Yearly Archives: 2016

In brief

Br J Cardiol 2016;23:10–11 Leave a comment
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News in brief from the world of cardiology

Approval for new heart failure treatment

A breakthrough drug for the treatment of chronic heart failure is now available in the UK.  The new drug sacubitril/valsartan (Entresto®, Novartis) has been approved for the treatment of adults with symptomatic heart failure with reduced left ventricular ejection fraction (HFREF).

Sacubitril/valsartan – the first drug in the angiotensin receptor neprilysin inhibitor (ARNI) class of drugs – was found to be superior to an evidence-based dose of the angiotensin-converting enzyme (ACE) inhibitor, enalapril, in the PARADIGM-HF study, the largest heart failure study conducted to date.

PARADIGM-HF (Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure trial), which involved 8,442 patients with HFREF, was stopped early due to a clear benefit of sacubitril/valsartan over enalapril. It significantly reduced the risk of cardiovascular death and first hospitalisation for heart failure by 20% when compared to enalapril (absolute risk reduction: 4.7%). Analysis of safety data showed that sacubitril/valsartan had a similar tolerability profile to enalapril.

The availability of sacubitril/valsartan may change the way heart failure patients are treated. Outlook for many patients with heart failure remains poor with current treatments. Heart failure costs the NHS about £2.3 billion a year, accounts for one million in-patient bed days and 5% of all emergency and medical admissions to UK hospitals; hospital admissions are projected to rise by 50% over the next 25 years, largely as a result of an ageing population.

New guidelines for managing blood pressure before surgery

The Association of Anaesthetists of Great Britain and Ireland (AAGBI) and the British Hypertension Society (BHS) have released the first-ever National Guidelines for managing patients with high blood pressure before surgery.  Published in the journal Anaesthesia, the guideline aims to reduce unnecessary cancellations for surgery because of a patient’s blood pressure.

Dr Terry McCormack, General Practitioner and co-Chair of the Guidelines Working Party, states: “This is the first time that there has been a collaboration between hypertension specialists, anaesthetists and general practitioners to produce a clear set of guidelines as to how we manage blood pressure before elective anaesthesia”. Dr Mike Durkin, National Director of Patient Safety, NHS England, added: “We welcome the intention of these new National Guidelines to improve patient safety through the collaborative work of primary and secondary healthcare”.

Cancellations and postponements of planned surgery are a major, long-standing problem for NHS – nearly 1% of planned operations are cancelled at the last minute. The quantifiable loss of resource is pitted against unquantifiable and significant psychological, social and financial implications of postponement for patients and their families. Some cancellations are unavoidable, but this Guideline will go a long way towards reducing cancellations overall, by ensuring that surgery is only cancelled because of the patient’s blood pressure when the evidence supports this.

The guidelines can be accessed at:
http://onlinelibrary.wiley.com/doi/10.1111/anae.13348/full

BHF calls for national rollout of genetic testing for FH

As many as 250,000 people in the UK may be living with the inherited gene which causes familial hypercholesterolaemia (FH). Now the British Heart Foundation (BHF) is calling on health services across the country to urgently rollout a nationwide cascade testing programme.

Only around 20,000 people are thought to be receiving full treatment in lipid clinics. On average, FH can shorten life expectancy by 20 to 30 years if left untreated.

Despite recommendations by the National Institute for Health and Care Excellence (NICE) that NHS Trusts and health boards roll out cascade testing for FH for families across the UK, setting up of FH services has been slow in England and Scotland.

To start tackling the problem, the BHF have funded 25 FH nursing posts across 13 different locations to make sure millions of people have access to testing. Since these posts have been set up over the past two years, 974 people have been tested and 374 people (38% of those tested) have been shown to have FH, ensuring they get the treatment they need. The charity believes that the slow response by health services is putting thousands of people across the UK at an unnecessary risk of heart attacks early in life.

New BJC editorial board member

Dr Aynsley Cowie (British Association for Cardiac Prevention and Rehabilitation)
Dr Aynsley Cowie (British Association for Cardiac Prevention and Rehabilitation)

Dr Aynsley Cowie, Scientific Officer for the British Association for Cardiac Prevention and Rehabilitation (BACPR), has joined the BJC editorial board.

Aynsley has worked as cardiac rehabilitation physiotherapist within NHS Ayrshire and Arran for 11 years.  In 2011, she completed a PhD examining effects of home- versus hospital-based exercise training in chronic heart failure. Aynsley has recently started in a new post as consultant physiotherapist in cardiology. One of her first tasks is to lead on a Scottish Government funded project to develop a patient-reported outcome measure (PROM) for cardiology

Wide differences in UK prescribing rates for NOACs

Stark differences in access to new medicines such as non-vitamin K oral anticoagulant (NOACs) to reduce the risk of strokes in people atrial fibrillation (AF) are revealed today in a new report from the Atrial Fibrillation Association.

The chance of receiving the newer treatments varies 16-fold across England, the report says. In one part of England 69% of patients receive the newer treatments compared to just 4% in another part of the country.

The report, In pursuit of excellence in the prevention of AF-related stroke, which was supported by an unrestricted educational grant from Daiichi Sankyo UK, points out that more than half (56%) of Clinical Commissioning Groups (CCGs) are at or below the national average in England for NOAC use of 16.5% compared to warfarin. Within this 56%, 53 CCGs (25%) have NOAC prescribing rates of 10% or less.

Just seven CCGs have reached or exceeded the recommended level of 35% NOAC use as set out by the National Institute for Health and Care Excellence (NICE) in June 2014.

Trudie Lobban, Founder of the AF Association, said: “This variation is completely unacceptable. It makes a mockery of the concept of a National Health Service that patients with the same condition living just miles apart receive such dramatically different rates of the newer therapies”.

Dabigatran reversal agent available

Idarucizumab (Praxbind®, Boehringer Ingelheim), a reversal agent specifically designed for the non-vitamin K oral anticoagulant (NOAC), dabigatran etexilate (Pradaxa®, Boehringer Ingelheim), has been approved for use in adult patients when rapid reversal of the anticoagulant effect is required for emergency surgery/urgent procedures and in life-threatening or uncontrolled bleeding. Dabigatran is the first NOAC to have a specific reversal agent – idarucizumab specifically binds to dabigatran molecules only, neutralising their effect without interfering with the coagulation cascade.

Eating eggs does not increase risk of heart attack

A new study from the University of Eastern Finland shows that a relatively high intake of dietary cholesterol, or eating one egg every day, is not associated with an elevated risk of coronary heart disease (CHD) in this population.

The findings published in the American Journal of Clinical Nutrition (doi: 10.3945/ajcn.115.122317) also show no association was found among those with the APOE4 phenotype, which affects cholesterol metabolism and is common among the Finnish population, in whom the effect of dietary cholesterol on serum cholesterol levels is greater.  Research data on the association between a high intake of dietary cholesterol and the risk of cardiovascular diseases in this population group has not been available until now.

In the study, the dietary habits of 1,032 men aged between 42 and 60 years and with no baseline diagnosis of a cardiovascular disease were assessed at the onset the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) in 1984–1989 at the University of Eastern Finland. During a follow-up of 21 years, 230 men had a myocardial infarction, and 32.5% of the study participants were carriers of APOE4. A high intake of dietary cholesterol was found not to be associated with the risk of incident CHD in either the entire study population or in those with the APOE4 phenotype.

The consumption of eggs, a significant source of dietary cholesterol, was also found not to be associated with risk of incident CHD. No link was found between dietary cholesterol (or eating eggs) with thickening of the common carotid artery walls. In the highest control group, the study participants had an average daily dietary cholesterol intake of 520 mg and they consumed an average of one egg per day, which means that the findings cannot be generalised beyond these levels, the authors suggest.

Sedentary CHD patients have worse health even if they exercise

Sedentary coronary heart disease (CHD) patients have worse health even if they exercise, reveals research published in the European Journal of Cardiovascular Prevention (doi: 10.1177/2047487315617101).

“Limiting the amount of time we spend sitting may be as important as the amount we exercise,” says lead author Dr Stephanie Prince, (Division of Prevention and Rehabilitation, University of Ottawa Heart Institute, Ontario, Canada).

Previous research has shown that being sedentary increases the risk of cardiovascular disease but until now its effect on patients with established heart disease was unknown. The current study investigated levels of sedentary behaviour and the effect on health in 278 CHD patients who had been through a cardiac rehabilitation programme, which taught them how to improve long-term exercise levels.

The researchers, from using activity monitors, found that CHD patients spent an average of eight hours each day being sedentary. Men spent more time sitting than women – an average of one hour more each day. This was primarily because women tended to do more light intensity movement – things like light housework, walking to the end of the drive, or running errands. Recent research suggests that, at around the age of 60, men become more sedentary than women and may watch more TV.

The researchers have provided the following practical tips to help to get moving more:

  • get up and move every 30 minutes
  • stand up during TV commercials or, even better, do light exercises while watching TV
  • set a timer and take regular breaks from your desk
  • take lunch breaks outside instead of in front of the computer
  • go to bed instead of sitting in front of the TV and get the benefits of sleeping
  • monitor your activity patterns to find out when you are most sedentary.

Book review: Hypertension, 2nd edition

Br J Cardiol 2016;23:15 Leave a comment
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Editors: Nadar S, Lip GY

EHRA bookPublisher: Oxford Cardiology Library, Oxford University Press, Oxford, 2015
ISBN: 9780198701972 Price: £19.99

I have always been fascinated by how primary care and secondary care look at hypertension in different lights. This pocket reference, written by cardiologists, demonstrates those differences and will mainly be of interest to their specialist colleagues. Examples of this are the inclusion of echocardiograms as basic investigations, whilst home blood pressure monitoring is never mentioned.

Mostly written by Sunil Nadar, it is a collection of chapters that often repeat statements from previous chapters, particularly involving the epidemiological and pathophysiological aspects of the subject. Whilst this detracts from reading the book as a continuous text, it does facilitate its use as a handy reference. You can easily dip in and out.

Of particular note, specialists will find the summary of imaging studies for renal artery stenosis in chapter three very useful. Chapter eight gives a comprehensive account of target organ damage whilst chapter nine, on left ventricular hypertrophy, and chapter 10, on atrial fibrillation, are also excellent. As one would expect from our cardiology colleagues, beta blockers are extensively covered. Chapter 18 covers renal denervation, the very subject that reignited interest in hypertension among cardiologists, until Simplicity HTN-3 put this treatment concept on ‘hold’. The part that I most appreciated was in chapter 20, which covers risk assessment, where Sunil Nadar recommends that the decision to treat should be based on relative risk, not absolute risk alone.

All books are out of date as soon as they are published and the authors of this tome have been particularly unlucky because after several lean years in terms of new discovery in hypertension, we have just had a flurry of activity. PATHWAY 2 and 3 (featured in our BJC report from ESC 2015, available at https://bjcardio.co.uk/podcasts/) will change future guidelines and SPRINT will at the very least cause plenty of discussion. Sadly they all arrived long after this book was put to bed at the printers.

Terry McCormack

General Practitioner, and Honorary Reader at Hull York Medical School

Whitby Group Practice, Spring Vale Medical Centre, Whitby, North Yorkshire, YO21 1SD

Win a free copy of above book for your practice or department!

Watch our podcast featuring Terry McCormack from the 2015 ESC at:

https://bjcardio.co.uk/2015/10/european-society-of-cardiology-congress-2015-highlights-1/

…and answer the following questions:

1. In the PATHWAY 2 study, what drug was compared against placebo?

2. What is the new suggested definition of resistant hypertension?

3. Which two diuretics were included in the PATHFINDER 3 study?

The first 10 healthcare professionals who return the correct answers to: [email protected] (subject: Hypertension quiz) will receive the book

Good luck!

Correspondence: ‘You look dishevelled’ – MI in a cardiologist diagnosed by his secretary

Br J Cardiol 2016;23:14 Leave a comment
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Correspondence from the world of cardiology

Dear Sirs,

A few months ago, I arrived in the cardiology office around midday on Monday after a short ward round. One of our secretaries voiced the view “You don’t look right”. I was surprised when she qualified this as “looking dishevelled”. When asked what she meant, she was instantly apologetic and said “Oh I mean you look wide-eyed and agitated”.

The background was that I had felt nauseous whilst driving the car early Saturday afternoon and had, in fact, stopped the car to vomit on three occasions. I assumed I had eaten something that had upset me. The following day (Sunday) I continued doing minor jobs around the house and on the Monday went to work when the aforesaid conversation took place. Having previously arranged to check a PSA (prostrate-specific-antigen) level on myself, a cardiology colleague suggested I add a troponin to this blood request. 

Blood taken, I drove home and received a phone call to tell me my troponin-I had come back at 1,800 ng/L (normal range 0–40 ng/L). Feeling perfectly well and having experienced no discomfort at any time, I then drove to my local tertiary centre to undergo coronary angiography. This showed unobstructed coronary arteries. A cardiac MRI scan confirmed an apical left ventricular infarct. There followed further discussion and investigations concerning the possibility of a paradoxical embolic event, which remained unproven.

Whilst I had experienced no discomfort, I had been suffering anxiety due to a lack of junior staff support. This had manifested as me waking in the night and ruminating about who might appear for the team in the morning. After 32 years of clinical practice, the ‘lack of any consistency in team support’ was a far bigger concern than any clinical issues arising amongst my patients. I can only conclude this event was precipitated by stress, in much the same way as the condition Takutsubo syndrome (a usually reversible cardiomyopathy most frequently seen in middle-aged women who have experienced psychosocial trauma).

The overriding messages seem to be that your facial appearance often helps in diagnosing cardiac events. As a cardiologist and well aware of a ‘cardiac face,’ how could I have missed this in myself? And how many have such an event without ever being aware?

Conflict of interest

None declared.

Simon Dubrey
Consultant Cardiologist
Hillingdon Hospitals NHS Trust, Uxbridge, UB8 3NN

Correspondence: Aldosterone levels and oedema score in a small series of HF patients

Br J Cardiol 2016;23:14 Leave a comment
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Correspondence from the world of cardiology

Dear Sirs,

Acute decompensated heart failure (HF) is the most common cause of hospital admission among patients older than 65 years of age.1 Such patients present with dyspnoea and variable degrees of fluid retention. Although aldosterone is known to be elevated in patients with HF, it is not yet established whether aldosterone levels affect clinical presentation. We have performed a preliminary study to investigate the degree of variation in baseline aldosterone and whether there is any relationship between aldosterone levels and the extent of peripheral oedema.

Methods and results

We enrolled 29 patients (mean age: 76 years; range: 43−90) admitted to the cardiology ward with a diagnosis of acutely decompensated chronic HF (based on Framingham criteria).2 Following informed consent, blood samples for aldosterone levels were taken on the first morning after admission with the patient recumbent. Serum creatinine and brain natriuretic peptide (BNP) were measured simultaneously to control for renal function (GFR) and severity of HF respectively.3 The extent of oedema was assessed using a standard scoring system (see table 1) and patients were assessed clinically for the presence of ascites.

Table 1. Oedema scoring system
Table 1. Oedema scoring system

All patients had moderate or severe impairment of left ventricular function and were either New York Heart Association (NYHA) class 2 (n=8) or 3 (n=21). The majority had ischaemic heart disease (n=18) and were taking beta blockers (n=19), angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs) (n=25) and mineralocorticoid receptor antagonists (MRAs) (n=18). Aldosterone levels varied widely (mean: 496; range 60–2775 pmol/dl) and there was no correlation between aldosterone and BNP (Pearson’s correlation coefficient r² = 0.02) or between aldosterone and GFR (r² = 0.13).

Aldosterone levels were significantly higher in patients with oedema score 3-4 than in those with oedema score 1−2 [mean (SEM): 688 (214) vs. 289 (41) pmol/dl; p=0.04 one-tailed unpaired t-test]. See figure 1. Aldosterone levels were highest in patients (n=5) with oedema score 3−4 together with clinically detectable ascites [mean (SEM): 1019 (394) pmol/dl].

Figure 1. Aldosterone (pmol/dl) versus oedema score (oedema score 1–2 compared with oedema score 3–4)
Figure 1. Aldosterone (pmol/dl) versus oedema score (oedema score 1–2 compared with oedema score 3–4)

Conclusion

The results of this preliminary investigation suggest that aldosterone levels vary widely in patents presenting with acutely decompensated HF but appear to be highest in those with gross peripheral oedema. This relationship appears to be independent of renal function and overall severity of HF. Our data also suggest that aldosterone is particularly elevated in patients with ascites though the small numbers preclude meaningful statistical analysis.

Although oedema formation in HF is a complex and multifactorial process, our preliminary data suggest that aldosterone elevation may play a pivotal role in its pathophysiology. In this regard a comparison may be made with advanced cirrhotic liver disease, a condition in which aldosterone levels are also elevated in conjunction with ascites formation and peripheral oedema.  Although the pathophysiology is similarly complex, impaired hepatic metabolism of aldosterone is a key factor, in addition to stimulation of the renin angiotensin axis in response to reduced circulating volume.4 It may be hypothesised that similar mechanisms apply in heart failure with hepatic function compromised by congestion and chronic ischaemia.

The comparison may have therapeutic implications in that aldosterone antagonists (MRAs) are prescribed at substantially higher doses for cirrhotic liver disease than for congestive cardiac failure.5 In contrast, loop diuretics are the mainstay of treatment for heart failure with MRAs added at relatively low doses.6–8 We suggest that a more definitive study should be undertaken in a larger cohort of patients. If our initial findings are confirmed, further studies investigating the targeted use of high dose MRAs may be justified in patients with severe oedema and/or ascites.

Acknowledgements

Dr Paul Sainsbury for refereeing the ethics submission and Dr Lindsey Yeoman for statistical analysis.

Conflict of interest

None declared.

Gareth Archer
Specialist Registrar in Cardiology

Stephanie Hughes
Specialist Registrar in Cardiology

Haqeel Jamil
Specialist Registrar in Cardiology

Edward Bounford
Senior House Officer in Cardiology

Robert Stevenson
Consultant Cardiologist
Department of Cardiology, Huddersfield Royal Infirmary, Huddersfield

[email protected]

References

1. Fonarow GC, Adams KF Jr, Abraham WT, Yancy CW, Boscardin WJ. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. J Am Med Assoc 2005;293:572e80.

2. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993;22(4 Suppl A):6A−13A.

3. Hobbs R. Using BNP to diagnose, manage and treat heart failure. Cleveland Clinic J Med 2003;70:333−6.

4. Bansal S, Lindenfeld JA, Schrier RW. Sodium retention in heart failure and cirrhosis: potential role of natriuretic doses of mineralocorticoid antagonist? Circulation Heart Failure 2009;2:370−6.

5. Bernardi M. Optimum use of diuretics in managing ascites in patients with cirrhosis. Gut 2010;59:10−11.

6. Felker GM, Lee KL, Bull DA, Redfield MM, Stevenson LW. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med 2011;364:797−805.

7. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 1999;341:709−17.

8. Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003;348:1309−21.

Correspondence: Surviving an out-of-hospital arrest after negative tests: a GP’s experience

Br J Cardiol 2016;23:14 Leave a comment
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Correspondence from the world of cardiology

Dear Sirs,

I recently, at the age of 49, survived an out-of-hospital cardiac arrest. It helped that I am a GP and was on a ward round in a local care home. The nurse sitting next to me started cardiopulmonary resuscitation (CPR) immediately and I was defibrillated within a few minutes by a team of paramedics. It was strange to wake up somewhere else and told to “keep the oxygen on”. I thought I was in a dream. 

It is hard to thank sufficiently the teams in the acute cardiac unit, the ITU and CCU. Usually only 5% survive such an event. Often survivors suffer cognitive deficit that, hopefully, for me is minimal. I did not really have any major risk factors except a strong family history: four generations of heart disease presenting at a young age. My mother and uncle are still alive after their heart attacks at ages 46 and 36 years, respectively. The emergency angiography showed my coronary arteries were 100%, 95% and 90% blocked. I now have three stents, hopefully doing a grand job.

Because of my family history and some atypical sensations at the age of 48 years, I thought it would be a good idea to get screened for heart disease. So within the year before my event, I had an exercise tolerance test. This result was equivocal to the cardiologist, although I thought I could see some ST depression, so he recommended I have a thallium scan. This showed no evidence of significant risk for ischaemic heart disease. 

I was seen in an outpatient clinic four months later by the registrar, who counselled me on lifestyle modification and then she discharged me from the clinic. It was an odd consultation. I did not think she knew I was a doctor. I left the room feeling unhappy with how our encounter went but I know this can happen sometimes for all of us and shows how important the consultation is.

In one sense, I have been lucky and I am doing well. If I had not, my family would have been left asking how and why, especially as nothing had been found before. As for me, I keep trying to make sense of it all. I was unaware, for example, that the sensitivity of thallium scanning locally is 93%, i.e. a false negative rate of 7%. I wonder if this had been discussed with me whether I would have requested further tests. 

It has left me thinking about patients I knew with negative investigations and subsequent drastic events – often advanced cancer. I have had difficult consultations when they have asked why nothing was found before. From the cardiologist’s point of view, it has made me see how difficult their jobs are, especially when National Institute of Health and Care Excellence (NICE) guidelines are based on risk scores. For lower risk cases, minimally invasive tests are recommended. For atypical presentations, it is also less likely to recommend invasive tests. Since angiography comes with a risk of complications, it is only performed for higher risk cases. The atypical pain meant I had a thallium scan. If it had been based on family history, I would have had a CT angiogram.

This leaves me wondering about the use of our sixth senses and the importance of medical acumen. This has to be balanced against the risk of over investigating a population and the harm that this could cause. I usually avoid going to see a doctor but in this case it was my strong family history that made me seek help. If I had been offered further invasive tests and I knew the risks involved, would I have declined them? I found that, even as a doctor, I reverted to the patient role and relied on specialist advice.

Three months post-event, I went to see my first consultant to try and understand what had happened. Being human, I was stern and somewhat angry. It must have been hard for him to sit and listen to me. Although nothing could be changed, I hope he realised that I thought communication could be changed for future throughout the process and that it might protect him more.

The lessons I have drawn from this are:

  • the use of a good consultation
  • that screening tests have pitfalls and 
  • patients may need to be more aware. 

In the future for my patients’ sake, I will endeavour to be better informed on the sensitivity or specificity of each test. Finally  I have learned when to use your acumen and sixth sense.

Anonymous

Heart valve disease module 10: transcatheter valve treatment and other future developments

Released 1 March 2016     Expires: 01 March 2018      Programme: Heart valve disease 1 CPD/CME credit

Sponsorship Statement: This module has been sponsored by Edwards Lifesciences with an unrestricted educational grant

Designed to give healthcare professionals an understanding of future trends and treatments in the care of heart valve disease. It is one of several modules in our heart valve disease programme

1 CPD/CME credit

Module originally published July 2013. Revised module released March 2016

Learning objectives

Upon completing this module, participants should be better able to understand:

  • Transcatheter approaches to the mitral and aortic valves
  • Patient selection for aortic valve devices
  • Delivery approaches for replacement valves
  • Potential complications in such a procedure
  • Mitral valve techniques

Faculty

Dr Paul Aifesehi, Fellow Cardiovascular Surgery, Mount Sinai Medical Center, New York, USA

Dr Stephen Spindel, Resident Cardiothoracic Surgery, Mount Sinai Medical Center, New York, USA

Dr Jacob Kriegel, Medical Student, Colombia Presbyterian College of Physicians and Surgeons, New York, USA

Dr Joanna Chikwe, Associate Professor Cardiothoracic Surgery, Mount Sinai Medical Center, New York, USA

Accreditation

1 CPD/CME credit, 1 hour
BJC Learning has assigned one hour of CPD/CME credit to this module
The European Board for Accreditation in Cardiology (EBAC) has assigned one CME credit to this module. German participants should contact EBAC to receive a German VNR code for this course.
email: [email protected]
website: http://www.ebac-cme.org/

Produced in collaboration with:

You need to login to take this module

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Heart valve disease module 9: surgery for heart valve disease

Released 1 March 2016     Expires: 01 March 2018      Programme: Heart valve disease 1 CPD/CME credit

Sponsorship Statement: This module has been sponsored by Edwards Lifesciences with an unrestricted educational grant

Designed to give healthcare professionals an understanding of surgery for heart valve disease. It is one of several modules in our heart valve disease programme.

1 CPD/CME credit, 1 hour

Module originally published July 2013. Revised module released March 2016

Learning objectives

Upon completing this module, participants should be better able to understand:

  • the indications for surgery with impaired LV function
  • the indications for surgery in asymptomatic disease
  • The indications for surgery at the time of coexistent CABG.

Faculty

Professor John Chambers, St Thomas’ Hospital, London

Accreditation

1 CPD/CME credit, 1 hour
BJC Learning has assigned one hour of CPD/CME credit to this module
The European Board for Accreditation in Cardiology (EBAC) has assigned one CME credit to this module. German participants should contact EBAC to receive a German VNR code for this course.
email: [email protected]
website: http://www.ebac-cme.org/

Produced in collaboration with:

You need to login to take this module

You need to be a registered member to view this page. It's quick, free and offers you a host of other benefits, including the facility to print and download articles and supplements, access our archived issues and receive email updates when new issues and other content are online.

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Heart valve disease module 8: endocarditis

Released 1 March 2016     Expires: 01 March 2018      Programme: Heart valve disease 1 CPD/CME credit

Sponsorship Statement: This module has been sponsored by Edwards Lifesciences with an unrestricted educational grant

Designed to give healthcare professionals a clear understanding of how and why endocarditis is important. It is one of several modules in our heart valve disease programme.

1 CPD/CME credit, 1 hour

Module originally published July 2013. Revised module released March 2016

Learning objectives

Upon completing this module, participants should be better able to:

  • To understand when infective endocarditis should be suspected
  • To understand the criteria for diagnosis
  • To understand the principles of management
  • To understand the criteria for surgery.

Faculty

Dr Jonathan Sandoe, Department of Microbiology, Leeds Teaching Hospitals NHS Trust, Leeds
Professor John Chambers, St Thomas’ Hospital, London

Accreditation

1 CPD/CME credit, 1 hour
BJC Learning has assigned one hour of CPD/CME credit to this module
The European Board for Accreditation in Cardiology (EBAC) has assigned one CME credit to this module. German participants should contact EBAC to receive a German VNR code for this course.
email: [email protected]
website: http://www.ebac-cme.org/

Produced in collaboration with:

You need to login to take this module

You need to be a registered member to view this page. It's quick, free and offers you a host of other benefits, including the facility to print and download articles and supplements, access our archived issues and receive email updates when new issues and other content are online.

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Heart valve disease module 7: anti-thrombotic therapy for valvular heart disease

Released 1 March 2016     Expires: 01 March 2018      Programme: Heart valve disease 1 CPD/CME credit

Sponsorship Statement: This module has been sponsored by Edwards Lifesciences with an unrestricted educational grant

Designed to give healthcare professionals a clear understanding of how and why anti-thrombotic therapy is important. It is one of several modules in our heart valve disease programme.

1 CPD/CME credit

Module originally published July 2013. Revised module released March 2016

Learning objectives

Upon completing this module, participants should be better able to:

  • Introduce anticoagulation options in patients with native or prosthetic heart valves
  • Review early antithrombotic therapy after valve surgery
  • Understand the challenges of interrupting anticoagulation in valve patients
  • Review anticoagulation options during pregnancy.

Faculty

Dr Louise Tillyer, Consultant Haematologist, Royal Brompton Hospital, London.
Dr Pu-Lin Luo, Research Clinical Fellow, St George’s, University of London.

Accreditation

1 CPD/CME credit, 1 hour
BJC Learning has assigned one hour of CPD/CME credit to this module
The European Board for Accreditation in Cardiology (EBAC) has assigned one CME credit to this module. German participants should contact EBAC to receive a German VNR code for this course.
email: [email protected]
website: http://www.ebac-cme.org/

Produced in collaboration with:

You need to login to take this module

You need to be a registered member to view this page. It's quick, free and offers you a host of other benefits, including the facility to print and download articles and supplements, access our archived issues and receive email updates when new issues and other content are online.

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Heart valve disease module 6: organisation of care for valve disease

Released 1 March 2016     Expires: 01 March 2018      Programme: Heart valve disease 0.5 CPD/CME credits

Sponsorship Statement: This module has been sponsored by Edwards Lifesciences with an unrestricted educational grant

Designed to give healthcare professionals an understanding of the organisation of care for heart valve disease. It is one of several modules in our heart valve disease programme.

0.5 CPD/CME credits

Module originally published July 2013. Revised module released March 2016

Learning objectives

Upon completing this module, participants should be better able to:

  • The limitations of detection
  • The limitations in current surveillance systems
  • The limitations in non-specialist surgical centres
  • The advantages of a specialist valve clinic.

Faculty

Professor John Chambers and Mrs Denise Parkin, St Thomas’ Hospital, London

Accreditation

0.5 CPD/CME credits, 0.5 hours
BJC Learning has assigned half an hour of CPD/CME credit to this module

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