Only recently the FAME-2 trial1 showed for the first time that, in
patients with stable coronary artery disease (SCAD) and "significant"
myocardial ischemia, there is a prognostic advantage of PCI over optimal
medical therapy (OMT), and that this advantage is consistent in patients
with either single or multi-vessel coronary artery disease. The clinical
outcome of patients with coronary stenoses not associated with signi...
Only recently the FAME-2 trial1 showed for the first time that, in
patients with stable coronary artery disease (SCAD) and "significant"
myocardial ischemia, there is a prognostic advantage of PCI over optimal
medical therapy (OMT), and that this advantage is consistent in patients
with either single or multi-vessel coronary artery disease. The clinical
outcome of patients with coronary stenoses not associated with significant
ischemia is favorable with OMT alone, which is therefore a safe and
convenient therapeutic strategy.
Among patients with SCAD the risk of death and MI is proportional to the
extent of ischemic myocardium/number of diseased vessels. Only patients
with significant ischemia benefit from revascularization. Several studies
however, including the COURAGE and BARI-2D trials2,3, failed to
demonstrate a mortality benefit of PCI over OMT, most likely because of
the inclusion on these studies of low risk patients with only limited
ischemia or even no ischemia.
It's common practice, in most cath-labs, to stent intermediate coronary
stenoses only based on an angiographic estimation of severity. This meta-
analysis and the FAME-2 trial shows, instead, that revascularization with
PCI is safer and only confers a survival benefit when a given coronary
lesion is associated with significant myocardial ischemia, as proven by
FFR measurements. The use of FFR technique, which is simple and
relatively safe, should be therefore implemented in every day practice.
1- Fractional flow reserve-guided PCI for stable coronary artery
disease.
De Bruyne B, Fearon WF, Pijls NH, Barbato E, Tonino P, Piroth Z, Jagic N,
Mobius-Winckler S, Rioufol G, Witt N, Kala P, MacCarthy P, Engstr?m T,
Oldroyd K, Mavromatis K, Manoharan G, Verlee P, Frobert O, Curzen N,
Johnson JB, Limacher A, N?esch E, J?ni P; FAME 2 Trial Investigators. N
Engl J Med. 2014 Sep 25;371(13):1208-17.
2- Optimal medical therapy with or without PCI for stable coronary
disease.
Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson
M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz
S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman
DS, Mancini GB, Weintraub WS; COURAGE Trial Research Group.
N Engl J Med. 2007 Apr 12;356(15):1503-16.
3- A randomized trial of therapies for type 2 diabetes and coronary
artery disease.
BARI 2D Study Group, Frye RL, August P, Brooks MM, Hardison RM, Kelsey SF,
MacGregor JM, Orchard TJ, Chaitman BR, Genuth SM, Goldberg SH, Hlatky MA,
Jones TL, Molitch ME, Nesto RW, Sako EY, Sobel BE.
N Engl J Med. 2009 Jun 11;360(24):2503-15.
In recent article of Candilio and colleagues assessing effect of
remote ischemic preconditioning (RIPC) on postoperative outcomes in
patients undergoing cardiac surgery, they showed that RIPC reduced amount
of perioperative myocardial injury by 26% and incidence of acute kidney
injury by 48%, respectively. They should be applauded for trying to
control most of risk factors affecting postoperative myocardial and kidney
in...
In recent article of Candilio and colleagues assessing effect of
remote ischemic preconditioning (RIPC) on postoperative outcomes in
patients undergoing cardiac surgery, they showed that RIPC reduced amount
of perioperative myocardial injury by 26% and incidence of acute kidney
injury by 48%, respectively. They should be applauded for trying to
control most of risk factors affecting postoperative myocardial and kidney
injury. However, to differentiate the effects of one factor on study
endpoints, all of the other factors have to be standardised. In this
study, several important issues were not well addressed.
First, perioperative hemoglobin levels were not included in data analysis.
Actually, preoperative anemia is common among patients undergoing cardiac
surgery and is associated with independently increased risks of
postoperative adverse myocardial and renal events.2 Furthermore, the
lowest hemoglobin level during cardiopulmonary bypass has been associated
independently with the postoperative low-output syndrome, renal failure
and mortality.3
Additionally, their study design did not include the detail of
intraoperative complications and managements, such as hemodynamic
instability, blood loss and blood transfusion. It has been shown that
postoperative myocardial injury correlates with changes in blood pressure
and heart rate during cardiac surgery.4 Furthermore, it is well know that
perioperative blood transfusion is associated with increased troponin I
release after cardiac surgery, and increased risks of postoperative short-
and long-term mortality. Thus, we cannot exclude possibility that
existence of any imbalance in the above factors would have confounded
interpretation of their results.
Finally, the study by Candilio and colleagues was not powered to show a
difference in postoperative short-term clinical outcomes that occurred
during the follow-up period. Thus, it is unclear whether favorable effect
of RIPC on myocardial and kidney injury after cardiac surgery can be
translated to postoperative benefits on mortality and severe adverse
events. To address this issue, we agree the authors that the large-scale
clinical trials are still required. These new studies should have enough
power for postoperative mortality and severe adverse events. If further
studies show consistent beneficial effect of RIPC on postoperative
myocardial and kidney injury and mortality following cardiac surgery, the
implications for practice are immense.
REFERENCES
1 Candilio L, Malik A, Ariti C, et al. Effect of remote ischaemic
preconditioning on clinical outcomes in patients undergoing cardiac bypass
surgery: a randomised controlled clinical trial. Heart 2015; 101:185-92.
2 Kulier A, Levin J, Moser R, et al; Investigators of the Multicenter
Study of Perioperative Ischemia Research Group; Ischemia Research and
Education Foundation. Impact of preoperative anemia on outcome in patients
undergoing coronary artery bypass graft surgery. Circulation 2007; 116:471
-9
3 Loor G, Li L, Sabik JF 3rd, et al. Nadir hematocrit during
cardiopulmonary bypass: end-organ dysfunction and mortality. J Thorac
Cardiovasc Surg 2012; 144:654-62.
4 Ketenci B, Enc Y, Ozay B, et al. Myocardial injury during off-pump
surgery. The effect of intraoperative risk factors. Saudi Med J 2008;
29:203-8.
We thank Laukkanen et al. for their interest in our recent report titled "Obesity related risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) study" (1). We agree that regular moderate physical activity reduces the risk of sudden cardiac death (SCD) and all-cause mortality. Physical activity, but not fitness, was captured in the ARIC study via questionnaires. However, adjustment for this variable in our...
We thank Laukkanen et al. for their interest in our recent report titled "Obesity related risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) study" (1). We agree that regular moderate physical activity reduces the risk of sudden cardiac death (SCD) and all-cause mortality. Physical activity, but not fitness, was captured in the ARIC study via questionnaires. However, adjustment for this variable in our multivariable analysis did not change the results of the study. In the analysis for BMI, after adjustment for physical activity in addition to all variables in our Model 2, the HR (95% CI) for SCD were 1, 1.24 (0.75-2.04), 1.05 (0.59-1.85), and 1.42 (0.76-2.68) among non- smokers with BMI of 18.5-24.9, 25-29.9, 30-34.9 and 35+, respectively (p for trend 0.45). In the analysis for waist-hip-ratio, after additional adjustment for physical activity in our Model 2, the HR (95% CI) for SCD were 1, 0.98 (0.53-1.81), 1.45 (0.86-2.43), and 1.93 (1.13-3.30) among non -smokers with waist-hip-ratio of reference (<0.8 in women, <0.95 in men), high category 1, 2 and 3, respectively (p for trend 0.005).
REFERENCES
1. Adabag S, Huxley RR, Lopez FL, Chen LY, Sotoodehnia N, Siscovick D, Deo R, Konety S, Alonso A, Folsom AR. Obesity related risk of sudden cardiac death in the atherosclerosis risk in communities study. Heart. 2015;101:215-21
The paper by Patterson et al (1) illustrates why the NICE and ESC
guidelines (2,3) recommend no non-invasive testing in patients presenting
with undifferentiated chest pain in whom a non-cardiac cause is suspected
or the probability of coronary artery disease (CAD) is judged to be very
low (NICE <10%, ESC <15%). Table 5 shows there were 351 such
patients, of whom 24 were subsequently diagnosed with CAD. Even if we...
The paper by Patterson et al (1) illustrates why the NICE and ESC
guidelines (2,3) recommend no non-invasive testing in patients presenting
with undifferentiated chest pain in whom a non-cardiac cause is suspected
or the probability of coronary artery disease (CAD) is judged to be very
low (NICE <10%, ESC <15%). Table 5 shows there were 351 such
patients, of whom 24 were subsequently diagnosed with CAD. Even if we
accept that the chest pain in all 24 of these "false negative" cases was
in fact caused by myocardial ischaemia, this is equivalent to a diagnostic
sensitivity of 93% for clinical judgment in ruling out coronary disease,
better than could be achieved by exercise electrocardiography or perfusion
imaging in such a low risk population (4).
It is unclear from the manuscript exactly how "the subsequent CAD
diagnosis" was determined and how sound was that determination. There were
only 11 hospital admissions with "angina" so it presumably involved some
form of non-invasive testing in most cases. The fact that CAD was
"excluded" or "inconclusive" in nearly all (>90%) of these patients is
entirely predictable given the initial clinical diagnosis of non-cardiac
chest pain or low probability CAD. This begs the question what
contribution the testing made to patient care? Certainly, the tests were
unhelpful in failing to prevent 6 MACE events, although it is hard to know
whether this 1.7% event rate should be seen as a cause for "alarm".
Finally, Patterson et al warn against using the NICE guidance to
"justify excluding (low risk) patients from further investigation if CAD
is still suspected based on all available clinical information". There was
no intention that the guideline should be used in this way but a more
selective approach to investigation than apparently used by Patterson et
al is surely needed to address increasing concerns about the overuse of
noninvasive diagnostic tests in patients with chest pain (5).
References
1. Patterson CM, Nair A, Ahmed N, Bryan L, Bell D, Nicol ED. Clinical
outcomes when applying NICE guidance for the investigation of recent-onset
chest pain to a rapid-access chest pain clinic population. Heart
2015;101:113-118
2. Chest pan of recent onset: Assessment and diagnosis of recent onset
chest pain or discomfort of suspected cardiac origin. NICE guidelines
[CG95] Published date: March 2010. http://www.nice.org.uk
3. Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C, Budaj A,
et al. 2013 ESC guidelines on the management of stable coronary artery
disease: The Task Force on the management of stable coronary artery
disease of the European Society of Cardiology. Eur Heart J. 2013;
34(38):2949-3003
4. Detrano R, Gianrossi R, Mulvihill D, Lehman K, Dubach P, Colombo A,
Froelicher V. Exercise-induced ST segment depression in the diagnosis of
multivessel coronary disease: a meta analysis. J Am Coll Cardiol
1989;14:1501-8.
5. Ladapo JA, Blecker S, Douglas PS. Physician decision making and trends
in the use of cardiac stress testing in the United States: An analysis of
repeated cross-sectional data. Ann Intern Med 2014;161:482-490
Conflict of Interest:
I chaired the NICE guideline group: Chest pan of recent onset: Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. NICE guidelines [CG95] Published date: March 2010. http://www.nice.org.uk
I am rather surprised that the authors did not take into account more
clinical features of the history in their model.(1) Pleuritic features and
relief when sat up suggest pericarditis, whilst there are of course
specific features that suggest reflux oesophagitis; timing is important,
as pain lasting less than a minute is really not suggestive of ischaemic
disease.
The authors state 'we included consenting adults...
I am rather surprised that the authors did not take into account more
clinical features of the history in their model.(1) Pleuritic features and
relief when sat up suggest pericarditis, whilst there are of course
specific features that suggest reflux oesophagitis; timing is important,
as pain lasting less than a minute is really not suggestive of ischaemic
disease.
The authors state 'we included consenting adults aged >25 years
who presented to the ED within 24h of experiencing chest pain suspected to
be cardiac in origin by the initial treating physician' and thus I take
this to assume they trusted the history of the initial physician as one
that suggested cardiac disease - even then, I assume 'cardiac' means
ischaemic, not pericarditic or indeed dissection-type of pain.
Similar work to this paper has been done in stable angina, where the
description of angina pain as typical is associated with coronary
outcomes.(2) Clearly unstable angina lacks the exertional component of
stable angina and is thus harder perhaps from simple history-taking alone
to be sure of a diagnosis, but that does not mean chest pain descriptors
(character, site, duration) don't play a diagnostic, and hence potentially
prognostic role in unstable angina.
1. Body R, Carley S, McDowell G, Pemberton P, Burrows G, Cook G,
Lewis PS, Smith A, Mackway-Jones K. The Manchester Acute Coronary
Syndromes (MACS) decision rule for suspected cardiac chest pain:
derivation and external validation. Heart 2014;100:18 1462-1468
2. Zaman MJ, Junghans C, Sekhri N, et al. Presentation of stable
angina pectoris among women and South Asian people. CMAJ 2008;179:659-67
The 6.3% prevalence of left bundle branch block(LBBB) among 17,488
subjects with type 1 acute myocardial infarction(AMI) translates into 1101
subjects with this manifestation of AMI(1). This represents a golden
opportunity to document the prevalence of concordant ST segment deviation
in those 1101 subjects so as to enable a comparison to be made with the
study which reported a low prevalence of acute coronary occlusion in...
The 6.3% prevalence of left bundle branch block(LBBB) among 17,488
subjects with type 1 acute myocardial infarction(AMI) translates into 1101
subjects with this manifestation of AMI(1). This represents a golden
opportunity to document the prevalence of concordant ST segment deviation
in those 1101 subjects so as to enable a comparison to be made with the
study which reported a low prevalence of acute coronary occlusion in
patients with LBBB who did not have concordant ST segment deviation(2). An
even more important comparison would be a documentation of the sensitivity
and specificity of concordant ST segment deviation for type 1 AMI in those
1101 subjects vs the documentation of 16.7% sensitivity and 88.6%
specificity in the 120 subjects evaluated by Brown et al(3)
References
(1)Baron T., Hambraeus K., Sundstrom J et al
Type 2 myocardial infarction in clinical practice
Heatr 2015;101:101-106
(2)McMahon R., Siow W., Bhindi R et al
Left bundle branch block without concordant ST changes is rarely
associated with acute coronary occlusion
International Journal of Cardiology 2013;167:1339-1342
(3) Brown AJ., Hoole SP., McCormick LM et al
Left bundle branch block with acute thrombotic occlusion is associated
with increased myocardial jeopardy score and poor clinical outcomes in
primary percutaneous coronary activations
Heart 2013;99:774-778
The documentation of a rising incidence of cardiac resynchronisation
therapy(CRT)-related infection(1) calls for a reappraisal of the Class 1
level A recommendation for the use of this modality(2), given the fact
that the recommendation antedated the ground breaking introduction of
angiotensin-neprilysin inhibition in subjects with comparable severity of
systolic heart failure(3). In that study a significant(p < 0.00...
The documentation of a rising incidence of cardiac resynchronisation
therapy(CRT)-related infection(1) calls for a reappraisal of the Class 1
level A recommendation for the use of this modality(2), given the fact
that the recommendation antedated the ground breaking introduction of
angiotensin-neprilysin inhibition in subjects with comparable severity of
systolic heart failure(3). In that study a significant(p < 0.001)
reduction in mortality and hospitalisation for heart failure was
documented in subjects randomised to angiotensin-neprilysin inhibition vs
counterparts randomised to optimum dose enalapril with comparable
background therapy(3). Over and above the risk of infection(1), CRT has
the added disadvantage of unpredictability of response(4), and, in 36% of
cases, poor retention on mean follow up of 2.5 years(5). Accordingly, to
justify CRT in the unique subgroup of symptomatic systolic heart failure
subjects with left bundle branch block(QRS duration > 150 ms) and sinus
rhythm(2) that modality will have to be shown to be superior to
angiotensin-neprilysin inhibition when the latter is used in a comparable
group of subjects , both groups being on comparable background therapy.
References
(1) Harrison JL., Prenedergast BD., Sandoe JAI
Guidelones for diagnosis management and prevention of implantable cardiac
electronic device infection
Heart 2014 doi 10.1136/heartjnl-2014-306873
(2) Brignole M., ASuricchio A., Baron Equivas G et al
2013 ESC guidelines on cardiac pacing and cardiac resynchronisation
therapy
Europace 2013;15:1070-1118
(3) McMurray JJV., Packer M., Desai AS et al
Angiotensin-neprilysin inhibition versus enalapril in heart fdailure
2014;371;993-1004
(4) Clelenad J., Freemantle N., Ghio S et al
Predicting the long term effects of cardiac resynchronisation therapy on
mortality from baseline variables and early response
J Am Coll Cardiol 2008;52:430-444
(5) Knight B., Desai A., Coman J Faddis M., Yong P
Long term retention of cardiac resynchronisation therapy
J Am Coll Cardiol 2004;44:72-77
We read with great interest the recent report, published in Heart,
entitled "Obesity related risk of sudden cardiac death in the
Atherosclerosis Risk in Communities (ARIC) study" by Adabag et al.1
Among a large cohort of middle-aged adults (n = 14,491 African American
and white men and women; 55% female), baseline measures of obesity,
including body mass index (BMI), waist circumference (WC), and waist-to-
hip ratio (W...
We read with great interest the recent report, published in Heart,
entitled "Obesity related risk of sudden cardiac death in the
Atherosclerosis Risk in Communities (ARIC) study" by Adabag et al.1
Among a large cohort of middle-aged adults (n = 14,491 African American
and white men and women; 55% female), baseline measures of obesity,
including body mass index (BMI), waist circumference (WC), and waist-to-
hip ratio (WHR), were related to the incidence of sudden cardiac death
(SCD, 253 cases) over a 12.6 year follow up. BMI was indirectly
associated with SCD through its adverse effects on cardiovascular risk
factors, diabetes and heart disease, whereas abdominal obesity, measured
by WHR, appeared to be the strongest predictor of SCD in non-smokers. In
contrast, the relation between measures of obesity and SCD were
inconsistent in current smokers, perhaps due to the relatively small
number of SCD cases in this population subset. It was suggested that this
finding may reflect the 'obesity paradox.'
Although the ARIC investigators attempted to adjust for potential
confounding variables to clarify the impact of obesity per se on SCD,
there was no mention of physical activity or cardiorespiratory fitness
(CRF), potential mortality modulators in SCD cohorts. Adherence to a
regular exercise regimen (> 30 minutes/day) is strongly and
independently associated with a lower risk of SCD in women.2 Numerous
previous studies have also shown that low fitness is an independent
predictor of mortality in normal-weight, overweight, and obese men and
women, regardless of the risk factor profile.3 Similarly, we reported
that CRF was inversely related to the risk of SCD in a population-based
long-term follow-up study.4
Hu et al5 examined whether higher levels of physical activity can counter
the elevated risk of death associated with excess adiposity. During a 24-
year follow-up of 116,564 women (30-55 years of age) who free of known
cardiovascular disease and cancer, there were 10,282 deaths. The relative
risk of death of lean (BMI < 25 kg/m2)-active, lean-inactive, obese
(BMI > 30 kg/m2)-active, and obese-inactive was 1.00, 1.55, 1.91, and
2.42, respectively. It was concluded that both increased adiposity and
reduced physical activity are strong and independent predictors of death.
In conclusion, we wonder whether the ARIC study included assessments of
physical activity or CRF and, if so, why these variables were not
considered in their multivariate adjusted model? Furthermore, we question
whether the association between WHR and SCD would have persisted after
adjusting for these variables. Collectively, these data and other recent
reports,6 suggest that the deleterious health impact of obesity may be
markedly overestimated, unless physical activity and CRF are appropriately
accounted for.
REFERENCES
1.Adabag S, Huxley RR, Lopez FL, Chen LY, Sotoodehnia N, Siscovick D,
Deo R, Konety S, Alonso A, Folsom AR. Obesity related risk of sudden
cardiac death in the atherosclerosis risk in communities study. Heart.
2014 Nov 19.
2.Chiuve SE, Fung TT, Rexrode KM, Spiegelman D, Mason JE, Stampfer
MJ, Albert CM. Adherence to a low-risk, healthy lifestyle and risk of
sudden cardiac death among women. JAMA 2011;306:62-69.
3.Lavie CJ, McAuley PA, Church TS, Milani RV, Blair SN. Obesity and
cardiovascular diseases: implications regarding fitness, fatness, and
severity in the obesity paradox. J Am Coll Cardiol 2014;63:1345-54.
4.Laukkanen JA, M?kikallio TH, Rauramaa R, Kiviniemi V, Ronkainen K,
Kurl S. Cardiorespiratory fitness is related to the risk of sudden cardiac
death: a population-based follow-up study. J Am Coll Cardiol 2010;56:1476-
83.
5.Hu FB, Willett WC, Li T, et al. Adiposity as compared with
physical activity in predicting mortality among women. N Engl J Med
2004;351:2694-703.
6.Lee CD, Sui X, Blair SN. Combined effects of cardiorespiratory
fitness, not smoking, and normal waist girth on morbidity and mortality in
men. Arch Intern Med 2009;169:2096-101.
Sae Young Jae, PhD, Department of Sport Science, University of Seoul,
Seoul, South Korea.
Sudhir Kurl, MD, Department of Medicine, Institute of Public Health
and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Jari A. Laukkanen, MD, Department of Medicine, Institute of Public
Health and Clinical Nutrition, University of Eastern Finland, Kuopio,
Finland (jariantero.laukkanen@uef.fi).
Barry A. Franklin, PhD, Preventive Cardiology and Cardiac
Rehabilitation, William Beaumont Hospital, Royal Oak, MI, USA.
We believe that we have identified a methodological issue related to
the procedure that Pieters et al. [1] used to combine studies using
different types of regression models. In some studies heart rate
variability parameters were modeled as a linear model but in others they
were modeled as log-linear (i.e., where the outcome was log-transformed).
To combine effect estimates from these two types of models, the authors
co...
We believe that we have identified a methodological issue related to
the procedure that Pieters et al. [1] used to combine studies using
different types of regression models. In some studies heart rate
variability parameters were modeled as a linear model but in others they
were modeled as log-linear (i.e., where the outcome was log-transformed).
To combine effect estimates from these two types of models, the authors
converted the effect estimate into a "percent change" for an increment of
10 ug/m3.
We consider that the procedure Pieter et al. [1] used to compute
percent change from un-transformed model to be incorrect. For a log-linear
model of an outcome, y, regressed on exposure x and adjusted for
covariates, z, the percent change of the expected value of y, E(y), is:
E((y2-y1)/y1) = exp(b(x2-x1))-1. But it cannot be computed for a simple
linear model because it includes the intercept (a) and covariates:
{E(y(x2))-E(y(x1))}/E(y(x1)) = b(x2-x1)/[a+bx1+cz].
Because the value of these covariates z depends on each subject in
the study, percent change from an untransformed model cannot be computed
and used in a meta-analysis. Replacing the mean value of the outcome with
the value of the entire linear predictor in the denominator, as Pieters et
al. [1] did, is not correct because it assumes that none of the covariates
have an effect on the outcome. Effectively, they have computed the
difference and standardized it by the mean value of the outcome.
We also found that the same conversion procedure in Pieters et al.[1]
has been used in others studies [e.g., 2, 3, 4], also yielding spurious
estimates of percent change. In summary, effect estimates derived from
regression models using different functional forms for outcomes cannot be
combined and used in a meta-analysis.
References:
[1] Pieters N, Plusquin M, Cox B, Kicinski M, Vangronsveld J, Nawrot
TS. An epidemiological appraisal of the association between heart rate
variability and particulate air pollution: a meta-analysis. Heart (British
Cardiac Society) 2012; 98(15): 1127-35.
[2] Schneider A, Neas LM, Graff DW, et al. Association of cardiac and
vascular changes with ambient PM2.5 in diabetic individuals. Part Fibre
Toxicol 2010a; 7: 14.
[3] Rich DQ, Kipen HM, Huang W, et al. Association between changes in air
pollution levels during the Beijing Olympics and biomarkers of
inflammation and thrombosis in healthy young adults. JAMA : the journal of
the American Medical Association 2012; 307(19): 2068-78.
[4] Lipsett MJ, Tsai FC, Roger L, Woo M, Ostro BD. Coarse particles and
heart rate variability among older adults with coronary artery disease in
the Coachella Valley, California. Environ Health Perspect 2006; 114(8):
1215-20.
We thank the authors for their letter. The question is raised whether
our study is able to distinguish between the effect of using antiepileptic
medications (AEMs) and epilepsy on SCD risk. We studied SCD risk among AEM
users (with and without epilepsy).1 We show in multiple ways that AEM use
increases SCD risk, independently from epilepsy and other confounders.
Notably, SCD risk in non-epilepsy pa...
We thank the authors for their letter. The question is raised whether
our study is able to distinguish between the effect of using antiepileptic
medications (AEMs) and epilepsy on SCD risk. We studied SCD risk among AEM
users (with and without epilepsy).1 We show in multiple ways that AEM use
increases SCD risk, independently from epilepsy and other confounders.
Notably, SCD risk in non-epilepsy patients using AEMs was 2.3 (1.01-5.2),
while SCD risk in all patients using AEMs was also 2.3 (1.4-3.9), with
correction for epilepsy and confounders.
Additionally, we show among epilepsy patients (who were all AEM users)
that uncontrolled seizures determined SCD risk. Epilepsy patients with
controlled seizures (=stable epilepsy) had an SCD risk of 1.6 (0.7-4.1),
while epilepsy patients with uncontrolled seizures had an SCD risk of 6.4
(2.4-17.4). Therefore, we believe that SCD is associated with both
epilepsy and AEM use.
Another question is raised whether sudden unexpected death in epilepsy
(SUDEP) could be an alternative diagnosis for SCD. We have previously
studied SCD risk in epilepsy in a large population-based study, with ECG-
documentation of ventricular fibrillation (VF).2 In that study, 1.4% of
all cases (n=1019) had epilepsy. In the current study, SCD was defined by
established clinical criteria. Here we found epilepsy in 1.5% of SCD cases
(n=926). Thus, proportions of epilepsy are comparable between the
populations. For this reason we assume that SCD misclassification is
minimal. If SUDEP would be misclassified as SCD, one would expect the
proportion of epilepsy to be higher.
Importantly, autopsy-negative sudden death (the hallmark of SUDEP)
does not help to exclude cardiac causes of sudden death. Potentially fatal
arrhythmia syndromes (e.g., Idiopathic VF, Brugada Syndrome, Long QT
syndrome) are often accompanied by negative autopsy.
The OR for Gabapentine is indeed based on small numbers, however
significant. Although residual bias cannot be excluded, we would like to
underline that diabetes and stroke were no major confounders in this
association.
In conclusion, we believe that SUDEP has both cardiac and non-cardiac
causes. Acknowledging that SCD is part of SUDEP is the first step in the
battle against sudden death in epilepsy.
REFERENCES
1. Bardai A, Blom MT, van Noord C, Verhamme KM, Sturkenboom MC, Tan HL.
Sudden cardiac death is associated both with epilepsy and with use of
antiepileptic medications. Heart Published Online First: 16 Jul 2014
doi:10.1136/heartjnl-2014-305664
2. Bardai A, Lamberts RJ, Blom MT, Spanjaart AM, Berdowski J, van der
Staal SR, Brouwer HJ, Koster RW, Sander JW, Thijs RD, Tan HL. Epilepsy is
a risk factor for sudden cardiac arrest in the general population. PLoS
One. 2012;7:e42749
Only recently the FAME-2 trial1 showed for the first time that, in patients with stable coronary artery disease (SCAD) and "significant" myocardial ischemia, there is a prognostic advantage of PCI over optimal medical therapy (OMT), and that this advantage is consistent in patients with either single or multi-vessel coronary artery disease. The clinical outcome of patients with coronary stenoses not associated with signi...
In recent article of Candilio and colleagues assessing effect of remote ischemic preconditioning (RIPC) on postoperative outcomes in patients undergoing cardiac surgery, they showed that RIPC reduced amount of perioperative myocardial injury by 26% and incidence of acute kidney injury by 48%, respectively. They should be applauded for trying to control most of risk factors affecting postoperative myocardial and kidney in...
The paper by Patterson et al (1) illustrates why the NICE and ESC guidelines (2,3) recommend no non-invasive testing in patients presenting with undifferentiated chest pain in whom a non-cardiac cause is suspected or the probability of coronary artery disease (CAD) is judged to be very low (NICE <10%, ESC <15%). Table 5 shows there were 351 such patients, of whom 24 were subsequently diagnosed with CAD. Even if we...
I am rather surprised that the authors did not take into account more clinical features of the history in their model.(1) Pleuritic features and relief when sat up suggest pericarditis, whilst there are of course specific features that suggest reflux oesophagitis; timing is important, as pain lasting less than a minute is really not suggestive of ischaemic disease.
The authors state 'we included consenting adults...
The 6.3% prevalence of left bundle branch block(LBBB) among 17,488 subjects with type 1 acute myocardial infarction(AMI) translates into 1101 subjects with this manifestation of AMI(1). This represents a golden opportunity to document the prevalence of concordant ST segment deviation in those 1101 subjects so as to enable a comparison to be made with the study which reported a low prevalence of acute coronary occlusion in...
The documentation of a rising incidence of cardiac resynchronisation therapy(CRT)-related infection(1) calls for a reappraisal of the Class 1 level A recommendation for the use of this modality(2), given the fact that the recommendation antedated the ground breaking introduction of angiotensin-neprilysin inhibition in subjects with comparable severity of systolic heart failure(3). In that study a significant(p < 0.00...
We read with great interest the recent report, published in Heart, entitled "Obesity related risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) study" by Adabag et al.1 Among a large cohort of middle-aged adults (n = 14,491 African American and white men and women; 55% female), baseline measures of obesity, including body mass index (BMI), waist circumference (WC), and waist-to- hip ratio (W...
We believe that we have identified a methodological issue related to the procedure that Pieters et al. [1] used to combine studies using different types of regression models. In some studies heart rate variability parameters were modeled as a linear model but in others they were modeled as log-linear (i.e., where the outcome was log-transformed). To combine effect estimates from these two types of models, the authors co...
To the Editor,
We thank the authors for their letter. The question is raised whether our study is able to distinguish between the effect of using antiepileptic medications (AEMs) and epilepsy on SCD risk. We studied SCD risk among AEM users (with and without epilepsy).1 We show in multiple ways that AEM use increases SCD risk, independently from epilepsy and other confounders. Notably, SCD risk in non-epilepsy pa...
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