We read with interest the article by Varcoe et al (Heart Jan 15 th 20917) “Impact of call-to-balloon time on 30-day mortality in contemporary practice” We were not surprised by the results which indicate yet again that patients with delays to reperfusion suffer worse mortality rates - the concept of timely reperfusion in STEMI has been previously very well documented, and its importance recognised for some time. Thus de Lucca (1), Cannon (2) and others (3) reported data >10 years ago which supported the concept that mortality rates increase when important time metrics are not achieved. Time dependent infarct size is considered the cause (4)
When the National Infarct Angioplasty Project (NIAP) was established in 2008 with the explicit aim of rolling out P-PCI in the UK, everyone involved in care of STEMI patients thought it was a good idea to go with a policy of one STEMI management strategy, for simplicity. No-one doubted that P-PCI should become the standard of care. Some (including the authors of this letter - one of whom served on NIAP) voiced concerns however that, based on the published data, achieving guideline mandated times was essential, and that this might be difficult to achieve with P-PCI in patients transferred from more rural regions. There was assurance from Department of Health that >95% of patients were “within distance” of a P-PCI centre. We tried to point out that being “within distance”, and being within the mandated times were very differe...
We read with interest the article by Varcoe et al (Heart Jan 15 th 20917) “Impact of call-to-balloon time on 30-day mortality in contemporary practice” We were not surprised by the results which indicate yet again that patients with delays to reperfusion suffer worse mortality rates - the concept of timely reperfusion in STEMI has been previously very well documented, and its importance recognised for some time. Thus de Lucca (1), Cannon (2) and others (3) reported data >10 years ago which supported the concept that mortality rates increase when important time metrics are not achieved. Time dependent infarct size is considered the cause (4)
When the National Infarct Angioplasty Project (NIAP) was established in 2008 with the explicit aim of rolling out P-PCI in the UK, everyone involved in care of STEMI patients thought it was a good idea to go with a policy of one STEMI management strategy, for simplicity. No-one doubted that P-PCI should become the standard of care. Some (including the authors of this letter - one of whom served on NIAP) voiced concerns however that, based on the published data, achieving guideline mandated times was essential, and that this might be difficult to achieve with P-PCI in patients transferred from more rural regions. There was assurance from Department of Health that >95% of patients were “within distance” of a P-PCI centre. We tried to point out that being “within distance”, and being within the mandated times were very different indeed. We predicted that about 20% of patients could not achieve the call to balloon times in the UK probably for reasons in part related to transport times. And so it turns out. Data from the USA (5) indeed suggested that while door to balloon times fall, mortality does not, supporting the concept that it is the total ischaemic time that is crucial . This has thus again been confirmed by the data reported in this Heart paper.
In this context there are issues with these data in addition: In particular we are not provided with any data on total ischaemic times. It is clear that total ischemic time is best metric so the following is not an excuse to minimize its importance - quote “The STB time is a measure of total ischemic time, but symptom onset may be difficult to define accurately because of recall bias, prodromal anginal symptoms and silent or atypical presentations”. Other data bases manage to report this metric. Thus the authors cannot say “In our study, symptom-to-call time was not associated with 30-day mortality, whereas call-to-door and DTB times were (table 4), thus suggesting that pre-hospital and hospital-based emergency care are equally important contributors to patient outcome” since they havn’t considered the time from symptom onset. Again it is total ischaemic timer that is the issue. Furthermore whilst there is of course some value in measuring the 150 or 120 min CTB, time alone fails to recognize the key prognostic variables of territory at risk or demographics (anterior, young patient).
Inability to attain Guideline mandated times may occur for a number of reasons some of which are suggested in this paper. However since it is not patient level data, important issues such as individual transport times, other than inter-hospital transfer, which has always shown been shown to add time and lead to worse outcomes, cannot be determined. For the 18.5% patients in the ‘transfer’ cohort, the mean DTB time from first hospital admission was an unacceptable 133 min (median 123 min, IQR 95–161 min).
Difficulty in attaining Guideline agreed optimal times to reperfusion is not uncommon in other countries such as Australia, USA and parts of South America where geography and local conditions (e.g known times of traffic congestion) mean these times may be regularly missed, with the consequent impact on outcomes.
It was for the reasons of difficulty in achieving symptom to balloon times, because of transport delays that we devised, ran and published in 2013 the STREAM trial (6) which showed that if P-PCI could not be delivered within one hour of first medical contact, then a pharmaco-invasive strategy (immediate pre-hospital thrombolysis (with a reduced dose>75 years), then transfer to a PCI capable centre and intervention on those who needed rescue angioplasty and routine angiography+/- angioplasty between 6 and 24 hours in all others) resulted in equivalent outcomes to those randomised to timely P-PCI. As such recommendations, based on this study and others (7), have been incorporated into the European Guidelines (8). The authors allude to all of this a mere last sentence of their discussion.
The concept of pre-hospital timings are worth emphasizing more than this however. If those who could not receive timely P-PCI had in fact received a pharmaco-invasive strategy then the robust published data suggests they would have had the same outcomes as if they had received timely P-PCI (6).
Rather than one line in a discussion, we should robustly address the issue of whether it is indeed time (if transport delays because of geography are an issue in the UK) to re-think the reperfusion strategy and be a bit smarter and nuanced as to how we deliver reperfusion to ensure all patients do as well as those who receive timely P-PCI. They and all the others who missed the mandated Guideline time metrics may have done better with the pharmaco-invasive strategy. We worried about this previously, now UK data also supports this. Mixed models work in other countries who struggle to meet total ischaemic time challenges, why shouldn’t they in the UK?
Tony Gershlick
Frans van der Werf
Paul Armstrong
1) De Luca G1, Suryapranata H, Ottervanger JP, Antman EM. Time delay to treatment and mortality in primary angioplasty for acute myocardial infarction: every minute of delay counts. Circulation. 2004 Mar 16;109(10):1223-5. Epub 2004 Mar 8.
2) Cannon CP1, Gibson CM, Lambrew CT, Shoultz DA, Levy D, French WJ, Gore JM, Weaver WD, Rogers WJ, Tiefenbrunn AJ. Relationship of symptom-onset-to-balloon time and door-to-balloon time with mortality in patients undergoing angioplasty for acute myocardial infarction. JAMA. 2000 Jun 14;283(22):2941-7.
3) McNamara RL, Herrin J, Bradley EH, Portnay EL, Curtis JP, Wang Y, Magid DJ, Blaney M, Krumholz HM; NRMI Investigators.Hospital improvement in time to reperfusion in patients with acute myocardial infarction, 1999 to 2002.J Am Coll Cardiol. 2006 Jan 3;47(1):45-51.
4) Francone M, Bucciarelli-Ducci C, Carbone I, Canali E, Scardala R, Calabrese FA, Sardella G, Mancone M, Catalano C, Fedele F, Passariello R, Bogaert J, Agati L Impact of primary coronary angioplasty delay on myocardial salvage, infarct size, and microvascular damage in patients with ST-segment elevation myocardial infarction: insight from cardiovascular magnetic resonance. J Am Coll Cardiol. 2009 Dec 1;54(23):2145-53. doi: 10.1016/j.jacc.2009.08.024.
5) A Flynn, M Moscucci, D Share, Smith D, LaLonde T, Changezi H, Riba A, Gurm HS. Trends in door-to-balloon time and mortality in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention Arch Intern Med, 170 (2010), pp. 1842–1849
6) Armstrong PW, Gershlick AH, Goldstein P, Wilcox R, Danays T, Lambert Y, Sulimov V, Rosell Ortiz F, Ostojic M, Welsh RC, Carvalho AC, Nanas J, Arntz HR, Halvorsen S, Huber K, Grajek S, Fresco C, Bluhmki E, Regelin A, Vandenberghe K, Bogaerts K, Van de Werf F; STREAM Investigative TeamFibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013 Apr 11;368(15):1379-87
7) Bonnefoy E, Steg PG, Boutitie F, Dubien PY, Lapostolle F, Roncalli J, Dissait F, Vanzetto G, Leizorowicz A, Kirkorian G; CAPTIM Investigators, Mercier C, McFadden EP, Touboul P Comparison of primary angioplasty and pre-hospital fibrinolysis in acute myocardial infarction (CAPTIM) trial: a 5-year follow-up. Eur Heart J. 2009 Jul;30(13):1598-606. doi: 10.1093/eurheartj/ehp156. Epub 2009 May 8.
8) Eur Heart J. 2012 Oct;33(20):2569-619. doi: 10.1093/eurheartj/ehs215. Epub 2012 Aug 24.
9) Steg PG, James SK, Atar D, Badano LP, Blömstrom-Lundqvist C, Borger MA, Di Mario C, Dickstein K, Ducrocq G, Fernandez-Aviles F, Gershlick AH, Giannuzzi P, Halvorsen S, Huber K, Juni P, Kastrati A, Knuuti J, Lenzen MJ, Mahaffey KW, Valgimigli M, van 't Hof A, Widimsky P, Zahger D ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012 Oct;33(20):2569-619.
On reading the review on coronary revascularisation in the elderly by
Cockburn et al (1) I must agree that more trials are needed to focus on
the benefit of PCI in elderly populations.
When assessing these patients, clinicians should consider the impact
of symptom relief versus procedural risk. If a patient is experiencing
recurrent and debilitating chest pain requiring frequent hospital
a...
On reading the review on coronary revascularisation in the elderly by
Cockburn et al (1) I must agree that more trials are needed to focus on
the benefit of PCI in elderly populations.
When assessing these patients, clinicians should consider the impact
of symptom relief versus procedural risk. If a patient is experiencing
recurrent and debilitating chest pain requiring frequent hospital
admission then the risks of PCI, despite multiple comorbidities, could
easily be rationalised when the benefit to the patient is clear. In such
patients this "palliative PCI" approach, aiming to improve quality of life
but not necessarily prolong it, should be at the forefront of the
clinicians mind. Each patient should be assessed with consideration of the
benefits to the individual and with a clear understanding of the values of
the patient.
An interesting additional consideration not mentioned in the review
is the potential benefit of PCI in elderly patients in terms of cost to
hospitals. Although complications and poor outcomes may be increased in
this population, the burden of elderly patients deemed unfit for PCI
presenting with recurrent admissions due to chest pain must be taken into
account. I noted that in a paragraph on future research the authors
mentioned further trials of PCI in elderly patients that looked at
myocardial infarction and mortality as their primary outcomes. This may no
longer be as relevant in elderly patients where quality of life is more
important than quantity. A trial involving predominantly elderly patients
assessing quality of life both before and after PCI as the primary outcome
could be useful.
References:
1.Cockburn J, Hildick-Smith D, Trivedi U, de Belder A. Heart 2016;0:1-9.
doi:10.1136/heartjnl-2015-308999
We would like to thank Sarah Blake et al, for their thoughtful and insightful comments.
Firstly, we agree that "palliative PCI" can be a very useful treatment in this elderly patient population. Locally at our institution, via our heart team meeting, we can offer an elderly symptomatic patient with multiple co-morbidities percutaneous coronary intervention (PCI), which often fails to achieve complete re-vasculari...
We would like to thank Sarah Blake et al, for their thoughtful and insightful comments.
Firstly, we agree that "palliative PCI" can be a very useful treatment in this elderly patient population. Locally at our institution, via our heart team meeting, we can offer an elderly symptomatic patient with multiple co-morbidities percutaneous coronary intervention (PCI), which often fails to achieve complete re-vascularisation (even with small territories left ischaemic) but offers significant improvement in symptoms and can leave them safer in the presence of left main stem (LMS) or proximal left anterior decending (LAD) disease. Unlike the younger population, these patients prioritise symptomatic relief, and quality of life (Qol) over prognostic benefit, preferring a quick and immediate return over life years gained.
Secondly, in elderly patients with chest pains treated medically who re-present to the emergency department , a more definitive intervention can certainly help prevent re-admissions. However a careful and full discussion of the risks and benefits of PCI in this high risk cohort needs to be made often in conjunction with family members and it is crucial to consider bleeding risk from DAPT.
Finally, interventional cardiology in general has realised the need to shift outcomes away from procedural success to more patient orientated outcomes, such as QoL and angina status. The only issue with these is that they are qualitative rather than quantitative outcomes and often subjective. However we agree that this may need to be the focus along with bleeding risk in elderly interventional trials.
I read with great interest the article by Morris et al entitled,
"Marginal role for 53 common genetic variants in cardiovascular disease
prediction" (1). The article analyzed a large sample of 11, 851
individuals from 7 prospective studies aimed at primary prevention of
fatal or non-fatal coronary heart disease (CHD) or stroke.
The study incorporated susceptibility variants for CHD and str...
I read with great interest the article by Morris et al entitled,
"Marginal role for 53 common genetic variants in cardiovascular disease
prediction" (1). The article analyzed a large sample of 11, 851
individuals from 7 prospective studies aimed at primary prevention of
fatal or non-fatal coronary heart disease (CHD) or stroke.
The study incorporated susceptibility variants for CHD and stroke
into a genetic risk score (GRS), to match the two conditions predicted by
a conventional risk score QRISK-2. Results for population-wide utility of
the GRS, and estimates from a sequential screening strategy proposed for
individuals at intermediate risk, were provided. The study extrapolated
that 462 intermediate-risk individuals would need to be screened in order
to prevent one coronary heart disease or stroke event in 10 years.
Based on these results, a GRS could become a novel method for
determining which intermediate-risk individuals should be managed
aggressively, if reclassified to high-risk. However, before these results
are adopted in clinical practice, the following should be considered.
First, the extrapolated estimates should be confirmed prospectively.
Second, the 53 variants include 46 for CHD and 7 for stroke. The CHD
variants are not necessarily found to associate with stroke, and vice
versa. This may limit predictions for each disorder. Third, 46 CHD
variants account for 10% of heritability, and do not capture the entire
contribution of genetics estimated at 40-60% (3). Fourth, the GRS included
29 variants unique for CHD, as well as 17 additional variants that also
associate with CHD risk factors, such as cholesterol, blood pressure, and
diabetes (3); these risk factors are already accounted for in QRISK2 and
are not providing independent information. Fifth, the GRS did not
incorporate 10 additional variants recently discovered (4).
Reclassification and discrimination analyses should be redone with only 29
variants (then adding in the 10 new variants) in population-wide analysis
and for intermediate-risk individuals. Finally, a weak effect on mortality
was reported. This is likely due to the GRS being developed using case-
control prevalence and not incidence.
Overall, there is still work to be done before these excellent
results can be implemented.
References
1. Morris RW, Cooper JA, Shah T, Wong A, Drenos F, Engmann J, et al.
Marginal role for 53 common genetic variants in cardiovascular disease
prediction. Heart. 2016 Jun 30. 2. Kullo IJ, Jouni H, Austin EE, Brown SA,
Kruisselbrink TM, Isseh IN, et al. Incorporating a Genetic Risk Score Into
Coronary Heart Disease Risk Estimates: Effect on Low-Density Lipoprotein
Cholesterol Levels (the MI- GENES Clinical Trial). Circulation. 2016
Mar;133(12):1181-8. 3. Deloukas P, Kanoni S, Willenborg C, Farrall M,
Assimes TL, Thompson JR, et al. Large-scale association analysis
identifies new risk loci for coronary artery disease. Nat Genet. 2013
Jan;45(1):25-33. 4. Nikpay M, Goel A, Won HH, Hall LM, Willenborg C,
Kanoni S, et al. A comprehensive 1,000 Genomes-based genome-wide
association meta-analysis of coronary artery disease. Nat Genet. 2015
Oct;47(10):1121-30.
We have read with interest the article written by Emdin et al (1)
using multilevel regression analysis of variance to investigate hospital
performance for heart failure management. We were pleased to note that the
authors apply and refer to our previous methodological work concerning the
use of the Intraclass Correlation (ICC) and Median Odds Ratio (MOR).(2)
However, the authors did not consider a re...
We have read with interest the article written by Emdin et al (1)
using multilevel regression analysis of variance to investigate hospital
performance for heart failure management. We were pleased to note that the
authors apply and refer to our previous methodological work concerning the
use of the Intraclass Correlation (ICC) and Median Odds Ratio (MOR).(2)
However, the authors did not consider a recent paper of ours investigating
survival after heart failure hospitalization and applying a modern
multilevel analytical framework.(3)
Nevertheless, the article by Emdin et al (1) actually applies a
similar way of reasoning that we presented in our previous article.(3) In
this respect, we would like to take this opportunity to comment on their
study.(1)
First, much of variation in performance identified by the authors
could be attributed to the ward rather than to the hospital level since
the ward-level is where the genuine organisational effect could take
place. In our recent study we found that the ward ICC (around 5.3%) was
much larger than the hospital ICC (0.04%).(3)
Second, while the issue of confounding, and hence the need to adjust
for patient case-mix, is a cause of concern in the case of outcome
indicator, it is normally not a concern when it comes to process
indicators (4) and the authors should have discussed this aspect.
Third, the authors used backward stepwise single-level regression to
identify the hospital characteristics that "were significantly associated
with a better performance score". We think this identification should be
based on a priori theory rather than on a posteriori finding of
statistical significance. Besides, the use of single level regression
analysis for this task is unsuitable as it does not consider the intra-
hospital correlation and provides spurious "significant" associations.(2)
Otherwise we agree with Emdin et al(1) methodological approach and
interpretation of the results. However, a reference to our previous
article (3) should have been made.
Kind Regards,
Nermin Ghith, PHD candidate, Research Unit of Chronic Conditions,
Bispebjerg Hospital, Copenhagen.
Prof. Juan Merlo MD, PhD, Head of the Research Unit for Social
Epidemiology, Dept. Clin. Sci.(Malmo), Faculty of Medicine, Lund
University, Sweden
-References
1. Emdin CA, Conrad N, Kiran A, Salimi-Khorshidi G, Woodward M,
Anderson SG, et al. Variation in hospital performance for heart failure
management in the National Heart Failure Audit for England and Wales.
Heart. 2016.
2. Merlo J, Chaix B, Ohlsson H, Beckman A, Johnell K, Hjerpe P, et
al. A brief conceptual tutorial of multilevel analysis in social
epidemiology: using measures of clustering in multilevel logistic
regression to investigate contextual phenomena. Journal of Epidemiology
and Community Health. 2006;60(4):290-7.
3. Ghith N, Wagner P, Fr?lich A, Merlo J. Short Term Survival after
Admission for Heart Failure in Sweden: Applying Multilevel Analyses of
Discriminatory Accuracy to Evaluate Institutional Performance. PLoS ONE.
2016;11(2):e0148187.
4. Rubin HR, Pronovost P, Diette GB. The advantages and disadvantages
of process?based measures of health care quality. International Journal
for Quality in Health Care. 2001;13(6):469-74.
We read with great interest the manuscript by Faden et al. (1)
entitled "A nationwide evaluation of spontaneous coronary artery
dissection in pregnancy and the puerperium" when it was published online
July 13. Using the Healthcare Cost and Utilization Project national
database, the authors evaluated over 4 million pregnancy-related
discharges, looking at the prevalence and outcomes of pregnancy-associated
spontaneous cor...
We read with great interest the manuscript by Faden et al. (1)
entitled "A nationwide evaluation of spontaneous coronary artery
dissection in pregnancy and the puerperium" when it was published online
July 13. Using the Healthcare Cost and Utilization Project national
database, the authors evaluated over 4 million pregnancy-related
discharges, looking at the prevalence and outcomes of pregnancy-associated
spontaneous coronary artery dissection (P-SCAD). By applying the
International Classification of Diseases, 9th Revision (ICD-9) 79 cases of
P-SCAD were identified, resulting in a prevalence of 1.81 per 100,000
pregnancies. Although this study stands out as the largest cohort thus far
assessing P-SCAD, a few shortcomings should be highlighted. First, the
methodology for P-SCAD search and identification included the ICD-9
medical code 412.12 represents a general definition of coronary artery
dissection; there is no specific classification for SCAD in either the ICD
-9 or in the recent ICD-10-CM (diagnosis code I25.42). Therefore, the 79
cases identified by the investigators may have included coronary artery
dissections arising from other causes including atherosclerosis. The
genuine classification of SCAD should be non-atherosclerotic. In addition,
other ambiguous findings by angiography, such as thrombus, may also mimic
SCAD (2). Prior study evaluating pregnant and postpartum women with
myocardial infarction showed that its pathophysiology includes SCAD in 43%
of cases, atherosclerosis in 27%, intracoronary thrombus in 17%, and
normal coronary arteries in 11% (3). Second, despite its well-known
limitations, invasive coronary angiography is still the main tool for
recognizing this condition; other intravascular imaging such as
intravascular ultrasound and optical coherence tomography have been
recently used to enhanced its diagnostic accuracy. Of note, the
pathognomonic appearance of SCAD on angiography--contrast dye staining of
arterial wall with multiple radiolucent lumen--is less prevalent among all
the findings, making the diagnostic ability of invasive angiography
limited and challenging (5). In the present study by Faden et al. there is
no mention about the angiographic findings of those patients, making the
definite and final diagnosis of P-SCAD debatable. Had the authors
reassessed all coronary invasive angiography, the ability to definitively
diagnosis SCDA would have been improved; indeed, 10% of cases did not
undergo invasive angiography, so the final diagnosis P-SCDA could only be
extracted from the data set alone. Finally, when assessing the risk
factors for P-SCAD, the authors demonstrated that chronic hypertension and
lipid profile abnormalities were highly prevalent in relation to SCAD,
which is in disagreement with prior studies showing that most patients had
no risk factors for coronary artery disease (4). Likewise, a high rate of
prior coronary angioplasty and, specifically, coronary artery bypass graft
surgery (34%) in this cohort may suggest the inclusion of patients with
coronary atherosclerosis.
References:
1. Faden MS, Bottega N, Benjamin A, Brown RN. A nationwide evaluation
of spontaneous coronary artery dissection in pregnancy and the puerperium.
Heart 2016;0:1-6. doi:10.1136/heartjnl-2016-309403.
2. Cade JR, Abizaid A, Caixeta A. Organized Thrombus Mimicking
Spontaneous Coronary Artery Dissection. JACC Cardiovasc Interv. 2014;
7(12):1458.
3. Elkayam U, Jalnapurkar S, Barakkat MN, Khatri N, Kealey AJ, Mehra
A, et al. Pregnancy-associated acute myocardial infarction: a review of
contemporary experience in 150 cases between 2006 and 2011. Circulation.
2014;129(16):1695-702.
4. Cade JR, Szarf G, de Siqueira ME, Chaves A, Andrea JC, Figueira
HR, et al. Pregnancy-associated spontaneous coronary artery dissection:
insights from a case series of 13 patients. Eur Heart J Cardiovasc
Imaging. 2016 [Epud ahead of print].
5. Saw J. Coronary angiogram classification of spontaneous coronary
artery dissection. Catheter Cardiovasc Interv. 2014;84(7):1115-22.
We read with great interest the elegant work of Kasula et al.
recently published on Heart [1]. The Authors showed that fractional flow
reserve (FFR) may be an effective tool to discriminate the long-term
functional outcome after percutaneous coronary intervention (PCI) in
patients with acute coronary syndrome (ACS) [1].
This retrospective study included exclusively ACS patients for whom FFR
evaluation resulted "flow lim...
We read with great interest the elegant work of Kasula et al.
recently published on Heart [1]. The Authors showed that fractional flow
reserve (FFR) may be an effective tool to discriminate the long-term
functional outcome after percutaneous coronary intervention (PCI) in
patients with acute coronary syndrome (ACS) [1].
This retrospective study included exclusively ACS patients for whom FFR
evaluation resulted "flow limiting" (<0.80). All patients were treated
with PCI and the main finding of the study was that FFR value after PCI
was able to discriminate those at higher risk of adverse events. The
Authors concluded that FFR reliably estimates baseline ischemia and its
subsequent reduction post-PCI in patients with ACS. We totally agree with
the significance of the post-PCI FFR assessment, but any comment regarding
the FFR role in the determination of baseline ischemia in ACS patients
should not be taken for granted. Recently, Lee et al. showed that
deferring the treatment of intermediate coronary stenosis based only on
the FFR value, without taking into account the features of coronary
microcirculation, exposes the patient to an increase of adverse events
[2]. Kasula et al. did not report the long-term outcome of patients for
whom FFR result was "no flow limiting" [1]. Accordingly, the conclusion
that "FFR alone may be an invaluable tool in identifying ischemia
producing lesions" is methodologically incorrect. It is well established
that microvascular disfunction may be the result of: i) pre-existing
condition (e.g. microvascular angina), ii) chronic damage (e.g chronic
kidney disease [3]), iii) acute injury (e.g. ACS) or iv) a mix of these.
Therefore, the impairment in the coronary microcirculation may differ
significantly across ACS patients. Some patients show a partial impairment
that allows an effective adenosine action and then a proper FFR
determination. Contrarily, other patients have an extensive damage and FFR
assessment may result misleading. For this reason, in our opinion, it
seems important to focus our attention on ACS patients with "no flow
limiting" FFR assessment. In these cases, the simultaneous assessment of
the coronary microcirculation (e.g. index of microcirculatory resistance)
may help physicians in the decision-making process [4].
References
1. Kasula S, Agarwal SK, Hacioglu Y, et al. Clinical and prognostic
value of poststenting fractional flow reserve in acute coronary syndromes.
Heart. 2016 Aug 4 doi: 10.1136/heartjnl-2016-309422
2. Lee JM, Jung JH, Hwang D, et al. Coronary Flow Reserve and
Microcirculatory Resistance in Patients With Intermediate Coronary
Stenosis. J Am Coll Cardiol. 2016 15;67(10):1158-69
3. Tebaldi M, Biscaglia S, Fineschi M, et al. Fractional flow reserve
evaluation and chronic kidney disease: Analysis from a multicenter Italian
registry (the FREAK study). Catheter Cardiovasc Interv. 2015 Dec 31. doi:
10.1002/ccd.26364
4. Tebaldi M, Biscaglia S, Pecoraro A, et al. Fractional flow reserve
implementation in daily clinical practice: A European survey. Int J
Cardiol. 2016 15;207:206-7.
I read the article by Kasula and colleagues with great interest. I
firmly believe that this is a novel finding and of great clinical
significance (1).
Utility of Fractional flow reserve (FFR) is firmly established in
stable coronary artery disease but has been widely debated in patients
with acute MI particularly in the culprit vessel (2, 3). FFR measurements
require maximal coronary hyperaemia which may be les...
I read the article by Kasula and colleagues with great interest. I
firmly believe that this is a novel finding and of great clinical
significance (1).
Utility of Fractional flow reserve (FFR) is firmly established in
stable coronary artery disease but has been widely debated in patients
with acute MI particularly in the culprit vessel (2, 3). FFR measurements
require maximal coronary hyperaemia which may be less readily achieved in
patients with acute coronary disease because of coronary microvascular
dysfunction. This in turn may result in a falsely higher FFR value. This
will be of particular concern while assessing FFR value post-PCI since
coronary stenting of a 'hot' culprit lesion in acute coronary syndrome
would inevitably carry risk of some distal embolization which may further
exacerbate this issue.
Since, microvascular obstruction carries a poor prognosis, a direct (in
contrast to an inverse relationship) relationship between post-PCI FFR
value and adverse outcome would have supported this theoretical limitation
of FFR in patients with MI (4). However, it was reassuring to see that
these concerns appear unfounded in the current study. The fact that FFR
value had an inverse relationship with future adverse events is an in-
direct evidence that FFR value is still valid even in culprit vessel in
patients with NSTEMI.
References:
1) Clinical and prognostic value of poststenting fractional flow reserve
in acute coronary syndromes
2) Pijls NH, De Bruyne B, Peels K, Van Der Voort PH, Bonnier HJ,
Bartunek J, Koolen JJ, Koolen JJ. Measurement of fractional flow reserve
to assess the functional severity of coronary-artery stenoses. N Engl J
Med 1996;334:1703-1708.
3) Tonino P.A., De Bruyne B., Pijls N.H., et al; Fractional flow
reserve versus angiography for guiding percutaneous coronary intervention.
N Engl J Med. 2009;360:213-224
4) Fearon W.F., Low A.F., Yong A.S., et al; Prognostic value of
the Index of Microcirculatory Resistance measured after primary
percutaneous coronary intervention. Circulation. 2013;127:2436-2441.
In this interesting article, Lipworth and colleagues report that beta
-blockers are underused in patients with heart failure (HF) and COPD,
compared to those with HF alone. However, they do not quote the
proportion of "HF" patients within their dataset who had HF with reduced
ejection fraction (HFrEF; left ventricular ejection fraction (LVEF)
<40%) and HF with preserved ejection fraction (HFpEF; LVEF >50%).
This d...
In this interesting article, Lipworth and colleagues report that beta
-blockers are underused in patients with heart failure (HF) and COPD,
compared to those with HF alone. However, they do not quote the
proportion of "HF" patients within their dataset who had HF with reduced
ejection fraction (HFrEF; left ventricular ejection fraction (LVEF)
<40%) and HF with preserved ejection fraction (HFpEF; LVEF >50%).
This distinction is important, as beta-blockers are only recommended in HF
guidelines for patients with HFrEF (1), owing to a lack of trial data to
support their efficacy in patients with HFpEF.
Furthermore, patients with HFpEF tend to have a higher prevalence of
co-morbidities compared to patients with HFrEF, including COPD,
hypertension and diabetes (2). Thus, it is possible that "HF and COPD"
patients in this dataset may have a higher proportion of HFpEF to HFrEF,
in comparison to patients with "HF alone", and the rates of ACE/ARB
prescribing may be increased in this group owing to treatment of
hypertension and diabetes rather than HF. These considerations may
therefore confound the strength of the authors' conclusions regarding
underuse of beta-blockers in patients with HF and COPD.
References
1. Ponikowski P, Voors AA, Anker SD et al. 2016 ESC Guidelines for
the diagnosis and treatment of acute and chronic heart failure. Eur Heart
J 2016; DOI:
10.1093/eurheartj/ehw128.
2. Ather S, Chan W, Bozkurt B et al. Impact of non-cardiac
comorbidities on morbidity and mortality in a predominantly male
population with heart failure and preserved versus reduced ejection
fraction. J Am Coll Cardiol 2012;59:998-1005.
We would like to thank Dr Cunnington for his interest in our study
and raising some potentially interesting points . We do not have a
breakdown of patients with heart failure ( HF) who had either preserved
(HFpEF) or reduced ejection fraction (HFrEF) . Since beta-blockers only
have a licensed indication for HFrEF on the basis of an echocardiogram ,
we do not believe that this is likely to be a relevant factor withi...
We would like to thank Dr Cunnington for his interest in our study
and raising some potentially interesting points . We do not have a
breakdown of patients with heart failure ( HF) who had either preserved
(HFpEF) or reduced ejection fraction (HFrEF) . Since beta-blockers only
have a licensed indication for HFrEF on the basis of an echocardiogram ,
we do not believe that this is likely to be a relevant factor within our
dataset . The relative prevalence of hypertension within our cohort was
13.3% verses 11.6% ,and for diabetes was 47.4% verses 41.9% respectively
for HF alone verses HF with COPD . Hence the assertion made regarding a
higher putative comorbidity is not supported by the data presented here .
Consequently prescribing of ACEI/ARB in HF with COPD was not confounded
by comorbidity due to treatment for either diabetes or hypertension . The
higher use of ACEI/ARB without beta-blocker in HF with COPD compared to HF
alone is more likely to reflect a reticence of physicians to prescribe add
on therapy with beta-blockers in the presence of airflow obstruction due
to fears of bronchoconstriction . As such we remain confident in the
strength of our conclusions regarding underuse of beta-blockers in HF with
COPD .
We read with interest the article by Varcoe et al (Heart Jan 15 th 20917) “Impact of call-to-balloon time on 30-day mortality in contemporary practice” We were not surprised by the results which indicate yet again that patients with delays to reperfusion suffer worse mortality rates - the concept of timely reperfusion in STEMI has been previously very well documented, and its importance recognised for some time. Thus de Lucca (1), Cannon (2) and others (3) reported data >10 years ago which supported the concept that mortality rates increase when important time metrics are not achieved. Time dependent infarct size is considered the cause (4)
Show MoreWhen the National Infarct Angioplasty Project (NIAP) was established in 2008 with the explicit aim of rolling out P-PCI in the UK, everyone involved in care of STEMI patients thought it was a good idea to go with a policy of one STEMI management strategy, for simplicity. No-one doubted that P-PCI should become the standard of care. Some (including the authors of this letter - one of whom served on NIAP) voiced concerns however that, based on the published data, achieving guideline mandated times was essential, and that this might be difficult to achieve with P-PCI in patients transferred from more rural regions. There was assurance from Department of Health that >95% of patients were “within distance” of a P-PCI centre. We tried to point out that being “within distance”, and being within the mandated times were very differe...
Dear Editor
On reading the review on coronary revascularisation in the elderly by Cockburn et al (1) I must agree that more trials are needed to focus on the benefit of PCI in elderly populations.
When assessing these patients, clinicians should consider the impact of symptom relief versus procedural risk. If a patient is experiencing recurrent and debilitating chest pain requiring frequent hospital a...
We would like to thank Sarah Blake et al, for their thoughtful and insightful comments.
Firstly, we agree that "palliative PCI" can be a very useful treatment in this elderly patient population. Locally at our institution, via our heart team meeting, we can offer an elderly symptomatic patient with multiple co-morbidities percutaneous coronary intervention (PCI), which often fails to achieve complete re-vasculari...
Dear Editor,
I read with great interest the article by Morris et al entitled, "Marginal role for 53 common genetic variants in cardiovascular disease prediction" (1). The article analyzed a large sample of 11, 851 individuals from 7 prospective studies aimed at primary prevention of fatal or non-fatal coronary heart disease (CHD) or stroke.
The study incorporated susceptibility variants for CHD and str...
Dear Editor,
We have read with interest the article written by Emdin et al (1) using multilevel regression analysis of variance to investigate hospital performance for heart failure management. We were pleased to note that the authors apply and refer to our previous methodological work concerning the use of the Intraclass Correlation (ICC) and Median Odds Ratio (MOR).(2) However, the authors did not consider a re...
We read with great interest the manuscript by Faden et al. (1) entitled "A nationwide evaluation of spontaneous coronary artery dissection in pregnancy and the puerperium" when it was published online July 13. Using the Healthcare Cost and Utilization Project national database, the authors evaluated over 4 million pregnancy-related discharges, looking at the prevalence and outcomes of pregnancy-associated spontaneous cor...
We read with great interest the elegant work of Kasula et al. recently published on Heart [1]. The Authors showed that fractional flow reserve (FFR) may be an effective tool to discriminate the long-term functional outcome after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) [1]. This retrospective study included exclusively ACS patients for whom FFR evaluation resulted "flow lim...
I read the article by Kasula and colleagues with great interest. I firmly believe that this is a novel finding and of great clinical significance (1).
Utility of Fractional flow reserve (FFR) is firmly established in stable coronary artery disease but has been widely debated in patients with acute MI particularly in the culprit vessel (2, 3). FFR measurements require maximal coronary hyperaemia which may be les...
In this interesting article, Lipworth and colleagues report that beta -blockers are underused in patients with heart failure (HF) and COPD, compared to those with HF alone. However, they do not quote the proportion of "HF" patients within their dataset who had HF with reduced ejection fraction (HFrEF; left ventricular ejection fraction (LVEF) <40%) and HF with preserved ejection fraction (HFpEF; LVEF >50%). This d...
We would like to thank Dr Cunnington for his interest in our study and raising some potentially interesting points . We do not have a breakdown of patients with heart failure ( HF) who had either preserved (HFpEF) or reduced ejection fraction (HFrEF) . Since beta-blockers only have a licensed indication for HFrEF on the basis of an echocardiogram , we do not believe that this is likely to be a relevant factor withi...
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