a significant increase in both incidence and prevalence of coronary heart disease (CHD) in subjects with periodontal disease.1,8 This has led to calls for robust and rigorous study of the association between periodontal disease and cardiovascular disease in order to establish, or refute, causation, and this is reflected in a consensus view on the implications for current clinical practice.8

Old ideas to new ideas

That severe periodontal infection could have systemic health implications is not a new concept.9 For centuries the mouth has been recognised as an important site for infection and an indicator of a person’s general health status. In terms of pathophysiological rationale, there is now contemporary evidence to suggest that people with severe periodontal infections have increased concentrations of circulating inflammatory markers such as C-reactive protein,10,11 adverse changes in blood pressure and serum cholesterol,11 and it has been suggested that periodontal pathogens could be linked with carotid intima-media thickening.12,13

Is the relationship causal?

What the current evidence does not allow, however, is certainty of a causal relationship between periodontal disease and cardiovascular disease.

Large-scale observational studies can provide some insights into the epidemiological importance of risk factors. The Atherosclerosis Risk in Communities (ARIC) study for example, has reported that the host response to oral bacterial infection has bearing on systemic atherothrombotic events, and that systemic exposure to more than one oral pathogen involved in periodontitis is related to an increased risk for CHD.11,14 However, substudies within observational datasets are fraught with methodological difficulties and influenced by confounding risk factors that are hard to control for, such as poverty, smoking, diet and level of education.

Is periodontal disease a potentially modifiable cardiovascular risk factor?

There is some suggestion that the treatment of periodontal disease might reduce cardiovascular risk, but little current evidence to support that this might reduce cardiovascular events.15,16

The way forward

The evidence is tantalising in suggesting that an oral infection might confer systemic cardiovascular risk – not least, as periodontal disease is very much a treatable and manageable condition. An estimated 8–10% of the population may have severe periodontal disease, yet the condition is amenable to dental treatment and potentially avoidable through good oral hygiene.

Specifically designed prospective studies are needed to clarify whether periodontal disease and cardiovascular disease simply share risk factors or whether there is a true causal relationship. These studies will need to control for confounding factors such as age, gender, smoking, family history and diabetes mellitus. Ultimately, the goal of such research will be to establish the population-attributable risk of periodontal disease with respect to cardiovascular disease, which would allow it to be used in calculating risk.

If the evidence is clear that periodontal disease is a cardiovascular risk factor, prospective intervention studies will need to assess whether intervention to prevent periodontitis in the general population reduces the risk of cardiovascular disease. Additionally, prospective studies will be needed to prove that treatment of established periodontal disease has demonstrable effects on accepted, cardiovascular disease end points such as death, fatal and non-fatal myocardial infarction and other coronary or cerebrovascular events. Research into whether treatment of periodontal disease has a beneficial effect on surrogate end points such as glycosylated haemoglobin (HbA1c) and lipid profile may be helpful in the time before the large end point studies report.

Although the research task may seem challenging, robust evidence could see oral health assume a place within the list of lifestyle-related and modifiable risk factors that contribute to cardiovascular disease.

Implications for current practice

So are there implications for current medical practice? It seems reasonable to suggest that good oral health may contribute to good general health, and in turn, that poor oral health could be viewed as a marker of an unhealthy lifestyle. Physicians should encourage any patients with poor oral health to consult with a dentist and there may be a case for dentists to consider referrals to GPs. Cardiovascular disease is born of multiple chronic risk factors that interact and compound to affect an individual’s risk for clinical events. When we assess a patient’s global cardiovascular risk, we routinely consider lifestyle factors together with an evaluation of well-recognised, potentially modifiable physiological and biochemical risk factors.

Our management involves attempting to control hypertension, dyslipidaemia and poor glycaemic control. Pharmacotherapies do much to reduce cardiovascular risk and the role of successful lifestyle interventions – helping patients to stop smoking, eat healthily, exercise more and avoid becoming overweight – is proven. To add oral health status to the list of patient lifestyle considerations would not add greatly to physician workload and could be seen as a natural extension of healthy lifestyle messages designed to help reduce the burden of cardiovascular disease.

Conflict of interest

MD received an honorarium by Colgate-Palmolive for work on the consensus document.

References

  1. Bahekar AA, Singh S, Saha S et al. The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis. Am Heart J 2007;154: 830–7.
  2. Michaud DS, Liu Y, Meyer M, Giovannucci E, Joshipura K. Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study. Lancet Oncol 2008;9: 550–8.
  3. Grau AJ, Becher H, Ziegler CM et al. Periodontal disease as a risk factor for ischemic stroke. Stroke 2004;35:496–501.
  4. Khader YS, Dauod AS, El-Qaderi SS et al. Periodontal status of diabetics compared with nondiabetics: a meta-analysis. J Diabetes Complications 2006;20:59–68.
  5. Saremi A, Nelson RG, Tulloch-Reid M et al. Periodontal disease and mortality in type 2 diabetes. Diabetes Care 2005;28:27–32.
  6. Shultis WA, Weil EJ, Looker HC et al. Effect of periodontitis on overt nephropathy and end-stage renal disease in type 2 diabetes. Diabetes Care 2007;30:306–11.
  7. Bobetsis YA, Barros SP, Offenbacher S. Exploring the relationship between periodontal disease and pregnancy complications. J Am Dent Assoc 2006;137(10S):7s–13s.
  8. Williams RC, Barnett AH, Claffey N et al. The potential impact of periodontal disease on general health: a consensus view. Curr Med Res Opinion 2008;24:1635–43.
  9. Hunter W. Oral sepsis as a cause of disease. BMJ 1900;1:215–16.
  10. D’Aiuto F, Parkar M, Nibali L et al. Periodontal infections cause changes in traditional and novel cardiovascular risk factors. Am Heart J 2006;151:977–84.
  11. Slade DG, Ghezi EM, Heiss G et al. Relationship between periodontal disease and C-reactive protein among adults in the atherosclerosis risk in communities study. Arch Intern Med2003;163:1172–9.
  12. Desvarieux M, Demmer RT, Rundek T et al. Relationship between periodontal disease, tooth loss, and carotid artery plaque: the oral infections and vascular disease epidemiology study (INVEST). Stroke 2003;34:2120–5.
  13. Engebretson SB, Lamster IB, Elkind MSV et al. Radiographic measures of chronic periodontitis and carotid artery plaque. Stroke 2005;36:561–6.
  14. Beck JD, Eke P, Heiss G et al. Periodontal disease and coronary heart disease. A reappraisal of the exposure. Circulation 2005;112:19–24.
  15. Ioannidou E, Malekzadeh T, Dongari-Bagtzoglou A. Effect of periodontal treatment on serum c-reactive protein levels: a systematic review and meta-analysis. J Periodontol 2006;77:1635–42.
  16. Offenbacher S, Beck JD. A perspective on the potential cardioprotective benefits of periodontal therapy. Am Heart J 2005;149: 950–4.

The mouse is mightier than the pen

Br J Cardiol 2009;16:13-14 Leave a comment
Click any image to enlarge
Authors:

We continue our series in which Consultant Interventionist Dr Michael Norell takes a sideways look at life in the cath lab… and beyond. In this column, he considers electronic communication.

The era of electronic communication has spawned a host of previously unimagined problems with regard to the written word. A recent news item revealed that Google has come up with a system that avoids an email being sent if the writer might, shall we say, be tired and emotional (a euphemism often used in the satirical – and iconic – periodical Private Eye, in place of the term ‘sloshed’). Before you are allowed to ‘send’ you have to solve a number of mathematical problems and thereby demonstrate that you are in reasonable possession of your faculties. Now there’s an idea …

In what other ways could the art of e-letter writing be even further enhanced? How might we fine tune our software in order to improve our missives as they fly about the ether? And, in the ever-threatening climate of computer viruses and identity theft, how might we better protect ourselves from others … and others from ourselves?

Suggested areas for improvement

In order to give William Gates esq. some help, I have listed below some suggestions that could be easily introduced into our network in the hope that value would be added to our e-writing experience. (For all I know some, many, or all of these modifications might be available already from your local family computer store, but … what the heck. I was stuck for copy with this issue and the BJC was hassling me over the deadline.) See what you think, but bear in mind that these top tips all come under author’s copyright, intellectual property legislation and patent law.

1. When you receive an email and press ‘reply’, the system recognises the manner in which the sender signed off, e.g. “Yours sincerely, Emily Chuckleberry (Ms)” or, “All the best, Chuck”, and begins your response accordingly: “Dear Ms Chuckleberry” or, “Hi, Chuck”.

Get the idea?

2. On returning from a week’s annual leave you come in early on a Monday morning to trawl your mail before the official day begins. As you work through the list in the order in which mail was received, you are particularly taken with one to which you are urged to respond immediately. Having accomplished this task and pressed ‘send’ with a satisfying sense of efficiency, you are then deflated when, a few mails further up the list (and therefore received subsequently), you see a supplementary message from the same source indicating that any response is unnecessary.

My system would alert you with the phrase, “Before responding, see later mail from same sender”. You hit ‘return’ and see additional information that might modify, if not nullify, your response.

Impressed?

3. If you wish to insert an ellipsis (…) the computer will not let you type more than three dots in a row. Even if you choose to override spell-check and request to ‘ignore all’ after your ludicrous construction of incessant full stops has been highlighted, it will steadfastly resist. After a series of increasingly severe warnings, it will shut down until you see common sense, at which point it will insist that you complete a short grammar test before you are ever allowed to press ‘send’ again.

You can envisage a similar approach being taken with inappropriate use of the apostrophe, let alone the semicolon, but I thought it would be preferable to start with a straightforward example, which as you can see, is a bit of a bete noir of mine.

4. While I understand the reasoning behind setting up a ‘firewall’, the security in place in our own institution might still need some tweaking. Occasionally I am notified that incoming jottings from my more ‘jovial’ correspondents have been barred, and that there is a process of appeal I could pursue if I am minded to (I am usually not). However, I am more puzzled as to why communication from more upstanding sources, such as ‘theheart.org’ for heaven’s sake, is siphoned off to be scrutinised and, presumably, verbally cleansed in the literal equivalent of Guantanamo Bay.

5. On the same note, and acknowledging that it is our Government’s declared intention to monitor and log the content of all electronic communication, I can think of a further software modification. When we use certain, shall we say, ‘sensitive’ words or phrases (I won’t mention them here for obvious reasons), a message box springs up and advises “If you use this letter sequence, be aware that you may be visited by Special Branch at four in the morning”.

Pause for thought

The following suggestions all relate to a major downside of our modern era, so pay attention.

Responding in writing to letters that cause us to become enraged, used to incorporate what might be regarded as the communication equivalent of the atrioventricular node. An automatic brake was put into the system to avoid rapid conduction and protect the ventricle from overstimulation. We would dictate our infuriated reply but then have to wait for it to be typed, and this pause would give us the opportunity to ponder as to the wisdom of actually posting our vitriol.

This vital delay in the system no longer applies and the result is that all too soon we have sent something that we will live to regret. My system protects us, and the recipients, from such hasty transmissions.

6. First, the audio component of our desktop detects if the email we have opened is producing a higher than normal volume in terms of our welcoming verbal comment (as in, “What the h*** is he on about? He’s got a b****y nerve; I’ll show him!”).

7. The time at which the provocative mail is opened is noted, and the computer does not allow you to send a response without administering a preset time delay to run. (Admit it, you’re impressed. But there are even more sophisticated algorithms yet to come into play).

8. The software can detect the phrasing and tone of your response and, as you vent your spleen, will display pop-ups with cautious advice like, “Are you sure you want to use that term?” or, “Suggest you check the anatomical possibility of actually doing that”.

In addition, when you press ‘reply to all’, it will ask you whether you are absolutely sure that you want your response to be seen by all the members of the British Cardiovascular Society (who were rather stupidly copied into the original correspondence you received). A sobering message will be displayed: “Two wrongs don’t make a right”.

9. Let us assume that, as the red mist descends, you plough on with only one goal in mind. As you bang away, touch sensitive keys translate the pressure applied to gradually emphasise the appearance of words on the screen. With slightly increased force, it converts to italics and a little more effort produces ‘bold’ as well. Finally, when you are hammering as hard as you can with blood oozing from your nail beds, it also underlines, thereby leaving no doubt in the mind of our thus far innocent recipient that you are distinctly unimpressed with his comments.

10. In severe cases these measures may prove insufficient in distracting you from your single-minded crusade. The modifications described above can be overridden or circumvented, but there is one programme I have devised that is foolproof: the computer screen is not only touch sensitive (just in case, as a result of unrestrained anger, you bash it), but is also chemically coated so as to detect the presence of … saliva. As you type and yell at the top of your voice, spluttering as you do so, the deposit of spittle on the screen and keyboard is detected and as a result the computer shuts down.

11. Finally, a piece of advice: instead of touching ‘send’, hit ‘save’ instead. The software then will not allow you to transmit until the following morning, or next working day, thereby permitting you to ‘sleep on it’. (The computer will also eject a 5 mg tablet of diazepam at this point – an updating of its ‘snooze’ function). When you next open the document in the cold light of day, an ingenious device comes in to play: when you press ‘send’ the computer is programmed to interpret this instruction instead as ‘delete’. Think yourself lucky.

New sources of vascular disease information

Br J Cardiol 2009;16:16-14 Leave a comment
Click any image to enlarge
Authors:

A new on-line resource from the National Library for Health – the Vascular Specialist Library – has been launched to provide information for both health care professionals and the general public on the prevention, diagnosis and management of diseases of the arteries, veins and the lymphatic system.

The core content of the Vascular Library includes systematic reviews, National Institute for Health and Clinical Excellence (NICE) guidelines, health policy initiatives, evaluated patient information, key vascular-related information from general medical and specialist vascular journals and data from national standards, statistics and audits. Visit: www.library.nhs.uk/vascular

The Department of Health has also published guidance for PCTs regarding risk assessment and management for vascular checks. Visit: www.dh.gov.uk/en/Publicationsandstatistics/Publications/ PublicationsPolicyAndGuidance/DH_090277

NHS Choices and NHS Direct join forces

Br J Cardiol 2009;16:16-14 Leave a comment
Click any image to enlarge
Authors:

Two government websites – NHS Choices and NHS Direct – have joined forces to provide the public with a one stop health information service: www.nhs.uk. The website will give public advice and information about anything from which hospital to choose (including data on hospital comparisons) to checking what symptoms might mean. NHS guides will cover long-term conditions, a health A-Z will cover more than 700 conditions and treatments, answers to common health questions will be given and there will also be an online enquiry service for non-emergency health questions.

National search for ‘the face of diabetes’

Br J Cardiol 2009;16:16-14 Leave a comment
Click any image to enlarge
Authors:

As one person is diagnosed with diabetes every three minutes, faster than ever before, according to the charity Diabetes UK, the pharmaceutical company MSD is trying to build a ‘face of diabetes’ mosaic to highlight the impact of type 2 diabetes on patients.

People with diabetes are being asked to send photographs or images of themselves, or what diabetes means to them, to be used in the mosaic. Boxes have been placed in selected GP surgeries throughout the UK for pictures to be posted alongside any personal thoughts patients may have on living with diabetes.

Images and comments can also be emailed, text or uploaded to the following link: www.facingdiabetes.co.uk or posted to Facing Diabetes, Merck Sharp & Dohme Ltd, Hertford Road, Hoddesdon, Hertfordshire, EN11 9BU.

Panic attacks linked to higher risk of heart attacks and heart disease

Br J Cardiol 2009;16:16-14 Leave a comment
Click any image to enlarge
Authors:

People who have been diagnosed with panic attacks or panic disorder have a greater risk of subsequently developing heart disease or a myocardial infarction (MI) than the normal population, with higher rates occurring in younger people, according to a recent study (Eur Heart J 2008:29:2981–8)

The study – which looked at 57,615 adults diagnosed with panic attacks/disorders and 347,039 adults who did not have the condition – found that people who were younger than 50 when first diagnosed had a significantly higher risk of MI but this was not the case in older people. It also found there was a significantly higher incidence of subsequent coronary heart disease (CHD) in people diagnosed with panic attacks/disorders at all ages, but this was more marked in the under 50s.

Interestingly, amongst people of all ages, the research showed that the risk of dying from CHD was actually reduced.

New lipid-modifying therapy phase 3 study shows reduced flushing

Br J Cardiol 2009;16:16-14 Leave a comment
Click any image to enlarge
Authors:

Phase III clinical study results with a nicotinic acid/laropiprant combination (Tredaptive®), show that in the treatment of patients with dyslipidaemia and primary hypercholesterolaemia, this new lipid-modifying therapy produced less flushing compared with those patients who were treated with extended-release nicotinic acid (Int J Clin Pract 2008;62:1959–70).

Treatment with 2 g of the nicotinic acid/laropiprant combination produced a significant 18% reduction from baseline in low-density lipoprotein cholesterol (LDL-C) and a 26% reduction in triglycerides compared to placebo across weeks 12-24. In addition, patients treated with the combination experienced significantly less flushing compared with those treated with extended-release nicotinic acid (0.2 days/week versus 0.7 days/week respectively).

Some 69% of patients treated with 1 g of the combination reported either no flushing symptoms, or mild flushing symptoms during the first week of treatment, compared to 44% of those who received extended-release nicotinic acid alone. More than twice as many patients on extended release nicotinic acid (22%) discontinued treatment due to flushing compared with those patients taking the combination (10%).

The nicotinic acic/laropiprant combination has recently received EU marketing authorisation.

New heart failure report

Br J Cardiol 2009;16:16-14 Leave a comment
Click any image to enlarge
Authors:

A new report Focus on heart failure, by the NHS Institute for Innovation and Improvement, aims to provide primary and secondary care services with guidance on how to achieve high quality care for all heart failure patients. The report is one of a series which highlights best practice within key services in the NHS in order to improve delivery.

Heart failure currently affects one in 1,000 people, and is rising by at least 10% each year. When combined with other heart diseases, the annual cost to the NHS of supporting these patients is £625 million.

For further information and to view a copy of the Focus on heart failure document visit www.institute.nhs.uk/heartfailure

Future of PAH: what does success look like?

Br J Cardiol 2009;16(Suppl 1):S13-S14 Leave a comment
Click any image to enlarge
Authors:
Sponsorship Statement: The symposium was sponsored by GlaxoSmithKline, who also sponsored the writing of this report and this supplement. Volibris™ ▼ is a registered trademark of Gilead (Nasdaq: GILD), used under license by the GlaxoSmithKline group of companies. Ambrisentan has been licensed to GlaxoSmithKline by Gilead Sciences Inc. in all countries of the world, except the United States (US).

Professor Jean-Luc Vachiéry, Université Libre de Bruxelles, Belgium, began by looking at progress in the management of PAH over the last 50 years. Current therapies are now based on experience with earlier treatments, including calcium channel blockers1 and surgery,2 and by more recent, evidence-based RCTs with newer drugs (figure 1).3-5

We are facing different needs in a rapidly evolving field, according to Professor Vachiéry. He outlined the many emerging issues in PAH (table 1), which is an incurable disease.6 Unequivocally, patients need a cure and better quality of life with enhanced survival, while clinicians need evidence to guide treatment strategies. This must be balanced by healthcare regulators, who will be under pressure to control the costs, and also by industry, which has a huge responsibility in this field, especially as PAH is considered to be an orphan disease.7

Table 1: Emerging issues in pulmonary arterial hypertension (PAH)
Table 1: Emerging issues in pulmonary arterial hypertension (PAH)

A likely first step might be to understand new targets. Evidence to guide clinical decision-making in how to measure success is coming from RCTs, but sometimes it can be difficult to translate this evidence into clinical experience. Professor Vachiéry discussed some of these new targets and investigational therapies, including vasoactive intestinal peptide (VIP)8 and antiproliferative agents.9 As cancer and PAH may share similar pathophysiology of aberrant cell proliferation, growth factor inhibition could play a role in the treatment of PAH, said Professor Vachiéry. But these new agents which target, for example, platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) are not yet fully proven in his view. Another concept is to transplant autologous endothelial progenitor cells which, one Chinese study suggests,10 may be beneficial in patients with idiopathic PAH. The technique is being further assessed in a larger Canadian trial, the Pulmonary Hypertension: Assessment of Cell Therapy (PHACeT) trial.

Table 1: Emerging issues in pulmonary arterial hypertension (PAH)
Table 1: Emerging issues in pulmonary arterial hypertension (PAH)

What evidence can be derived from RCTs and will success derive from combination therapy? These are important questions to assess as the impact of treatments on disease progression is not yet known. We will have to change and redefine success and update clinically relevant end points, in Professor Vachiéry’s opinion, with robust demonstrations of safety and efficacy. Clinical trial end points over the past 15 years have included exercise capacity, haemodynamics, quality of life, time to clinical worsening, NYHA class, biomarkers and imaging.3-5 Time to clinical worsening as assessed in clinical trials has evolved from event recording (death and transplantation) to more complex end points such as;

  • refractory systolic hypertension
  • worsening right ventricular failure
  • rapidly progressing end-organ damage
  • decrease in six-minute walk duration.
  • It has been used as a secondary end point in drug trials.3-5, 11

Composite end points in RCTs may have several components (table 2).5, 12-14 Composite end points have been used to evaluate treatments for heart failure, as seen in large trials such as SOLVD,15 MERIT16 and CHARM.17 It is likely too in PAH that combinations of drugs will be assessed utilising composite end points.

Table 2: Composite end points in RCTs
Table 2: Composite end points in RCTs

How can the evidence gained translate into practice? Professor Vachiéry considered that clinical judgement was paramount. Clinical assessment may be derived from measures including NYHA FC, signs of right heart failure, aetiology and rate of progression; whereas the degree of exercise (in)tolerance can be assessed by six-minute walk duration.18 Right ventricular (dys)function may be evaluated using biological surrogate markers and/or imaging (echocardiography, magnetic resonance imaging) and/or invasive techniques.18 What is missing may come down to the definition of treatment failure, the type and timing of combination therapy, future targets and the definition of specialised centres. Clearly, more clinical trials are needed to provide evidence of significant, safe and clinically meaningful interventions. This will in the future be increasingly difficult as there are relatively few patients with this so-called orphan disease.

We have made such progress over the past 20 years that, when deciding on treatment, we have the luxury of choice, said Professor Vachiéry: we definitely need specialised centres. “The future of PAH starts today” and the bar has been raised very high. Now “it’s our responsibility to make it happen” and to concentrate efforts on finding better tools to improve the quality of life and survival of these patients, said Professor Vachiéry •

Conflict of interest

J-LV is consultant to GSK and Encysive Europe. He is an advisory board member to and has received speaker fees from Actelion, Encysive Europe, GSK, Pfizer and United Therapeutics.

References

  1. Sitbon O, HymbertM, Ioos V et al. Who benefits from long-term calcium-channel blocker therapy in primary pulmonary hypertension? Am J Respir Crit Care Med 2003;167:A440.
  2. Klepetko W, MayerE, Sandoval J et al. Interventional and surgical modalities of treatment for pulmonary arterial hypertension. J Am Coll Cardiol 2004;34:73S–80S.
  3. Rubin LJ, Badesch DB, Barst RJ et al. Bosentan therapy for pulmonary arterial hypertension. N Engl J Med 2002; 346:896–903.
  4. Barst RJ, Langleben D, Badesch D et al. STRIDE Study Group. Treatment of pulmonary arterial hypertension with the selective endothelin-A receptor antagonist sitaxsentan. J Am Coll Cardiol 2006;47:2049–56.
  5. Galie N, Olschewski H, Oudiz RJ et al. Ambrisentan for the treatment of pulmonary arterial hypertension. Results of the ARIES Study 1 and 2. Circulation 2008;117:3010–19.
  6. Humbert M, Sitbon O, Simonneau G. Treatment of pulmonary arterial hypertension. N Engl J Med 2004;351:1425–36.
  7. Humbert M, Khaltaev N, Bousquet J et al. Pulmonary hypertension. From an orphan disease to a public health problem. Chest 2007;132:365–7.
  8. Petkov V, Mosgoeller W, Ziesche R et al. Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension. J Clin Invest 2003;111:1339–46.
  9. Souza R, Sitbon O, Parent F et al. Long-term imatinib treatment in pulmonary arterial hypertension. Thorax 2006;61:736.
  10. Wang XX, Zhang FR, Shang YP et al. Transplantation of autologous endothelial progenitor cells may be beneficial in patients with idiopathic pulmonary arterial hypertension. J Am Coll Cardiol 2007;47:1566–71.
  11. Galie N, Ghofrani HA, Torbicki A et al. Sildenafil citrate therapy for pulmonary arterial hypertension. N Engl J Med 2005;353:2148–57.
  12. Simonnean. Am J Respir Crit Care Med 2002;165:800–04.
  13. Olschewski H. N Engl J Med 2002;347:322–9.
  14. Barst RJ. J Am Coll Cardiol 2003;41:2119–25.
  15. SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fraction and congestive heart failure. N Engl J Med 1991;325:293–302.
  16. MERIT-HF Study Group. Effect of metoprolol CR/XL in congestive heart failure: Metoprolol CR/XL Randomized Intervention Trial (MERIT-HF). Lancet 1999;353:2001–07.
  17. Pfeffer MA, Swedberg K, Granger CB et al. Effects of candesartan on mortality and morbidity in patients with congestive heart failure: the CHARM-Overall programme. Lancet 2003;362:759–66.
  18. Galie N, Torbicki A, Barst R et al. Guidelines on diagnosis and treatment of pulmonary arterial hypertension. The Task Force on Diagnosis and Treatment of Pulmonary Arterial Hypertension of the European Society of Cardiology.Eur Heart J 2004;25:2243–78.
Disclaimer: UK prescribing information current at the date of publication of this supplement can be found by downloading the PDF. Medinews Cardiology Limited advises healthcare professionals to consult up-to-date Prescribing Information and the full Summary of Product Characteristics available from the manufacturers before prescribing any product. Medinews Cardiology Limited cannot accept responsibility for any errors in prescribing which may occur.

Combating vascular disease in Scotland: 20 years of SHARP

Br J Cardiol 2009;16:17-19 Leave a comment
Click any image to enlarge
Authors:

The Scottish Heart and Arterial Risk Prevention Group (SHARP) was launched in 1988 with the aim of helping to reduce and prevent premature morbidity and mortality from cardiovascular disease (CVD) in Scotland. The programme for the 20th anniversary meeting – held on the 20th–21st November 2008 in the Hilton Hotel Dunkeld – examined the likely future direction for cardiovascular disease prevention and management but also reflected on achievements over the past 20 years. Dr Alan Begg, Chairman of SHARP reports.

Heart disease in Scotland

The age standardised mortality rate for the under 75s for coronary heart disease (CHD) continues to fall in Scotland from a rate of 124.6 per 100,000 population in 1995 to 61.3 in 2007.1 The 30-day survival for acute myocardial infarction (MI), however, has remained constant over the last few years at 85%. Evidence of major differences in service provision, activity and approach between the devolved nations has been previously highlighted.2 As the Department of Health Vascular Screening Programme for cardiovascular disease (CVD) and diabetes gathers momentum in the years ahead, this difference is likely to become more apparent. Deprivation as measured by the Scottish Index of Multiple Deprivation is associated with higher rates of CHD mortality. In the 15% most deprived areas in Scotland, the under 75s mortality rate from CHD (standardised by age) increased slightly from 110.2 in 2006 to 112.4 per 100,000 in 2007. This rate had previously fallen year on year from 2000 to 2006, with the prevalence rate in men aged 45–64 in East Glasgow at 9.1% being almost twice that of the rate in Aberdeenshire which is 4.7%. For women aged 45–64 the prevalence rate in north Glasgow is 4.4% compared with the equivalent rate of 1.5% in Shetland.1

Speakers at the conference were asked to highlight some important aspects and pressing developments that are required in the forthcoming years.

Acute coronary syndrome

Managing patients with acute coronary syndrome by a specialist cardiology service with access to continuous cardiac rhythm monitoring is now accepted as the norm, Dr John Maclean (GP, National Stadium Sports Medicine Centre, Glasgow) told the conference. There is evidence that patients managed in a specialist cardiology service are more likely to receive evidence-based therapy, compared to general physician care with prompt defibrillation and treatment of arrhythmias. On discharge from a specialist unit, patients are much more likely to be taking appropriate effective preventative drugs.

He felt the move to the use of primary percutaneous coronary intervention (PCI) for acute ST-elevation myocardial infarction (STEMI) will continue since it shows a mortality/reinfarction benefit and a reduced subsequent need for coronary artery bypass grafting. The use of intracoronary stent implantation at the time of primary PCI to reduce reinfarction and improve prolonged revascularisation needs to be encouraged and the use of drug-eluting stents, when clinically relevant, should be considered. There is also a need to ensure easy access to rescue PCI where there is apparent failure of reperfusion with thrombolysis.

Stroke care

Turning to stroke, Professor Peter Langhorne (Professor of Stroke Care, Royal Infirmary, Glasgow) said its rapid recognition and diagnosis was essential to ensure early acute treatment and secondary prevention, including the increased use of early recognition scores by those seeing patients at initial presentation. Early recognition and treatment offers the promise of preventing recurrent stroke or of limiting the extent of stroke damage. One challenge is in selecting patients in the acute phase who will benefit from the use of recombinant tissue plasminogen activator (rtPA) and in how to develop the service to encompass expanding applicability.

Managing patients in stroke units manned by a co-ordinated multidisciplinary team is now well established, he said, with the majority of patients being able to access such services in a timely manner. Rehabilitation needs to be a continuum with facilitation of the process from hospital to home, which requires all components of the stroke service to be fully integrated to ensure collaborative working between all health professional groups including social care.

Familial hypercholesterolaemia

The introduction of a programme of cascade testing to identify patients with familial hypercholesterolaemia will be a welcome development, according to Dr Robert Finnie (General Practitioner, Livingston). This, he said, involves screening and testing all first-degree relatives of an affected case and repeating the process when another affected individual is identified. This screening, carried out in conjunction with genetic testing for the common mutations and gene sequencing, will help to identify the normal mutations apparent within the Scottish population.

Peripheral arterial disease

On the basis of their increased CVD risk, Professor Jill Belch (Professor of Vascular Medicine, Ninewells Hospital, Dundee) told the meeting that there is an urgent need for patients with peripheral arterial disease (PAD) to be included in the Quality and Outcomes Framework (QOF) for general practitioners, either within its own disease category or as a directly enhanced service.

The REACH registry has shown that patients with PAD experience the highest rates of cardiovascular death and major cardiovascular events due to atherothrombosis and these higher event rates in patients with PAD may reflect a higher proportion of disease in other vascular beds.3 She said this level of risk makes them one of the highest priority group of patients for intensive risk reduction.

Chronic kidney disease

Dr Chris Isles (Consultant Physician, Dumfries and Galloway Royal Infirmary) spoke about how the management of chronic kidney disease (CKD), especially to minimise cardiovascular risk, will gain increasing importance in primary care as general practitioners bring its management into their chronic disease portfolio. He told delegates that he felt the benefits of renin angiotensin system blockade in reducing progression in those with proteinuric nephropathy needed to be balanced against their potential nephrotoxic effects. Better outcomes from longer periods of dialysis is likely to lead to more nocturnal home dialysis with refinement of immunosuppressant therapy likely in those with a renal transplant. End-of-life issues and palliative care are an important aspect of the patient’s management and need to be considered in appropriate cases.

Erectile dysfunction

The association between erectile dysfunction (ED) and its risk factors cannot be ignored with ED predicting the presentation of both acute and chronic CHD, Dr Graham Jackson (Consultant Cardiologist, Guy’s and St Thomas’s Hospital London) told the meeting. For those men with no cardiac symptoms, there is a window of between two to three years from the onset of ED in which their overall vascular risk can be actively reduced. Those at highest risk should undergo further investigations and intensive preventative therapy.

Cardiovascular risk reduction

Professor Lewis Ritchie (Professor of General Practice, University of Aberdeen) said he believed that traditional boundaries of care, currently demarcated by sectors of provision, will give way to more integrated care focused on the patient journey.

High risk and population strategies will continue to have complementary roles for cardiovascular morbidity/mortality reduction – the likely beneficial effects of the ban of smoking in public places is already being seen in reducing emergency cardiac admissions, for example. Other novel approaches to public and childhood education will also need to be pursued and the Quality and Outcomes Framework (QOF) should continue to evolve to meet the challenges of CVD management and prevention. Aligned to this will be the development and refinement of national standards for the prevention and optimal management of cardiovascular disease, as currently being developed by NHS Quality Improvement Scotland (QIS).

Cardiovascular risk scoring is an inexact science and needs to be refined not only in terms of scientific accuracy, but in addressing equity through deprivation correction. Risk-scoring tools need to be embedded seamlessly within computer systems and used actively to prompt more effective management and targeting. Patient-centred records should be available throughout the NHS and national guidelines also need to be embedded more seamlessly into electronic records in a context sensitive fashion.

Adequate training and learning for the primary care team is essential and there is potential for an extended role for pharmacists along with empowering patients for supported self-care.

Medical research

If patients are to continue to receive the benefit of medical advances and new treatments, it is important that they are encouraged to become involved in medical research, said Professor Tom MacDonald (Professor of Clinical Pharmacology, Ninewells Hospital Dundee). The ‘Get Randomised’ campaign, which has the backing of four medical school faculties in Scotland, as well as the support of the Chief Scientist in Scotland, aims to highlight the importance of medical research, increase public awareness of clinical trials, and encourage people to become involved so that present and future generations can benefit from effective treatments.5

Atherosclerosis

“With time, genetics may have an increased role in determining the pathogenesis of atherosclerosis and an association with future events,” Professor Peter Weissberg (Medical Director, British Heart Foundation) told the meeting. While biomarkers and molecular imaging may assume an increased role in future diagnosis, he said, drug therapy will continue to be the most important for prevention, The role of statins in changing our approach to heart disease prevention cannot be underestimated and the lower the cholesterol level, the better, he concluded. The concern now is that in the future our ability to predict risk may outstrip our ability to modify it.

Conclusion

In the years to come, SHARP will continue to have an important role in facilitating the implementation of guidelines and evidence-based practice, as well as auditing clinical practice. The Scottish Intercollegiate Guidelines Network (SIGN) published in February 2007 updates previous SIGN CHD and CVD prevention guidelines. Nationally agreed standards relevant to CHD management and CVD prevention are currently being developed by NHS QIS and are due to be finalised later this year.5

H.E.A.R.T UK, the cholesterol charity, has recently presented the findings of a review into the implementation of the SIGN cardiovascular prevention guideline in Scotland.6 Awareness of the guideline was high and GPs continue to use traditional risk-screening tools based on the Framingham function. There are clear concerns, however, about resources for carrying out primary prevention of CHD, as well as concerns about the levels and consistency of specific training for heart disease prevention. In the short term, this lack of educational opportunities is something that SHARP aims to rectify with its use of regional training sessions across Scotland throughout 2009 and 2010. Health Service organisations, clinical networks and public charities all need to work in unison towards the common goal of better prevention and disease reduction. Challenges in vascular disease prevention still remain and SHARP remains committed to rising to that challenge. Where we will be in another 20 years, however, is impossible to predict.

References

  1. Information Services Division Scotland. Coronary Heart Disease http://www.isdscotland.org/isd/5762.html
  2. Brooks N, Norell M, Hall J et al. on behalf of a working group of the British Cardiac Society. National variations in the provision of cardiac sevices in the United Kingdom. Br J Cardiol2005;12:192–8.
  3. Steg PG, Bhatt DL, Wilson PW et al. REACH Registry Investigators. One-year cardiovascular event rates in outpatients with atherothrombosis. JAMA 2007;297:1197–206.
  4. Get randomised – medical research – do we really need it? http://www.getrandomised.org/home.htm
  5. NHS Quality Improvement Scotland Coronary Heart Disease Programme http://www.nhshealthquality.org/nhsqis/files/HeartDisease_CHD_SEP08.doc
  6. HEART UK The Cholesterol Charity Scotland – SIGN 97 guideline review. http://www.heartuk.org.uk/index.php?/news_and_campaigns/breaking_new/