Medical Clinic II-Department of Cardiology, Angiology and Intensive
Care Medicine, University Heart Center Luebeck, University of Luebeck,
Luebeck, Germany
Medical Clinic II-Department of Cardiology, Angiology and Intensive
Care Medicine, University Heart Center Luebeck, University of Luebeck,
Luebeck, Germany
Corresponding author:
Georg Fuernau, M.D.
Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine)
University Heart Center Luebeck
University Hospital Schleswig-Holstein, Ratzeburger Allee 160
23538 Luebeck, Germany
Mail: georg.fuernau@gmx.at
Tel.: +49 451 500 2501; Fax: +49 451 500 6437
We read with great interest the manuscript by Park and co-workers
published epub ahead of print in Heart [1]. The authors investigated an
important and controversial issue, interventional treatment of multi-
vessel disease in patients with cardiogenic shock complicating acute
myocardial infarction. Yet, we have some concerns if the population
studied in this manuscript reflects a population with real cardiogenic
shock. Although using established definitions for cardiogenic shock
(systolic blood pressure <90 mmHg for >30 min or the need for
supportive management to maintain systolic blood pressure >90 mmHg and
evidence of end-organ hypoperfusion) the one-year mortality (~16%) in the
study by Park et al. was much lower than in all other studies
investigating cardiogenic shock. In other trials mortality rates of 50% up
to 63% after 1 year were reported [2, 3]. Therefore, we believe that the
population studied is a cohort at minor risk and the results cannot be
extrapolated to patients with severe cardiogenic shock. Furthermore, the
discussion is slightly selective with not all trials being cited comparing
multi-vessel versus culprit lesion only PCI in cardiogenic shock. The
current evidence has recently been reviewed [4]. To clarify the important
question of multi-vessel vs. culprit lesion percutaneous coronary
intervention in patients with cardiogenic shock complicating myocardial
infarction a randomized European multi-center study is currently
recruiting patients (Culprit Lesion Only PCI Versus Multivessel PCI in
Cardiogenic Shock - CULPRIT-SHOCK; ClinicalTrials.gov Identifier:
NCT01927549).
Conflict of Interest:
None declared
References
1 Park JS, Cha KS, Lee DS, et al. Culprit or multivessel
revascularisation in ST-elevation myocardial infarction with cardiogenic
shock. Heart 2015. pii: heartjnl-2014-307220. doi: 10.1136/heartjnl-2014-
307220. [Epub ahead of print].
2 Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon
counterpulsation in acute myocardial infarction complicated by cardiogenic
shock (IABP-SHOCK II): final 12 month results of a randomised, open-label
trial. Lancet 2013;382:1638-45.
3 Aissaoui N, Puymirat E, Tabone X, et al. Improved outcome of
cardiogenic shock at the acute stage of myocardial infarction: a report
from the USIK 1995, USIC 2000, and FAST-MI French nationwide registries.
Eur Heart J 2012;33:2535-43.
4 Thiele H, Ohman EM, Desch S, et al. Management of cardiogenic
shock. Eur Heart J 2015. pii: ehv051. [Epub ahead of print].
Dear Editor
Gholap et al confirmed a surprising observation that South Asians,
compared to White British populations, have lower or similar, rather than
higher mortality, following myocardial infarction, as Fischbacher et al
first demonstrated in Scotland.(1;2) As the chief investigator of that
Scottish study I found the result perplexing given South Asians' high
prevalence of type 2 diabetes. A literature review showed...
Dear Editor
Gholap et al confirmed a surprising observation that South Asians,
compared to White British populations, have lower or similar, rather than
higher mortality, following myocardial infarction, as Fischbacher et al
first demonstrated in Scotland.(1;2) As the chief investigator of that
Scottish study I found the result perplexing given South Asians' high
prevalence of type 2 diabetes. A literature review showed the mortality
following MI in Scottish South Asians was similar to international reports
and concluded that White Scottish people had unusually high post-MI
mortality.(2) This showed how studies on minorities may, paradoxically,
throw light on health of the majority.
Possibly, compared to White Scottish people, South Asians may have
having smaller, less lethal MIs given their tendency to diffuse
atherosclerosis. We hypothesised that South Asians may reach hospitals
quicker than the White Scottish populations given they tended to live in
the inner city. Given heterogeneity in South Asian populations (Indians,
Pakistanis; men, women) we were keen to disaggregate them. We have
published our results, and they show further surprises. The survival
following MI was, compared to White Scottish people, similar in Indian men
and women, but better in Pakistanis, especially women. Our conclusions
were unaltered by adjustment for socio-economic factors, travel times,
hospitalisation for diabetes, or cardiovascular procedures. We had no
cardiovascular risk factor data but Gholap et al's data show these are not
explanatory.
The results are reassuring from a clinical and public health
perspective but they remain surprising. Possibly, they relate to lower
cardiovascular risk factors over a lifetime, as many of South Asians came
to the UK as adults having had little exposure to risk factors when young.
It will be interesting to see whether the new generations of South Asians
will also enjoy this 'protection', given their lifelong exposure to
cardiovascular risk factors and a high risk of diabetes.
In the Netherlands ethnic minority groups (defined by parental and
own birthplace) have relatively worse outcomes, with gaps increasing over
time.(4) Overall, in the UK we can be proud of these results as they
reflect, at least partially, equitable health care.
Reference List
1 Gholap NN, Khunti K, Davies MJ, Bodicoat DH, Squire IB. Survival in
South Asian and White European patients after acute myocardial infarction.
Heart 2015; 101/8: 630-636.
2 Fischbacher CM, Bhopal R, Povey C, Steiner M, Chalmers J, Mueller G et
al. Record linked retrospective cohort study of 4.6 million people
exploring ethnic variations in disease: myocardial infarction in South
Asians. BMC Public Health 2007; 7/1: 142.
3 Bansal N, Fischbacher CM, Bhopal RS, Brown H, Steiner MF, Capewell S et
al. Myocardial infarction incidence and survival by ethnic group: Scottish
Health and Ethnicity Linkage retrospective cohort study. BMJ Open 2013;
3/9.
4 van Oeffelen AAM, Agyemang C, Stronks K, Bots ML, Vaartjes I. Prognosis
after a first hospitalisation for acute myocardial infarction and
congestive heart failure by country of birth. Heart 2014; heartjnl-2013.
We have read with interest the article by Choi and colleagues
entitled "Myocardial fibrosis progression on cardiac magnetic resonance in
hypertrophic cardiomyopathy" published on Heart" (1).
In this study, the Authors evaluated the increment of the extent of late
gadolinium enhancement (LGE) in patients with hypertrophic cardiomyopathy
(HCM). This study reproduces our previous paper entitled "Progression of
myocardial fi...
We have read with interest the article by Choi and colleagues
entitled "Myocardial fibrosis progression on cardiac magnetic resonance in
hypertrophic cardiomyopathy" published on Heart" (1).
In this study, the Authors evaluated the increment of the extent of late
gadolinium enhancement (LGE) in patients with hypertrophic cardiomyopathy
(HCM). This study reproduces our previous paper entitled "Progression of
myocardial fibrosis assessed with cardiac magnetic resonance in
hypertrophic cardiomyopathy", published in 2012 (2) and cited in the
current ESC guidelines for HCM.
Choi found a fast progression of fibrosis in HCM, confirming our previous
results.
However, there are some differences between the studies that deserve a
discussion.
Choi and colleagues used a cut-off of >4% of LGE to assess the
increment of fibrosis, whereas we used a cut-off of ?1 gram increment.
In HCM the left ventricular mass may change significantly from the
baseline to the follow-up magnetic resonance and a change in % of
ventricular mass may not necessarily be consequence of a real increase in
LGE but only secondary to variation of left ventricular mass.
We found that apical HCM had higher LGE rate of progession, but this
was not found by Choi who underlines this difference asserting that
our"results are in clear contrast with common belief that the prognosis of
apical HCM is generally good". However, in both studies the prognosis was
not evaluated and the populations are different because Choi and
colleagues excluded apical HCM with apical anuerysm. Apical anuerysms may
be the evolution of the fast progression of LGE in apical HCM and are
associated to worse prognosis (3). Yet, there are some recent evidences
demonstrating the worse prognosis of apical HCM than other patterns of
hypertrophy in caucasian patients (4). European and Asiatic apical HCM
might be different diseases, with similar phenotype but different rate of
progression of LGE and maybe prognosis. Unfortunately, because of the lack
of genotype in both the studies, we cannot assess whether the different
rate of LGE progression between the two populations of apical HCM is
secondary to geographical/ethnic differences or to a selection bias
performed by the Authors.
References
1. Choi HM, Kim KH, Lee JM, Yoon YE, Lee SP, Park EA, Lee W, Kim YJ, Cho
GY, Sohn DW, Kim HK. Myocardial fibrosis progression on cardiac magnetic
resonance in hypertrophic cardiomyopathy. Heart. 2015;101:870-876.
2. Todiere G, Aquaro GD, Piaggi P, Formisano F, Barison A, Masci PG,
Strata E, Bacigalupo L, Marzilli M, Pingitore A, Lombardi M. Progression
of myocardial fibrosis assessed with cardiac magnetic resonance in
hypertrophic cardiomyopathy.J Am Coll Cardiol. 2012;60:922-929.
3. Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR,
Udelson JE, Ackerman MJ, Maron BJ.Prevalence, clinical significance, and
natural history of left ventricular apical aneurysms in hypertrophic
cardiomyopathy. Circulation. 2008;118:1541-1549
4. Klarich KW, Attenhofer Jost CH, Binder J, Connolly HM, Scott CG,
Freeman WK, Ackerman MJ, Nishimura RA, Tajik AJ, Ommen SR.Risk of death in
long-term follow-up of patients with apical hypertrophic cardiomyopathy.
Am J Cardiol. 2013;111:1784-1791
We read the paper of Bhatnagar P. et al. 1 and were impressed by
great success of the UK health care on control of cardiovascular disease
(CVD). In the UK during last decade, CVD decreased from top to 2nd row on
mortality of men in whom, lipid lowering drugs were the most prescribed
medicine. 1 In this report, importance of primary care and increased
number of less invasive approaches like angioplasty compared to surge...
We read the paper of Bhatnagar P. et al. 1 and were impressed by
great success of the UK health care on control of cardiovascular disease
(CVD). In the UK during last decade, CVD decreased from top to 2nd row on
mortality of men in whom, lipid lowering drugs were the most prescribed
medicine. 1 In this report, importance of primary care and increased
number of less invasive approaches like angioplasty compared to surgery
were pointed out. We compared some data here with performance-based
procedure-dependent income model for physicians in Turkey during the last
decade. All individuals can apply to a tertiary hospital since absence of
compulsory referral system in this model.
Decreased number of referred patients may not eliminate low risk
group and high risk patients may not be treated effectively, then more
severely ill patients may be detected in a vicious circle. Since the
health autority has started to act in 2002, the number of refered patients
from primary care has decreased and operations has increased from 22 %,
1.598.362 to 3 %, 4.684.237 respectively in 2013. 2 Nevertheless, CVD
continues to be the biggest killer in Turkey. In this model, increased
applications may be seen as a profitable investment. In fact, the total
number of private hospitals has gradually increased from 271 in 2002 and
to 550 in 2013 in Turkey. 2 Interestingly, instead of encouraging
preventive approach, it was tried to settle a mandatory on call
arrangement for primary care physicians differently from UK. Fortunately,
that was blocked by social consciousness.
Limited time for diagnostic tests in Turkish model may be a
disadvantage for prevention of organ damage in hypertension. One of five
patients with previously undiagnosed hypertension, the leading risk for
CVD is associated with subclinical target organ damage including cardiac
remodelling. 3 Early determination of cardiac remodelling and exercise
hypertension have gained more importance, 4 however, they may be ignored
in clinical practice. Exercise hypertension may be missed even in large
national registiries, therefore, we recently have mentioned its importance
in healthy individuals who develope early cardiac remodelling in British
registry (LARGE). 4
1. Bhatnagar P, Wickramasinghe K, Williams J, et al. The epidemiology
of cardiovascular disease in the UK 2014. Heart 2015;0:1-8.
doi:10.1136/heartjnl-2015-307516.
2. Kose MR, Basara BB, Guler C, Yentur GK. Turkish Republic, Ministry of
Health. Annual Health Statistics, Ankara, 2013.
3. Korhonen PE, Kautiainen H, Jarvenpaa S, Kantola I. Target organ damage
and cardiovascular risk factors among subjects with previously undiagnosed
hypertension. Eur J Prev Cardiol 2013; 21:980-8.
4. Yalcin F, Abraham TP, Gottdiener JS. Letter regarding the article by
Lee PT, et al. Left ventricular wall thickness and the presence of
asymmetric hypertrophy in healthy young army recruits: data from the LARGE
heart study. Circ Cardiovasc Imaging 2013;6:e28.
In their review of the epidemiology of cardiovascular disease (CVD)
in the UK, Bhatnagar et al considerably underestimate the prevalence of
CVD.[1] They used data from the Clinical Practice Research Datalink
(CPRD), an extract of primary care electronic health records (EHRs) of a
representative sample of patients registered with UK general practices,
and data from the Quality & Outcomes Framewor...
In their review of the epidemiology of cardiovascular disease (CVD)
in the UK, Bhatnagar et al considerably underestimate the prevalence of
CVD.[1] They used data from the Clinical Practice Research Datalink
(CPRD), an extract of primary care electronic health records (EHRs) of a
representative sample of patients registered with UK general practices,
and data from the Quality & Outcomes Framework (QOF), the UK general
practice pay for performance scheme. However data from two other sources
demonstrate a higher incidence or prevalence of CVD than that obtained
from CPRD or QOF.
For example, using CPRD data, Bhatnagar et al report a prevalence of
stroke of 2.53% in men and 1.99% in women. This is higher than the overall
stroke prevalence of 1.7% quoted by the authors using QOF data, probably
because data and care quality is better in CPRD practices. However the
Health Survey for England (HSfE) 2013 report includes time trends in CVD
prevalence up to 2011,[2] and the corresponding figures, based on patient-
reported doctor-diagnosed disease, are 2.7% and 2.1%. Patient reports of
stroke prevalence have been well-validated in longitudinal cohort
studies.[3-5]
Record linkage studies have also shown that primary care EHRs
underestimate the prevalence of CVD. For example, using data from CPRD,
hospital admissions from Hospital Episode Statistics, and the national
registry of acute coronary syndromes (Myocardial Ischaemia National Audit
Project, MINAP), and the mortality registry, Herrett et al showed that the
crude incidence of acute myocardial infarction was 25% lower using only
Clinical Practice Research Datalink data compared with using all three
sources. Payne et al showed considerably higher CVD incidence rates when
general practice and hospital data was combined.[6]
We have used HSfE data to model the prevalence of CVD in small
populations,[7] and have shown strong evidence of spatial clustering of
CVD under-diagnosis, particularly in deprived inner city areas.[8] In
order to reduce CVD mortality further and tackle health inequalities,
there should be much higher awareness of under-diagnosis in primary care.
References
1. Bhatnagar P, Wickramasinghe K, Williams J, Rayner M, Townsend N.
The epidemiology of cardiovascular disease in the UK 2014. Heart 2015.
Link: http://heart.bmj.com/content/early/2015/05/06/heartjnl-2015-
307516.abstract.
2. Health & Social Care Information Centre. Health Survey for
England - 2013, Trend tables 2014. Link:
http://www.hscic.gov.uk/catalogue/PUB16077/HSE2013-Adult-trend-tbls.xls.
3. Walker MK, Whincup PH, Shaper AG, Lennon LT, Thomson AG.
Validation of Patient Recall of Doctor-diagnosed Heart Attack and Stroke:
A Postal Questionnaire and Record Review Comparison. American Journal of
Epidemiology 1998;148(4):355-61. Link:
http://aje.oxfordjournals.org/cgi/content/abstract/148/4/355
4. Glymour MM, Avendano M. Can Self-Reported Strokes Be Used to Study
Stroke Incidence and Risk Factors?: Evidence From the Health and
Retirement Study. Stroke 2009;40(3):873-79. Link:
http://stroke.ahajournals.org/cgi/content/abstract/40/3/873
5. Kazumasa Y, Ai I, Hiroyasu I, Manami I, Shoichiro T. Self-reported
stroke and myocardial infarction had adequate sensitivity in a population-
based prospective study JPHC (Japan Public Health Center)?_"based
Prospective Study. Journal of clinical epidemiology 2009;62(6):667-73.
Link: http://www.sciencedirect.com/science/article/pii/S0895435608002345
6. Payne RA, Abel GA, Simpson CR. A retrospective cohort study
assessing patient characteristics and the incidence of cardiovascular
disease using linked routine primary and secondary care data. BMJ Open
2012;2(2). Link: http://bmjopen.bmj.com/content/2/2/e000723.abstract.
7. Public Health England (Association of Public Health
Observatories). Browsing Disease prevalence models: modelled estimates of
prevalence of CHD by GP Practice. 2009. Link:
http://www.apho.org.uk/resource/view.aspx?RID=48308.
8. Soljak M, Samarasundera E, Indulkar T, Walford H, Majeed A.
Variations in cardiovascular disease under-diagnosis in England: national
cross-sectional spatial analysis. BMC Cardiovascular Disorders
2011;11(1):12. Link: http://www.biomedcentral.com/1471-2261/11/12.
The journal, Heart, recently published a meta-analysis(1) and a
commentary(2) on the association of obesity and mortality in patients with
Coronary Heart Disease (CHD). Lavie begins his commentary with a story of
two hypothetical patients with CHD. One has a BMI of 23 kg/m2 (normal)
and the other has a BMI of 32 kg/m2 (obese).(2) Lavie asks about their
prognosis. The meta-analysis by Wang et al(1) suggests that the obese...
The journal, Heart, recently published a meta-analysis(1) and a
commentary(2) on the association of obesity and mortality in patients with
Coronary Heart Disease (CHD). Lavie begins his commentary with a story of
two hypothetical patients with CHD. One has a BMI of 23 kg/m2 (normal)
and the other has a BMI of 32 kg/m2 (obese).(2) Lavie asks about their
prognosis. The meta-analysis by Wang et al(1) suggests that the obese
patient has the better prognosis. Given that numerous primary prevention
studies document that obesity is a cause of CHD, Lavie labels it a
"paradox" that the prognosis would be better for the obese patient.
It is true that obesity is a cause of CHD, and, as shown by Wang et
al,(1) it is true that the obese people with CHD have a better prognosis
than the non-obese people with CHD. However, this is not a paradox. The
results are a function of the well-described phenomenon called, "collider
stratification bias."(3) Consider that a person contracts CHD due to
either (a) obesity or (b) factors unrelated to obesity (e.g. genetics or
infectious diseases). If the causes unrelated to obesity are more strongly
associated with the outcome of interest (i.e. mortality), then obesity
appears protective. This is similar to analyses finding that maternal-
smoking appears protective against infant mortality if one evaluates only
low birth weight babies.(4)
It is misleading to imply that obesity is protective in people with
CHD. In the example by Lavie, the non-obese subject is not similar to the
obese subject in ways other than obesity.(2) The non-obese subject with
CHD must have contracted CHD from factors unrelated to obesity such as
genetics or infectious disease. The apparent "obesity paradox" occurs
because of confusion with the groups being compared. The comparison is not
between obese people and non-obese people. Rather, the comparison is
between people who have CHD presumably due to the ramifications of obesity
and people who have CHD due to causes unrelated to obesity. The
conclusion is not that obesity is protective, but rather that there are
other causes of CHD that are more life-threatening than obesity.
1. Wang ZJ, Zhou YJ, Galper BZ, Gao F, Yeh RW, Mauri L. Association
of body mass index with mortality and cardiovascular events for patients
with coronary artery disease: A systematic review and meta-analysis.
Heart. 2015. doi: heartjnl-2014-307119.
2. Lavie CJ, De Schutter A, Milani RV. Body composition and the obesity
paradox in coronary heart disease: Can heavier really be healthier? Heart.
2015. doi: heartjnl-2015-307966.
3. Banack HR, Kaufman JS. Does selection bias explain the obesity paradox
among individuals with cardiovascular disease? Ann Epidemiol.
2015;25(5):342-349.
4. Hernandez-Diaz S, Schisterman EF, Hernan MA. The birth weight "paradox"
uncovered? Am J Epidemiol. 2006;164(11):1115-1120.
Georg Fuernau, Holger Thiele
Medical Clinic II-Department of Cardiology, Angiology and Intensive Care Medicine, University Heart Center Luebeck, University of Luebeck, Luebeck, Germany
Keywords: acute myocardial infarction, cardiogenic shock, multivessel percutaneous coronary intervention
Corresponding author: Georg Fuernau, M.D. Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine)...
Dear Editor Gholap et al confirmed a surprising observation that South Asians, compared to White British populations, have lower or similar, rather than higher mortality, following myocardial infarction, as Fischbacher et al first demonstrated in Scotland.(1;2) As the chief investigator of that Scottish study I found the result perplexing given South Asians' high prevalence of type 2 diabetes. A literature review showed...
We have read with interest the article by Choi and colleagues entitled "Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy" published on Heart" (1). In this study, the Authors evaluated the increment of the extent of late gadolinium enhancement (LGE) in patients with hypertrophic cardiomyopathy (HCM). This study reproduces our previous paper entitled "Progression of myocardial fi...
We read the paper of Bhatnagar P. et al. 1 and were impressed by great success of the UK health care on control of cardiovascular disease (CVD). In the UK during last decade, CVD decreased from top to 2nd row on mortality of men in whom, lipid lowering drugs were the most prescribed medicine. 1 In this report, importance of primary care and increased number of less invasive approaches like angioplasty compared to surge...
Dear Editor
In their review of the epidemiology of cardiovascular disease (CVD) in the UK, Bhatnagar et al considerably underestimate the prevalence of CVD.[1] They used data from the Clinical Practice Research Datalink (CPRD), an extract of primary care electronic health records (EHRs) of a representative sample of patients registered with UK general practices, and data from the Quality & Outcomes Framewor...
The journal, Heart, recently published a meta-analysis(1) and a commentary(2) on the association of obesity and mortality in patients with Coronary Heart Disease (CHD). Lavie begins his commentary with a story of two hypothetical patients with CHD. One has a BMI of 23 kg/m2 (normal) and the other has a BMI of 32 kg/m2 (obese).(2) Lavie asks about their prognosis. The meta-analysis by Wang et al(1) suggests that the obese...
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