A busy and varied programme discussing some of the hottest topics in cardiovascular disease was presented at the 11th Primary Care Cardiovascular Society (PCCS) Annual Scientific meeting, held in Chester on 25th – 27th September 2008. It attracted over 250 people and inspired great interest and debate.
More than just a postcode
The keynote session, ‘Cardiovascular disease and deprivation; more than a postcode’, heard from public figures and leading clinicians defining deprivation as it relates to cardiovascular disease from various perspectives. Professor Roger Boyle (National Director, Coronary Heart Disease and Stroke) said that, despite the “considerable progress” seen across all age groups and genders in cardiovascular disesase (CVD) reduction, there remains a gap between deprived and non-deprived areas, and between different social classes.
“Deprivation and social class are key risks for mortality in CVD, yet, the map of spend on CVD does not reflect the map of deprived areas and social class status across the UK.” He concluded “Primary care must take the opportunity to manage the health of all of their patients and tackle inequalities”.
Professor Klim McPherson (Chair, National Heart Forum) highlighted mortality trends according to deprivation. “There is an eight to nine year gap in mortality trends between deprived and less deprived areas,” he said, stressing the importance of long-term diet in the development of CVD.
Dr Kiran Patel (Consultant Cardiologist, Sandwell) highlighted inequalities of care within ethnic groups. He noted that CVD presentation is often atypical across different ethnic groups meaning that diagnosis can be missed or delayed. This, together with other factors, such as language barriers, the absence of support, access issues and long working hours can mean that the patient pathway is prolonged. “In order to address disparities, we need to focus on awareness, acceptability, accessibility and acquisition of services,” concluded Dr Patel.
Finally, Professor Richard Hobbs (Professor of Primary Care and General Practice, University of Birmingham) highlighted deprivation in the elderly and inequalities in the management of women with CV events. Quoting results from the OXVASC study, he noted that CV events increase with increasing age, with women presenting typically 10 years later than men and less likely to receive acute interventions.
If we know who and where they are, are they really that hard to reach?
A fascinating and lively session heard four successful risk assessment projects conducted in the community setting.
Deirdre Doogan (Lloyds Pharmacy) described a project in which Lloyds Pharmacy were part of an initiative to tackle inequalities in CV screening in deprived areas of Birmingham. The project reviewed 10,000 men in seven months. “The challenge is to engage specific groups in the community,” she said. This was achieved by inviting men identified from GP practice registers, to football grounds, church halls and health centres. “Community pharmacy has a key contribution to make in such CVD risk reduction projects,” she concluded.
Jane Deville-Almond (Wolverhampton) stressed “We need to understand men, their drivers, interests and language when trying to sell a health service to them”. Having taken her various heart, prostate and weight risk assessment clinics around the country, to such diverse places as farmers markets, barber shops, fishing fairs, truckers’ cafes and Harley Davidson showrooms, Ms Deville-Almond concluded: “We need to find new ways to motivate our patient populations so that they ultimately have the tools they need to look after their own health”.
Peter Heywood (Middlesbrough) described how social marketing techniques can be used in the health care arena. “Once we identify the type of patient that we want to target, such as younger males, older females, we can start to target our messages appropriately,” he advised. Such techniques are being implemented in the Tees Vascular Assessment Programme.
Catriona Jennings (London) described the 16-week ‘MyAction’ programme, a nurse-led, multi-disciplinary, family-based model of vascular prevention, already successfully running in the Bromley area. “With shared lifestyles between partners, we recognised that including the entire family is key to the success of this vascular prevention programme,” she said. Close co-operation between the Primary Care Trust (PCT) and local services is also important.
Keynote address
Chris Brinsmead (President of the Association of the British Pharmaceutical Industry [ABPI]) gave a rousing address, encouraging industry and clinicians to work together for maximal patient outcomes. He noted the advances in cardiovascular care over the last two decades stressing that cardiovascular disease remains a major priority for industry, as well as Government. Giving examples of successful projects with industry working closely with PCTs, Mr Brinsmead highlighted the importance of the ABPI Code of Practice to provide a clear framework for partnerships between industry and health care professionals.
Creative plenary sessions
Several creative plenary sessions kept the audience enlivened and educated throughout the meeting. ‘High risk high school’ (sponsored by Boehringer Ingelheim) saw four cardiovascular ‘pupils’ from primary care, nursing and secondary care (Dr Henry Purcell, London; Dr Terry McCormack, Whitby; Dr Michael Norton, Sunderland, and Delyth Williams, Hitchen) highlight projects they have undertaken over the past year to further advance CV risk prevention in their area. Chairing the session, ‘Headmistress’ Dr Kathryn Griffiths (General Practitioner, York) concluded: “It is fascinating to hear what others are doing and how much we can learn from one another.”
‘Lipids on trial’ (sponsored by Merck Sharp and Dohme) turned the audience into the ‘jury’ to vote on the debate entitled ‘By focusing on total cholesterol alone, primary care is guilty of not going far enough to address CV residual risk.’ The trial, adjudicated by TV presenter, Sue Lawley, heard from the ‘prosecution’, Professor Richard Hobbs and Dr Marc Evans (Cardiff), and the ‘defence’, Dr Mark Davis (Leeds) and Professor Julian Halcox (Cardiff). The prosecution noted that, despite a reduction in cardiovascular risk, many patients still suffer morbidity and mortality from CVD. They therefore argued that low-density lipoprotein (LDL) “cannot be the only CVD risk factor”. Furthermore, they pointed out, high-density lipoprotein (HDL) has as strong a correlation as LDL with CV risk. The defence argued that, despite there being epidemiological evidence that HDL is a risk factor for CVD, there is, as yet, no definitive clinical trial evidence that raising HDL leads to a reduction in CV events. After strongly argued battles, intermingled with heckling from the judge, 50% of the ‘jury’ voted for the motion and 50% against!
‘Welcome to the CV risk clinic’ (sponsored by the Merck Sharp & Dohme/Schering Plough Partnership) heard opinions from Dr Mike Norell (Wolverhampton), Dr Jonathan Morrell (Hastings) and Michaela Nuttall (Bromley) on patient case studies including patients with acute coronary syndrome, peripheral arterial disease, and obesity. The variety of issues that were discussed amongst the panel included patient compliance, drug choices and doses, cardiac rehabilitation, statin non-responders and intolerance, and random vs. fasting triglycerides.
In ‘Know your 3 ‘S’s: statins, sartans and savings’ (sponsored by Takeda), Professor Mike Kirby (Letchworth) highlighted the huge pressures on primary care that make switching more desirable. He presented data showing cost savings that can be made by switching surgery patients from atorvastatin 10 mg to simvastatin 30 mg, and losartan 50 mg to candesartan 8 mg. Of 122 patients, there were no significant differences in cholesterol control when switching, and blood pressure improved when switching to candesartan. Two years on, there were no increased adverse events from the switches. This exercise has resulted in five-year savings to the practice of £71,000 from the statin switch and three-year savings of £41,000 from the sartan switch.
Professor Richard Hobbs then argued for the case that ‘The wholesale substitution of drugs in the same class is safe and effective’ with Dr Sarah Jarvis (London) arguing against this. “We need to substitute our drugs to the cheapest options possible so we can treat more patients,” he said. Dr Jarvis argued “We can only do this if quality of care is not compromised and if financial gains are sufficient to warrant the time and cost of switching.” She cautioned, “We must consider efficacy, adverse effects, licensed indications and discontinuation rates”. The majority of the audience agreed.
Interactive cases: clinical problems and solutions
Dr Kathryn Griffith stressed that earlier stage chronic kidney disease (CKD) – up to stage 3b – is a primary care condition that can be diagnosed with simple blood tests. She noted that it is invariably part of a wider vascular disease picture, and reminded “we must always refer patients if needed, particularly those with more severe CKD”.
Professor Mike Kirby highlighted that erectile dysfunction (ED) is closely linked to CVD, and should also be considered an indicator of wider vascular issues. He advised that angiotensin-converting enzyme (ACE) inhibitors can make ED worse, and PD-5 inhibitors can help to improve endothelial function if given regularly – for three to six months, for example. “Our patients are often reluctant to talk about ED so we need to be proactive due to its important link with heart disease”.
Dr Khalid Khan (Wrexham) discussed ECG and atrial fibrillation. He advised that, generally, patients should be referred to secondary care if they have syncope >3 seconds, 2nd or 3rd degree block with symptoms, and tachycardia or bradycardia. He noted the low use of warfarin in older patients with AF, and advised “Using the CHADS 2 score, we can risk stratify who needs warfarin”.
Finally, Dr Matt Capehorn (Rotherham) highlighted the issues surrounding obesity in primary care. He said “We spend a lot of time in primary care treating the complications of obesity, and not enough time treating the actual cause, i.e. the excess weight”.
Summary
As the meeting drew to a close, everyone agreed that the 11th PCCS Annual Scientific meeting had been varied, educational, informative, interactive, entertaining and memorable. Planning is already underway for next year’s meeting on 1st–3rd October 2009 in Nottingham.
Authors: Ibrahim Ali, Trudie Lobban, Richard Sutton, Alex Everitt, Darrel P Francis
Ibrahim Ali
Medical student
Richard Sutton
Professor of Clinical Cardiology
Darrel P Francis
Clinical Senior Lecturer in Cardiology
Imperial College, South Kensington, London, SW7 2AZ
Trudie Lobban
Chief Executive Officer
STARS and Arrhythmia Alliance, PO Box 175, Stratford-Upon-Avon, CV37 8YD
Alex Everitt
Consultant Neurologist
Imperial College Healthcare NHS Trust, St Mary’s Hospital, Praed Street, London, W2 1NY
Correspondence to:
Mr I Ali, c/o Office of Dr D Francis, ICCH building, 59–61 North Wharf Road, London, W2 1LA [email protected]
Blackout is a common, alarming symptom occurring across patients of all ages, and can create enormous psychological and social distress. In this review, we describe a new clinical approach that improves healthcare delivery to patients suffering blackouts.
Introduction
Case history 1
PL is a 19-year-old female who presented with two episodes of blackout accompanied with convulsions. She was diagnosed with epilepsy and prescribed carbamazepine. Episodes continued, however, and one year later she was further investigated by tilt-testing and discovered to have cardioinhibitory vasovagal syncope. A dual-chamber rate-drop-response pacemaker was implanted and no further episodes occurred during five years of follow-up. Anticonvulsant medication was stopped without ill effect.
Case history 2
CM is a 72-year-old male admitted for pain control following an unwitnessed fall, which although initially believed to be a mechanical fall, was later revealed to be unexplained. He denied any prodromal symptoms or loss of consciousness and had suffered five previous falls in the last 12 months, developing symptoms of depression as a result. Previous investigations (Holter monitoring, echocardiogram and Doppler studies) were unremarkable. Tilt-testing, however, confirmed a diagnosis of vasodepressor vasovagal syncope. After being given preventive advice, he remained asymptomatic after two years of follow-up, regained confidence and no longer suffers from depressive symptoms.
Diagnosis
Table 1. Definitions
Blackout (a sudden, transient loss of consciousness, table 1) is a frightening symptom for many patients. The current convention of having entirely separated cardiological and neurological pathways is hampering speedy, accurate and cost-effective diagnosis. As a consequence, a significant proportion of sufferers are either not assessed or are misdiagnosed (for example, with epilepsy) with potentially disastrous effects on their well-being.
In this review, we highlight the challenges in managing patients presenting with transient loss of consciousness, the implications of misdiagnosis, and present the concept of rapid access blackout clinics – a novel clinical pathway that can streamline and improve the healthcare delivery to patients suffering blackouts.
The scale of the problem
Epilepsy
Even though epilepsy (the principal neurological cause of blackout) is one of the most common serious neurological conditions in the UK with a prevalence between 0.7–1%,1 only one to two new cases occur per year within the average list size of a UK general practitioner.2 The condition, nevertheless, can confer significant morbidity and mortality for patients. For instance, important medical complications include status epilepticus, injuries from falls, aspiration and sudden unexpected death, which is estimated to account for 500 deaths per year in the UK.3 In addition, patients are faced with a high social burden including mistreatment, social stigma, educational difficulties and driving and employment restrictions.
Syncope
Syncope, in contrast to epilepsy, is far more common: it affects half of the UK population at some point in their lives, and is responsible for 3% of accident and emergency admissions and 1% of all admissions to hospital.4 It shows a similar bi-modal incidence to epilepsy5 as it appears to be increased in two age clusters – the young and the elderly.6 In the young, there is a peak around 15 years of age, with females having more than twice the incidence of males. In the elderly, it affects 35% of adults over 65 years and 45% over 80 years.7 Syncope, therefore, just like epilepsy, imposes an important medical, social and economic burden on the general population.
Table 2. Causes of blackout and their underlying mechanism
Among the causes (table 2), the most common is neurally-mediated syncope, which refers to a group of cardiovascular disturbances that are characterised by the triggering of a reflex response. Despite extensive research, the afferent arc remains to be elucidated but the efferent arc involves a reduction in sympathetic outflow to the vasculature and the heart and activation of vagal efferents, causing vasodilatation and a variable degree of bradycardia, which causes transient global cerebral hypoperfusion leading to transient loss of consciousness.8
The most common form of neurally-mediated syncope is ‘vasovagal syncope’, which causes 40% of syncopal events.9 Precipitating factors include emotional distress, fear, or prolonged standing, and there are usually early symptoms and signs such as pallor, weakness or nausea. On regaining consciousness, the patient may complain of persistent weakness.8 Indeed, in common with other causes of syncope, although there is rapid and complete recovery from the transient loss of consciousness, patients may continue to experience unpleasant symptoms such as exhaustion, dizziness and dyspnoea for hours or days after the syncopal episode.10
Syncope as a disability
Recurrent syncopal events, which affect one in three patients, can dramatically impair all aspects of physical and social functioning, affecting activities of daily living, driving, employment, and impacting on interpersonal relationships.10 Affected patients are also predisposed to sustain injury from collapse11 and the functional impairment has been reported to be similar to patients suffering from rheumatoid arthritis or chronic back pain. Psychologically, there is a high prevalence of chronic anxiety and depression.12
Prognosis
Decisive management of patients can reverse the physical and psychosocial morbidity associated with syncope. Nevertheless, patients affected by recurrent episodes of vasovagal syncope have a favourable prognosis, as they are at no increased risk of cardiovascular mortality.13 In contrast, patients with an underlying cardiac cause, which includes those with structural heart disease and arrhythmias, are at an increased risk of non-fatal and fatal cardiovascular events,13 especially sudden cardiac death. Indeed, syncope is a key early symptom in children and young adults who have congenital life-threatening arrhythmias such as long QT syndrome and Brugada syndrome. Such patients need to be accurately diagnosed as life-saving treatment can be offered. However, evidence reveals that diagnostic difficulties hinder the effective management of patients who present with transient loss of consciousness.
Diagnostic challenges
Half of all patients presenting with syncope do not attain a diagnosis while in hospital despite investigation.14 Even for the half receiving a diagnosis, that diagnosis can often be wrong, with blackouts wrongly attributed to epilepsy or a mechanical fall (especially in the elderly).
A presumptive diagnosis of epilepsy is often made initially in a patient presenting with syncope, and may be discovered to be incorrect later.15 This bias may be because a number of cardiovascular causes of blackouts, such as vasovagal syncope or primary cardiac arrhythmia, can masquerade as epilepsy. It is important to remember that prolonged syncope can result in secondary seizures. Even in the absence of secondary seizures, there can be urinary incontinence.16 Such similar features arise because transient global cerebral hypoperfusion in syncope causes cerebral anoxia that may result in myoclonic jerks and sometimes a full reflex anoxic seizure. Indeed, Lempert et al.17 reported that myoclonic activity, predominantly multifocal jerking in proximal and distal muscles, occurred in 90% of healthy subjects in whom syncope was induced using a combination of hyperventilation, orthostasis and the Valsalva manoeuvre. The underlying mechanism of epilepsy is different, with seizures resulting from neuronal hyper-excitability rather than transient hypoperfusion. Regardless of underlying mechanisms, the manner of presentation understandably causes a diagnostic hindrance, although there is a propensity towards overdiagnosing epilepsy.
Syncope masquerading as epilepsy
Around 20–30% of adults and 40% of children18 who are diagnosed with epilepsy do not actually have the condition. In children, syncopal events are commonly due to ‘neurally-mediated syncope,’ also called ‘reflex asystolic seizures,’ which highlight a cardiorespiratory disturbance, not a neurological disturbance like epilepsy. Diagnosis is particularly difficult in children because a clear first-person history is often unavailable in the very young, and clinical features are easily mistaken to be due to epilepsy.
This is a critical public health issue, therefore, due to the number of patients affected, approximately 100,000 in the UK alone, and due to the consequences of misdiagnosis for patients, such as:
denial of potentially life-saving treatment, such as a pacemaker or defibrillator
commencement on potentially harmful anticonvulsant therapy
symptom recurrence may lead to more expensive drugs being employed (with high cost to both the patient and the hospital budget)
symptom recurrence may also lead to diagnostic ambiguity, further investigative costs and further delay for correct treatment to be initiated
impingement of high social burden in education, employment, driving and life insurance.
Substantial financial savings could be made from correct management of patients, as reported by the All Parliamentary Group on Epilepsy in 2007:19 the annual cost of epilepsy misdiagnosis in England is estimated at around £189 million a year, which takes into account unnecessary treatment costs, economic costs of lost work and payments of the Disability Living Allowance, which itself totals £55 million a year.
Syncope masquerading as mechanical fall
Syncope and mechanical falls are the most common reasons for elderly patients to present at an accident and emergency department.20 Misdiagnosis of mechanical falls is most problematic in this group of patients and represents another challenge in obtaining a correct diagnosis: 30% of patients aged ≥ 65 may not admit to loss of consciousness due to retrograde amnesia, but the resultant fall will be reported.21 This is further hampered by the lack of an eyewitness account in 50% of cases.22 As a result, doctors may be swayed to diagnose a fall and patients will not be treated for the actual precipitating cause, such as an arrhythmia. This increases the likelihood of more falls with an allied increase in morbidity and mortality, and also contributes to the rising costs of managing falls, estimated to cost the NHS over £1 billion each year.
The rapid access blackout clinic
Historic assessment and management pathways appear to be failing patients presenting with transient loss of consciousness. One study8 reported that the length of stay in hospital after acute admission for those over 65 years was 5–17 days, highlighting the implementation of variable management plans. This has been contributed to by disparity among hospitals in the investigative approach to patients and highlights the difficulty in acquiring the correct diagnosis.14
Effective handling of patients with blackouts comes from early clinical evaluation by specialist staff trained to do this rapidly and efficiently, and who have access to all necessary facilities without requiring elaborate inter-referrals, which create confusion and delay. Within this model of care is the opportunity to apply management strategies to patients presenting with blackouts that deliver diagnostics decisions.
The Department of Health Heart Team Expert Reference Group for the National Service Framework for Arrhythmias and Sudden Cardiac Death23 formulated algorithms for the management of patients presenting with blackout at four points of call: ambulance service, accident and emergency department, general practitioner, and secondary referral. The rapid access blackout clinic is the secondary referral care pathway, a single out-patient clinic accessible within two weeks of referral that eliminates referral delays arising from uncertainty about the mechanism of the presenting symptom. In some localities there are rapid access seizure clinics and syncope clinics, which make it easy for referrers to get patients through to specialist review. However, even in these regions, referrers may hesitate, especially in the many patients where they cannot be immediately confident of which group of aetiologies to suspect more strongly. Access to a blackout clinic eliminates this final block to specialist assessment of the patient.
By making diagnostic clarity its paramount interest, the aim of the clinic is simple: to complete a global assessment of patients (referred by accident and emergency or their general practitioner) that will secure a definitive diagnosis efficiently and cost-effectively.
Clinical expertise
A dedicated, specialist nursing team with blackout skills will provide the first stage of the diagnostic service. The nursing team may include separate neurologically and cardiologically trained specialist nursing sisters or, as these skills become more widespread, individual specialist nurses who possess both sets of skills. Other members of the multi-disciplinary team are brought in after initial evaluation including specialist neurology and cardiology doctors, geriatricians, and (where available) clinical autonomic scientists.
Initial assessment
Figure 1. Imperial College Healthcare NHS Trust Blackout ProtocolTable 3. Focused questions relating to transient loss of consciousness
As highlighted in the Imperial College Healthcare NHS Trust protocol for the rapid access blackout clinic (figure 1), modelled on the European Society of Cardiology guidelines,24 the initial assessment is primarily focused on deciding whether the patient is likely to have syncope or epilepsy. It involves four key components: medical history with the aid of a computer-based extended questionnaire, a physical examination, electrocardiogram (ECG) and supine and upright blood pressure, and thus ensures that the various causes of syncope are all taken into account; suspicion of epilepsy is principally raised through an accurate medical history.
The questionnaire acts as a pre-assessment form, establishing the patient’s background medical history, which includes past cardiac and neurological history. An eyewitness account is a very valuable way to ascertain an accurate history, and patients will be asked to answer the questionnaire with the help of any eyewitnesses before attending the clinic. The questionnaire also contains focused questions regarding the transient loss of consciousness: the circumstances and experiences before, during and after the episode (table 3). To help guide diagnosis, the most important clinical features differentiating between epilepsy and various causes of syncope are outlined in the protocol.25 This initial approach, which may result in a diagnosis or a suspected diagnosis, can thus discover quickly if and where further investigative priorities need to be placed (table 4), and will help avoid unnecessary hospital admissions, which alone are responsible for 74% of the cost of investigating patients.7
Table 4. Equipment that needs to be accessible to the blackout clinic for the diagnostic work-up of patients
Appropriate further investigation
With regards to syncope, further investigations will be most necessary in determining if the mechanism is neurally-mediated or of a cardiac origin. The most valuable tests at present for neurally-mediated syncope include the use of tilt-testing (figure 2) to diagnose and categorise vasovagal syncope and performing carotid sinus massage to diagnose carotid sinus hypersensitivity. For patients who are young, in whom there is no suspicion of cardiac or neurological disease, there is a strong likelihood that vasovagal syncope is the culprit for transient loss of consciousness, and so tilt-testing can be particularly helpful in securing a positive diagnosis.
A variety of protocols are employed for tilt-testing among clinical institutions, and many incorporate pharmacological provocation if the initial tilt-test is negative. Our centre uses the Westminster protocol.26
Figure 2. Patient undergoing a tilt-test at 60°
Carotid sinus hypersensitivity is a disease of the elderly and so older patients (over 50 years) are most likely to respond to carotid sinus massage, especially those without features suggesting the existence of cardiac or neurological disease or in those who have a typical history of syncope during neck turning. A standardised safe technique exists although there are contraindications, such as previous ventricular tachyarrhythmias or carotid bruit.27 Some centres use carotid duplex ultrasound, rather than clinical examination, to exclude carotid disease before carotid sinus massage.
Ultimately, the protocol places most stress on evaluating patients suspected of cardiac syncope as they have a poorer prognosis than patients with neurally-mediated syncope. For instance, an abnormal ECG creates a strong suspicion of an arrhythmic cause of syncope, especially important for some potentially life-threatening inherited arrhythmias in children. Further investigation of patients likely to have cardiac syncope may involve echocardiography (if structural heart disease is suspected) or the implantable loop recorder, which provides a new opportunity to diagnosing arrhythmias in patients in whom tilt-testing does not usefully reproduce the presenting symptom.28 Once implanted, the patient simply activates the device with a hand-held control after any subsequent episode of syncope and the device automatically retains the previous 40 minutes of ECG to memory, which almost always includes the period of syncope itself. The ‘Additional testing’ section under ‘syncope’ is a supplementary list of specific recommendations that are all directed at appropriately investigating the underlying cardiac cause of syncope, emphasising the need for a comprehensive investigative approach in this group of patients.
In contrast, further investigations for epilepsy are not essential for diagnosis but instead are used to classify the type of epilepsy, which is important when considering the best treatment approach. Investigations include the electroencephalogram (EEG) and magnetic resonance imaging (MRI). EEG may be useful in assessing the likelihood of further epileptic seizures after an isolated seizure as well as assisting syndromic classification. MRI is often useful for identifying aetiology, especially in localisation-related cases, such as in hippocampal sclerosis, focal cortical scars, malformations of cortical development, tumours, cavernomas and arteriovenous malformations.
Impact of STARS
The blackout charity, Syncope Trust And Reflex anoxic Seizures (STARS – www.stars.org.uk), is the leading resource for support and information for both patients and medical professionals on syncope and reflex anoxic seizures. The STARS Medical Advisory Committee developed a blackouts checklist, a patient-directed checklist of important information regarding blackouts that aims to educate and empower patients. Almost 10,000 downloads of this document were made in less than three months. Components of this checklist have also been used to structure the questionnaire that forms part of the initial assessment of patients.
Conclusion
The effective management of patients presenting with transient loss of consciousness is an important clinical challenge. Pioneered at the Manchester Royal Infirmary, and developed further into a multi-disciplinary cardiology–neurology collaboration at Imperial College Healthcare NHS Trust (part of the UK’s first Academic Health Science Centre), the rapid access blackout clinic creates a single entry point through which every patient can undergo a cohesive and thorough assessment. It establishes an easy referral pathway (for general practitioners and accident and emergency departments), and attempts to overcome common diagnostic difficulties, which otherwise lead to high rates of clinical uncertainty, misdiagnosis and unnecessary financial costs. Widespread availability of these clinics, now a national priority in the UK as part of the National Service Framework, will provide improved healthcare for all patients affected by blackouts.
Acknowledgements
The authors are grateful for support from Sister Andrea Meyer, Sister Kicki Franzen-McManus and from the NIHR Biomedical Research Centre funding scheme.
Conflict of interest
None declared.
Editors’ note
An editorial on the rapid access blackout clinic by Byrne and O’Shea can be found on pages 9–10 of this issue.
Key messages
The assessment of transient loss of consciousness is a common clinical problem
A substantial proportion of patients presenting with syncope are either not diagnosed or are misdiagnosed, for instance with epilepsy or, especially in the elderly, a mechanical fall
The rapid access blackout clinic attempts to overcome important diagnostic challenges by providing an integrated and complete evaluation of patients that aims to secure a definitive diagnosis efficiently and cost-effectively
References
Stokes T, Shaw EJ, Juarez-Garcia A et al. Clinical guidelines and evidence review for the epilepsies: diagnosis and management in adults and children in primary and secondary care. London: Royal College of General Practitioners, 2004.
Macdonald BK, Cockerell OC, Sander JW, Shorvon SD. The incidence and lifetime prevalence of neurological disorders in a prospective community-based study in the UK. Brain 2004;123(Pt 4):665–76.
Petkar S, Cooper P, Fitzpatrick AP. How to avoid a misdiagnosis in patients presenting with transient loss of consciousness. Postgrad Med J 2006;82:630–41.
Ammirati F, Colivicchi F, Minardi G et al. The management of syncope in the hospital: the OESIL Study (Osservatorio Epidemiologico della Sincope nel Lazio). G Ital Cardiol 1999;5:533–9.
Sander JW, Hart YM, Johnson AL, Shorvon SD. National general practice study of epilepsy: newly diagnosed epileptic seizures in general population. Lancet 1990;336:1267–71.
Wieling W, Ganzeboom KS, Krediet CTP et al. Initiele diagnostische strategien bij wegrakingen: het belang van de anamnese (Initial diagnostic strategy in the case of transient losses of consciousness: the importance of the medical history). Ned Tijdschr Geneesk 2003;147:849–54.
Kenny RA, O’Shea D, Walker HF. Impact of a dedicated syncope and falls facility for older adults on emergency beds. Age & Ageing 2002;31:272–5.
Fenton AM, Hammill C, Rea RF, Low PA, Shen WK. Vasovagal syncope. Ann Intern Med 2000;133:714–25.
Kapoor WN. Evaluation and outcome of patients with syncope. Medicine (Baltimore) 1990;69:160–75.
Shaffer C, Jackson L, Jarecki S. Characteristics, perceived stressors, and coping strategies of patients who experience neurally mediated syncope. Heart Lung 2001;30:244–9.
Kapoor W, Petersen J, Wieand HS, Karpf M. Diagnostic and prognostic implications of recurrences in patients with syncope. Am J Med 1987;83:700–08.
Kapoor WN, Foruanto M, Hanusa BH, Schulberg HC. Psychiatric illnesses in patients with syncope. Am J Med 1995;99:505–12.
Soteriades ES, Evans JC, Larson MG et al. Incidence and prognosis of syncope. N Engl J Med 2002;347:878–85.
Kapoor WN, Karpf M, Wieand S, Peterson JR, Levey GS. A prospective evaluation and follow-up of patients with syncope. N Engl J Med 1983;309:197–203.
Zaidi A, Clough P, Cooper P, Scheepers B, Fitzpatrick A. Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol 2000;36:181–4.
Fitzpatrick AP, Cooper P. Diagnosis and management of patients with blackouts. Heart 2006;92:559–68.
Lempert T, Bauer M, Schmidt D. Syncope: a videometric analysis of 56 episodes of transient cerebral hypoxia. Ann Neurol 1994;36:233–7.
Uldall P, Alving J, Buchholt J, Hansen L, Kibak M. Evaluation of a tertiary referral epilepsy centre for children. Epilepsia, Proceedings of International League Against Epilepsy, 2001.
Kenny RA, Richardson DA, Steen N, Bexton RS, Shaw FE, Bond J. Carotid sinus syndrome is a modifiable risk factor for non-accidental falls in older adults. J Am Coll Cardiol 2001;38:1491–9.
Benditt DG, Blanc JJ, Brignole M, Sutton B, eds. The evaluation and treatment of syncope. A handbook of clinical practice. New York: Blackwell, 2003.
Shaw FE, Kenny RA. The overlap between syncope and falls in the elderly. Postgrad Med J 1997;73:635–9.
European Society of Cardiology Task Force on Syncope. Guidelines on Management (Diagnosis and Treatment) of Syncope – Update 2004. Eur Heart J 2004;25:2054–72.
Sheldon R, Rose S, Ritchie D et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol 2002;40:142–8.
Fitzpatrick AP, Theodorakis G, Vardas P, Sutton R. Methodology of head-up tilt testing in patients with unexplained syncope. J Am Coll Cardiol 1991;17:125–30.
Munro NC, McIntosh S, Lawson J, Morley CA, Sutton R, Kenny RA. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc 1994;42:1248–51.
Farwell DJ, Freemantle N, Sulke AN. Use of implantable loop recorders in the diagnosis and management of syncope. Eur Heart J 2004;14:1547–63.
Congestive heart failure (CHF) is an increasingly widespread condition, the prognosis for moderate and severe heart failure is almost identical to colorectal cancer1 and worse than breast2or prostate cancer.3 CHF has an overall population prevalence of approximately 1–3% rising to approximately 10% in the very elderly
CHF accounts for about 5% of all medical admissions and approximately 2% of total healthcare expenditure.4 Nearly one million new cases are diagnosed annually worldwide, making it the most rapidly growing cardiovascular disorder.
The consequences of heart failure for primary care are profound. CHF has been reported to be second only to hypertension as a cardiovascular reason for a surgery appointment.5Despite improvements in medical management, undertreatment is common, many patients with CHF still do not receive treatment optimised according to current guidelines.4,6
The introduction of the 2009/10 heart failure Quality Outcomes Framework (QOF) additions will bring financial incentives for the prescribing of beta blockers for patients with a diagnosis of heart failure. This will apply to all diagnosed heart failure patients. There are, however, no additional QOF points for optimising medication or maximum tolerated levels, therefore, patient care will rely on good practice and receiving treatment according to current guidelines.
The prevalence of heart failure nationally in QOF is just over 1%. Because of the increase in survival after acute myocardial infarction and ageing of the population, the number of patients with heart failure will increase rapidly in most industrialised countries. Heart failure will continue to be a challenge to healthcare.
The profile of heart failure management has been raised with the publication of the Coronary Heart Disease (CHD) National Service Framework (NSF)
Chapter 6 in 20007 and the National Institute for Health and Clinical Excellence (NICE) Heart Failure Clinical Guideline 2003.8 The heart failure publications have supported the development of community heart failure services, and heart failure specialist nurse roles.
The development of the General Practitioner with Special Interest (GPSI) in cardiology qualification and the accreditation in community echocardiography in 2004 has enabled the development of community heart failure services. The training and development of the workforce in primary care has led to improvements in the treatment and management of heart failure patients. A referral to a community specialist heart failure service or secondary care will still be relevant in certain instances, however, the 10 steps will assist in the decision to continue the management in primary care or refer for expert advice and a future management plan.
The amyloidoses comprise a collection of disorders in which proteins, some native and some mutated, are deposited in tissues. These proteins self-assemble themselves to form an ordered fibrillar matrix termed amyloid. Currently, more than 20 different proteins have been identified, the most common with as many as 100 different mutations per protein. Despite these figures, the conditions that arise clinically are not that common. This undoubtedly results in a number of such individuals not being identified, or typically only when it is too late to effect a cure.
This article describes the features, diagnosis and treatments for the different types of amyloid that affect the heart.
Cardiovascular magnetic resonance (CMR) is a safe and accurate imaging modality, with an established role in current cardiology practice. It is becoming essential for cardiologists in other non-imaging sub-specialities to acquire a working knowledge of the potential of CMR in both structural and in ischaemic heart disease. In the current specialist registrar training environment, however, it is difficult to gain that expertise unless wholly committed to an imaging career.
Editors: Varghese A, Pennell D Publisher: Churchill Livingstone Elsevier, 2008 ISBN 978-0-443-10301-8Price £19.99
This book affords the opportunity to derive a comprehensive overview of this highly technical field in a concise and yet easy-to-read format. Edited by Dr Anitha Varghese and Professor Dudley Pennell, from the Royal Brompton Hospital in London, one of the world’s foremost clinical and academic CMR departments, it also draws upon the experience of a number of international experts.
The first chapter, written by Dr Varghese, introduces the reader to the principles of CMR. It sets the tone of the book with sufficient technical information to introduce the reader to the basics of magnetic resonance imaging with an exhaustive description of the indications for CMR and the associated level of evidence for the assessment of different cardiac pathologies. It serves well as a reference and has well-annotated figures for a visual appreciation of the technique.
All the chapters are well-designed – ischaemic heart disease, heart failure and cardiomyopathy, valvular heart disease, cardiac masses, pericardial disease and myocarditis, the aorta, adult congenital heart disease, and magnetic resonance angiography are all covered sufficiently to give the reader a full overview of the potential of CMR. There is a separate chapter on CMR angiography with an honest caveat on the limitations of the technique compared to invasive angiography, aside from the determination of an anomalous coronary circulation. It would have been helpful to describe the role of CMR angiography in enhancing the diagnosis of vulnerable atherosclerotic plaque, although this indication is largely an academic one at present and not yet in regular clinical practice. The book finishes with a simple description of the common artefacts seen with CMR and how to avoid them in routine practice, again with excellent images presented which are easy to interpret.
In summary, this book is an excellent read and delivers to the reader a full appreciation of the full potential of CMR. It is well written by experts in the field and the quality of the images presented are superb. CMR is truly made easy by Varghese and Pennell and is a worthy addition to this series.
A 52-year-old man presented to the emergency department with increasingly frequent anginal chest pain. He had had an anterior ST elevation myocardial infarction two years previously, for which he received thrombolysis. He was an ex-smoker, hypercholestrolaemic and had a family history of ischaemic heart disease. During stress electrocardiography, he developed chest pain at nine minutes of a standard Bruce protocol, but no significant ST changes.
A computed tomography (CT) coronary angiogram (CTA) was performed, as the patient was not keen on an invasive angiogram, and demonstrated sub-endocardial hypoattenuation at rest in the anterior wall, apex and apical inferior walls (figure 1B). It was not clear if there was any reversible ischaemia so a myocardial perfusion scintigraphy (SPECT) was performed, and demonstrated a partial thickness infarction involving the anterior wall, apex and apical inferior wall (figure 1A). A research cardiac magnetic resonance (CMR) scan demonstrated late Gadolinium enhancement in the same territories as the other two studies (figure 1C).
Figure 1. A. Myocardial perfusion scintigraphy (SPECT) scan demonstrating a partial thickness infarction involving the anterior wall, apex and apical inferior wall; B. computed tomography angiogram (CTA) demonstrating sub-endothelial hypoattenuation at rest in the anterior wall, apex and apical inferior walls; C. cardiac magnetic resonance (CMR) scan showing late Gadolinium enhancement in the same territories
Recent advances in non-invasive imaging have resulted in the ability to assess myocardial infarction with multiple modalities. Each technique relies on a different methodology for the assessment of irreversible myocardial injury. For SPECT, a comparison of images obtained at rest and during hyperaemic stress demonstrates the absence or delayed uptake of a radioisotope, while CMR detects infarction by the delayed clearance of a paramagnetic contrast agent. CTA may detect infarction by either reduced first-pass perfusion or via delayed clearance of iodinated contrast. Given these inherent differences, the relative strengths and weakness of these techniques for the detection of myocardial injury are likely to be clinically important.
Teaching and learning the three-dimensional anatomy of the heart can be challenging. The use of the hand to model structures in the heart has proven useful. In this article a more comprehensive model of the heart using a gloved hand is proposed.
Introduction
The teaching and learning of the three-dimensional (3-D) anatomy of the heart, and especially the coronary arteries and the interpretation of cardiac angiogram radiographs of patients, is challenging to most students.1,2 Studying the anatomy of the heart using specific shapes of the hand during bedside teaching in hospitals and demonstrations of the gross anatomy can be useful.3,4 Harvey appears to have been the first to introduce the concept of using hands to depict the 3-D anatomy of the heart (in the 1950s).5 A 3-D anatomy hand model representing the liver organ has also been developed.4
One hand model,3 which showed the three major arteries of the heart, mimicked the commonly used arteriographic viewing positions by rotation of the hand. A more detailed model,1 which used both left and right hands, demonstrated the 3-D anatomy of the six major arteries of the heart. Duytschaever et al.6 used the left-handed model to demonstrate the structures on the walls of the right atrium. In this report, a more comprehensive hand model of the heart is proposed.
The proposed hand model of the heart
Figure 1. Anterior view: borders along the anterior surface of the heartFigure 2. Posterior view: the left atrium and pulmonary veins
The proposed hand model of the heart illustrates up to 60 features about the heart, (figures 1 and 2). These include the chambers, coronary vessels, venous drainage, valves of the heart and the great vessels of the mediastinum.
In this model, a specific position of the left hand was used. The anterior surface of the heart is ‘constructed’ with the tips of the middle finger and the thumb, grasping the palmar and dorsal surfaces of the index finger tip respectively. The ‘ring’ finger is positioned such that, its proximal interphalangeal joint can be seen, while its distal interphalangeal joint is hidden behind the proximal interphalangeal joint of the middle finger, as shown in figure 1. The fifth digit is completely obscured by the ring finger. The thumb, index finger, middle finger and the last two fingers represent the right atrium, right ventricle, left ventricle and left atrium, respectively. The tips of the thumb, index finger and middle fingers form the inferior or diaphragmatic surface of the heart.
The proximal phalanx of the index finger should be anterior to the proximal phalanx of the middle finger. This will highlight the fact that the superior part of the right ventricle is anterior to the superior part of the left ventricle. This places the aortic valve to the right and posterior of the pulmonary valve, while keeping the inferior part of the left ventricle to the left of the inferior part of the right ventricle.
The posterior surface of the heart can be demonstrated in a similar position. The forearm is maximally supinated, until the finger tips of the thumb, index and middle fingers are pointing superiorly, the elbow flexed and the wrist held straight. The metacarpophalangeal and interphalangeal joints of the ‘ring’ finger and last digit need to be strongly flexed, until they are at right angles (figure 2). The ‘ring’ finger and fifth digit represent the left atrium and by strongly flexing them, enables the left atrium to ‘appear’ between the right atrium and left ventricle, while yet in the upper half of the posterior surface of the heart.
Figure 3. Anterolateral view: the structures of the right atrium. The fossa ovalis is indicated by an ‘X’
The right atrium is represented by the thumb (figure 3). The following anatomical structures can be labelled: the free wall, terminal crest, auricle, septal surface, tricuspid valve, opening of the coronary sinus, sinoatrial node and the orifices of the caval veins. A small circular piece of paper (about 2 cm2), held between the palmar surface of the interphalangeal joint of the thumb (right atrium) and the postero-lateral surface of the middle phalanx of the ring finger (left atrium) can represent the interatrial septum, on which the fossa ovalis lies.
The triangle of Koch is an area of surgical importance in which the atrioventricular node and its branches are found.6 The triangle of Koch lies between the antero-medial margin of the opening of the coronary sinus, the tendon of Todaro and the septal cusp of the tricuspid valve.6 The fossa ovalis lies just superior to the tendon of Todaro, so the triangle of Koch can be described as lying between the mark for the opening of the coronary sinus, the small circular paper (fossa ovalis) and the mark for the tricuspid valve.
The heart hand model by Duytschaever et al.6 represented most of the structures of the right atrium using the left hand. The proposed hand model has the advantage of showing the other chambers of the heart in relation to the right atrium, albeit on a smaller area of the hand than in the model by Duytschaever et al.6
Figure 4. Anterior view: great arteries of the mediastinumFigure 5. Anterolateral view: great veins of the mediastinum
The great arteries and veins of the mediastinum are not represented, but can be drawn on the dorsal surface of the metacarpals, as shown in figures 4 and 5. Several coronary arteries and veins, with their branches and tributaries, can be marked out on the proposed model of the heart as shown in figure 6. The 3-D conceptualisation of flow of blood through the heart can be emphasised by marking the direction of the flow of blood with arrows.
Implications of teaching the three-dimensional perspective
Figure 6. Anterior view: the blood supply of the heart
The practical application of this model is best done by students working in pairs. The model created by the hand of one student represents the correct anatomical configuration of the heart in the body of the observer, i.e. the second student, when facing each other. This also encourages students to interact, and to assist the weaker student in consolidating his or her knowledge.
The main strength of this hand model is that it provides a spatial framework for the relations of the anatomic structures of the heart. The left hand preserves the attitudinally correct anatomical configuration of the surfaces and borders of the heart, in relation to the anterior and posterior walls, superior and inferior surfaces and right and left borders. The majority of people are right handed, which enables the student to use the right hand to write on the left hand (with the heart model). However, the right hand can successfully represent the attitudinally correct anatomical configuration of the surfaces and borders of the dextrocordis heart organ.
Limitations
The hand model is meant to provide an approximation of the 3-D layout of the heart, but has some limitations. The upper right border of the right atrium is tilted more towards the right side and the lower right border of the right atrium tilts towards the left. The tilting is caused by poor representation of the transverse cross-section areas of the chambers by the thumb, index and middle fingers. The fingers are leaner than the chambers of the heart and this can be partially solved by separating the finger tips (which represent the inferior surface) by 3 cm from each other. The inferior surface of the heart has a transverse section diameter of 8–9 cm7 and separating the three fingers with 3 cm from each other will approximate the transverse dimension of the normal heart. The most difficult blood vessel to illustrate is the course of the posterior interventricular branch of the right coronary artery (right dominance). The normal course of this artery is to pass through the right anterior atrioventricular groove and then through the posterior interventricular groove. The artery in the hand model passes through the right anterior atrioventricular groove and then crosses the posterior surface of the right ventricle to reach the posterior interventricular groove. Notwithstanding the limitations of the hand model, it provides a readily available 3-D learning aid to the gross anatomy of the heart.
Conclusions
Hand models are virtually free of cost and can be ‘handy’ teaching aids for instructors who have poor quick drawing abilities. The knowledge gained from using the hand model can be easily applied in the clinical setting,3,4 e.g. the clinician can place his or her hand on the chest or upper abdomen of the patient to gain the correct 3-D perspective of the heart. Students may also use their hands during formal anatomy assessments, to represent the heart and to aid their recall of the anatomy of the heart4.
Acknowledgements This paper was helpfully reviewed by members of the Department of Human Biology of the University of Cape Town, before submission for publication.
Conflict of interest
None declared.
References
Sos TA, Kligfield PD, Sniderman KW. A method for understanding three-dimensional coronary anatomy. JAMA 1980;243:252–4.
Edvinsson L, Mackenzie E, McCulloch J (eds). Cerebral blood flow and metabolism. New York: Raven Press, 1993;1–683.
Spring DA, Thomsen JH. A model for teaching coronary artery anatomy. JAMA 1973;225:56.
Gangata H.A 3-dimensional anatomy model of the liver organ using a gloved hand. Liver International Journal 2008;28:532–3.
Hurst JW. The approach to the patient. In: Hurst JW, Logue BW. The heart, arteries and veins. New York: McGraw-Hill Book Co Inc, 1969;44–47. Quoted in: Spring DA, Thomsen JH. A model for teaching coronary artery anatomy. JAMA 1973;225:56.
Duytschaever M, Ho SY, Devos D, Tavernier R. The left hand as a model for the right atrium: a simple teaching tool. Europace 2006;8(4):245–50.
Standring S. Gray’s anatomy. 39th Ed. London: Churchill Livingstone, 2007;995–1027.
The cardiovocal syndrome was first described by Otner, a Viennese physician, in 1897.1 It refers to a clinical syndrome of hoarseness due to dysfunction of the left recurrent laryngeal nerve, caused by cardiac diseases. Here, we describe a case of Otner’s syndrome following the second revision of mitral valve replacement.
Case report
Figure 1. Echocardiogram showing dilated left atrium
A female patient was admitted to our unit after the second repair of her mitral valve, with breathlessness and hoarseness about 10 days after the operation. Prior to the last revision she was in left ventricular failure due to severe paravalvular mitral regurgitation and, despite severe pulmonary hypertension and dilated left atrium (figure 1), she did not have any vocal symptoms prior to the operation. Ear, nose and throat examination revealed left vocal cord palsy with normal pharynx and larynx. During her stay her voice steadily improved.
Discussion
Cases have been reported showing an improvement of voice hoarseness after repair of the leaking prosthetic valve.2 However, in our case, hoarseness occurred after the repair. Although hoarseness of voice is common after endotracheal intubations, it tends to occur in the immediate post-operative stage and should resolve within three to five days. In our case it started much later.
Slow compression of nerves might lead to a compensatory mechanism maintaining some function of the nerve until a late stage. We propose that the sudden change in the pressure on the nerve by the enlarged pulmonary artery and/or left atrium caused a temporary nerve dysfunction, probably due to some oedema of the myelin sheath with complete recovery afterwards.
The left recurrent laryngeal nerve branches off the left vagus nerve, as it crosses the arch of the aorta. Then it hooks around the ligamentum arteriosum medial to the arch and ascends in the groove between the trachea and oesophagus, to enter the larynx behind the cricoid cartilage. Not surprisingly, this long course around the aortic arch makes it more frequently involved than the right nerve in various pathologies. A unilateral lesion causes paralysis of the ipsilateral larynx and lower sphincter of the pharynx. The vocal cord becomes immobile and lies near the midline. The compensatory mechanism is so efficient that the voice may remain, or soon return to normal.
Conflict of interest None declared.
References
Otner N. Recuurens Lahmung bei Mitralstenose. Vienna: Klin Wechenschi 1897;10:753–5.
Silvia ZM, Fermin LB, Manuel AV. Paralysis of left recurrent laryngeal nerve palsy secondary to mitral periprosthesis insufficiency. Rev Esp Cardiol 1997;50:902–03.
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Editors: Varghese A, Pennell D
