Switching statins
BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7554.1344 (Published 08 June 2006) Cite this as: BMJ 2006;332:1344
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Sir,
I read with interest the article by Moon and Bogle (1) concerning
statin prescriptions and possible savings. The research of cost-effective
therapies is to be applauded. However, some conclusions in this article
appear too simplistic and over-estimated, and therefore could generate
wrong therapeutic decisions. In particular, three points should be better
defined.
First, author declared that “simvastatin 40 mg and atorvastatin
20 mg are equally effective”. This is not totally correct, as demonstrated
both by randomized trials and meta-analyses. In fact, in the CURVES study
(2), atorvastatin 20 mg was better that simvastatin 40 mg in reducing LDL
cholesterol (LDL-C) after 8 weeks of therapy (-46% vs -41%). In addition,
the 3T study (3) entirely confirmed these data (-49% vs -44%) also after a
longer period of treatment (52 weeks). Interestingly enough, in this study
75% of patients randomized to simvastatin but only 55% of those randomized
to atorvastatin required the increment of drug dose in order to achieve
the LDL-C target. Finally, a large meta-analysis (4) published by Law et
al on your Journal and based on 164 randomized studies involving 24.000
pharmacologically-treated and 14.000 placebo-treated patients again
confirmed the advantage of atorvastatin 20 mg with respect to simvastatin
40 mg (-43% vs -37%).
Second, authors asserted that “changing atorvastatin
20 mg to simvastatin 40 mg should no effect on health”. Also this
declaration is not supported by scientific evidences. In fact, the CAPISH
study (5) a retrospective study specifically aimed to investigate the
cardiovascular effect of the switch from a simvastatin-based regimen to an
atorvastatin-based regimen demonstrated a statistically significant
improvement in the lipid profile (LDL-C, HDL-C and TG) after the switch,
with and higher number of patients who met the therapeutic goal. On the
contrary, one observational study (6) performed on 100
hypercholesterolemic patients showed that the switch from simvastatin to
atorvastatin may negatively affect lipid profile, with a reduction in the
percent of patients efficiently treated.
Third, authors stated that one
meta-analysis (carried out by the same authors) of clinical trials using
simvastatin 40 mg and atorvastatin 10 mg showed no differences in
mortality, CHD deaths, or stroke. However, this declaration doesn’t
reflect the entire scientific evidences, as authors missed to say that
another recent meta-analysis (7) based on 8 randomized trials reported
that atorvastatin on average produces a greater reduction in the incidence
of major vascular events (-39% vs -28% for coronary events; -32% vs -24%
for cerebvrovascular events).
In general, the assumption of equivalence between simvastatin and
atorvastatin raised by the authors is perhaps the main caveat of their
article, as this conclusion is far from the evidence based medicine. In
fact, results generated from trials involving atorvastatin and simvastatin
appear not easily comparable for several reasons, namely:
1) studies
involving atorvastatin are essentially primary prevention studies [ASCOT-
LLA (8), CARDS (9)], whereas those involving simvastatin are prevalently
secondary prevention trials [4S (10) and HPS (11)]. In fact, despite the
HPS was a combined study (primary prevention + secondary prevention),
however the 65% of the study population had documented cardiovascular
disease. Now, according to the well demonstrated linear relationship
between LDL-C reduction and event reduction, it is clear that the clinical
benefit may be greater in patients with an higher baseline absolute risk
(i.e. secondary prevention) than in patients with a lower baseline
absolute risk (i.e. primary prevention). Thus, it is conjecturable that
patients recruited in the simvastatin trials were patients more likely to
receive a clinical benefit from statin therapy.
2) It is established that
duration of therapy is an important determinant of the overall clinical
benefit generated by statin therapy. In fact, Law and colleagues4 showed
that a LDL-C reduction of 0.2-0.7 mmol/L may generate only a 6% risk
reduction in the first 2 years of therapy, but a stronger -21% after sixth
years. Now, considering that the above trials with atorvastatin were
stopped prematurely (3.3 years in the ASCOT-LLA study; 3.9 years in the
CARDS study) whereas the studies with simvastatin had an average duration
of about 5 years, we can speculate that the clinical benefit associated
with atorvastatin was underweighted by limited duration of therapy.
In addition, we should consider also that recent evidences in lipid-
lowering therapy focus on absolute LDL-C reduction rather than on specific
LDL-C targets (12). In fact, a recent meta-analysis (13) comparing
intensive statin regimen versus standard statin regimen in randomized
controlled trials showed that intensive therapy (mean LDL-C 75 mg/dL) may
generate an additional 16% reduction in the incidence of coronary death of
non-fatal myocardial infarction when compared with standard therapy (mean
LDL-C 101 mg/dL). Now, as simvastatin 40 mg generates on average a 37%
reduction in LDL-C,4 so it could not permit the best possible reduction of
coronary death in patients with a LDL-C greater that 150 mg/dL.
Finally, if we desire to have a therapeutic approach strictly
supported by evidence based medicine, in this case we should remember that
atorvastatin (14) but not simvastatin (15) was able to reduce ischemic
events in patients with acute coronary disease, and again that at this
time atorvastatin is the only statin which produced significant stroke
reduction in patients with previous stroke or TIA but not coronary artery
disease (16).
In conclusion, whereas a cost-effective approach is meritorious and
must be always pursued, however we should not immolate the evidence based
medicine in the name of saving, and a lack of evidence for equivalence
should not be translated into evidence of lack of difference.
1. Moon JC and Bogle RG. Switching statins. BMJ 2006; 332: 1344-5.
2. Jones P, Kafonek S, Laurora I, Hunninghake D. Comparative dose
efficacy study of atorvastatin versus simvastatin, pravastatin,
lovastatin, and fluvastatin in patients with hypercholesterolemia (the
CURVES study). Am J Cardiol 1998; 81: 582-7.
3. Olsson AG, Eriksson M, Johnson O, Kjellstrom T, Lanke J, Larsen
ML, et al. A 52-week, multicenter, randomized, parallel-group, double-
blind, double dummy study to assess the efficacy of atorvastatin and
simvastatin in reaching low density lipoprotein cholesterol and
tryglyceride targets: The Treat to Target (3T) Study. Clinical
Therapeutics 2003.
4. Law MR, Waid NJ, Rudnicka R. Quantifyng effect of statins on low
density lipoprotein cholesterol, ischaemic heart disease, and stroke:
systematic review and meta-analysis. BMJ 2003; 326; 1423.
5. Krasuski RA, Doeppenschmidt D, Henry JS, Smith PB, Adinaro J, Beck
R, et al. Conversion to atorvastatin in patients intolerant or refractory
to simvastatin therapy. The CAPISH study. Mayo Clinic Proc 2005; 80: 1163-
8.
6. Raal FJ. A single centre retrospective observational study to
evaluate the change in total cholesterol and LDL cholesterol in
hyperlipidaemic patients switched from atorvastatin to simvastatin.
Cardiovasc J South Afr 2004; 15:118-123.
7. Zhou Z, Rahme E, Pilote L. Are statins created equal?. Evidence
from randomized trials of pravastatin, simvastatin and atorvastatin for
cardiovascular disease prevention. Am Heart J. 2006; 151: 273-81.
8. Sever PS, Dahlöf B, Poulter N, Wedel H, Beevers G, Caulfield M, et
al. Prevention of coronary and stroke events with atorvastatin in
hypertensive patients who have average or lower-than-average cholesterol
concentrations, in the Anglo- Scandinavian Cardiac Outcomes Trial--Lipid
Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial.
Lancet. 2003;361:1149-58.
9. Colhoun HM, Betteridge D, Durrington PN, Hitman GA, Neil HAW,
Livingtone J, et al. Primary prevention of cardiovascular disease with
atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes
Study (CARDS): multicentre, randomized placebo-controlled trial. Lancet
2004; 364: 685-96.
10. Scandinavian Simvastatin Survival Study Group. Randomized trial
of cholesterol lowering in 4444 patients with coronary heart disease: the
Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 1383-89.
11. MRC/BHF Heart Protection Study of cholesterol lowering with
simvastatin in 20536 high risk individuals: a randomized placebo-
controlled trials. Lancet 2002; 360: 7-22.
12. Cannon CP, Braunwald E, McCabe CH, Rader DJ, Rouleau JL, Belder
R, et al. Intensive versus moderate lipid lowering with statins after
acute coronary syndromes. N Engl J Med 2004; 350: 1495-1504.
13. Cholesterol Treatment Trialist (CTT) Collaborators. Efficacy and
safety of cholesterol lowering treatment: prospective meta-analysis of
data from 90056 poartecipants in 14 randomized trials of statins. Lancet
2005, 366; 1267-78.
14. Schwartz GG, Olsson AG, Ezekowitz MD, Ganz P, Oliver MF, Waters
D, et al. Effects of atorvastatin on early recurrent ischemic events in
acute coronary syndromes. The MIRACL study: a randomized controlled trial.
JAMA 2001; 285: 1711-8.
15. de Lemos JA, Blazing MA, Wiviott SD, Lewis EF, Fox KA, White HD,
et al. Early intensive versus a delayed conservative simvastatin strategy
in patients with acute coronary syndromes. Phase Z of the A to Z trial.
JAMA 2004; 292: 1307-1316.
16. Amarenco P, Bogousslavsky J, Callahan A 3rd, Goldstein LB,
Hennerici M, Rudolph AE, et al. High-dose atorvastatin after stroke or
transient ischemic attack. N Eng J Med. 2006; 355: 549-59.
Competing interests:
None declared
Competing interests: No competing interests
With regard to the editorial by Moon and Bogle (1) that reported how
using generic simvastatin as first line could save £2bn over five years
in England, we have some comments to the authors :
First, no data exist showing that statin treatment decreases the risk
of stroke among patients with a history of stroke or TIA with except of
SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels)
trial (2) that reported how in patients with recent stroke or TIA and
without known coronary heart disease, 80 mg of atorvastatin per day
reduced the overall incidence of strokes and of cardiovascular events ;
Second, primary prevention of cardiovascular risk in patients with
diabetes is based on evidence showing a significant reduction after
treatment with simvastatin 40 mg of this disorder in 2912 patients with
diabetes and no previous occlusive vascular disease in the HPS (Heart
Protection Study) (3), but CARDS(Collaborative Atorvastatin Diabetes
Study) study (4)showed that with atorvastatin 10 mg risk reduction in
major cardiovascular disease is larger (-36%) than the point estimates
seen in HPS (-31%) and that the average difference in LDLcholesterol
between treatment groups was with 1•20 mmol/L in comparison with 0•9
mmol/L of the HPS ;
Third, economic evaluation by Bloom and Bogle disagree with a
recent Spanish pharmacoeconomic analysis that showed that atorvastatin was
the most cost-effective treatment in the achievement of the NCEP (National
Cholesterol Education Program) ATP III (Adult Treatment Panel III), LDL-C
reduction objectives in patients with high (<_100 mg="mg" dl="dl" and="and" moderate="moderate" _130="_130" risk="risk" of="of" coronary="coronary" heart="heart" disease="disease" chd="chd" with="with" a="a" cost="cost" per="per" patient="patient" euro="euro" _747="_747" _405="_405" year="year" respectively="respectively" _5="_5" when="when" compared="compared" pravastatin="pravastatin" fluvastatin="fluvastatin" simvastatin.="simvastatin." finally="finally" generic="generic" drug="drug" is="is" the="the" term="term" used="used" for="for" products="products" that="that" contain="contain" same="same" medicinal="medicinal" ingredients="ingredients" as="as" original="original" brand="brand" name="name" but="but" which="which" are="are" generally="generally" cheaper="cheaper" in="in" price.="price." neverthelss="neverthelss" nonmedicinal="nonmedicinal" can="can" be="be" different="different" from="from" those="those" brand.="brand." normally="normally" manufacturers="manufacturers" have="have" to="to" provide="provide" studies="studies" prove="prove" effectiveness="effectiveness" has="has" not="not" changed.="changed." p="p"/> So before suggesting switching to generic simvastatin, it would
be more cautious to wait for studies that prove a comparable
effectiveness of the generic drug in terms of reduction of cardiovascular
events.
On this basis, did Blom and Bogle forget any important variables before
suggesting this switch ?
References
1.Switching statins.Moon JC, Bogle R.Using generic simvastatin as
first line could save £2bn over five years in England. BMJ 2006;332:1344–5
2.The Stroke Prevention by Aggressive Reduction in Cholesterol Levels
(SPARCL) Investigators*High-Dose Atorvastatin after Stroke or Transient
Ischemic Attack. N Engl J Med 2006;355:549-59.
3.Heart Protection Study Collaborative Group. MRC/BHF Heart
Protection Study of cholesterol-lowering with simvastatin in 5963 people
with diabetes: a randomised placebo-controlled trial. Lancet 2003; 361:
2005–16.
4.Colhoun HM, Betteridg DJ. Durrington PN, Hitman GA et al. Lancet
2004; 364: 685–96. Primary prevention of cardiovascular disease with
atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes
Study (CARDS): multicentre randomised placebo-controlled trial . Lancet
2004; 364: 685–96.
5.Plans-Rubio P. Cost-effectiveness analysis of cholesterol-lowering
therapies in Spain. Am J Cardiovasc Drugs. 2006;6(3):177-88.
Competing interests:
None declared
Competing interests: No competing interests
In their editorial Moon and Boogle have referenced the 3T study
saying a head to head comparison of atorvastatin and simvastatin, although
underpowered, showed no difference between the drugs. Although the first
statement that the study was underpowered is true as it had only 552
patients randomized to receive atorvastatin and 535 randomized to receive
simvastatin. However it is not entirely accurate to say that it showed no
difference between the two drugs. According to the 3T Study[1] abstract
the patients in the trial were started on once-daily oral treatment with
20 mg atorvastatin or 20 mg simvastatin The dose was doubled after 12
weeks if the target National Cholesterol Education Program level of LDL-C
(2.6 mmol/L [100 mg/dL]) was not reached at 8 weeks. Fewer atorvastatin
patients needed to have their dose doubled; nevertheless more atorvastatin
patients reached the LDL-C target after 52 weeks (61% vs 41%; P <
0.001).
The authors have mentioned in their editorial that an alternative
(Pravasatin)may be needed for patients who do not meet their target LDL-C
and Triglyceride level with Simvastatin. Atorvastatin although costly
might still provide a good alternative for these patients.
[1](Olsson AG, Eriksson M, Johnson O, Kjellstrom T, Lanke J, Larsen
ML, et al. A 52-week, multicenter, randomized, parallel-group, double-
blind, double-dummy study to assess the efficacy of atorvastatin and
simvastatin in reaching low-density lipoprotein cholesterol and
triglyceride targets: the treat-to-target (3T) study. Clin Ther 2003;25:
119-38)
Competing interests:
None declared
Competing interests: No competing interests
EDITOR - The June 10 issue of BMJ contained an editorial by J. Moon
and R. Bogle (1) entitled “Switching statins”. The editorial claims that
simvastatin 40 mg has the same lipid lowering effect as 10-20 mg
atorvastatin. However, the trials cited found atorvastatin superior to
simvastatin in lowering LDL-C. Therefore, the suggestion to replace
atorvastatin 10-20 with simvastatin 40 might not be appropriate since
clinical evidence points to the advantage of lowering cholesterol as far
as possible (2).
The editorial mentions a meta-analysis by the authors, based on RCT using
simvastatin 40 and atorvastatin 10, which found no difference between the
two molecules as regards total mortality, fatal coronary disease or
stroke. It is worth noting that in populations with stable ischemic heart
disease, clinical trials testing long-term statins, even at high doses,
have not found any reduction in cardiovascular mortality considered alone;
this might be because of the numbers of events. They did, however, find a
reduction in fatal and non-fatal events cumulatively (3).
The evidence of equivalence, therefore, mentioned in the editorial does
not appear comparable, as the trials with atorvastatin 10 mg (ASCOT-LLA
and CARDS) were in primary prevention, whereas those with simvastatin (4S
and HPS) were mainly for secondary prevention. Then there is also the
question of the duration. Both CARDS and ASCOT-LLA had a shorter median
follow-up than 4S and HPS (3.9 vs. 5 years). We have, however, to note
that the effect, in terms of reduction of events, rises with the duration
of treatment.(4)
It therefore seems clear that combining various studies with differences
in design, duration and types of patient is not really correct from the
methodological point of view, and is an inappropriate basis for guidelines
for clinical practice. The suggestion that one statin should automatically
be used in place of another, on the basis of equivalence that has not
really been demonstrated, is quite likely to be a source of harm to
patients, requiring them to return to their previous therapy, but with the
additional costs for seeking and correcting the damage.
REFERENCES
1. Moon JC, Bogle RG. Switching statins. BMJ 2006;332:1344-5.
2. Cannon C P, Braunwald E, McCabe C, Rader D J, Rouleaua J L, Belden R,
et al. Intensive versus moderate lipid lowering with statins after acute
coronary syndromes.
N Engl J Med 2004;350:1495-1504
3. Pedersen TR, Faergeman O, Kastelein JJP, Olsson AG, Tikkanen MJ, Holme
I, et al. High-Dose Atorvastatin vs Usual-Dose Simvastatin for Secondary
Prevention After Myocardial Infarction. The IDEAL Study: A Randomized
Controlled Trial. JAMA 2005; 294:2437-2445
4. Law MR, Wald NJ and Rudnicka A R. Quantifying effect of statins on low
density lipoprotein cholesterol, ischaemic heart disease, and stroke:
systematic review and meta-analysis. BMJ 2003;326:1423
Competing interests:
None declared
Competing interests: No competing interests
I read the article by Moon and Bogle with great interest as I had
been switched from atorvastatin to simvastatin when I registered with my
new GP. I experienced significant side effects of muscle pains and
stiffness, tiredness and interference with libido in spite of careful
titration downwards. After a few months, I asked my GP to put me back on
atorvastatin and the side effects vanished quickly. I now look forward to
becoming old enough to relinquish statins altogether, thus saving the NHS
some costs.
It may be worth offering a warning about side effects that could
well impede compliance.
Competing interests:
None declared
Competing interests: No competing interests
The leading article on "Switching Statins" 1 makes a powerful case
for the use of generic simvastatin both in primary and secondary care. We
support the concept that statin treatment, when indicated, should be
initiated with generic simvastatin, because of its extensive evidence base
and lengthy clinical usage, and the marked cost difference compared to the
other statins, which are still on patent. What the article fails to
address is the requirement to achieve reductions to target levels,
especially in the field of secondary prevention. The recent recommendation
of the Joint British Societies is that the total cholesterol level should
be brought down to <_4 mmol="mmol" l="l" and="and" the="the" ldl-cholesterol="ldl-cholesterol" to="to" _2="_2" _2.="_2." p="p"/>Simvastatin 40mg reduces total cholesterol levels by 23-33% 3 and so in
those patients with an initial cholesterol of >6 mmol/l the probability
that such monotherapy will achieve evidence based targets is <_50. p="p"/>This includes almost all patients with familial hypercholesterolaemia, and
many with polygenic dyslipidaemia as well. For these patients it is
important that there is still access to more potent statins such as
atorvastatin or rosuvastatin, with or without ezetimibe. In addition,
there is an argument that more potent statins may deliver additional
benefits in the longer term 3.
References
1. Moon JC, Bogle RG. Switching statins. Br Med J 2006;332:1344-5.
2. JBS2: Joint British Societies’ guidelines on prevention of
cardiovascular disease in clinical practice. Heart 2005;91[Suppl.V]:38.
3. Davies A, Hutton J, O'Donnell J, Kingslake S. Cost-
effectiveness of rosuvastatin, atorvastatin, simvastatin, pravastatin and
fluvastatin for the primary prevention of CHD in the UK. Br J Cardiol
2006;13:196-202.
Paul Nicholls
Hon. Professor of Medicine
Consultant Physician, Royal Victoria Hospital, Belfast
Ian Young
Professor of Medicine
The Queen’s University of Belfast
Competing interests:
None declared
Competing interests: No competing interests
Within Angus Community Health Partnership, which comprises 16 GP
practices and covers a population of 105,000 we have been actively
promoting the use of generic simvastatin as first line choice for patients
for over two years now. This decision was reached by the Medicines
Management Group due to the compelling evidence base and financial
arguements that have been well rehearsed in other responses.
Without pursueing a policy of active switches (which we are now
carrying out a risk/benefit analysis on) we have managed to increase the %
of generic simvastatin as a % of all equivalent statins from 65% in March
2004 to 74% in December 2005. Similar figures for a neighbouring
organisation who did not actively pursued this policy are 67% and 69%
respectively. Our performance in relation to GMS is no worse than our
neighbour and I ma not aware of any detrimental effect on admission rates
for CHD events
Up until now we have taken the view that switching of patients
already stable, and showing an apprioriate clinical response should be
avoided wherever possible but as indicated above, we are now reviewing
this position.
Competing interests:
Part of my role is to ensure the safe and effective use of medicines within available budgets
Competing interests: No competing interests
Duerden has highlighted that a number of prescribers firmly believe
that the optimum total and LDL cholesterol targets recommended in the
Joint British Societies’ revised guidelines on cardiovascular disease
prevention (JBS 2) should be adopted [1]. The affordability of doing so
seems questionable, given that it would entail giving many people
atorvastatin >20mg/day or other drugs that are more expensive than
generic simvastatin but not currently supported by outcome evidence on
cardiovascular events or mortality. If 5.2 million people in England are
now candidates for statin treatment [2] the drug cost of treating them for
1 year (using prices from the June 2006 Drug Tariff) would be:
£286 million if all take simvastatin 40mg daily
£1,096 million if half take simvastatin 40mg daily and half
atorvastatin 40mg daily.
NICE expects to issue a clinical guideline on modification of blood
lipids in December 2007. In light of JBS 2 it would be desirable to have
a clear national policy on target cholesterol concentrations much sooner.
In particular, in our view, it would be inappropriate for the cholesterol
targets in the GMS contract’s quality and outcomes framework to be brought
into line with JBS 2 targets without consideration by national policy
makers of the answers to the following questions:
- How many people taking a statin need to achieve JBS 2 cholesterol
targets rather than coronary heart disease National Service Framework
(NSF) targets to avoid one cardiovascular event or one death in a
specified period?
- What is the incremental cost per quality adjusted life year (QALY)
associated with achieving the JBS 2 cholesterol targets rather than the
NSF targets, given the available evidence on the rate of non-compliance
with statin treatment [3, 4]?
- What would be the total cost of achieving the JBS 2 cholesterol
targets rather than the NSF targets in all 5.2 million people considered
to be eligible for statin treatment and is this affordable?
1. Duerden M G. Switching statins works with ‘an adequate dose’ but
not ‘target chasing’. BMJ rapid response
http://bmj.bmjjournals.com/cgi/eletters/332/7554/1344 (accessed 15 June
2006)
2. Moon J C, Bogle R G. Switching statins. BMJ 2006; 332: 1344-5.
3. Jackevicius C A, Mamdani M, Tu J V. Adherence with statin therapy
in elderly patients with and without acute coronary syndromes. JAMA 2002;
288: 462-7.
4. Blackburn D F, Dobson R T et al. Adherence to statins, beta-
blockers and angiotensin-converting enzyme inhibitors following a first
cardiovascular event: a retrospective cohort study. Can J Cardiol 2005;
21: 485-8.
Competing interests:
All authors are tax payers and work for the NHS. CC and HM work to contain prescribing expenditure within budgets.
Competing interests: No competing interests
Dear Sir
Your previous correspondents demonstrate learning and ability which
eclipse mine as a rural general practitioner.
A rather more potent influence to general practitioners using statins
other than simvastatin is the tyranny of "treating to target(s)". Evidence
based medicine as thoughtfully demonstrated by Sackett over three decades
will fail, when the over-riding concern of the general practitioner will
only be to achieve cholesterol targets decreed by central government.
Readers of the British Medical Journal outwith the United Kingdom,
and even UK based hospital readers, may not realise that the Department of
Health runs a "name and shame" campaign by publicising those miscreant
general practitioners who fail to achieve prescribed targets.
British general practice has deteriorated to such an extent that the
Chairman of the Royal College of General Practitioners claimed to have
been misunderstood recently by readers of The Times and listeners to BBC
Radio, when he suggested that GPs' target "achievements" should be
advertised to the general public by rosettes, somewhat akin to Michelin
stars for restaurants.
Bogle's editorial should be commended for its clear syntax and
message.
Michael G Bamber
Competing interests:
I have received honoraria from Astra Zeneca in relation to advice on design of GP meetings
Competing interests: No competing interests
Response to prof. Cipollone: mortality versus 'event' based cardiology.
Professor Cipollone may well be right in his Dec. 5, 2006, eBMJ
response that atorvastatin is the only statin to have shown a benefit in
repeat stroke but he somewhat misrepresents his reference 16, the SPARCL
study, where a total stroke decrease was marred by an increase in
hemorrhaging stroke and a numerical increase in on-drug deaths.
We may forever argue 'event' benefit and 'lipid goals' but we would
argue instead that atorvastatin has now conclusively shown not to reduce
overall deaths in anyone with or at high risk of vascular disease. THAT
is the bottom line based on the combined outcomes of ASCOT and SPARCL with
about 28,000 on-drug patient-years and a mortality difference of 22 over
placebo, with numbers needed to treat well over 1000, drug costs well over
one million dollars per death and a probability of saving any patient's
life in the realm of wishful thinking.
Competing interests:
no conflict by either author
Competing interests: No competing interests