Magill v Panel Systems (DB Limited)

This claim is brought by Deborah Magill both in her own right and as personal representative of the estate of her late husband Colin Magill. Mr Magill (the deceased) died on 18^th July 2016 when he was sixty years of age. The deceased had been employed by the Defendant as a saw man between 1975 and 1978. During that time the Defendant accepts that it exposed the deceased to asbestos dust and fibres in breach of their duty of care. The deceased developed mesothelioma which was diagnosed in June 2015. The Defendant accepts it is liable for any damage which flows from the contraction of mesothelioma by the deceased but not otherwise. The deceased did not die directly from the mesothelioma but from a cardiac arrest. The Claimant claims that were it not for the mesothelioma the deceased would have undergone a coronary artery bypass graft (CABG) which would then have prevented his death from hypoxia following cardiac arrest. The Defendant does not accept this and the purpose of the trial was to resolve this dispute and other related issues.

The agreed factual background

The investigation of the pleural problem caused the second planned operation to be postponed and on 5^th May 2015 a thoracoscopic biopsy led to the deceased being given a diagnosis of mesothelioma. He then underwent five cycles of chemotherapy over the following year. On 17^th July 2015, he was at home and complained of breathlessness. He went outside to get some air and collapsed shortly afterwards. An ambulance was called and arrived within seven minutes. He was in cardiac arrest characterised by ventricular fibrillation but was shocked back into sinus rhythm. He had to be shocked again in the ambulance on route to the hospital. His heart was stabilised and performed adequately for twenty-four hours. He had suffered severe anoxic brain injury however and treatment was withdrawn. He died on 18^th July 2016. A post-mortem was performed and both experts comment on the result of the post mortem.

The factual evidence

The Claimant made two witness statements dated 18^th March 2016 and 21^st September

The Claimant gave evidence at the trial and was cross-examined briefly and sympathetically by leading counsel for the Defendant. She was taken to two documents which the deceased had completed in 2012 and 2014 called “Limited capability for work questionnaire” in connection with a claim for state benefits . This form revealed a considerable level of disability at a time well before the diagnosis of mesothelioma was made. She candidly conceded that she was giving the deceased a great deal of personal care in even those days amounting to about 35 hours per week. She agreed that the deceased would not have been capable of decorating a room at home given the level of disability. After the diagnosis of mesothelioma, the level of care was roughly the same but she had to spend more time dealing with and organising his medication which was much more complex than previously. She was a patently truthful and impressive witness.

The issues in the case

What was the cause of the cardiac arrest?

Dr Robin Rudd was instructed initially to deal with the diagnosis of the deceased’s condition of mesothelioma and his life expectancy but for the contraction of the disease. In relation to the issue concerning the cause of the deceased’s cardiac arrest Dr Rudd agreed with Dr Witte that the cause of death was an arrhythmia leading to the loss of cardiac output and thereby perfusion to the brain. Dr Rudd doubted whether the deceased had acute left ventricular failure as opined by Professor Channer because this would have caused pulmonary oedema which was not described by the treating clinicians, nor found on autopsy. The deceased was not given intravenous diuretics which would have been standard treatment for a patient present with fluid on the lungs. Dr Rudd was also of the view that the anaemia caused by the reduced output from the right lung would have reduced the effectiveness of resuscitation after the cardia arrest. In most other respects, he deferred to the opinion of the cardiologists on this issue. It seems to me however that he can validly comment about the treatment for and effects of pulmonary oedema as a chest physician.

Dr Klaus Witte was called by the Claimant to give expert evidence on this issue. He is a consultant cardiologist at Leeds General Infirmary. He prepared four reports and contributed to the expert’s joint statement. His overall view was that the deceased’s cardiac condition had been stable and mild for the previous 10 years or more. On the 17^th July 2016, the deceased suffered a cardiac arrest in ventricular fibrillation resulting from an acute myocardial infarction. Although the pathologist at post mortem diagnosed left ventricular failure Dr Witte disagrees because of the lack of pulmonary oedema found either by treating physicians or at post mortem. He felt that the symptoms of breathlessness reported by the Claimant shortly before the deceased’s collapse could be evidence of a myocardial infarction in a patient with diabetes mellitus who often do not present with classic chest pain. An acute (permanent or transient) occlusion of a distal coronary artery would not be seen on autopsy, and with death occurring so abruptly, there would be no evidence of tissue damage. He felt the most common cause of ventricular fibrillation is cardiac ischaemia and the raised troponin levels suggest that ischaemia or infarction was the origin of the arrhythmia and the cause of the ultimate death due to cerebral hypoxia.

His initial view was not only that coronary artery bypass surgery (which was cancelled because of mesothelioma) would have prevented this acute coronary event and thereby the arrhythmia that led to his death but also the mesothelioma increased the chances that he would suffer hypoxic brain damage during the cardiac arrest.

Dr Witte was asked to comment on Professor Channer’s report in particular his conclusion that the deceased had died of acute left ventricular failure. Dr Witte did not accept this as a diagnosis in that left ventricular failure, whether acute or chronic is always the consequence of a change. Professor Channer had not identified what change had caused the suggested left ventricular failure he opined.

Professor Channer also prepared four reports in this case and contributed to the experts’ joint statement. He is a consultant cardiologist and physician formerly of the Royal Hallamshire Hospital. He was asked for his opinion on the cause of the cardiac arrest and he opined that from the history as recorded in the Claimant’s statement of a sudden onset of breathlessness this almost certainly represented acute left ventricular failure. Although the treating physician had diagnosed a myocardial infarction Professor Channer felt this was unlikely because there was no preceding history of chest pain, and no evidence of acute thrombotic occlusion of a coronary artery found at post mortem. There was no evidence of acute changes within the myocardium at post mortem to suggest myocardial infarction and that the raised troponin could have been caused by the cardiac arrest. His overall opinion was that the cardiac arrest occurred because of acute left ventricular failure which occurred in association with the natural history of dilated cardiomyopathy in this case.

Professor Channer also pointed out the dismal survival rate from out of hospital cardiac arrests. The main reason why the survival rate is so poor is the time before defibrillation is done in cases of ventricular fibrillation. In the current case the earliest that defibrillation could have been done was at least seven minutes after the cardiac arrest. In Professor Channer’s view hypoxic brain injury was inevitable given the cessation of circulation during that period.

In his fourth report Professor Channer replied to some Part 35 questions which had been put by the Claimant’s solicitors. He was asked to explain why there would be a sudden deterioration in relation to the deceased’s cardiomyopathy which had been diagnosed over 20 years previously and remained stable. His reply was that heart failure is relentlessly progressive. All individuals with impairment of cardiac contractile function will develop heart failure over time. This is called the “natural history” of the condition. The time to deterioration varies with the underlying condition and the progress of the aetiological factors. Professor Channer felt there was evidence of deterioration of the deceased’s heart condition over time. He was diagnosed with severe obstructive coronary artery disease which can itself cause heart muscle damage from ischaemia. He relied on the enlargement of the heart found at post-mortem together with myocardial fibrosis which is the scar tissue left after muscle death, a sign of heart muscle cell deterioration. He relied on the fact that the heart surgeon treating the deceased described him as a “high risk” patient for surgery.

The expert’s joint statement runs to some sixteen pages and I can only give a brief summary of the expert’s views on the most relevant issues. Professor Channer was of the view that the deceased’s heart failure was at least “moderate” prior to his death whereas Dr Witte described it as “mild”. Professor Channer felt that his heart condition was deteriorating whereas Dr Witte felt it was stable. To the extent that his coronary artery disease was causing damage to his heart muscle Dr Witte felt this would be improved by revascularisation following CABG surgery. When surgery was being considered Professor Channer agreed that the deceased had a high perioperative risk as his surgeon recorded whereas Dr Witte felt his risk was merely higher than average in that the pleural effusion which had been noted at that stage was actually due to the mesothelioma and not the heart condition (as the surgeon had understandably assumed). The chances of the deceased not surviving the surgery would have been 1.34% according to Dr Witte and more than 2% according to Professor Channer.

Professor Channer was asked to address the diagnosis of left ventricular failure which he did having seen the hospital records relating to the final admission for the first time. He opined that the cause of the acute left ventricular failure was an arrhythmia, probably ventricular tachycardia, which is supported by the recurrent ventricular tachycardia he had after initial successful resuscitation. He felt there was radiological evidence of pulmonary oedema on 17^th July 2016 but treatment on the Intensive Therapy Unit (if only positive pressure artificial ventilation) would clear the lungs of oedema from left ventricular failure. He only had the necessary IV fluids to maintain insensible losses.

Dr Witte agreed that the cause of death was an arrhythmia leading to a loss of cardiac output but disagreed there was a left ventricular failure. Pulmonary oedema was not recorded by the treating clinicians nor on autopsy. He was not given intravenous diuretics which would have been standard treatment for pulmonary oedema and was given a litre of fluids over time, again treatment inconsistent with pulmonary oedema.

Professor Channer felt there was an acute arrhythmic event of ventricular tachycardia which then precipitated ventricular fibrillation. Dr Witte felt it was more likely that there was a myocardial ischaemic event which triggered ventricular fibrillation. Both agreed that the immediate cause of death was hypoxic brain damage.

Dr Witte conceded in the joint statement that a reduced haemoglobin level and the pro-thrombotic effect of both mesothelioma and chemotherapy did not play a material part in the development of the arrhythmic event which led to the death of the deceased. He had previously raised these issues in his reports as possible contributory factors.

When directly asked, what was the cause of the deceased’s cardiac arrest Professor Channer replied “scar related VT (ventricular tachycardia) causing acute LVF (left ventricular failure) decompensation and degeneration to VF (ventricular fibrillation) and OOH (out of hospital) cardiac arrest”. Dr Witte (who was addressing this explanation for the first time) considered that there was no evidence of a focal myocardial scar on the MRI scan that would increase the chance of an untriggered short circuit and it was far more likely that an ischaemic event triggered ventricular fibrillation.

Both experts gave evidence at the trial for some time and were robustly but fairly cross-examined by counsel for both parties. They are both experienced and respected in their field and eminently qualified to give expert evidence on this case. Neither expert made significant concessions in relation to the core issues in this case and were not shaken from their views. Dr Witte was asked why in the joint statement he had conceded that the reduced haemoglobin levels and the pro-thrombotic effects of mesothelioma and chemotherapy did not play a material part in the cause of the cardiac arrest. He replied “we all agreed that there were more major issues”. I felt this was a sensible concession and an example of the concept of the joint meeting of experts working well to narrow the issues. These issues might have had a theoretical effect but it was not likely to be material and so it was right to exclude them. He had also argued in his report that the respiratory impairment caused by mesothelioma would have reduced the effectiveness of resuscitation and increased the risk and extent of brain damage. When it was put to him in cross-examination that after seven minutes’ delay in an out of hospital cardiac arrest case the chance of resuscitation without brain damage was slim he accepted that on balance of probabilities the reduced respiratory effect would have made no difference. Again, I felt this was a sensible and reasonable concession to make and reflected well on Dr Witte’s independence as an expert witness. Professor Channer was a more combative witness who seemed determined to put across his point of view forcibly. On the morning of the third day of trial he asked permission to make three extra points which had occurred to him since giving his evidence the previous day. It may have been the case that he wanted to make sure that his arguments had the necessary clarity to them but it did rather give the impression of a witness who wished to add weight to his client’s cause.

Analysis

Professor Channer opines that these readings show objective evidence of both deterioration in the deceased’s cardiac status and of progressive ischaemic heart disease. Dr Witte opines that they show stable heart failure and left ventricular function as there is no evidence of deterioration of renal function or change in diuretic requirement which would be expected if there was a marked deterioration in heart function. There seems to be no objective measured change in either the LVEDD or LVEF from 2004 to 2014. Whilst the reference to the mild dilation of the right ventricle and impaired function of free wall motion is a new symptom in 2014 this could be explained by ischaemia due to the coronary artery disease according to Dr Witte. Professor Channer disagreed with this due to the site of the damage to the free wall but this is not an issue I have the knowledge or capacity to resolve. Standing back from the technical issues’ the measurements which these various scans reveal do not, in my view, appear to support a substantial worsening of the deceased’s cardiac condition (other than due to the new coronary heart disease symptoms).

Professor Channer relies heavily on the conclusion expressed by Mr Javangula the consultant thoracic surgeon treating the deceased in his letter of 14^th January 2015 (page 1571 of the trial bundle) where he stated “he has poor LV and he is a high-risk patient for surgery because of the previous MI’s and very poor right ventricle and left ventricle with a diagnosis of? cardiomyopathy…”. Just leaving aside the rather poorly expressed letter I agree with Dr Witte by this point the patient’s clinical condition would have been deteriorating because of the undiagnosed mesothelioma and this would have been the cause of the pleural effusion reported on the cardiac MRI. He also appears to have concluded that the deceased had suffered two previous myocardial infarctions which was agreed during the trial to be incorrect. I accept the deceased’s mortality risk was perhaps higher than average due to his diabetic status and heart condition but otherwise not indicative of a worsening cardiac status.

If I accept that there was no real objective evidence of a worsening in the deceased cardiac condition, then Dr Witte would say that a myocardial ischaemic event against a background of known coronary artery disease sufficient to justify CABG surgery is a much more likely explanation for the episode of ventricular fibrillation which caused the cardiac arrest than a sudden left ventricular failure triggered by a scarrelated ventricular tachycardia leading to ventricular fibrillation. This was Professor

At trial Professor Channer expanded on the brief explanation he gave in the joint statement by explaining how in his view an ectopic beat triggered ventricular tachycardia. The heart must pump from the bottom upwards and an electrical impulse triggers the contraction of the heart muscles. The heart has its own pacemaker which is a modified cell which sends electrical impulses and causes the atrium to contact. There is a delay at the atrioventricular node to allow time for blood to go from atrium to the ventricle. There is then an impulse to the bottom of the heart which contracts from the bottom in a corkscrew fashion. The cells wait for the next electric signal to contract again. When they are electrically silent they are building up their battery and are exquisitely sensitive. If there is an extra beat the cells themselves spontaneously contract and can send the message to the next cell. It is called ventricular ectopy, which is this unexpected beat that can sometimes occur. If there is scar tissue where there is a dead cell the impulse must go around the scar to the next cell. When there is scar tissue the delay caused by the travelling of the impulse around the scar may cause it to hit the cell just when it is ready to depolarise. This can occur randomly, but it can trigger an unfortunate reaction such as ventricular tachycardia.

If this summary of the explanation is not clear it is because I was making a note of it for the first time at the trial as it had not actually figured in any of the expert evidence submitted in writing. Whilst I appreciate that this type of ectopic beat can only occur in the presence of scar tissue there was a debate between Professor Channer and counsel for the Claimant whether the scarring was caused by ischaemia. Eventually it appeared that Professor Channer accepted that ischaemia could be the cause of the fibrosis but he opined that ventricular tachycardia would not occur unless there was pre-existing cardiac muscle disease. This explanation which is complex and difficult for a layman to follow does not seem to me to be the same as the “natural history” of heart failure as previously expressed. Dr Witte considers this an unlikely explanation in any event because there was no evidence of a focal myocardial scar on the MRI that would increase the chance of an untriggered short circuit. He also appeared to opine that it would require an actual scar (dead tissue) to produce this reaction not merely fibrosis.

Another issue which separates the parties is whether there was pulmonary oedema when the deceased was admitted to hospital after his cardiac collapse. Both experts agreed that if there had been left ventricular failure then there would have been pulmonary oedema which would have been noticeable in the healthy left lung. Professor Channer is of the view that the deceased’s complaints of breathlessness before his collapse are classic for pulmonary oedema and the chest X Ray taken on 17^th July 2016 (page 2222 of the trial bundle) reveals patchy airspace shadowing at the left midzone (of the lung). Dr Witte was dismissive of the diagnostic quality of X rays particularly a supine view of an unwell patient. Dr Knights the consultant pathologist who conducted the post-mortem concluded that there was acute ventricular failure but not because of a finding pulmonary oedema in the healthy left lung which was normal (page 632 of the trial bundle). He perhaps reached his view because he found no evidence of coronary artery thrombosis or myocardial infarction. Dr Witte disagrees with this diagnosis and points out that the hospital medical team were not treating the deceased for pulmonary oedema as they were continuing to give him fluids (100 ml per hour) and did not prescribe diuretics which would be the normal treatment for pulmonary oedema. Dr Atkinson the consultant anaesthetist responsible for the deceased’s treatment in the Intensive Care Unit opined that the cause of death was myocardial infarction caused by ischaemic heart disease the management of which condition was influenced by the mesothelioma as a contributory factor (page 638 of the trial bundle). He makes no mention of pulmonary oedema even though he presumably

Dr Witte points out that whilst the deceased was defibrillated both at the scene and in the ambulance after application of amiodarone he settled into sinus rhythm and his cardiac condition was stable thereafter. It was only after extensive anoxic brain damage was discovered that treatment was withdrawn. This is not consistent with left ventricular failure. Professor Channer points out that the deceased kept returning to ventricular tachycardia after being shocked until amiodarone was administered adding weight to his theory of scar related tachycardia but I conclude that the relatively stable cardiac condition shown by the deceased for the 24 hours after his admission is not consistent with left ventricular failure.

I therefore conclude that on balance the deceased did not suffer from pulmonary oedema and I am not satisfied that there was left ventricular failure. The evidence that the deceased’s heart condition (other than coronary artery disease) was deteriorating is not strong objectively. Whilst I have carefully considered the two competing theories, on balance I feel the theory put forward by Dr Witte is more likely. There was evidence of coronary artery disease which was worsening and Dr Witte has explained why evidence of a thrombotic event may not have been evident on post-mortem. The relative recovery of the deceased from a cardiac point of view in hospital is consistent with a transient thrombotic event creating a myocardial infarction which was successfully treated by defibrillation and medication. Professor Channer’s theory as developed at trial is in my view overly complex and by continuing to embrace the notion of left ventricular failure in the absence of convincing evidence of pulmonary oedema less convincing than Dr Witte’s explanation. I therefore decide the first issue that the cause of the deceased’s cardiac arrest was an acute ischaemic event triggering ventricular fibrillation as proposed by Dr Witte.

If the deceased had undergone CABG surgery in March / April 2015 would he have avoided the cardiac arrest in July 2016?

Professor Channer opined that there is a time lag for the benefits of coronary artery bypass graft surgery of about three years and accordingly the deceased would not have reached the stage of experiencing the benefit from surgery before he died. Even if the death had occurred in association with coronary artery disease the scientific evidence is that coronary artery bypass does not reduce the risk of death initially. There is a lag time of nearly three years before the survival curves separate indicating a benefit from surgery (Footnote: ¹). Because the deceased died less than two years after he would have undergone bypass surgery the effect of mesothelioma made no difference to his prospects of avoiding the fatal cardiac arrest which he experienced in July 2016.

Dr Witte accepted that all treatments, especially serious surgical interventions are associated with a lag time to benefit since each is associated with side effects or complications which are more common in those patients with more severe disease. The Kaplan-Meier survival curve relied on by Professor Channer described the survival rate of a population with a worse underlying heart condition than the deceased and with a range of co-morbidities not shared by the deceased. Dr Witte felt that the deceased would have benefitted much earlier than three years from the coronary bypass surgery.

Professor Channer’s opinion is based upon a study entitled “Coronary Artery Bypass Surgery in Patients with Ischaemic Cardiomyopathy” first published in the New England Journal of Medicine in April 2016. It sought to assess the survival benefit of a strategy of CABG added to guideline-directed medical therapy as compared with medical therapy alone, in patients with coronary artery disease, heart failure, and severe ventricular systolic dysfunction. The conclusion of the study was that the rates of death were significantly lower over ten years among patients who underwent CABG in addition to receiving therapy than those who received medical therapy alone. His conclusions can perhaps best be understood by considering certain graphs which were included as part of the study to illustrate the results:

Professor Channer relied on the first of the graphs reproduced above to show that whilst CABG improved mortality rates over the lifetime of the study (58.9% after bypass surgery compared with 66.1% in those treated medically only) the Kaplan Meier survival curves show that the improvement in survival occurred only after nearly three years following randomisation.

Dr Witte had several principled objections to this analysis, the first one being that the patients who were eligible for this trial were significantly unhealthier than the deceased. Patients were only eligible for this trial if they had coronary artery disease that was amenable to CABG and an ejection fraction of 35% or lower. Dr Witte considers that the deceased who had a stable ejection fraction of 45% could not have qualified to be part of the trial. In addition, there were patients who were part of the trial who had comorbidities not shared by the deceased which would have been poor prognostic indicators of mortality. The characteristics of the patients who were the subject of the test are revealed in the following table:

It can be seen from this table that there were several patients with diabetes (as did the deceased) but other complicating factors such as previous myocardial infarctions, hypertension, strokes, renal problems and current smokers (not shared by the deceased). The most significant distinguishing factor according to Dr Witte is that these were patients effectively in heart failure whereas the deceased’s condition was virtually stable (save for the coronary disease) based upon his EF of 45% and theirs of 35% or less.

It was also suggested that the graph which Professor Channer utilised was not the most accurate or appropriate from those published in the study. He used the primary outcome graph whereas the “as treated analysis” would produce a more accurate view of mortality rates because this analysis shows the results in accordance with the treatment they received, not determined by the sample group they were originally allocated to:

Another point made by counsel for the Claimant and endorsed by Dr Witte is that the time lag before the benefits of surgery are seen is caused by the increased mortality involved in surgery itself compared with medicine alone. Even the graph used by Professor Channer shows the very early increased mortality and the fact that once the mortality surrounding the original surgery is removed the death rate of the CABG

Professor Channer was not able to express any particular medical reason why it would take three years to see any benefit from CABG, for example that it would take that long for ischaemic heart tissue to re-vascularise. Dr Witte pointed out that heart surgeons find the operation very satisfying because the moment the clamp is removed it is possible to see the blood flowing freely into the heart whereas previously it had enjoyed interrupted flow due to stenosis of the vessels or arteries. Logically, once the obstruction is removed the heart will immediate benefit from an uninterrupted supply of blood which, if properly oxygenated, should prevent any further damage from anaemia. I was told that previously anaemic cardiac muscle may possibly recover if is re-vascularised provided the cells are not already dead. Both experts confirmed that a CABG operation tends to have an immediate benefit for patients in the removal of angina pectoris pain. These arguments were put to Professor Channer who merely pointed out that there was no improvement in the heart function at rest, which may be relevant to the removal of angina pectoris pain (which would only occur on exertion) but seems to ignore the benefit both of increased oxygenated blood supply to the heart and the re-vascularisation of ischaemic tissue.

The graph prepared by counsel for the Claimant was shown to Professor Channer but he said it was scientifically inappropriate to manipulate the figures in this way. The authors of the report may agree with that but I accept that the less than 10% of the 600 patients in the CABG group who died within 30 days may well be distorting the position if the court wishes to look at the graph to see if there would be any benefit to this particular deceased if he had been given the opportunity to have CABG surgery in early 2015. According to Dr Witte his chances of not surviving the operation were only 2.4 % and Professor Channer accepted that a bare statistical analysis would be no more than 4%. As he was overwhelmingly likely to survive the surgery in my view it is permissible to look at those patients who survived for longer than 30 days to establish whether his chances of survival would have increased if he had undergone CABG surgery 15 months before his death. The answer appears to be that his chances of survival would have been twice as good as without the surgery.

Even ignoring the statistical analysis a logical examination of what the surgery is intended to achieve leads to the conclusion that there are very likely to be early and significant benefits from CABG surgery, a proposition that Professor Channer did not seem able to accept. On balance, I prefer Dr Witte’s view that the deceased would have benefitted from surgery and the prospects of his suffering a cardiac arrest due to an acute ischaemic event would have been significantly reduced.

I therefore accept that there was a doubling of the risk of death due to the absence of CABG surgery caused by the deceased contraction of mesothelioma. Both counsel agreed that if I made this finding, I would inevitably find that the Defendant had caused or contributed to an indivisible injury, namely the arrhythmia, which caused the death of the deceased. This means the Defendant is liable in law for the death of the deceased and any consequences which flowed from that event even though there may have been other competing causes.

What was the deceased’s life expectancy had he not developed mesothelioma?

In his report dated December 2015 Dr Witte adopts what might be termed as the conventional approach in personal injury litigation when there are co-morbidities which might mean that it would be appropriate to deviate from the life expectancy of the population. He reduces the deceased’s expectation of life by two years because of his coronary artery disease, a further two years because of his diabetes and in his 2016 report he agreed to deduct a further two years to reflect the mild left ventricular failure. This would make the deceased’s life expectancy 19.5 years. Professor Channer does not criticise these individual discounts (although he may well have chosen to do so) but would prefer to approach the problem from a completely different perspective.

Professor Channer is critical of the method of discounting from the average population as used by Dr Witte which he describes as a retrospective assessment. It

In the case of the deceased Professor Channer says there are data on survival after triple bypass surgery in association with impaired left ventricular function, and in the presence of diabetes and atrial fibrillation and so it is possible to predict average survival from those data sets. The data from coronary artery bypass surgery suggest the mortality rate is 4% per annum (Footnote: ²). Patients with diabetes do better with CABG than without but still have double the mortality of those without diabetes (Footnote: ³). Generally, the lower the ejection fraction measured on echocardiography the higher the annual mortality (Footnote: ⁴). He also relied on the Velazquez study that I have referred to earlier which showed a mortality at 6 years of follow up after CABG of over 40%. On this basis Professor Channer calculates that if the deceased had not developed mesothelioma when he did he would have survived for about eight years after bypass surgery in 2015.

I had some assistance on this issue in the form of an expert report from Mr Chinu

I also had some assistance on this issue from Dr Robin Rudd the consultant chest physician. He accepted that on the issue of life expectancy he had deferred to Dr Witte in relation to the cardiac components of the assessment. He accepted that he had prospectively assessed the deceased actual life expectancy as result of the contraction of mesothelioma at between 3 – 9 months. He said that when life expectancy is very short the best way to approach it is by using the median survival period for patients with that condition coupled with any particular factors that might affect the individual patient. He accepted that Professor Channer’s method was a legitimate way to approach life expectancy for someone who had the characteristics of the study which was being used to fix the median. His view was that where there were multiple comorbidities it was more difficult to find a study which reasonably matched the patient under consideration and it was therefore more sensible to use the retrospective method and to make deductions from the normal life expectancy to reflect each factor. I gave him an example of dealing with a mesothelioma patient who smoked and he confirmed that he would deal with his theoretical life expectancy absent mesothelioma by the retrospective method making a deduction to reflect the additional health risks appropriate for patients who smoke.

Whilst I accept from what the experts have told me that both the prospective and retrospective methods of assessment are scientifically legitimate I reach the view that the prospective method is very much dependant on finding data or studies which accurately match the patient concerned. Where this is difficult, the retrospective method would appear to be more appropriate method, accepting as I do that it is very rough and ready method depending mainly on the clinical judgment of the physician making the assessment. The issue in this case then is whether the data relied on by Professor Channer are a close enough match to the deceased to mean that the prospective method of assessment is likely to be more accurate than the retrospective method.

I am satisfied that the studies relied on by Professor Channer prove the individual points that he wishes them to make but they are not wholly supportive, in my judgment, of his overall conclusion. For example, whilst the Weintraub paper quoted in paragraph 48 above does suggest a mortality rate of 4% per annum for CABG patients this would not lead to a 50% mortality in the population for 17 years. Similarly, whilst the Hlatky paper does show that CABG patients with diabetes do half as well as those who do not have diabetes the graph shown at paragraph 4.6 of

From this graph, it can be seen that the patients in the 43-52% category into which the deceased would have fallen have an annual mortality of about 4% when noncardiovascular causes are removed. One of the conclusions of the Solomon paper was:

“All cause mortality, cardiovascular death, and all components of cardiovascular death declined with increasing ejection fraction of 45%, after which the risk of these outcomes remained relatively stable with increasing LVEF”

The importance of the ejection fraction as a tool for assessing the condition of the heart is emphasised by this study.

The Claimant relies on a paper by Michael E Farkouh and others (Footnote: ⁵) which was a study about patients with diabetes and the relative benefits of CABG compared with percutaneous coronary intervention. The study found that CABG had a lower overall mortality rate which is perhaps best illustrated by the following table:

It against this background that I must consider Professor Channer’s reliance on the Velazquez paper that I considered in more detail in paragraphs 35-40 of this judgment. The concerns I explored about the applicability of that paper to the deceased are clearly relevant to the issue of life expectancy as well. The fact that the deceased had an LVEF of 45 % whereas all the patients in the study had an LVEF of less than 35% is clearly relevant particularly given the issues I have explored in the last few paragraphs. Professor Channer had to concede that the deceased could not have participated in the Velazquez trial because his LVEF reading was too high (and therefore he had better cardiac function than the subjects). Professor Channer was asked in cross-examination why he chose that study and he replied that it was recent and it was the study which was the best fit for the deceased constellations of problems. The difficulty with this argument is that all of the patients in that study had worse LVEF readings than the deceased and many of them had other co-morbidities that he did not have.

In my judgment, the prospective method of life expectancy can only be preferable to the retrospective method where the data or studies used to make the assessment are as near a fit as possible to the actual medical condition of the Claimant or deceased being assessed. In this case the constellation of the deceased’s symptoms and comorbidities mean that it is impossible to approach the prospective method of assessment with any real confidence given the material I have considered in the preceding paragraphs of this judgment. The retrospective method of assessment is a rough and ready approach based not upon scientific study but on clinical judgment of experienced and qualified practitioners. I doubt it is a method they use in their clinical practice but it is a genuine attempt to answer a question which lawyers put to them to assist the court in a way it can understand. In this case I prefer the retrospective method of assessment as put forward by Dr Witte for the reasons I have expressed.

Counsel for the Claimant submitted that it would be open to me to make a finding of life expectancy which is somewhere between the two estimates. This is tempting as my gut reaction is that Dr Witte’s estimate may be too optimistic whereas Professor Channer’s may be too pessimistic. I have however chosen a method of assessment which is reliant on the clinical experience and judgment of a properly qualified clinician. I have no experience or expertise in this area and I believe it would be wrong for me to substitute my view for his where I have no sound basis for doing so. I accordingly find that the deceased’s life expectancy, but for the mesothelioma would have been 19.5 years from the date of trial.

Counsel for the Defendant addressed me briefly about the application of the various tables when dealing with a fixed period of life expectancy but I got the impression that this would only be an issue if I preferred Professor Channer’s view about life expectancy. On this basis, I will merely say that I prefer the use of Table 1 of the Ogden Tables as adjusted for the reasons expressed by Mr Justice Cranston in paragraphs 40-43 of his judgment in Smith v LC Windows Fashions Ltd [2009] EWHC 1532 (QB).

The claim for dependency on the deceased’s services

In his first witness statement dated 18^th July 2015 the deceased stated:

“We also have a nice garden at the front and a large garden at the rear. I mainly take care of this and mow the lawn and look after the plants but I don’t know how I am going to do this now”

This suggests he had been mowing the lawn up to his mesothelioma diagnosis. His statement also suggested that he and the Claimant were planning on doing quite a lot of decorating and DIY in their new home. The Claimant had to concede however that prior to the mesothelioma diagnosis she was giving him a lot of personal care, up to 35 hours per week. She said “he could do a few things but very, very slowly” and she also agreed that he was incapable of decorating the house at this stage. Whilst I accept the deceased did mow the lawn at some point in the past I am not convinced he was doing this before his diagnosis of mesothelioma. The two questionnaires he completed in 2012 and 2014 reveal extensive disability such that the Claimant was awarded a carer’s allowance. In January 2014, he was asked if he could safely move 50 metres (page 715 of the trial bundle). His reply was:

“I cannot go any distance unless I take it slowly and stop for rests. Any kind of effort can bring on shortness of breath and chest pain. I do need a walking stick sometimes”

He was then asked about going up or down two steps and his reply was:

“I can manage two steps as long as I take it slowly. I can go upstairs ok but I usually have to stop and catch my breath a few times”

In my view these answers are not consistent with a man who is carrying out DIY decorating and gardening at home. The impression I got was that the Claimant was acting as the deceased’s full time carer before the diagnosis of mesothelioma and that she carried on doing just the same afterwards, albeit with the need to devote more time to his complicated medication regime. The burden of proof is on the Claimant and I am not satisfied on balance of probability that she has lost the benefit of the deceased services in any meaningful way as a consequence of his death.

Loss of partner’s care and attention

This claim is expressed simply in the schedule of special damages as follows:

“It is claimed that compensation should be awarded for loss of partner’s care and attention and an appropriate award under this heading is £4500 see Bath v Highgate [2004] EWHC 707 (Ch)”

This type of claim found its origins in Regan v Williamson [1976] 1 W.L.R. 305 where it was held that, in determining the pecuniary value to be put on the services of the deceased, acknowledgement should be given to the constant attendance of a mother on her children, and accordingly the value placed on such services should not be limited to a mere computation of the cost of services of a housekeeper less the cost of the deceased wife’s maintenance. So, too in Mehmet v Perry [1977] 2 All E.R. 529 an additional sum was awarded because “the children have lost the attention of their mother and …now have only one parent to look after them instead of two”. In the same case the husband was awarded a modest sum because he had lost the care and attention of his wife.

The development of this principle to widows and widowers in addition to children was recognised by Mr Justice Hamblen (as the then was) in Beesley v New CenturyGroup Ltd [2008] EWHC 3033 (QB):

Whilst recognising that awards of this nature have become commonplace in fatal accident claims Mr Justice Garnham in Mosson questioned the jurisprudential foundation for this type of claim:

“71.

I have had careful regard to these previous cases, in particular to the reasoning of Hamblen J and Mackay J. I take on board the fact that the making of awards of this sort has become increasingly commonplace. However I regret to say that, for two reasons, I find myself in disagreement with the conclusions of the other judges of this Court to whom I have referred. I can see no proper jurisprudential foundation for this claim.

72.

First, damages for personal injuries are intended, so far as money can achieve it, to put the claimant in the position he or she would have been in had the tort not occurred. But that is an art not a science, especially in the case of claims for future loss. There can be no precise equivalence in money terms of every loss that flows from an injury or a death. The Court fixes on a sum, often by reference to commercial costs, but recognises that that is unlikely to be a precise reflection of all the future consequences of the event. In the case of claims for services, the award is the Court’s best estimate of the value, rather than the cost, of the services lost.

73.

I have already made an award in respect of the services the deceased would have provided his family had he not contracted mesothelioma. I have done so by seeking to estimate the cost of providing commercially what would otherwise have been provided by the deceased. Obtaining services commercially, rather than from a member of the family, has both advantages and disadvantages. The disadvantages are those to which Mr Steinberg refers. But since few individuals, even caretakers, possess all the skills of all trades people, there are also advantages in having work carried out commercially. The work can be provided by specialist contractors at times that are convenient to the claimant; it may be of a better quality; its provision does not necessarily detract from other activities the family may wish to carry out. The award I have already made recognises both the advantages and disadvantages of having services provided commercially rather than by the deceased.

74.

In my judgment, there is no room here for an additional award for the loss of intangible benefits over and above the claim for the lost services.

75.

Second, what the claimant seeks is further financial compensation for the inconvenience of having to pay someone to do what her husband would have done voluntarily. In other words, she seeks financial compensation for what is a nonfinancial loss consequent upon her husband’s death. That, it seems to me, is a claim of the sort which bereavement damages were intended to cover.”

I recognise that these claims have become commonplace but I find myself in agreement with Mr Justice Garnham for the same reasons he gives. My personal view on the jurisprudential basis of this type of claim is however irrelevant in this case. This is a case where the deceased was unwell at the time he was diagnosed with mesothelioma. He was receiving personal care from the Claimant for at least 35 hours per week as he was too unwell to manage without that care. I have already found that his medical condition was such that he was unable to provide services such as DIY, gardening and decorating by 2014 and made no award for the loss of those services. As a consequence of this finding, even if a claim pursuant to Regan v Williamsoncould be validly made it could not be justified on the facts of this case as the deceased would not have been fit enough to do the various “jobs round the house” which formed the factual foundation for the successful claim made by the Claimant in Beesley v New Century Group Ltd. I have no doubt that the Claimant has lost the care

Counsel for the Claimant felt that Mr Justice Garnham had been led into error by claimant’s counsel in Mosson expressing the claim as “loss of intangible benefits” rather than loss of love and affection. It is clear however from my analysis above that the genesis of this claim is based upon the perceived advantages of having a service performed by a member of the family rather than a commercial provider (and compensation for that loss). If a claim was in fact put forward, simply for loss of love and affection, in my view it would fail for being encompassed in the bereavement award whichever school of thought prevails about claims pursuant to Regan vWilliamson.

For the reasons I have expressed I make no award for this head of loss.

Both counsel kindly indicated that if I ruled on the two outstanding issues in relation to quantum they would perform and agree a calculation of the Claimant’s claim which could be incorporated in an agreed order. I would like to express my thanks to them for this help and their assistance generally.

This Judgment will be handed down on a date to be fixed by the court in public. The time for appealing the Judgment shall not start to run until it is handed down. CPR Practice Direction 40E shall apply. If the parties can agree the form of an order and any consequential directions arising from this Judgment then the attendance of leading and junior counsel and solicitors will be excused.

The heart comprises four chambers: two upper collecting chambers (atria) and two pumping chambers (ventricles). Blood from the body enters the right atrium and flows to the right ventricle, from where it is pumped to the lungs. It returns to the left atrium, whence it passes to the left ventricle to be pumped into the aorta and round the body.

A cardiac cycle comprises the relaxation phase, diastole, during which the chambers fill passively, and the ejection phase, systole. In systole, the atria contract first, contributing about 20% to ventricular filling; the ventricles contract a fraction of a second later. The proportion of blood in the left ventricle (LV) which is ejected during systole is the ejection fraction (EF), normally around 55 to 70%.

Cardiac muscle fibres normally contract in unison. A state of uncoordinated contraction of the muscle fibres is known as fibrillation. Atrial fibrillation (AF) causes loss of the atrial contribution to ventricular filling and may lead to a rapid heart rate but is compatible with long-term survival. Ventricular fibrillation (VF) causes complete loss of cardiac output and death within minutes: it is one rhythm seen in cardiac arrest, the other being asystole (absence of any ventricular activity).

The heart itself is supplied with blood from the coronary arteries (left and right; the left divides after a short main stem into anterior descending and circumflex branches). Coronary artery disease (CAD; also ischaemic heart disease, IHD), in which the coronary arteries are narrowed (stenosed) by atheroma (fatty deposits in the walls), is a cause of angina (pain in the chest arising from inadequate oxygen supply to heart muscle). Angina usually occurs when the heart is called upon to work harder than normal, for example on exertion. The stenoses may be seen on coronary angiography, a procedure in which contrast medium is injected into the coronary arteries and a video x-ray taken. If a branch of a coronary artery becomes blocked, for example by rupture of an atheromatous plaque, the portion of heart muscle it supplies may die (myocardial infarction, MI) and be replaced by a scar. In coronary artery bypass grafting (CABG), vein is attached to the aorta and to the coronary artery, bypassing the narrowed section and improving distal blood flow. Arterial conduit may also be used.

IHD can cause diminution in function of the LV (left ventricular failure, or heart failure). The EF is diminished and the left ventricle dilates: the latter is reflected in an increased left ventricular end-diastolic diameter (LVEDD) seen usually on echocardiography (cardiac ultrasound). Increased pressures required to fill the failing LV can lead to fluid leaking into the lung (pulmonary oedema) and breathlessness.

Oxygen is carried in the blood bound to haemoglobin contained in the red blood cells. Only minimal quantities are dissolved in the plasma. A reduction in the haemoglobin concentration in the blood (anaemia) causes a proportionate reduction in the capacity of the blood to carry oxygen.