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The recently published article by Chan et al. questions the value of AAA screening.  We question the validity of the arguments and the data they use to support it, which we believe are either irrelevant or support the case for screening. Furthermore, the Chan et al. paper completely neglects the important equity gains that AAA screening can produce in the New Zealand (NZ) population.
Chan and his co-authors’ critique of AAA screening is based on 3 arguments: (i) patients with AAA are too sick with other comorbidities to benefit from screening and die of these other illnesses; (ii) most patients with AAA would be diagnosed by the health system anyway without a screening programme; and (iii) the size of the population that can benefit from screening is too small for it to be cost effective. Let us look more closely at each of these.
Co-morbidities in patients with AAA
The authors emphasise the point that co-morbidities in AAA patients might limit the benefit they attain from screening. They calculate that 77% of those dying of AAA had some other comorbidity. However, to imply that these were fulminant conditions and that preventing AAA death in this group would have been futile because they are moribund is highly misleading. The collection of co-morbidities includes: atrial fibrillation (a condition very prevalent in any elderly population), cardiovascular disease (CVD), also highly prevalent especially for Māori (which could range in severity f...
The authors emphasise the point that co-morbidities in AAA patients might limit the benefit they attain from screening. They calculate that 77% of those dying of AAA had some other comorbidity. However, to imply that these were fulminant conditions and that preventing AAA death in this group would have been futile because they are moribund is highly misleading. The collection of co-morbidities includes: atrial fibrillation (a condition very prevalent in any elderly population), cardiovascular disease (CVD), also highly prevalent especially for Māori (which could range in severity from stable angina or transient ischaemic attacks to severe stroke), diabetes (which in fact has a negative association with AAA ), bronchiectasis (which is acquired in childhood by many in NZ) and previous hip fracture (also a common event in the elderly and one which would not normally on its own be considered a contraindication to life-saving intervention).
Even for the 25.6% with “evidence of malignant cancer” the majority (24.5% of the 25.6%) were non-metastatic cancers and the group excludes two of the most lethal tumour sites (lung, upper gastrointestinal). The malignant cancer group would have included (among others): successfully treated malignant melanoma; chronic haematological malignancies that can remain in remission for many years; and non-metastatic prostate cancer, which is rarely lethal. Note that the five-year net survival in England at ages 55-74 for Stage 1-3 cancers of the anus, colon and rectum, urinary tract including kidney and bladder, liver, and thyroid, plus Hodgkin lymphoma, myeloma, and malignant melanoma (weighted by incidence) is 78%. 
Although the authors do not provide a general population comparison of the prevalence of the conditions listed in Table 2, they use the M3 co-morbidity index to argue that the AAA deaths had higher co-morbidities than the general population. The authors fail to countenance the possibility that this could be attributable to reverse causality: in a country without population screening, those with high co-morbidities are far more likely to have their AAA diagnosed than those with AAA and low co-morbidities. It would clearly be difficult for AAA not to be diagnosed in someone with stage 3 renal disease whose abdomen will almost certainly have been imaged by CT or ultrasound as part of the diagnostic work-up. And why compare morbidities in patients who have died from AAA rather than with patients who have been diagnosed with AAA but not died from it? Clearly patients who are dead are likely to have much higher rates of co-morbidity than age-matched peers who are still alive, no matter what the patient died of. Why not compare the co-morbidity index in patients diagnosed with colorectal cancer as a similar screening programme?
Other arguments in relation to co-morbidities in fact support the case for screening. Stating that “out of a group of people with AAA… there were eight times more deaths from other cardiovascular causes than AAA rupture” only serves to underline the high efficacy of modern treatment of AAA disease. They go on to say, “For people with known AAA, the absolute risk of AAA rupture resulting in death is actually low”. That is exactly why screening is effective in preventing those deaths.
The issue of co-morbidities becomes even less relevant if good systems exist to exclude patients with limited life expectancy or poor quality of life from participating in screening. We have piloted a screening programme based in primary care in Auckland, NZ that has ample scope to do just that. 
Capacity of the health system to diagnose AAA without a screening programme
A crucial element to Chan et al.’s case against AAA screening is that 31.3% of patients had been diagnosed prior to the acute event resulting in death. This implies that the vast majority – 68.7% – had not been diagnosed before their death and highlights how poor the existing health system is at identifying this treatable disease. Without doubt, a high proportion of deaths in the large undiagnosed majority (of this group) could have been prevented by diagnosis in a screening programme, not to mention all of those who died of AAA without the death being recorded as AAA (see below). And even so, this figure was calculated only in those patients with AAA as their primary cause of death, which is biased to those who had a known history of AAA.
In a country with no population screening many, perhaps even the majority of, AAA deaths will never be recorded as such because the underlying cause of death documented in sudden fatalities frequently relies on a person’s medical history. Sudden deaths in older people, particularly those with a history of CVD, are most often classified as ischaemic heart disease or stroke, and the autopsy rate in NZ, like many other Western countries, is now very low (approximately 13% of all deaths in 2010, but likely to be much lower in older age groups).  So just as those with AAA cited as the cause of death are more likely to have previously been diagnosed with AAA and more likely to have had prior aortic surgery, there is likely to be a significant degree of under-reporting of AAA deaths in people without a prior diagnosis of AAA in NZ, since death is more likely to be attributed to AAA in those who have a pre-existing diagnosis of AAA.
Even this low proportion of 31% with a prior AAA diagnosis exaggerates the extent that this might undermine the case for screening. Chan et al. fail to disaggregate the proportion of these cases that would have been diagnosed prior to screening, in which case they would be excluded as ineligible. Our screening pilots have now produced more accurate data on the prevalence of undiagnosed AAA in the NZ population. In just one large rural practice in the north of Auckland we identified 34 previously undiagnosed AAA screening 480 men and women using a risk-based algorithm (set at a threshold of 2%). Three of these undiagnosed aneurysms were large and at significant risk of imminent rupture.
The authors are remarkably sanguine about the likelihood that AAA will be diagnosed (and followed up) as an incidental finding in abdominal CT and ultrasound imaging. It has been our experience that when AAA is not the reason for abdominal imaging, the size of the abdominal aorta is often not examined and/or reported. Others are reported but not followed up by referral to either the patient’s general practitioner or the vascular service. Khashram et al’s NZ study of aneurysms detected through CT colonography noted that 65 of 223 (29.1%) were not reported and only 84 (37.6%) were in surveillance.  Similarly, Claridge et al, performed a retrospective audit of all abdominal CT scans in those over 50 years of age in the Otago Southland region of NZ in 2013-14.  Of the 187 AAA were identified, 35% were not documented on the original radiology report, including 48% of small (30-39mm) aneurysms. Having a prior diagnosis is manifestly no guarantee of adequate surveillance and treatment. Conversely, formal screening programmes provide the structure and quality control systems to ensure that diagnosed patients receive appropriate follow-up.
The lack of structured surveillance of patients diagnosed with AAA as an incidental finding may help to explain the fact that, according to Chan et al., 89.1% of those who died from AAA had not undergone surgical repair Given this high proportion it is surprising that the authors chose to focus on the small proportion who died with a previously repaired AAA, rather than the huge proportion who, for whatever reason, did not benefit from this highly effective procedure.
Size of benefit and cost-effectiveness
The third theme of Chan et al.’s paper is that AAA does not have a large population health benefit. They claim that “One of the primary objectives for screening for AAA is to reduce all-cause mortality at a population level”. In fact, the aim of screening for AAA is to produce a net benefit in those who are screened (at an acceptable cost), and in NZ at least, to reduce health inequities. AAA is a deadly but relatively uncommon disease that has high prevalence among groups with extensive exposure to tobacco smoke – as is the case for the indigenous Māori population in NZ, as we have ascertained in our recent AAA prevalence research. While there is legitimate debate about whether screening programmes should be required to demonstrate an impact on all-cause mortality , there is no doubt that existing programmes, which the authors have not gone on record to criticise, fail to meet their requirement in this regard. For example, evidence is lacking for an all-cause mortality benefit in screening colorectal cancer, a disease with a far higher incidence and mortality than AAA, and one where population screening programmes now exist in many countries, including NZ. The Cochrane Collaboration report on colorectal cancer screening found that “combining the four trials did not show any significant difference between the screening and control groups”.  Similarly breast screening may not even reduce breast cancer mortality. 
Contrast this with the finding from the most recently published meta-analysis of AAA screening “Invitation to AAA screening in ≥64-year-old men significantly reduced both all-cause and AAA-related mortalities.”  In fact, Chan et al. argue that instead of screening for AAA we should be “designing interventions to more directly improve systematic CVD risk management in primary care”. Their inconsistency is ironic given a recently published overview of system reviews of using cardiovascular risk scoring in routine risk assessment in primary prevention of CVD which noted that “none of the included [systematic reviews] reported changes in all-cause mortality” and it concluded that there is “a possible lack of effectiveness of [total risk assessment] in reducing CVD events and mortality, as well as a clinically insignificant influence on individual risk factor levels.” 
Space does not permit us to respond point by point to each of the authors’ comments on the cost-effectiveness of AAA screening. We note that of the numerous published studies of AAA screening cost-effectiveness, most of which have reported favourable ratios, a recent one examined it from a NZ perspective and concluded that “a UK-style AAA screening programme would be cost-effective in New Zealand.”  Crucially, their cost-effectiveness analysis did not assume that all participants with screen-detected AAA would receive what Chan et al call “the full benefit”; it accounted for not only co-morbidity and opportunistic detection, but also treatment failure, lower life expectancy in AAA cases, non-attendance at screening, complication costs and even unrelated healthcare costs. Rather than simply speculating about the negative impact that certain factors may have had, whilst ignoring the positive effect that others might have had (e.g. the life expectancy gain of almost 3 years in 65-year old men between 1999 and 2017 when the MASS trial ended recruitment),  it would have been more useful if Chan et al. had published their own cost-effectiveness estimates.
Other methodological flaws and inaccuracies
Chan et al. incorrectly suggest that there was evidence of rapidly falling prevalence of AAA prior to commencement of screening in the UK. There was evidence of falling rates of mortality and hospital admission, but not of prevalence. The authors have excluded the proportion of patients with an acute AAA presentation that died within 2 days of the admission which further reduces the number of AAA-related deaths in this analysis.
There is not a single mention of equity in the paper by Chan et al. and none of the published cost-effectiveness studies of AAA screening assign any value to the reductions in health inequities that AAA screening might produce. AAA, like lung cancer, places a disproportionate burden on specific ethnic groups and is also patterned by deprivation and gender. While AAA prevalence rates in 65 year old men in the UK range from 1.0-1.3%, in NZ Māori men it was 3.6% in our own study.  The Chan et al paper completely ignores the impact that differential access to primary care, diagnostics and surgery [15-17] contributes to the well-documented inequity in AAA outcomes for Maori compared to non-Māori. 
NZ has yet to take the steps required for elimination of unfair, avoidable and remedial health inequalities between its Indigenous and non-Indigenous populations. Such poorly thought through studies illustrate how deeply entrenched and unexamined bias against Māori creates and continues to maintain health inequities in New Zealand.
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