![]() Are you confused about what to eat? It can't be because of lack of information. Search Google today for the word "diet" and it will give you over 136 million hits with over 4 million in the News section alone. Most stories are here today and gone tomorrow and who bothers to look at the evidence behind the headline. Take the one on today's front pages: "Eating too much meat and eggs is as deadly as smoking." Really? Taken at face value this should be a public health emergency. Warnings on plates used to serve the full English breakfast ought to be introduced, we might even call for an ingestion charge on meat and eggs! But probably what will happen is that we will forget the headline by tomorrow certain in the knowledge there will always be another story this time telling us that too much fat or sugar or carbohydrate or this or that is bad. Confused about what the best diet is? Of course you are who wouldn't be? With so much conflicting information it is difficult to know what to believe. So what of the study reported today? Should we worry about meat and eggs? Are they really as dangerous as smoking?The story comes from a paper published in Cell Metabolism. This is a "good journal" with a very high impact factor. In other words you would be proud to have your research published there. The study followed 6.381 adults, 50 years old and over for 18 years. So far so good, a large study sample with long follow up. They found that people with diabetes were more likely to die from diabetes if they had a high protein intake. They assessed protein intake using a diary card for 24h at the start of the study ie about 20 years ago. Are you still eating the same diet as you were 20 years ago? I thought so but anyway not to worry the authors assumed that the people's diet remained unchanged for 20 years. When the results were analysed there were no differences in death rates overall, cancer or cardiovascular deaths. Now this ins interesting because the group eating a lot of protein had a much higher proportion of diabetic patients and you would have though that the cardiovascular death rate would be higher in that group. Then if you look at the data more carefully you notice that the death rate from diabetes in the study is very low indeed (about 1in 100). Most people died of cancer or cardiovascular disease as expected The proportion of diabetics in the high protein group was 17% whereas it was only 2.6% in the low protein group. Presumably this reflects the advice given previously by diabetes specialists to recommend high protein diets to diabetics as it was thought that the blood sugar levels were easier to control. So this group has far higher numbers of diabetics and if you look at the proportion of diabetics in each group which died of diabetes then it is 7.7 for the low, 8.7 for the intermediate and 11.8 for the high protein groups. Not so different and because the numbers are small the accuracy is low. Not withstanding this the investigators analysed the data some more and managed to find an association between age, protein consumption and cancer mortality. If you are 50–65 years you get benefit from a low protein intake but once you are over 65 then it is harmful. Is this biologically plausible? So that's just one headline on one day. But there is a message there: Meat and eggs are as deadly as smoking. This is confusion at best and harmful at worst as this study really doesn't support that conclusion. In the end it is likely that the public, seeing so many stories which apparently contradict each other, will decide that no-one really knows what the best diet is and carry on eating their usual food.
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![]() When doctors are asked to classify atrial fibrillation (AF) they usually start by describing it as paroxysmal (coming and going) or persistent. When they are asked about the causes of AF they will usually list high blood pressure, ischaemic and valvular heart disease, alcohol and over active thyroid. These things are definitely associated with AF but what triggers episodes. Another way of classifying AF is Sympathetic or adrenergic AF and vagal AF. The initiator of the AF episodes can often be overlooked in the consultation but is very important particularly as vagal AF will gets worse when treated with beta blockers. The vagus nerve wanders from the brainstem throughout the chest and abdomen innervating the heart, lungs and intestines. It is part of the autonomic nervous system and its cardiac action is to slow the heart. For some patients increased vagal activity is associated with the initiation of atrial fibrillation. So called vagal AF is enigmatic but should be more recognised. This is important because it needs to be managed differently from other more common types of atrial fibrillation. When to suspect vagal AF: If the arrhythmia occurs at rest, after meals or during sleep then it is more likely to be vagal stimulated. Commonly this type of AF stops in the morning or during periods of exercise and can be precipitated by cough, nausea, after eating, swallowing and ingestion of cold foods and drinks. Vagal AF is more frequently seen in younger patients (30-50 years old), typically men and usually the heart is structurally normal on echocardiography. If the patient participates in endurance sports such as cycling, marathon running or cross country skiing then AF is also more common. ECG recordings often show a combination of atrial flutter alternating with atrial fibrillation. When a 24h ECG monitor is performed sinus bradycardia usually occurs before the onset of the AF. The ventricular rate during the AF is generally not fast. It is possible to measure the activity of the autonomic nervous system but it is difficult. One way is to assess heart rate variability which can assess the balance between the sympathetic and parasympathetic or vagal tone. Vagal stimulation shortens atrial effective refractory period and augments the ability of a single atrial premature beats to induce AF. How should vagal AF be managed? Anticoagulation as per the underlying stroke risk predicted by CHAD2VASC score should be considered. With respect to reducing vagal AF episodes there are only anecdotal data about the best way to manage this. Drugs which block the sympathetic nervous system commonly used in the management of AF such as beta blockers and digoxin should be avoided. Alternative drugs such as those which reduce vagal tone should theoretically be effective. These drugs include flecainide, quinidine, and disopyramide. The pulmonary veins are a well-recognised source of AF in many patients and ablation can be effective in reducing paroxysmal AF. In contrast there are no specific studies reporting the success of ablation in vagal AF. One recent development is the awareness of increased activity of the If channels which raises the possibility that blockade of these channels with ivabradine might have an anti-arrhythmic in vagal AF patients. This is still an area for research and further information will be needed before this can be used routinely in the clinic. ![]() Yesterday the 2014 AHA/ACC Guidelines for the Management of Patients with Valvular Heart Disease were released. Last published as a full guideline in 2006 and updated in 2008 the new guideline occupies 235 pages and is supported by 939 references. The guideline development group have sifted, weighted and considered all the evidence and come up with 226 recommendations for you and me to follow. In this type of guideline the strength of evidence supporting each recommendation is graded as A, B or C. A recommendation supported by evidence graded as an A is derived from multiple randomised trials or meta-analyses, Evidence graded as B comes from a single randomised trial or more usually non-randomised trials and evidence graded as C is expert opinion. In this new guideline just 7 out of the 226 recommendations are supported by A grade evidence and of the remainder, over half (112 to be precise) are the product of just expert opinion. The 7 recommendations supported by top class evidence a straightforward enough. For example they recommend replacing the aortic valve in people with an indication for aortic valve replacement who have acceptable surgical risk, seems logical. They recommend treating patients with heart failure who also have mitral regurgitation with guideline directed medical therapy and using resynchronisation therapy for those who meet the indications for this treatment; again this seems logical and derives from clinical trials of heart failure rather than valve disease. They recommend giving warfarin to patients with mechanical prosthetic valves; Is there anyone who wouldn't do that? They also recommend giving aspirin in addition to warfarin to patients with mechanical valve prosthesis; I don't think that practice is very widespread even though it comes from a trial published in 1993. It seems cardiologist ignore some evidence when it suits them. They also recommend treating symptomatic severe mitral stenosis with balloon valvuloplasty provided there are no contraindications and tell us not to give statins to reduce progression of aortic stenosis - they don't work. Actually this latter recommendation is interesting since there were a large number of retrospective and case-controlled studies which indicated that statins reduced progression of aortic stenosis. When the blinded clinical trials were done however these drugs were without effect. What of the recommendations based on level B and C evidence. As the guideline document states just because the level of evidence is C does not necessarily mean that the evidence is weak but they would say that wouldn't they. In fairness some clinical questions are not suited to randomised clinical trials so I don't think there will ever be a trial to investigate whether taking blood cultures before antibiotics are given for endocarditis is appropriate or not. Currently the biggest challenge and difficult decision is when to refer asymptomatic patients for valve replacement or repair. The guideline helps us here recommending various cut-offs of left ventricular size and function but what of the evidence supporting these recommendations. Lets take one as an example: On page 56 the guideline says: Aortic valve replacement is reasonable for asymptomatic patients with severe aortic regurgitation and normal LV function (EF>50%) but with severe LV dilatation (LVESD >50mm or 25mm/m2). [Class IIb, Level B]. This recommendation is supported with evidence from three studies. The first (reference 226, Van Rossem et al), is an imaging study describing a comparison of MRI and angiography for the assessment of LV ejection fraction and it doesn't seem to have too much to do with when to operate for aortic regurgitation. The other two studies (Bonow et al, reference 243 and Gaasch et al, reference 244) are actually about aortic regurgitation which is a good start. The Bonow paper looked at 61 patients all with dilated ventricles who had an aortic valve replacement. They found that after the operation the diastolic dimensions decreased. In this study a third of the patients could not complete an exercise test to 8METS of workload so they were anything but asymptomatic and more importantly everyone got an operation so the study doesn't tell you when to operate. The other study was an extensive treatise on 31 patients with severe aortic regurgitation. In this study 23 had NYHA class 2 or 3 symptoms - so again not asymptomatic. The authors concluded that LV enlargement could be detected by echocardiography. Again not a study of when to operate. So these papers don't really support the guideline recommendation and we need to be cautious because there is a tendency for weak recommendations based on little evidence to gain strength when they enter a guideline. Guidelines are disseminated at meetings and internet presentations. Some people will read the executive summary, some will skim though the guideline document. Only a very few will read the guideline and then go back to the original studies that support the recommendations to evaluate them in detail - we assume the guidelines development group will have done due diligence. Although we chant the mantra of evidence based medicine in many cases we are still practicing eminence based medicine. ![]() This is the angiogram of a 48 year old man who exercises regularly and has no cardiac symptoms. His story is not uncommon. He has a medical up every 2 years including an exercise stress test. He completes 9 minutes of exercise without symptoms but there are some ECG changes and cardiology referral is recommended. The cardiologist agrees the exercise ECG is abnormal and requires further investigation. In the absence of symptoms or risk factors for coronary artery disease a CT coronary angiogram was recommended. This surprisingly to the patient indicated a stenosis in the proximal LAD which was then confirmed with an invasive angiogram. Now the cardiologist and patient are faced with a decision: What to do next? There are few things cardiologists agree on but I reckon if you showed 10 interventional cardiologist this angiogram they would all say that something must be done. There might be a discussion about the long term pros and cons of drug eluting stents versus surgical revascularisation but most would agree that medical therapy alone in the absence of revascularisation would represent a sub-standard level of care. Most would agree that a 3.5x23mm drug eluting stent could be placed efficiently with very small risk of complication and an excellent result. There would be complete relief of vessel obstruction and at the same time a reduction in patient and physician anxiety. When it comes to the decision to place a stent are we too strongly influenced by our heart rather than our head. Is it a case of emotion trumping science! The COURAGE study compared optimal medical therapy with stenting in patients with significant coronary disease. After 7 years of follow up in COURAGE study was there was no significant difference between stent treatment and medication. But what of patients with 90% stenosis in the proximal LAD the so called "widow-maker" lesion. Surely patients with this pattern of coronary disease benefit from revascularisation? ![]() A recent paper from the COURAGE study looked at just this group of patients and found that there was no significant difference between the patient treated with stents or optimal medical therapy. The figure on the left shows the that the group of patients with >90% stenosis in the proximal LAD did not fair well over the 7 years. The surprising thing is that those treated with angioplasty and bare metal stenting (lowest solid green line) appeared if anything to fair less well than those treated with optimal medical therapy (second lowest green dotted line). The presence of proximal LAD disease as a rationale for favouring stenting was therefore not proven. This finding is provocative and instructive. If you ask interventional cardiologists (and this has been done in focus groups) they will acknowledge that stenting offers no reduction in the risk of death or heart attack in patients with stable coronary artery disease but despite this they generally believe that stenting does benefit such patients. One senior cardiologist said to me that he preferred to treat the cause of coronary artery disease with a stent rather than merely manage the symptoms with tablets. Reasons for performing stenting include belief in the benefits of treating ischaemia, the open artery hypothesis, potential regret for not intervening if a cardiac event could be averted, alleviation of patient anxiety and medico-legal concerns. If asked, most cardiologists believe that the oculo-stenotic reflex prevails and all significant and amenable stenosis should receive intervention even in asymptomatic patients. When cardiologists are challenged about the lack of evidence of adding stenting to optimal medical therapy in preventing future coronary events most still feel that any patient with significant coronary disease should get a stent even whilst acknowledging the evidence. This disconnect between knowledge and behaviour reflects the discordance between cardiologists’ clinical knowledge and their beliefs about the benefits of angioplasty and that non-clinical factors have substantial influence on cardiologists' decision making. So what happened to this patient? I will leave you to decide and to post your thoughts and comments. ![]() Many patients seek advice from a cardiologist because of palpitations. Sometimes the cause can be worked out from the clinical history and description of the symptoms with a reasonable degree of certainty (e.g. ectopic beats) but often it is necessary to try and correlate the patients symptoms with an ECG recorded at the same time. Classically this involved fitting the patient with a Holter monitor. These portable devices, named after Norman Holter, American biophysicist, continuously monitoring the electrical activity of the heart. Originally recording onto cassette tape they now use digital technology which has reduced their size. The 24h tape is a useful investigation provided that symptoms occur frequently. However in my experience most patients with palpitations do not have daily symptoms and therefore the value of a short period of recording is low. The other growing use of these devices is to detect asymptomatic arrhythmias such as atrial fibrillation (AF) which is a very common cause of stroke. Detection of episodes of this arrhythmia and offering anticoagulation can dramatically reduce the risk of recurrent stroke. Again a 24h period of recording has limited utility to detect episodes of AF which may occur infrequently. Of course it is possible to record cardiac rhythm for upto 7 days using these monitors or single lead cardiac event recorders such as the Novacor device however these become uncomfortable when worn for long periods of time due to the adhesive electrodes causing skin irritation. Also the electrodes often displace or contact is lost limiting the quality of the recording. An alternative would be an implantable device to record the ECG. Such a device has existed in the form of the implantable loop recorder also known as a Reveal since 1998. Over the last 14 years the device, which is about the size of a USB stick, has become more sophisticated in terms of algorithms for the detection and assessment of arrhythmia although the size remained the same. However all that is about to change because In the last few days Medtronic have launched the new Reveal LINQ device. 90% smaller than the old one and more sophisticated it occupies a volume of one cubic centimetre and can be inserted through a tiny nick in the skin in with a special applicator. The whole process takes but a moment and yet once in place the device can record the ECG continuously for 3 years and the data can be downloaded to a computer wirelessly and transmitted to the physician for interpretation. The easy insertion, small size and long battery life put this device centre stage for the management of patients with arrhythmia. If you have paroxysmal AF then using this device to monitor frequency of occurrence and adjust treatment would be very helpful for the doctor and patient since we know that symptoms are not a good guide to the frequency of arrhythmias. With the advent of Smartphone technology it won't be long before we see implantable devices able to monitor all aspect of a patients physiology and communicate it to doctor and patient. Reveal LINQ ![]() In December 2009 The Telegraph ran an article describing a revolutionary new procedure which was aimed to be able to effectively cure high blood pressure. Like many people I was excited to find out more. A clinical trial been published in April 2009 in the Lancet describing the effects of destroying the nerves which supply the kidneys in 50 patients with resistant hypertension. This observational study had shown impressive and sustained blood-pressure reduction without serious adverse events. Following that a randomised clinical trial of 110 patients was started and the Telegraph article was prompted by the first patient in the UK being treated at the London Chest Hospital as part of the trial. When the study was finally published in December 2010 again it showed impressive and sustained reductions in blood pressure. These results stimulated excitement amongst interventional cardiologists who wanted access to this new treatment for their patients. Research was quoted by experts in the field estimating that there were huge numbers of patients with resistant hypertension for whom this therapy was potentially an option. Ardian, the company which made the ablation catheter, was valued at 800 million dollars and rapidly acquired by Medtronic one of the largest medical device companies in the world. Ablation devices were rapidly and widely promoted in Europe. Courses and international meetings were established by proponents of the device and sponsored by the device company. Reputations and CVs of the organisers and speakers were enhanced and by August 2012 it was though that over 5000 procedures had been performed. In particular German cardiologists embraced the technology with hundreds of patients being treated. Enthusiasm spread and papers started to appear proposing that renal denervation might be a potential treatment for metabolic syndrome, type 2 diabetes, sleep apnoea and heart failure. Much of this based on uncontrolled studies in a few highly selected patients. It all seemed to good to be true. UK cardiologists, including myself, started to work out how they could begin to perform this novel procedure. Interventional cardiologists like technology and the prospect of being able to perform a new procedure was very attractive. In many cases charitable funding was raised to purchase the catheters and ablation system. Collaborations were established between radiologists, hypertension experts and cardiologists, a NICE technology appraisal was published, followed by guidelines from the British Hypertension Society and the prospect of "Commission by Evaluation" from NHS England. Centres, including my own at St Helier Hospital in Carshalton, started to perform the procedure in small numbers. Our initial enthusiasm for the procedure was tempered by a difficulty in finding the apparently huge number of patients we were told had resistant hypertension. We were referred many patients for evaluation but usually simple medication adjustment such as the addition of spironolactone or treatment of other factors such as sleep apnoea were able to control the blood pressure. Sometimes patients simply had white coat hypertension and proper assessment with ambulatory monitoring revealed well controlled blood pressure. Sometimes the patient did have resistant hypertension but the renal artery anatomy wasn't suitable for ablation. Overall only about 1 in 10 patients we screened were suitable and we started to think that the epidemic of resistant hypertension (defined in guidelines as BP>140mmHg on 3 drugs including a diuretic but for the purposes of the denervation trials a BP threshold of >160mmHg was required) did not really exist. In the USA things were a little different. The Food and Drug Administration (FDA) concluded that the clinical trials which Ardian had performed were not adequate for licencing the technology since there was no sham treated group. Without this it is possible that significant bias has crept into the trials especially when the end point being measured was office blood pressure. The FDA required a double blind, sham controlled trial and we all awaited eagerly for the results. This week our wait ended earlier than expected when Medtronic put out a press release to say that their pivotal trial had failed to meet its primary efficacy endpoint. In other words there was no difference in the office blood pressure measurement from baseline to 6 months in patients treated with the ablation versus sham treated patients. Fortunately no safety concerns were raised from the trial. The data and full results have not been published yet and so it is difficult to comment in detail but at this stage it is certainly very disappointing that the blood pressure effects seen previously were not reproduced in a sham controlled double blind clinical trial. There are two lessons here. First, the placebo effect and bias are strong factors which influence clinical outcomes. The bigger the procedure, the more invasive it is and the more enthusiastic the doctor the greater is the chance of a very significant placebo effect. The only way to avoid this is a sham or placebo controlled trial. Second, it is often said that history repeats itself and there are parallels here with renal artery angioplasty. This procedure started in the 1970s with case series suggesting it reduced blood pressure in everybody with renal artery stenosis. The first randomized trial was published in 1998 and since then all the trials comparing medical treatment with renal angioplasty were negative. So where does that leave us with renal denervation. It's early days but we should be cautious and I think that in general renal denervation should now only be performed as part of blinded sham controlled research clinical trials. ![]() When a patient has a coronary angiogram the cardiologist will report the results in terms of the degree of narrowing of the arteries. For example a 60% stenosis in the LAD, a 40% stenosis in the circumflex. But what does that really mean? Is the stenosis flow limiting? Is it responsible for the patients symptoms? Is the lesion prognostically significant? Should a stent be place? Is a bypass indicated? Many questions but the fundamental one is: "Would this patient's outcome be better with or without revascularisation or is medical therapy more appropriate?" When there is mild or critical coronary artery disease then the decision making is straightforward. However in many cases there are moderate areas of coronary narrowing. Showing the angiogram to several cardiologists will usually result in differing opinions about whether a lesion is flow limiting or not. For some cardiologists the "Oculostenotic reflex" is already potentiated leading to "iatrogenosis fulminans." In 1995 Steve Nissen and Eric Topol wrote about cardiologists preoccupation with luminography and eloquently showed how lesion assessment with angiography performed very poorly compared to intravascular ultrasound. They also wrote of the dissociation between the angiogram and clinical outcome and called for a shift in our with luminology towards measures that improve survival, freedom from myocardial infarction and symptoms of angina. Whether a coronary lesion is flow limiting is not just dependent on the degree of arterial stenosis but also on the amount of cardiac muscle supplied, the presence of collateral vessels, the length of the lesion and the function of the endothelium. Some of these factors can be assessed subjectively by angiography but others cannot. What is required is a more functional or physiological assessment. Cardiologists have fooled themselves for too long that they are able to determine the functional significance of a moderate coronary stenosis from the angiogram alone. Recent data using the pressure wire has challenged some of this thinking although there are still some sceptics. The FAME studies showed that use of the pressure wire to measure fractional flow reserve (FFR) could be useful to help in selecting the appropriate therapy and guiding coronary revascularization in patients referred for a percutaneous coronary intervention (PCI) procedure. Very recently a real world study has been published using FFR in patients referred for diagnostic angiography and looking at its impact on the decisions involved in revascularization. In this study patients referred for diagnostic angiography had a treatment plan for intermediate lesions (35-65% by eye) made on the basis of the angiography alone. 55% of patients were recommended to receive medical therapy and 45% revascularization (PCI, 38%; CABG, 7%). FFR measurement was then performed with the pressure wire and after this 58% of patients were recommended for medical therapy and 42% for revascularization (PCI, 32%; CABG, 10%). The results were not so different overall but in individual patients the FFR strategy changed the recommended treatment in 43% of cases. Reclassification was observed in 33% medical patients, 56% of PCI patients and 51% of CABG patients. These results are hugely important since they indicate that even experienced cardiologists are unable to judge the flow limiting nature of moderate lesions. In the initial medical treatment group one third of patients met FFR criteria for revascularisation. In the PCI group, half of patients were due to receive inappropriate or a less optimal type of revascularisation. In the surgical group over half of patients could have avoided an operation. What this study is telling us is that using the eyeball technique to judge the severity of coronary disease is not the best way to decide on a management plan for cardiac patients. If the practice of using a pressure wire became standard in diagnostic coronary angiograms it would lead to more patients receiving medical therapy, less receiving angioplasty and more patients having CABG. The effects on the economics of management of coronary disease are complex. Assuming everyone gets medical therapy then the cost of the increased CABG although a more expensive procedure is offset by the reduction in expenditure on angioplasty. The repeat revascularisation costs are likely to be lower since this has been shown routinely in most of the CABG versus PCI studies. There is of course the cost of the pressure wire for every case. Overall the most improtant thing is that the patient receives the most appropriate treatment and not at the mercy of the oculostenotic reflex. ![]() Originally stable angina and acute myocardial infarction (MI) were believed to be different diseases. Then in the 1930s it was observed that some patients with severe and sometimes prolonged rest angina sometimes went on to have an MI. This disorder was referred to as pre-infarction or crescendo angina and then was renamed unstable angina in 1971. We still use this term today to describe a group of patients who have symptoms of angina at rest but who have normal cardiac biomarkers. The World Health Organization definition of MI requires 2 out of 3 of either typical symptoms of angina, a typical ECG pattern (e.g. Q waves, ST elevation) or a rise and fall in cardiac biomarkers of myocardial necrosis. In 1991 unstable angina was responsible for over half a million hospitalizations in the United States and it was one of the most common disorders leading to admission. Nowadays we refer to patients with chest pain as having acute coronary syndromes. This term encompasses all patients with unstable angina, non-ST elevation MI and ST elevation MI under one umbrella. However there is ambiguity since the operational definition of unstable angina is made when there are new or worsening symptoms of ischemia and ischemic ECG changes with normal biomarkers. The distinction between new angina, worsening angina and unstable angina is clinically very difficult since by this definition the first ever episode of angina is unstable angina. The differentiation of unstable angina and MI now rests on the identification of abnormal levels of cardiac biomarkers. When I first started in medicine we measured serial CK, AST and LDH over 3 days and looked for the typical rise and fall in these biomarkers. Later we started using the more specific but not more sensitive CK-MB and finally we started to use to troponin. Troponin is a highly specific biomarker of cardiac muscle injury. The sensitivity of troponin is now so high that we are detecting elevated levels in many patients who had they presented to physicians 20 years ago were told they had not had an MI. In the TIMI3 trial a quarter of patients originally classified as having unstable angina based on CK-MB measurements had elevated Troponin and as the years have gone on the sensitivities of troponin assays continues to reduce. In the TIMI3 trial the cut point for MI diagnosis was 0.4ng/mL, by 2010 in the MERLIN-TIMI 36 trial the cut point was 0.04 ng/ml. In the recent PROTECT-TIMI 30 trial the cut point was 0.003ng/mL and in this trial 44% of patients were defined as having an MI at presentation with 82% by 8h. It is now evident that a large majority of patients with clinical manifestations of myocardial ischemia will have elevated levels of troponin if an assay with high enough sensitivity is used. What is also important is not just that we are detecting more MIs but this newly identified group of patients do have higher risk than those patients with undetectable troponin and as such aggressive treatment is leading to improved clinical outcomes. So in the end with ultra high sensitive troponin assays emerging into clinical practice we will be able to confidently divided patients into a group with stable angina pectoris and a group with MI and the grey zone of unstable angina with most likely be banished forever. On the 29th October 1944 the first cardiac operation was performed at the Johns Hopkins Hospital for the treatment of congenital heart disease. Dr Alfred Blalock, the Chief of Surgery, carried out a pioneering surgical procedure designed to palliate a condition called Tetralogy of Fallot. This complex condition is characterised by a narrowing in the outflow tract of the right ventricle, thickening of the right ventricle, a ventricular septal defect and an over-riding aorta. In essence the blood flow to the lung is severely compromised and babies born with this condition are often deeply cyanosed and therefore known as "blue-babies." In the 1930’s the management of a blue baby was to place them in an oxygen tent. Children were advised to assume a squatting position to reduce venous return to the heart, and to try and keep as quiet and calm as possible to reduce infundibular spasm. The prognosis was terrible and the paediatric cardiologist at Johns Hopkins, Dr Helen Taussig, had to simply watch babies and children die. It was known that children with Fallot's who also had a patent ductus arteriosus were less cyanosed and this led to the idea of whether it might be possible to create a shunt between a great vessel and the pulmonary artery in order to supply blood to the lung. After painstaking laboratory work this resulted in the introduction of what is commonly called the "Blalock-Taussig shunt." In this procedure the left subclavian artery was anastomosed to the pulmonary artery. The operation was first performed at Johns Hopkins on 29th October 1944 and represented the first effective treatment for this condition and it is still used in a modified form today. It was published in JAMA in 1945. ![]() This story would in itself be interesting but what makes it fascinating is the contribution of another member of the team. If you look at the photograph of the operating room you can see there is a man on the far left of the picture standing behind Blalock who is operating. That man was called Vivien Thomas. Nowadays we would call him an African American but in 1940’s Baltimore things were different.Thomas left school at 14 with no college education and started work as a carpenter. After losing his job he obtained a position in Dr Blalock’s laboratory as a janitor. Soon Blalock recognised his exceptional talent with his hands and he became the technician who ran Dr Blalock’s experimental surgical laboratory. When it came to the scientific and the surgical technical aspects of the shunt his own autobiography and detailed research has demonstrated that the primary contribution was from Thomas. Most of the fundamental studies were done by him and Blalock only did one practice procedure in a dog before performing the first surgery on a 15-month-old girl. As the photograph shows Thomas stood behind Blalock during the procedure to provide advice. At a time of racial segregation and discrimination in America, Thomas’s contribution to the development of the shunt procedure remained relatively unknown outside Hopkins. He was ignored by the world’s press and media and the procedure became known as the Blalock-Taussig shunt. He was not even acknowledged for technical contributions in the original paper. However in time, as political and civil rights movements led to change in attitudes towards race, Thomas's exceptional contribution to the development of this pioneering heart surgery was recognised. His portrait now hands in the hallowed corridors of the Johns Hopkins Hospital alongside Dr Alfred Blalock, Sir William Osler, Dr Harvey Cushing and Dr William Halsted – legends of modern clinical medicine. October is Black History Month. You have probably heard of Rosa Parks, Mary Seacole and Claudia Jones but the story of Vivien Thomas is not well known outside of Johns Hopkins. Thomas made a huge contribution to the birth of cardiac surgery and thus plays an important part in the history of medicine. He is a wonderful example of how despite segregation a black man fought against the odds and was key in developing a life-saving operation used to treat thousands of children worldwide. Perhaps it’s time to officially rename the Blalock-Taussig shunt the Blalock-Thomas-Taussig shunt and give him his rightful place in Black History month. ![]() Medicine, according to Hippocrates, consists of three things – “the disease, the patient and the physician.” But what is disease? It is not simply a state of less than optimum physical health. As Charles Rosenberg says in the introduction to a set of essays on this subject: “In some ways a disease does not exist until we have agreed that it does by perceiving, naming and responding to it." In cardiology there are two diseases which have only been recently “framed." They are Brugada syndrome and Takotsubo cardiomyopathy. Brugada syndrome was first described in 1992 by the Brugada brothers. They reported the case of a child with recurrent episodes of ventricular fibrillation who had an abnormal pattern of right bundle branch block with ST elevation in the right precordial chest leads. Once this pattern had been described cardiologists looked back to patients they had been managing who were survivors of ventricular fibrillation and people with cardiac defibrillators and found that some of them also had this ECG pattern. Brugada syndrome had existed before this but was simply not recognised by mainstream cardiologists. The syndrome is commonly seen in young men originating from the Far East. In the Thai medical literature, long before the Brugada's description, doctors had described sudden adult death syndrome which was associated with night-time in episodes of ventricular fibrillation which had been called Lai Tai. Most victims were apparently otherwise healthy young men who died unexpectedly during sleep. In some families, similar deaths had occurred for over four generations. It was a local myth that these unexplained deaths were caused by a widow ghost who came to take the mens’ soul at night. It was tradition in some parts of Thailand for men to dress in women’s nightclothes to confuse the ghosts! In other countries similar syndromes were described including Tsob Tsuang in Vietnam and bangungut in the Philippines. Elsewhere the concept of "Voodoo Death" has been well described and may well be related to a cardiac arrhythmia. Another disease recently framed is the Takotsubo cardiomyopathy, also described first in the Far East this time in Japan. It is an unusual form of cardiomyopathy which is usually seen in women and often triggered by a severe emotional disturbance. It is characterised by chest pain and usually patients are usually thought to have an acute coronary syndrome. The first reports of this disease came from Japan possibly because this country is in an earthquake zone and earthquakes provoke severe emotional disturbances. Also Japan has a primary angioplasty service and the Takotsubo diagnosis is usually made when patients are studied in the catheter laboratory. This is because the coronary arteries are unobstructed and there is often a classical appearance of apical ballooning on the LV gram. This syndrome occurs reasonably commonly in clinical practice and until recently was simply not recognised. These two cardiac conditions have only recently been framed as diseases. In the past we would have simply labelled the patients as having idiopathic ventricular fibrillation or an acute coronary syndrome without obstructive coronary disease. I wonder how many other diseases there are waiting to be framed. |
Dr Richard BogleThe opinions expressed in this blog are strictly those of the author and should not be construed as the opinion or policy of my employers nor recommendations for your care or anyone else's. Always seek professional guidance instead. Archives
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