Atrial fibrillation (AF) constitutes a major risk factor for stroke and death.1 ,2 The potential of biomarkers to improve the prognostication concerning stroke and other cardiovascular events in patients with AF is gaining strength of evidence and clinical promise. In particular the biomarkers of cardiovascular stress and dysfunction such as cardiac troponin (cTn), a marker of myocardial cell damage; N-terminal B-type natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction; and growth-differentiation factor-15 (GDF-15), a marker of inflammation and oxidative stress, have been shown to be strong independent predictors.3–8 Although inflammatory activation has been linked to the occurrence of AF and to a prothrombotic state, the association with subsequent cardiovascular events during treatment with oral anticoagulation has not been fully established.9–14 Prior studies evaluating the relation between inflammation and cardiovascular events in patients with AF have often been exploratory and did not take into account the protective effect of oral anticoagulation. In addition the associations with outcomes have not been fully adjusted for other risk indicators, in particular other cardiovascular biomarkers, which recently have show
Atrial fibrillation (AF) constitutes a major risk factor for stroke and death.1 ,2 The potential of biomarkers to improve the prognostication concerning stroke and other cardiovascular events in patients with AF is gaining strength of evidence and clinical promise. In particular the biomarkers of cardiovascular stress and dysfunction such as cardiac troponin (cTn), a marker of myocardial cell damage; N-terminal B-type natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction; and growth-differentiation factor-15 (GDF-15), a marker of inflammation and oxidative stress, have been shown to be strong independent predictors.3–8 Although inflammatory activation has been linked to the occurrence of AF and to a prothrombotic state, the association with subsequent cardiovascular events during treatment with oral anticoagulation has not been fully established.9–14 Prior studies evaluating the relation between inflammation and cardiovascular events in patients with AF have often been exploratory and did not take into account the protective effect of oral anticoagulation. In addition the associations with outcomes have not been fully adjusted for other risk indicators, in particular other cardiovascular biomarkers, which recently have showed to be independent and powerful markers of adverse outcomes in patients with AF.4 In this predefined biomarker study within the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) trial we asse...
Atrial fibrillation (AF) constitutes a major risk factor for stroke and death.1 ,2 The potential of biomarkers to improve the prognostication concerning stroke and other cardiovascular events in patients with AF is gaining strength of evidence and clinical promise. In particular the biomarkers of cardiovascular stress and dysfunction such as cardiac troponin (cTn), a marker of myocardial cell damage; N-terminal B-type natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction; and growth-differentiation factor-15 (GDF-15), a marker of inflammation and oxidative stress, have been shown to be strong independent predictors.3–8 Although inflammatory activation has been linked to the occurrence of AF and to a prothrombotic state, the association with subsequent cardiovascular events during treatment with oral anticoagulation has not been fully established.9–14 Prior studies evaluating the relation between inflammation and cardiovascular events in patients with AF have often been exploratory and did not take into account the protective effect of oral anticoagulation. In addition the associations with outcomes have not been fully adjusted for other risk indicators, in particular other cardiovascular biomarkers, which recently have showed to be independent and powerful markers of adverse outcomes in patients with AF.4 In this predefined biomarker study within the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) trial we assessed the associations between levels of the inflammatory biomarkers interleukin 6 (IL-6) and C reactive protein (CRP) at baseline and clinical outcomes including adjustments for established clinical risk factors and other previously shown to be prognostically significant cardiovascular biomarkers in approximately 15 000 patients with AF treated with either warfarin or apixaban oral anticoagulation.15 ,16 Further, the prognostic information gained by the inflammatory biomarkers in relation to the currently used CHA2DS2VASc (risk model to assess risk of stroke) and HAS-BLED (risk model to asses risk of major bleeding) scores was evaluated, as well as potential interactions with the effects of apixaban as compared with warfarin on all outcomes.Atrial fibrillation (AF) constitutes a major risk factor for stroke and death.1 ,2 The potential of biomarkers to improve the prognostication concerning stroke and other cardiovascular events in patients with AF is gaining strength of evidence and clinical promise. In particular the biomarkers of cardiovascular stress and dysfunction such as cardiac troponin (cTn), a marker of myocardial cell damage; N-terminal B-type natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction; and growth-differentiation factor-15 (GDF-15), a marker of inflammation and oxidative stress, have been shown to be strong independent predictors.3–8 Although inflammatory activation has been linked to the occurrence of AF and to a prothrombotic state, the association with subsequent cardiovascular events during treatment with oral anticoagulation has not been fully established.9–14 Prior studies evaluating the relation between inflammation and cardiovascular events in patients with AF have often been exploratory and did not take into account the protective effect of oral anticoagulation. In addition the associations with outcomes have not been fully adjusted for other risk indicators, in particular other cardiovascular biomarkers, which recently have showed to be independent and powerful markers of adverse outcomes in patients with AF.4 In this predefined biomarker study within the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) trial we assessed the associations between levels of the inflammatory biomarkers interleukin 6 (IL-6) and C reactive protein (CRP) at baseline and clinical outcomes including adjustments for established clinical risk factors and other previously shown to be prognostically significant cardiovascular biomarkers in approximately 15 000 patients with AF treated with either warfarin or apixaban oral anticoagulation.15 ,16 Further, the prognostic information gained by the inflammatory biomarkers in relation to the currently used CHA2DS2VASc (risk model to assess risk of stroke) and HAS-BLED (risk model to asses risk of major bleeding) scores was evaluated, as well as potential interactions with the effects of apixaban as compared with warfarin on all outcomes.
Assessing effect of remote ischaemic preconditioning on clinical
outcomes in patients undergoing cardiac bypass surgery
To the Editor : In a recent article of Candilio et al.1 assessing the
effect of remote ischaemic preconditioning (RIPC) on postoperative
outcomes in patients undergoing cardiac surgery, they showed that RIPC
reduced the amount of perioperative myocardial injury by 26% and the
incidence of acute...
Assessing effect of remote ischaemic preconditioning on clinical
outcomes in patients undergoing cardiac bypass surgery
To the Editor : In a recent article of Candilio et al.1 assessing the
effect of remote ischaemic preconditioning (RIPC) on postoperative
outcomes in patients undergoing cardiac surgery, they showed that RIPC
reduced the amount of perioperative myocardial injury by 26% and the
incidence of acute kidney injury by 48%.The authors discuss the
limitations of their work.In our view, the following important issues in
this study seemed not to be well addressed.
Perioperative dexmedetomidine infusion was not included in data
analysis.Actually,perioperative dexmedetomidine infusion is common among
patients undergoing cardiac surgery.
Dexmedetomidine, a highly selective?2 adrenoreceptor agonist, has
advantages for reducing renal injury. Perioperative dexmedetomidine
infusion effectively reduces the incidence and severity of acute kidney
injury in cardiac surgery.2
Preoperative Contrast angiography was not included in data analysis.
Preoperative Contrast angiography is not rare among patients
undergoing coronary artery bypass grafting surgery.The contrast-induced
nephropathy is independently associated with increased postoperative risks
of adverse renal events 3.
Aminoglycoside, a commonly administered antibiotic in the operating
room, independently associated with increased risks of postoperative acute
renal injury(AKI) through intracellular processes such as mitochondrial
dysfunction and reduction of protein synthesis.4
We are concerned that if there is any disbalance in these factors
would have confounded the interpretation of the results.
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.Jin Sun Cho, Jae-Kwang Shim, Sara Soh , et al.Perioperative
dexmedetomidine reduces the incidence and severity of acute kidney injury
following valvular heart surgery. Kidney Int 2015; advance online
publication, 7 October 2015;doi:10.1038/ki.2015.306
3.Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium-
induced nephropathy. Kidney Int 2005; 68:14-22.
1.Department of Anesthesiology, the Affiliated Hospital of Qingdao
University ,Qingdao ,China
2.Department of nephrology ,the Affiliated Hospital of Qingdao
University , Qingdao ,China
Correspondence:
Wei Zhang, Department of Nephrology, The Affilitated Hospital of
Qingdao University,Qingdao266003, China.
E-mail:xfwwww@163.com
Contributors: Feng Xue read the manuscript of Candilio et al.;
analysed their methods and data; suggested comment points and drafted this
manuscript; responsible for this manuscript; and approved the final
manuscript. Hai chen Chu read the paper of Candilio et al.;analysed their
data; revised the comment points and this manuscript; and approved the
final manuscript.Wei Zhang read the manuscript of Candilio et al.;
analysed their methods and data; revised the comment points and this
manuscript; and approved the final manuscript.
Imazio et al. investigated the incidence and prognosis of presumably
new onset atrial fibrillation (AF) and flutter (AFl) in acute pericarditis
[1]. They showed that only 4% of the patients with acute pericarditis
developed new onset atrial arrhythmias [1]. The mean age of patients who
experienced AF in this study was 67 years. Notably, the age-stratified AF
prevalence in this study remains comparable to that in the gener...
Imazio et al. investigated the incidence and prognosis of presumably
new onset atrial fibrillation (AF) and flutter (AFl) in acute pericarditis
[1]. They showed that only 4% of the patients with acute pericarditis
developed new onset atrial arrhythmias [1]. The mean age of patients who
experienced AF in this study was 67 years. Notably, the age-stratified AF
prevalence in this study remains comparable to that in the general
population of a developed country [2-3]. The study findings strongly
suggested that acute pericarditis by itself may not be significantly
arrhythmogenic.
It apparently remains a common prevailing myth that acute idiopathic
pericarditis predisposes to AF due to an accompanying inflammatory state.
On the contrary, arrhythmias in acute idiopathic or viral pericarditis are
often related to alternate associated comorbidities such as ageing,
ventricular dysfunction, myocardial ischemia and/or factors predisposing
to left atrial abnormality [4-7]. This is supported by the data from
several prior controlled investigations [4-6]. Non-idiopathic forms of
pericarditis such as suppurative pericarditis and the ones complicated by
development of effusions or major hemodynamic alterations may be at a
higher risk for developing AF due to accompanying septic state and fluid
volume shifts. This perhaps may be partly the reason for why some studies
had shown higher rates of AF in patients with bacterial and tuberculous
pericarditis [8]. Similarly, in the current study presence of pericardial
effusion was associated with a higher risk of AF. Also, patients with
postoperative pericarditis and post-pericardiotomy syndrome may have a
higher incidence of AF due to the similar reasons associated with any
other form of post-surgical AF.
In summary, the presence of AF in acute idiopathic pericarditis
should not be perceived as a causal association and rather may reflect
unmasking of AF in a patient with prior asymptomatic paroxysmal AF or
simply reflect the presence of a prior underlying risk substrate for AF
such as left atrial enlargement or left ventricular systolic or diastolic
dysfunction. This well-designed study further in fact further clarifies
that the use of anticoagulation, when warranted, in patients with acute
pericarditis may not be as deleterious as it was previously thought.
References:
1. Imazio M, Lazaros G, Picardi E, Vasileiou P, Orlando F, Carraro M,
Tsiachris D, Vlachopoulos C, Georgiopoulos G, Tousoulis D, Belli R, Gaita
F. Incidence and prognostic significance of new onset atrial
fibrillation/flutter in acute pericarditis. Heart. 2015 Apr 29. pii:
heartjnl-2014-307398. doi: 10.1136/heartjnl-2014-307398.
2. Ball J, Carrington MJ, McMurray JJ, Stewart S. Atrial fibrillation:
profile and burden of an evolving epidemic in the 21st century. Int J
Cardiol. 2013;167(5):1807-24.
3. Lip GY, Brechin CM, Lane DA. The global burden of atrial fibrillation
and stroke: a systematic review of the epidemiology of atrial fibrillation
in regions outside North America and Europe. Chest. 2012;142(6):1489-98.
4. Spodick DH. Arrhythmias during acute pericarditis. A prospective study
of 100 consecutive cases. JAMA. 1976;235:39-41.
5. Spodick DH. Significant arrhythmias during pericarditis are due to
concomitant heart disease. J Am Coll Cardiol. 1998;32:551-2.
6. Spodick DH: The Pericardium: A Comprehensive Textbook, Marcel Dekker,
New York 1997.
7. Chhabra L, Spodick DH. Letter by Chhabra and Spodick regarding the
article, "Clinical Profile and Influences on Outcomes in Patients
Hospitalized for Acute Pericarditis" by Kyt? et al. Circulation. 2015. In
Press.
8.Syed FF, Ntsekhe M, Wiysonge CS, et al. Atrial fibrillation as a
consequence of tuberculous pericardial effusion. Int J Cardiol. 2012;
158:152-4.
To the Editor:
We have read with interest the article of Miranda WR and coauthors1, in
which a case of effusive-constrictive pericarditis is presented. This is a
comprehensive and educational case that provides clinicians with a
valuable message. Some points, however, require additional clarification
in order to further strengthen the impact of this case. In particular, it
is mentioned in the introduction that the patien...
To the Editor:
We have read with interest the article of Miranda WR and coauthors1, in
which a case of effusive-constrictive pericarditis is presented. This is a
comprehensive and educational case that provides clinicians with a
valuable message. Some points, however, require additional clarification
in order to further strengthen the impact of this case. In particular, it
is mentioned in the introduction that the patient was diagnosed with
'idiopathic pericarditis'. Nonetheless, the diagnosis of pericarditis is
established in the presence of at least 2 out of the 4 main criteria
including chest pain, pericardial friction, typical ECG changes and
pericardial effusion.2 CRP elevation and pericardial inflammation in the
cardiac magnetic resonance imaging (cMR) both constitute supportive
findings. Accordingly, since only one diagnostic criterion was fulfilled
(i.e. pericardial effusion), it should probably be more appropriate to
'label' the patient's disorder as 'idiopathic pericardial effusion' rather
than 'idiopathic pericarditis'.
Concerning treatment, the patient received initially colchicine as an
outpatient, despite normal baseline CRP values. However, in the absence
increased CRP levels, the efficacy of colchicine is questionable in
chronic idiopathic pericardial effusion.3 Furthermore, even in the setting
of idiopathic pericarditis, which this patient was presumed to have,
colchicine is beneficial when administered in conjunction with either
aspirin/non-steroidal anti-inflammatory (NSAID) medications or
corticosteroids, but not as monotherapy.3
Another intriguing finding in this case was the demonstration of active
pericardial inflammation in cMR. This is a quite unexpected finding in the
presence of normal baseline CRP levels. Since pericardiocentesis and
drainage catheters are potential triggers of pericardial inflammation, one
wonders if pericardiocentesis was the actual cause of pericardial
inflammation. Along this line, it would be interesting to know the post-
pericardiocentesis serum CRP levels.
Last but not least, the patient became asymptomatic and the jugular
pressure normalized within 72 hours after aggressive NSAID therapy. This
turn of events strongly suggests transient pericardial constriction,
namely a reversible cause of pericardial constriction, which is
occasionally observed towards the end of the effusive period of
pericarditis.4
In conclusion, a final diagnosis of idiopathic pericardial effusion
(possibly post-pericarditis) with transitory constriction probably unifies
all aspects of this challenging case.
References
1 Miranda WR, Newman DB, Nishimura RA. A not so typical pericardial
effusion case....Heart 2015 Jun 17. pii: heartjnl-2015-308115.
2 Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart 2015
Apr 8. pii: heartjnl-2014-306362.
3 Brucato A, Brambilla A, Adler Y, Spodick,D. Colchicine for Recurrent
Acute Pericarditis. Arch Intern Med 2006;166:696.
4 Haley JH, Tajik AJ, Danielson GK, et al. Transient constrictive
pericarditis: causes and natural history. J Am Coll Cardiol 2004;43:271-5.
a Division of Cardiology, University of Arkansas for Medical
Sciences, Little Rock, Arkansas; b Division of Cardiology, Winthrop
University Hospital, Mineola, New York.
Funding: None
Conflicts of interest: none
Word Count: 325
Corresponding author & (address for reprints)
Ramez Nairooz, MD...
a Division of Cardiology, University of Arkansas for Medical
Sciences, Little Rock, Arkansas; b Division of Cardiology, Winthrop
University Hospital, Mineola, New York.
Funding: None
Conflicts of interest: none
Word Count: 325
Corresponding author & (address for reprints)
Ramez Nairooz, MD
Division of Cardiology
University of Arkansas for Medical Sciences
4301 West Markham, Slot 532,
Little Rock, AR 72205-7199
Tel: (714)-606-5550; Fax: (501)-686-6439
Email: ramez.nairooz@gmail.com
Letter to editor
We read with interest the recently published meta-analysis by
Kowalewski and colleagues (1) titled "Complete revascularization in ST-
elevation myocardial infarction and multivessel disease: meta-analysis of
randomized controlled trials". However, we feel there are a few questions
that need addressing:
1. The authors define complete revascularization as "revascularization to
non-infarct-related artery lesions during index procedure" and non-
complete MV-PCI "encompassed culprit only revascularization and staged
approaches". Hence we ask the authors why they used the CvLPRIT (2) event
numbers for the total population in whom complete revascularization was
done both same setting and staged during index hospitalization? Shouldn't
they have used the clinical outcomes of immediate vs staged PCI (published
as supplementary material) to stay true to their definition?
2. Is staged PCI during index hospitalization same as after discharge
at later date revascularization? Can they be all added in one group "non-
complete MV-PCI"? Maamoun et al scheduled the second procedure at 7 days,
Ochala had the second procedure at average of 27 days while Politi et al
staged it at an average of 56 days. How did staged PCI become bundled in
the same group with infarct related artery only revascularization as seen
in PRAMI, CvLPRIT and HELP-AMI? Thus we ask the authors were there any
differences in outcomes of those who were staged in hospital vs staged at
a later time?
3. Finally we ask, what conclusion should clinicians draw from this
analysis based on the heterogeneous trials which constitute it? Can
clinicians conclude meaningful deductions regarding same setting complete
revascularization (CR) vs index hospitalization CR vs later date CR vs
infarct related artery only revascularization? These questions face the
interventional community on daily basis and have no conclusive answer,
with guidelines remaining equivocal on the topic. The COMPLETE trial
(NCT01740479), currently ongoing, may shed some light on index
hospitalization CR vs. infarct related artery only revascularization as
the initial strategy, but cannot entirely answer the question as to
optimal strategy.
References:
1. Kowalewski M, Schulze V, Berti S, et al. Complete revascularisation in
ST-elevation myocardial infarction and multivessel disease: meta-analysis
of randomised controlled trials. Heart. 2015 Jun 2. pii:heartjnl-2014-
307293. doi: 10.1136/heartjnl-2014-307293. [Epub ahead of print]
2. Gershlick AH, Khan JN, Kelly DJ, et al. Randomized trial of complete
versus lesion-only revascularization in patients undergoing primary
percutaneous coronary intervention for STEMI and multivessel disease: the
CvLPRIT trial. J Am Coll Cardiol. 2015;65:963-72.
The article entitled "The pathophysiology of hypertensive acute heart
failure"[1] provides a contemporary review of mechanisms involved in the
development of acute pulmonary oedema (APO). We wish to highlight the
potential key role of the right ventricle in the pathogenesis of APO.[2]
APO is often thought to result from backward pressure where a disease
of the left ventricle causes the left ventricular end-diasto...
The article entitled "The pathophysiology of hypertensive acute heart
failure"[1] provides a contemporary review of mechanisms involved in the
development of acute pulmonary oedema (APO). We wish to highlight the
potential key role of the right ventricle in the pathogenesis of APO.[2]
APO is often thought to result from backward pressure where a disease
of the left ventricle causes the left ventricular end-diastolic pressure
to rise resulting in elevated pulmonary venous pressure and hence
pulmonary capillary hydrostatic pressure. However, an increase in a given
pressure can only occur if there is energy is either added or converted
(eg kinetic to pressure energy). Since the conversion of kinetic energy to
pressure energy is too small to result in a significant rise in pressure,
the latter cannot be a dominant mechanism.
We suggest that extra pressure energy is added by the right
ventricle.[3] If the left ventricular stroke volume (LVSV) falls and the
right ventricular stroke volume (RVSV) is unchanged, there are two
effects: i) a beat by beat increase in the blood in the pulmonary
circulation, and ii) a progressive rise in left ventricular diastolic
pressure. The acute elevation of LVEDP must be a consequence of the
increased energy added by RV rather than due to back pressure as a direct
result of a LV disease.[2, 3]
In situations of a high afterload the contractile stress required to
maintain normal LVSV may be transiently exceeded. In the presence of a
relatively normal RV, a mismatch between LV and RV stroke volumes results.
An increased catecholamine drive causes augmented RV contractility and
systemic venous constriction, stimulating the RV Frank Starling mechanism
and increasing RVSV and pulmonary pressure. However, any disease of the
left ventricle results in a failure to increase the left heart output even
in the presence of adrenergic drive or LV Frank-Starling response.[4]
There is inevitably a fluid shift from the systemic circulation to the
pulmonary circulation and a rise in pulmonary artery pressure, capillary
hydrostatic pressure, and consequently, LVEDP. Any evaluation of
pathophysiology of APO that ignores the critical role of the right
ventricle is incomplete.
1 Viau DM, Sala-Mercado JA, Spranger MD, et al. The pathophysiology
of hypertensive acute heart failure. Heart 2015.
2 MacIver DH, Clark AL. The vital role of the right ventricle in the
pathogenesis of acute pulmonary edema. The American journal of cardiology
2015;115:992-1000.
3 MacIver DH, Dayer MJ, Harrison AJ. A general theory of acute and
chronic heart failure. Int J Cardiol 2013;165:25-34.
4 Kitzman DW, Higginbotham MB, Cobb FR, et al. Exercise intolerance
in patients with heart failure and preserved left ventricular systolic
function: failure of the Frank-Starling mechanism. J Am Coll Cardiol
1991;17:1065-72.
I appreciate Dr. Stovitz's interest in our editorial and on the topic
of the "Obesity Paradox". As I stated in my book, The Obesity Paradox,1 a
paradox can be defined "as a statement that is seemingly contradictory or
opposed to common sense and yet is perhaps true". Based on this, Stovitz
could have better titled his letter as "True, true, and is a true
paradox." As we previously demonstrated,2-4 despite that obese wit...
I appreciate Dr. Stovitz's interest in our editorial and on the topic
of the "Obesity Paradox". As I stated in my book, The Obesity Paradox,1 a
paradox can be defined "as a statement that is seemingly contradictory or
opposed to common sense and yet is perhaps true". Based on this, Stovitz
could have better titled his letter as "True, true, and is a true
paradox." As we previously demonstrated,2-4 despite that obese with
coronary heart disease (CHD) appeared to have a worse CHD risk profile,
including more abnormal lipids , more adverse glucose and blood pressure
values, and higher levels of inflammation, all of which suggest a worse
prognosis, the prognosis of the overweight/ obese with CHD was
"paradoxically" better. We believe that the fact that the obese were a
few years younger than their leaner counterparts with CHD did not
completely explain, or statistically explain, their better prognosis,
which represents a true paradox. However, no pun intended, I believe that
the rest of the letter by Dr. Stovitz is "true".
As we stated in our editorial, "supporting the obesity paradox,
however, does not mean that obesity is being promoted or that one is
suggesting that obesity is a good thing." As we also stated, "quite
possibly, many overweight and obese patients with CHD may not have
developed CHD in the first place had obesity been prevented." On the
other hand, although lean patients with CHD appear "healthier" than their
overweight/obese counterparts with similar CHD, they have a worse
prognosis, probably due to developing CHD from a different etiology, as
Dr. Stovitz suggests, which I believe is due to genetic predisposition.
Finally, as I started my editorial with the two CHD cases, one with
BMI of 23 kg/m2 and the other with BMI 32 kg/m2, my points of the
editorial remain true. Although many years ago I predicted that the thin
patient with CHD would have a better prognosis, fifteen years later the
data continues to show that overweight and obese (at least mildly obese)
with CHD "paradoxically" have a better short- and medium-term prognosis.
References:
1. Lavie CJ (with Loberg K). The Obesity Paradox - When Thinner Means
Sicker and Heavier Means Healthier. New York, NY:Hudson Street
Press;2014.
2. Lavie CJ, Milani RV, Artham SM, Patel DA, Ventura HO. The obesity
paradox, weight loss, and coronary disease. Am J Med 2009;122:1106-1114.
3. Lavie CJ, De Schutter A, Patel D, Artham SM, Milani RV. Body
composition and coronary heart disease mortality - an obesity or a lean
paradox? Mayo Clin Proc 2011;86(9):857-864.
4. Lavie CJ, De Schutter A, Patel DA, Romero-Corral A, Artham SM, Milani
RV. Body composition and survival in stable coronary heart disease.
Impact of lean mass index and body fat in the "obesity paradox". J Am
Coll Cardiol 2012;60(15):1374-80.
Conflict of Interest:
I am the author of the book "The Obesity Paradox" and I have served as a consultant and speaker for the Coca-Cola Company, but on fitness and not any of their products.
The timely restoration of flow in the culprit coronary artery lesion
remains the cornerstone of treatment in patients with evolving myocardial
infarction but with the inevitable cost of reperfusion injury. Cardiac
ischaemic conditioning (IC) is capable of reducing the extent of final
infarct size, but its actual benefit in improving clinical outcomes
remains to be established. In their excellent review article published...
The timely restoration of flow in the culprit coronary artery lesion
remains the cornerstone of treatment in patients with evolving myocardial
infarction but with the inevitable cost of reperfusion injury. Cardiac
ischaemic conditioning (IC) is capable of reducing the extent of final
infarct size, but its actual benefit in improving clinical outcomes
remains to be established. In their excellent review article published
recently in the Journal [1], Bulluck and Hausenloy describe elegantly the
expectations emerged from the different forms of IC (pre-, per- and post-
conditioning, applied locally or remotely). The authors present the
clinical conditions where IC has been tested and they also provide novel
thoughts regarding the potential to investigate its use in additional
clinical settings. We fully agree that IC can be applied in percutaneous
coronary intervention (PCI) during non-ST elevation myocardial infarction
(NSTMI), as outlined in Figure 2, but not only in the form of remote
ischaemic preconditioning (RIPC). Local ischemic postconditioning (IPost)
has also been successfully applied in patients presented with non-totally
occlusive coronary artery lesions; we have previously shown that IPost was
feasible in patients with unstable angina and NSTMI and effective in
reducing circulating biomarkers of oxidative stress, improving
microcirculatory function in the short term as well as wall motion score
index and left ventricular remodeling in the long term [2,3]. In addition,
the authors report that the Hoole's study was the first one that tested
the effect of limb remote ischaemic conditioning (RIC) in elective PCI.
However, our group published the successful application of the
intervention during elective PCI three years earlier, using actually a
more potent RIC protocol with cuff inflation in both arms and at more
appropriate timing [4]. Taking under consideration any piece of evidence
derived by the available IC studies, even with opposing results, may
enhance our efforts to recognize and overcome the obstacles that restrain
the translation of the benefits demonstrated by proof-of-concept trials
into the clinical setting.
References
1. Bulluck H, Hausenloy DJ. Ischaemic conditioning: Are we there yet?
Heart 2015;101:1067-77.
2. Iliodromitis EK, Paraskevaidis IA, Fountoulaki K, et al. Staccato
reperfusion prevents reperfusion injury in patients undergoing coronary
angioplasty: A 1-year follow-up pilot study. Atherosclerosis 2009;204:497
-502.
3. Ikonomidis I, Iliodromitis EK, Tzortzis S, et al. Staccato reperfusion
improves myocardial microcirculatory function and long-term left
ventricular remodeling: a randomized contrast echocardiography study.
Heart 2010;96:1898-1903.
4. Iliodromitis EK, Kyrzopoulos S, Paraskevaidis IA, et al. Increased C
reactive protein and cardiac enzyme levels after coronary stent
implantation. Is there protection by remote ischaemic preconditioning?
Heart 2006;92:1821-26.
Atrial fibrillation (AF) constitutes a major risk factor for stroke and death.1 ,2 The potential of biomarkers to improve the prognostication concerning stroke and other cardiovascular events in patients with AF is gaining strength of evidence and clinical promise. In particular the biomarkers of cardiovascular stress and dysfunction such as cardiac troponin (cTn), a marker of myocardial cell damage; N-terminal B-type natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction; and growth-differentiation factor-15 (GDF-15), a marker of inflammation and oxidative stress, have been shown to be strong independent predictors.3–8 Although inflammatory activation has been linked to the occurrence of AF and to a prothrombotic state, the association with subsequent cardiovascular events during treatment with oral anticoagulation has not been fully established.9–14 Prior studies evaluating the relation between inflammation and cardiovascular events in patients with AF have often been exploratory and did not take into account the protective effect of oral anticoagulation. In addition the associations with outcomes have not been fully adjusted for other risk indicators, in particular other cardiovascular biomarkers, which recently have show
Atrial fibrillation (AF) constitutes a major risk factor for stroke and death.1 ,2 The potential of biomarkers to improve the prognostication concerning stroke and other cardiovascular events in patients with AF is gaining strength of evidence and clinical promise. In particular the biomarkers of cardiovascular stress and dysfunction such as cardiac troponin (cTn), a marker of myocardial cell damage; N-terminal B-type natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction; and growth-differentiation factor-15 (GDF-15), a marker of inflammation and oxidative stress, have been shown to be strong independent predictors.3–8 Although inflammatory activation has been linked to the occurrence of AF and to a prothrombotic state, the association with subsequent cardiovascular events during treatment with oral anticoagulation has not been fully established.9–14 Prior studies evaluating the relation between inflammation and cardiovascular events in patients with AF have often been exploratory and did not take into account the protective effect of oral anticoagulation. In addition the associations with outcomes have not been fully adjusted for other risk indicators, in particular other cardiovascular biomarkers, which recently have showed to be independent and powerful markers of adverse outcomes in patients with AF.4 In this predefined biomarker study within the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) trial we asse...
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Assessing effect of remote ischaemic preconditioning on clinical outcomes in patients undergoing cardiac bypass surgery
To the Editor : In a recent article of Candilio et al.1 assessing the effect of remote ischaemic preconditioning (RIPC) on postoperative outcomes in patients undergoing cardiac surgery, they showed that RIPC reduced the amount of perioperative myocardial injury by 26% and the incidence of acute...
Imazio et al. investigated the incidence and prognosis of presumably new onset atrial fibrillation (AF) and flutter (AFl) in acute pericarditis [1]. They showed that only 4% of the patients with acute pericarditis developed new onset atrial arrhythmias [1]. The mean age of patients who experienced AF in this study was 67 years. Notably, the age-stratified AF prevalence in this study remains comparable to that in the gener...
To the Editor: We have read with interest the article of Miranda WR and coauthors1, in which a case of effusive-constrictive pericarditis is presented. This is a comprehensive and educational case that provides clinicians with a valuable message. Some points, however, require additional clarification in order to further strengthen the impact of this case. In particular, it is mentioned in the introduction that the patien...
Cover Letter
Complete revascularization in STEMI
a Ramez Nairooz, MD, b Srihari S Naidu, MD.
a Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas; b Division of Cardiology, Winthrop University Hospital, Mineola, New York.
Funding: None Conflicts of interest: none Word Count: 325 Corresponding author & (address for reprints) Ramez Nairooz, MD...
The article entitled "The pathophysiology of hypertensive acute heart failure"[1] provides a contemporary review of mechanisms involved in the development of acute pulmonary oedema (APO). We wish to highlight the potential key role of the right ventricle in the pathogenesis of APO.[2]
APO is often thought to result from backward pressure where a disease of the left ventricle causes the left ventricular end-diasto...
I appreciate Dr. Stovitz's interest in our editorial and on the topic of the "Obesity Paradox". As I stated in my book, The Obesity Paradox,1 a paradox can be defined "as a statement that is seemingly contradictory or opposed to common sense and yet is perhaps true". Based on this, Stovitz could have better titled his letter as "True, true, and is a true paradox." As we previously demonstrated,2-4 despite that obese wit...
The timely restoration of flow in the culprit coronary artery lesion remains the cornerstone of treatment in patients with evolving myocardial infarction but with the inevitable cost of reperfusion injury. Cardiac ischaemic conditioning (IC) is capable of reducing the extent of final infarct size, but its actual benefit in improving clinical outcomes remains to be established. In their excellent review article published...
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