We thank dr. Katsouras for his response to our long-term EXPLORE manuscript (1). We agree that in the ST-segment elevation (STEMI) population the presence of collaterals to the concurrent chronic total occlusion (CTO) is of prognostic relevance. We previously reported in 413 consecutive STEMI patients with a CTO that the presence of well-developed collaterals to the CTO compared to poorly developed collaterals was associated with improved outcome. We also assessed the influence of the collateral origin on survival, as collaterals coming distally from the culprit lesion are (partially) blocked during the acute phase of STEMI. In 16% of the patients the collaterals originated directly or distal from the culprit lesion and these patients had a lower survival compared to the patients in whom the collaterals were not blocked during STEMI (2).
In the EXPLORE trial patients with well-developed collaterals to the CTO had a significantly better left ventricular (LV) function at 4 months follow-up. Nonetheless, we did not find a significant treatment effect of CTO-PCI on global LV function nor on clinical outcome in patients with poorly developed nor with well-developed collaterals (3). On a regional level we found that the recovery of segmental wall thickening of the dysfunctional CTO myocardium was better in patients with well-developed collaterals. However, no significant interaction of collateral quality on the effect of CTO PCI was found (4). In EXPLORE there were 34 p...
We thank dr. Katsouras for his response to our long-term EXPLORE manuscript (1). We agree that in the ST-segment elevation (STEMI) population the presence of collaterals to the concurrent chronic total occlusion (CTO) is of prognostic relevance. We previously reported in 413 consecutive STEMI patients with a CTO that the presence of well-developed collaterals to the CTO compared to poorly developed collaterals was associated with improved outcome. We also assessed the influence of the collateral origin on survival, as collaterals coming distally from the culprit lesion are (partially) blocked during the acute phase of STEMI. In 16% of the patients the collaterals originated directly or distal from the culprit lesion and these patients had a lower survival compared to the patients in whom the collaterals were not blocked during STEMI (2).
In the EXPLORE trial patients with well-developed collaterals to the CTO had a significantly better left ventricular (LV) function at 4 months follow-up. Nonetheless, we did not find a significant treatment effect of CTO-PCI on global LV function nor on clinical outcome in patients with poorly developed nor with well-developed collaterals (3). On a regional level we found that the recovery of segmental wall thickening of the dysfunctional CTO myocardium was better in patients with well-developed collaterals. However, no significant interaction of collateral quality on the effect of CTO PCI was found (4). In EXPLORE there were 34 patients (11%) with no visible collaterals or collaterals originating from the IRA occluded during STEMI. These patients had a significantly lower LVEF (38% versus 45%, p=0.001) and a higher LVEDV (226ml versus 213ml, p=0.37) at 4 months follow-up. Long-term MACE rates were also numerically higher in this group (20% versus 12%, Log-rank p=0.21). Mortality rates were not different between both groups (9.4% versus 9.3%, Log-rank p=0.40). We did not find an effect of CTO-PCI on LV function nor on clinical outcome in the patients with collaterals blocked during STEMI nor in patients with present collaterals.
Therefore, data regarding the value of the collateral circulation are conflicting and their exact role remains controversial. Further CTO research should focus more on the collateral circulation to determine whether collaterals should be of influence on treatment strategies or whether they are just unmodifiable markers of prognosis in these complex patients.
References:
1. Elias J, van Dongen IM, Ramunddal T, et al. Long-term impact of chronic total occlusion recanalisation in patients with ST-elevation myocardial infarction. Heart 2018 doi: 10.1136/heartjnl-2017-312698
2. Elias J, Hoebers LPC, van Dongen IM, et al. Impact of Collateral Circulation on Survival in ST-Segment Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention With a Concomitant Chronic Total Occlusion. JACC Cardiovasc Interv 2017;10(9):906-14. doi: 10.1016/j.jcin.2017.01.026
3. Van Dongen IM, Elias J, Van Houwelingen KG, et al. P5156Impact of collateral filling on LVF and survival in STEMI patients with a concomitant CTO. An explorative subanalysis of the EXPLORE trial. European Heart Journal 2017;38(suppl_1):ehx493.P5156-ehx493.P56. doi: 10.1093/eurheartj/ehx493.P5156
4. Elias J, van Dongen IM, Hoebers LP, et al. Improved recovery of regional left ventricular function after PCI of chronic total occlusion in STEMI patients: a cardiovascular magnetic resonance study of the randomized controlled EXPLORE trial. J Cardiovasc Magn Reson 2017;19(1):53. doi: 10.1186/s12968-017-0369-z
I read with great interest the paper by Elias et al regarding the mid-term and long-term clinical outcome of the Evaluating Xience and left ventricular function in Percutaneous Coronary Interventions on occlusiOns afteR ST elevation myocardial infarction (EXPLORE) trial. [1] The authors are to be congratulated for this detailed analysis evaluating the effect of chronic total occlusions – percutaneous coronary intervention (CTO-PCI) compared with CTO-No PCI on clinical outcome, left ventricular function and angina status in patients with ST elevation myocardial infarction (STEMI) with a concurrent CTO. The message of their study is that early CTO-PCI in patients with STEMI presenting with a concurrent CTO during primary PCI should not be performed routinely.
The authors also analysed the study population combined and found higher long-term mortality in patients who were older (>60 years) (11% vs 3%; HR 3.74; 95% CI 1.37 to 10.21; P=0.01), who had diabetes (15% vs 6%; HR 2.94; 95% CI 1.19 to 7.30; P=0.02), had a higher left ventricular enddiastolic volume at baseline (12% vs 1%; HR 13.04; 95% CI 1.70 to 100.30; P=0.01) and who had a high SYNTAX score (10% vs 4%; HR 2.50; 95% CI 1.01 to 6.20; P=0.048). They also stated that cardiac death was more frequent in the CTO-PCI arm (6.0% vs 1.0%, P=0.02) with no difference in all-cause mortality. However, it is known that a major prognostic factor in STEMI patients with a concurrent CTO is the presence of collateral feeding...
I read with great interest the paper by Elias et al regarding the mid-term and long-term clinical outcome of the Evaluating Xience and left ventricular function in Percutaneous Coronary Interventions on occlusiOns afteR ST elevation myocardial infarction (EXPLORE) trial. [1] The authors are to be congratulated for this detailed analysis evaluating the effect of chronic total occlusions – percutaneous coronary intervention (CTO-PCI) compared with CTO-No PCI on clinical outcome, left ventricular function and angina status in patients with ST elevation myocardial infarction (STEMI) with a concurrent CTO. The message of their study is that early CTO-PCI in patients with STEMI presenting with a concurrent CTO during primary PCI should not be performed routinely.
The authors also analysed the study population combined and found higher long-term mortality in patients who were older (>60 years) (11% vs 3%; HR 3.74; 95% CI 1.37 to 10.21; P=0.01), who had diabetes (15% vs 6%; HR 2.94; 95% CI 1.19 to 7.30; P=0.02), had a higher left ventricular enddiastolic volume at baseline (12% vs 1%; HR 13.04; 95% CI 1.70 to 100.30; P=0.01) and who had a high SYNTAX score (10% vs 4%; HR 2.50; 95% CI 1.01 to 6.20; P=0.048). They also stated that cardiac death was more frequent in the CTO-PCI arm (6.0% vs 1.0%, P=0.02) with no difference in all-cause mortality. However, it is known that a major prognostic factor in STEMI patients with a concurrent CTO is the presence of collateral feeding donor arteries from an infarct-related artery (IRA). Of patients with CTO, those with collateral flow from the IRA have significantly higher mortality than the non-IRA group (at 30 days: 52.2% vs. 10.9%, P<0.0001).[2] Obviously, in acute phase of these unstable conditions, the myocardium in the “remote” zone of infarction (CTO-zone) also ceases to contract. It is uncertain whether primary angioplasty in the IRA led to recover in the contractile function in the CTO zone. It would be very helpful if Elias et al could provide additional angiographic data regarding the IRA and the donor artery of CTO in their population (and the impact of PCI-CTO in this group). Surprisingly, in most post-myocardial infarction PCI-CTO studies relevant data are lacking.
1. Elias J, van Dongen IM, Råmunddal T, Laanmets P, et al. Long-term impact of chronic total occlusion recanalisation in patients with ST-elevation myocardial infarction. Heart. 2018 Feb 20. pii: heartjnl-2017-312698. doi: 10.1136/heartjnl-2017-312698. [Epub ahead of print]
2. Fujii T, Sakai K, Nakano M, et al. Impact of the origin of the collateral feeding donor artery on short-term mortality in ST-elevation myocardial infarction with comorbid chronic total occlusion. Int J Cardiol. 2016;218:158-163.
Dear Editor,
With great interest, I read the article by Sainsbury and associates[1] and congratulate them for extensively reviewing the unsolved issue of refractory angina. How many suffer from this condition worldwide remains unclear. However, it is believed that hundreds of thousands of Americans are affected, and that this number increases annually. Likely, millions are affected worldwide. Diffuse coronary artery disease is the main reason for refractory angina, because such arteries are non-amenable to percutaneous interventions or bypass grafting. Comorbidities are a second reason, especially in our aging population. Yet history is a cycle; medicine’s history no exception. Old concept, experiments, and theories that have fallen by the wayside can sometimes be resurrected and re-explored, released from the technological constraints of their time. The coronary sinus reducer system is one good example, since the concept stems from studies on the effects of cardiac vein ligation performed in the 1930s by Canadian surgeon Mercier Fauteux[2]. Two additional concepts might be resurrected and adapted to modern technologies. One is the concept of internal mammary artery (IMA) occlusion which, at that time, was performed through a small bilateral incision between the second and third ribs. The belief was that localized hypertension superior to the obstruction increased perfusion pressure in channels leading to the heart, specifically through the peri-cardio-phrenic br...
Dear Editor,
With great interest, I read the article by Sainsbury and associates[1] and congratulate them for extensively reviewing the unsolved issue of refractory angina. How many suffer from this condition worldwide remains unclear. However, it is believed that hundreds of thousands of Americans are affected, and that this number increases annually. Likely, millions are affected worldwide. Diffuse coronary artery disease is the main reason for refractory angina, because such arteries are non-amenable to percutaneous interventions or bypass grafting. Comorbidities are a second reason, especially in our aging population. Yet history is a cycle; medicine’s history no exception. Old concept, experiments, and theories that have fallen by the wayside can sometimes be resurrected and re-explored, released from the technological constraints of their time. The coronary sinus reducer system is one good example, since the concept stems from studies on the effects of cardiac vein ligation performed in the 1930s by Canadian surgeon Mercier Fauteux[2]. Two additional concepts might be resurrected and adapted to modern technologies. One is the concept of internal mammary artery (IMA) occlusion which, at that time, was performed through a small bilateral incision between the second and third ribs. The belief was that localized hypertension superior to the obstruction increased perfusion pressure in channels leading to the heart, specifically through the peri-cardio-phrenic branch[3]. Recently, I have resurrected this concept and suggested performing endovascular occlusion of the IMAs[4]. More recently, others have demonstrated that occluding the IMAs arteries could increase the collateral flow index and fractional flow reserve ipsilaterally, while decreasing angina[5]. These data are encouraging and spur further investigations. However, I also feel that Vineberg’s operation, consisting of tunnelization of IMAs into the left ventricle wall, is worthy of resurrection. This procedure, performed for about two decades, once was successful at relieving angina[2]. A huge collateral network developed between the IMAs and coronary arteries, and the IMAs often remained patent even at long-term follow-up. There is no reason to a-priori exclude IMA intra-myocardial tunnelization in patients for whom bypass is contraindicated, and vast opportunities exist for novel experimental and clinical studies on this technique.
Words = 345
References
1. Sainsbury PA, Fisher M, de Silva R. Alternative interventions for refractory angina. Heart. 2017 ;103(23):1911-1922.
2. Picichè M. The history of myocardial revascularization before the advent of cardiopulmonary bypass, in: M. Picichè (Ed.), Dawn and Evolution of Cardiac Procedures:Research Avenues in Cardiac Surgery and Interventional Cardiology, Springer- Verlag, Heidelberg 2012, pp. 65–77.
3. Picichè M. Noncoronary Collateral Myocardial Blood Flow: The Human Heart’s Forgotten Blood Supply. The Open Cardiovasc Med J 2015; 9:105-113.
4. Picichè M. Embolization of the internal thoracic arteries in refractory angina. Int J Cardiol. 2016;212:310.
5. Stoller M, Seiler C. Effect of permanent right internal mammary artery closure on coronary collateral function and myocardial ischemia. Circ Cardiovasc Interv 2017;10:e004990.
We read with interest the excellent and timely article on increasingly detected cases of isolated tricuspid valve regurgitation (1) . The authors rightly note that there is an emerging population of adult patients without left-sided heart disease, pulmonary hypertension or congenital abnormalities who develop symptomatic isolated tricuspid regurgitation. While this is true, we believe that a proportion of these cases of isolated tricuspid regurgitation may well be congenital in origin.
The spectrum of congenital abnormalities of tricuspid valve abnormalities is large (2), and while Ebstein anomaly and tricuspid valve anomalies associated with atrioventricular septal defects and pulmonary atresia are the most commonly discussed, there is a group of patients with tricuspid valve dysplasia or congenitally abnormal tricuspid valves that are under-recognized. Said et al (3) and Dearani et al (4) from the authors’ institution have previously discussed the wide spectrum of congenital tricuspid valve anomalies. The importance of recognizing this group of cases as a separate entity is twofold. One that tricuspid valve dysplasia from failure of delamination of the tricuspid valve, like Ebstein anomaly can be associated with cardiomyopathy and arrhythmia and other congenital anomalies can be missed if focus if just on the valve. Secondly, surgical approach for tricuspid valve surgery, as authors suggest, should focus on the mechanisms of tricuspid regurgitation, which are uni...
We read with interest the excellent and timely article on increasingly detected cases of isolated tricuspid valve regurgitation (1) . The authors rightly note that there is an emerging population of adult patients without left-sided heart disease, pulmonary hypertension or congenital abnormalities who develop symptomatic isolated tricuspid regurgitation. While this is true, we believe that a proportion of these cases of isolated tricuspid regurgitation may well be congenital in origin.
The spectrum of congenital abnormalities of tricuspid valve abnormalities is large (2), and while Ebstein anomaly and tricuspid valve anomalies associated with atrioventricular septal defects and pulmonary atresia are the most commonly discussed, there is a group of patients with tricuspid valve dysplasia or congenitally abnormal tricuspid valves that are under-recognized. Said et al (3) and Dearani et al (4) from the authors’ institution have previously discussed the wide spectrum of congenital tricuspid valve anomalies. The importance of recognizing this group of cases as a separate entity is twofold. One that tricuspid valve dysplasia from failure of delamination of the tricuspid valve, like Ebstein anomaly can be associated with cardiomyopathy and arrhythmia and other congenital anomalies can be missed if focus if just on the valve. Secondly, surgical approach for tricuspid valve surgery, as authors suggest, should focus on the mechanisms of tricuspid regurgitation, which are unique to each given patient. For example, the surgical management of a cleft tricuspid valve (another well-known congenital entity) would be different from a case of tricuspid valve dysplasia when the mechanism of tricuspid regurgitation is a tethered anterior leaflet of tricuspid valve, which is failure of delamination issue.
We recognize this manuscript as an excellent resource for isolated tricuspid valve regurgitation; we would nonetheless underscore that congenital tricuspid valve disease (other than Ebstein anomaly) may be more common than anticipated, and may masquerade as primary idiopathic tricuspid regurgitation. We believe (likely as do the authors) that evaluation of all presumed isolated tricuspid valve disease deserves assessment by cardiologists expert in such distinction and classification.
1. Fender EA, Zack CJ, Nishimura RA. Isolated tricuspid regurgitation: outcomes and therapeutic interventions. Heart 2017.
2. Becker AE, Becker MJ, Edwards JE. Pathologic spectrum of dysplasia of the tricuspid valve. Features in common with Ebstein's malformation. Arch Pathol 1971;91:167-78.
3. Said SM, Burkhart HM, Dearani JA. Surgical management of congenital (non-Ebstein) tricuspid valve regurgitation. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2012;15:46-60.
4. Dearani JA, Danielson GK. Congenital Heart Surgery Nomenclature and Database Project: Ebstein's anomaly and tricuspid valve disease. Ann Thorac Surg 2000;69:S106-17.
We have read the interesting article from Bokma and colleagues [1] documenting the outcomes of pulmonary valve replacement (PVR) in patients with repaired tetralogy of Fallot (rTOF). In this large multi-centre rTOF cohort, PVR was not associated with a reduced rate of death at mid-term follow-up. Additionally, authors highlighted that there were more events after PVR compared with no PVR in subjects not meeting consensus criteria.
Currently, although the overall hemodynamic benefits of PVR are evident with broad consensus for surgery before clinical deterioration or symptoms develop, uncertainties remain about the optimal timing for PVR.
Haemodynamic assessment surrounding PVR has focused on assessment of the right ventricle (RV) size and function, with the goal of intervening in patient prior to the development of irreversible RV deterioration failure. However, although the concept of using RV volumes for decision-making for PVR is widely used, its evidence regarding its impact on long-term outcomes remains weak.
New information about optimal PVR timing has been continuously addressed. A cardiac magnetic resonance based study suggested that a preoperative RVESVi cutoff of ≤82 mL/m2 was equally sensitive and more specific for normalization of RV volumes compared with our preoperative RVEDVi threshold of ≤158 mL/m2, justifying the use of RVESVi for clinical timing for PVR [2]. In 2015, Bokma concluded that preoperative RVESVi < 80 mL/m2 was the best thr...
We have read the interesting article from Bokma and colleagues [1] documenting the outcomes of pulmonary valve replacement (PVR) in patients with repaired tetralogy of Fallot (rTOF). In this large multi-centre rTOF cohort, PVR was not associated with a reduced rate of death at mid-term follow-up. Additionally, authors highlighted that there were more events after PVR compared with no PVR in subjects not meeting consensus criteria.
Currently, although the overall hemodynamic benefits of PVR are evident with broad consensus for surgery before clinical deterioration or symptoms develop, uncertainties remain about the optimal timing for PVR.
Haemodynamic assessment surrounding PVR has focused on assessment of the right ventricle (RV) size and function, with the goal of intervening in patient prior to the development of irreversible RV deterioration failure. However, although the concept of using RV volumes for decision-making for PVR is widely used, its evidence regarding its impact on long-term outcomes remains weak.
New information about optimal PVR timing has been continuously addressed. A cardiac magnetic resonance based study suggested that a preoperative RVESVi cutoff of ≤82 mL/m2 was equally sensitive and more specific for normalization of RV volumes compared with our preoperative RVEDVi threshold of ≤158 mL/m2, justifying the use of RVESVi for clinical timing for PVR [2]. In 2015, Bokma concluded that preoperative RVESVi < 80 mL/m2 was the best threshold to achieve mid-to-late RV normalization [3]. The impact of abnormal RV mechanics on the LV has been appreciated, with the assessment of LV assuming higher priority in decision-making.
Interestingly, another study from INDICATOR cohort [4] found previous implantation of RV-pulmonary artery conduits was associated with adverse outcomes rather than RV volumes. Age at TOF repair was also identified as risk factor for post-PVR arrhythmia. It’s well summarized that TOF anatomical variants, trans-ventricular repair and preoperative cyanosis were also know as determinants for PVR outcomes [2].
Hence more information could be further illustrated, including the baseline anatomical and surgical features of TOF repair, the surgical techniques of PVR and their potential relationship with PVR outcomes. Moreover, additional comments about this issue would be helpful.
[1] Bokma JP, Geva T, Sleeper LA, et al. Heart Published Online First: [1-Nov-2017]. doi:10.1136/ heartjnl-2017-312048.
[2] Heng EL, Gatzoulis MA, Uebing A, et al. Immediate and Midterm Cardiac Remodeling After Surgical Pulmonary Valve Replacement in Adults With Repaired Tetralogy of Fallot: A Prospective Cardiovascular Magnetic Resonance and Clinical Study. Circulation. 2017;136:1703-1713.
[3] Bokma JP, Winter MM, Oosterhof T, et al. Pre-operative thresholds for mid-to-late haemodynamic and clinical outcomes after pulmonary valve replacement in tetralogy of Fallot. Eur Heart J. 2016;37(10):829-35.
[4] Valente AM, Gauvreau K, Assenza GE, et al. Contemporary predictors of death and sustained ventricular tachycardia in patients with repaired tetralogy of Fallot enrolled in the INDICATOR cohort. Heart 2014;100:247–253.
Title of E-letter: Intra coronary imaging to detect mal apposition: Are We Seeing Too Much!
Authors Name: Dr Yasir Parviz
Institution: Columbia University Medical Center
Intracoronary Imaging Heart 2017; 0: heartjnl-2015-307888v1
Link to the original paper: http://hwmaint.heart.bmj.com/cgi/content/full/heartjnl-2015-307888v1
Main Text:
We would like to congratulate Giavarini A et al on this comprehensive, educational article on intracoronary imaging. [1] Various modalities can be used to understand the mechanism of stent failure, and there is an ongoing debate on detection of stent mal-apposition, and whether this has any clinical impact. Acute stent mal-apposition on its own is not associated with adverse clinical events unless associated with under expansion or having inflow- outflow issues. Acute mal-apposition and its associated clinical events are possibly reduced due to negative remodelling.[2] The clinically events are non-significant may be due to the fact that newer generation of stents and stronger antiplatelets are performing very well. There is limited literature evidence to support that acute mal-apposition is associated with stent thrombosis. [3] Late acquired malaposition in combination with other contributing factors can be associated with stent failure. Most of the available literature looking into the mechanism of stent failure is from...
Title of E-letter: Intra coronary imaging to detect mal apposition: Are We Seeing Too Much!
Authors Name: Dr Yasir Parviz
Institution: Columbia University Medical Center
Intracoronary Imaging Heart 2017; 0: heartjnl-2015-307888v1
Link to the original paper: http://hwmaint.heart.bmj.com/cgi/content/full/heartjnl-2015-307888v1
Main Text:
We would like to congratulate Giavarini A et al on this comprehensive, educational article on intracoronary imaging. [1] Various modalities can be used to understand the mechanism of stent failure, and there is an ongoing debate on detection of stent mal-apposition, and whether this has any clinical impact. Acute stent mal-apposition on its own is not associated with adverse clinical events unless associated with under expansion or having inflow- outflow issues. Acute mal-apposition and its associated clinical events are possibly reduced due to negative remodelling.[2] The clinically events are non-significant may be due to the fact that newer generation of stents and stronger antiplatelets are performing very well. There is limited literature evidence to support that acute mal-apposition is associated with stent thrombosis. [3] Late acquired malaposition in combination with other contributing factors can be associated with stent failure. Most of the available literature looking into the mechanism of stent failure is from IVUS studies and newer technology, OCT due to superior resolution has the ability to detect a higher percentage of mal appositions.[4] There is on-going research on to the clinical significance of these findings.
We are presenting a summary of some evidence in detection of malapposition by IVUS /OCT and its clinical impact.
1)Im et al. Circ Cardiovasc Interv 2014;7:88-96.
356(n),62%(OCT), no impact.
2)Kubo et al. JACCCardiovasc Imaging 2013;6:1095-104.
100(n), 14%(IVUS), 39%(OCT), no impact
3)Kawamori et al. EHJ Cardiovasc Imaging 2013;14:865-75.
40(n), 65%(OCT), no impact
4)Bezerra et al. JACC Cardiovasc Interv 2013;6:228-36
26(n), 42% (IVUS), 96%(OCT), no impact
5)Ali ZA et al Lancet. 2016 Nov 26;388(10060):2618-2628.
304(n), 39% (IVUS), 41% OCT, no impact
6)Prati et al JACC Cardiovascular Imaging November 2015 2015;8:1297.
832(n), 50%(OCT), no impact
7)Prati F et al Am Heart J. 2015 Feb;169(2):249-56.
63(n), 52%(OCT), no impact
8)Hong et al, Circulation. 2006;113:414-9.
557(n), 12 %(IVUS),no impact
9)Steinberg et al J Am Coll Cardiol Intv 3:486-494.
1580(n), 7-10%(IVUS), no impact
10)Soeda et al Circulation. 2015 Sep 15;132(11):1020-9.
786(n), 39%(OCT), no impact
11)Kimura M Am J Cardiol. 2006;98:436-442.
168(n) 77% (IVUS), no impact
References.
1.Giavarini A, Kilic ID, Redondo Dieguez A, Longo G, Vandormael I, Pareek N, Kanyal R, De Silva R and Di Mario C. Intracoronary Imaging. Heart. 2017.
2. Guo N, Maehara A, Mintz GS, He Y, Xu K, Wu X, Lansky AJ, Witzenbichler B, Guagliumi G, Brodie B, Kellett MA, Jr., Dressler O, Parise H, Mehran R and Stone GW. Incidence, mechanisms, predictors, and clinical impact of acute and late stent malapposition after primary intervention in patients with acute myocardial infarction: an intravascular ultrasound substudy of the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial. Circulation. 2010;122:1077-84.
3. Alfonso F, Suarez A, Angiolillo DJ, Sabate M, Escaned J, Moreno R, Hernandez R, Banuelos C and Macaya C. Findings of intravascular ultrasound during acute stent thrombosis. Heart. 2004;90:1455-9.
4. Ali ZA, Maehara A, Genereux P, Shlofmitz RA, Fabbiocchi F, Nazif TM, Guagliumi G, Meraj PM, Alfonso F, Samady H, Akasaka T, Carlson EB, Leesar MA, Matsumura M, Ozan MO, Mintz GS, Ben-Yehuda O, Stone GW and Investigators IIOP. Optical coherence tomography compared with intravascular ultrasound and with angiography to guide coronary stent implantation (ILUMIEN III: OPTIMIZE PCI): a randomised controlled trial. Lancet. 2016;388:2618-2628.
We thank Xue et al for their interest in our article (1). The KDIGO classification (2) comprises 3 criteria in the diagnosis of acute kidney injury (AKI), namely an increase in serum creatinine (SCr) by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or an increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or urine volume <0.5 ml/kg/h for 6 hours. In our study, we had collected serial blood samples for the first 72 hours and the second KDIGO criterion (an increase in SCr to ≥1.5 times baseline) was applied over the 72 hours period to assess for AKI. As for the impact of perioperative fluid balance, this is not currently part of the recommendation, and the available evidence quoted (3) was taken from a retrospective, single-center study using the AKIN classification for AKI. Unfortunately the perioperative fluid balance was not collected in our study and we could not take this into account.
We did look at the Receiver Operating Characteristic curve analysis using sNGAL as a continuous variable. The area under the curve (AUC) was 0.57 (95%CI 0.54-0.60), very similar to that of sNGAL tertiles reported in our paper.(1) The diagnostic performance of sNGAL alone was quite low and therefore we did not provide cut-off values/sensitivity/specificity and predictive values. Expressing sNGAL as quartiles is more practical from a clinical point of view and we showed that by adding clinical factors, the c-statistic improved...
We thank Xue et al for their interest in our article (1). The KDIGO classification (2) comprises 3 criteria in the diagnosis of acute kidney injury (AKI), namely an increase in serum creatinine (SCr) by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or an increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or urine volume <0.5 ml/kg/h for 6 hours. In our study, we had collected serial blood samples for the first 72 hours and the second KDIGO criterion (an increase in SCr to ≥1.5 times baseline) was applied over the 72 hours period to assess for AKI. As for the impact of perioperative fluid balance, this is not currently part of the recommendation, and the available evidence quoted (3) was taken from a retrospective, single-center study using the AKIN classification for AKI. Unfortunately the perioperative fluid balance was not collected in our study and we could not take this into account.
We did look at the Receiver Operating Characteristic curve analysis using sNGAL as a continuous variable. The area under the curve (AUC) was 0.57 (95%CI 0.54-0.60), very similar to that of sNGAL tertiles reported in our paper.(1) The diagnostic performance of sNGAL alone was quite low and therefore we did not provide cut-off values/sensitivity/specificity and predictive values. Expressing sNGAL as quartiles is more practical from a clinical point of view and we showed that by adding clinical factors, the c-statistic improved to 0.69. We are aware that the value of 0.69 is not ideal for clinical application and our work was a post-hoc analysis of a randomized controlled trial (4) consisting of high-risk patients (EuroSCORE≥5). Therefore, further work remains to be done in a larger number of all-comers going for cardiac surgery to improve the identification of patients at risk of AKI.
References
1. Bulluck H, Maiti R, Chakraborty B, et al. Neutrophil gelatinase-associated lipocalin prior to cardiac surgery predicts acute kidney injury and mortality. Heart 2017 doi: 10.1136/heartjnl-2017-311760
2. James M, Bouchard J, Ho J, et al. Canadian Society of Nephrology commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. American journal of kidney diseases : the official journal of the National Kidney Foundation 2013;61(5):673-85. doi: 10.1053/j.ajkd.2013.02.350
3. Moore E, Tobin A, Reid D, et al. The Impact of Fluid Balance on the Detection, Classification and Outcome of Acute Kidney Injury After Cardiac Surgery. Journal of cardiothoracic and vascular anesthesia 2015;29(5):1229-35. doi: 10.1053/j.jvca.2015.02.004
4. Hausenloy DJ, Candilio L, Yellon DM. Remote Ischemic Preconditioning and Cardiac Surgery. The New England journal of medicine 2016;374(5):491-2.
The letter by Dr Al-Mohammad is welcomed by the study authors and highlights some of the important challenges with using single value cut-offs for diagnosis and in determining treatment options. This is particularly true for heart failure with preserved left ventricular ejection fraction (LVEF) (HFpEF) (and more recently mid-range ejection fraction [HFmrEF], 40-49%) where decisions on starting prognostic medications can be made based on subjective echocardiographic measurements, albeit with evidence of diastolic dysfunction (tissue Doppler, flow Doppler, and volumes). Clearly, additional patient-specific factors should be taken into account, including aetiology, co-morbidities, and underlying rhythm, which are nicely highlighted in the editorial piece accompanying our study[1 2].
The Study Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors With Heart Failure (SENIORS) trial investigated the effects of the beta-blocker nebivolol in the treatment of heart failure in patients aged 70 and over[3]. Patients were required to have a clinical diagnosis of heart failure with either hospitalisation for heart failure in the previous 12 months, or a documented LVEF ≤35%. Baseline LVEF was measured by transthoracic echocardiography in 94% of cases. While van Veldhuisen et al. used an LVEF cut-off of 35% to compare “reduced” with “preserved” ejection fraction, they also examined and reported on the effect of Nebivolol in 643 patients with an LVEF ≥40%....
The letter by Dr Al-Mohammad is welcomed by the study authors and highlights some of the important challenges with using single value cut-offs for diagnosis and in determining treatment options. This is particularly true for heart failure with preserved left ventricular ejection fraction (LVEF) (HFpEF) (and more recently mid-range ejection fraction [HFmrEF], 40-49%) where decisions on starting prognostic medications can be made based on subjective echocardiographic measurements, albeit with evidence of diastolic dysfunction (tissue Doppler, flow Doppler, and volumes). Clearly, additional patient-specific factors should be taken into account, including aetiology, co-morbidities, and underlying rhythm, which are nicely highlighted in the editorial piece accompanying our study[1 2].
The Study Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors With Heart Failure (SENIORS) trial investigated the effects of the beta-blocker nebivolol in the treatment of heart failure in patients aged 70 and over[3]. Patients were required to have a clinical diagnosis of heart failure with either hospitalisation for heart failure in the previous 12 months, or a documented LVEF ≤35%. Baseline LVEF was measured by transthoracic echocardiography in 94% of cases. While van Veldhuisen et al. used an LVEF cut-off of 35% to compare “reduced” with “preserved” ejection fraction, they also examined and reported on the effect of Nebivolol in 643 patients with an LVEF ≥40%. Results for this subgroup were included in our meta-analysis, ensuring that all patients included in our meta-analysis had an ejection fraction greater than this. Of note, inclusion of an additional 109 patients with an LVEF of 35-40% had minimal effect on the primary composite outcome of all-cause mortality or cardiovascular hospitalisation (LVEF ≥35%: HR 0.81, NS; LVEF ≥40%: HR 0.82, NS), or all-cause mortality (LVEF ≥35%: HR 0.91, NS; LVEF ≥40%: HR 0.92, NS). Indeed in SENIORS, the point estimate for reduction in the primary outcome was greater in those with an LVEF ≥40% (HR 0.82, NS) than in those with LVEF ≤35% (HR 0.86, NS).
We have tentatively concluded that beta-blockers may be of benefit in HFpEF, on the basis of pooled analysis from 3 trials, enrolling just 1046 participants. A large propensity-matched study from the Swedish Heart Failure registry (8244 patients) mirrored these findings with a 7% reduction in all-cause mortality at 5 years (P=0.04)[4]. Results from an individual patient data meta-analysis of beta-blockers in heart failure were recently presented at the European Society of Cardiology Congress and suggested reductions in all-cause and cardiovascular mortality in patients with HFmrEF (LVEF 40 to 49%) and sinus rhythm, but not in HFpEF (LVEF ≥50%) with sinus rhythm[5]. This study importantly highlights the importance of additional patient characteristics such as underlying rhythm. There is currently insufficient evidence to recommend widespread use of beta-blockers in HFpEF, and large prospective randomised controlled trial using a beta-blocker of proven benefit in reduced ejection fraction (e.g. bisoprolol, carvedilol, metoprolol[6]) is needed. It will be critically important to untangle and identify which specific patients with HFpEF may benefit from beta-blocker therapy.
1. Zheng SL, Chan FT, Nabeebaccus AA, et al. Drug treatment effects on outcomes in heart failure with preserved ejection fraction: a systematic review and meta-analysis. Heart 2017 doi: 10.1136/heartjnl-2017-311652published Online First: Epub Date]|.
2. Schnell F, Donal E. Pharmacological strategies in heart failure with preserved ejection fraction: time for an individualised treatment strategy? Heart 2017 doi: 10.1136/heartjnl-2017-312119published Online First: Epub Date]|.
3. van Veldhuisen DJ, Cohen-Solal A, Bohm M, et al. Beta-Blockade With Nebivolol in Elderly Heart Failure Patients With Impaired and Preserved Left Ventricular Ejection Fraction. Data From SENIORS (Study of Effects of Nebivolol Intervention on Outcomes and Rehospitalization in Seniors With Heart Failure). Journal of the American College of Cardiology 2009;53(23):2150-58 doi: http://dx.doi.org/10.1016/j.jacc.2009.02.046published Online First: Epub Date]|.
4. Lund LH, Benson L, Dahlstrom U, Edner M, Friberg L. Association between use of beta-blockers and outcomes in patients with heart failure and preserved ejection fraction. Jama 2014;312(19):2008-18 doi: 10.1001/jama.2014.15241published Online First: Epub Date]|.
5. Kotecha D. Efficacy of beta-blockers in heart failure according to left ventricular ejection fraction: An individual patient level analysis of double-blind randomised trials. Secondary Efficacy of beta-blockers in heart failure according to left ventricular ejection fraction: An individual patient level analysis of double-blind randomised trials 2017. http://congress365.escardio.org/Presentation/162249 - .WbHKsNOGMWo.
6. Chatterjee S, Biondi-Zoccai G, Abbate A, et al. Benefits of beta blockers in patients with heart failure and reduced ejection fraction: network meta-analysis. BMJ (Clinical research ed.) 2013;346:f55 doi: 10.1136/bmj.f55published Online First: Epub Date]|.
We thank Dr. Launey Y et al for their constructive comments regarding our recent report.[1] We also greatly appreciate their shared interests in traumatic intra-cranial hemorrhage (ICH) and the subsequent incidence of atrial fibrillation (AF).
Dr Launey and colleagues concerned about the acute effects of inflammation on the onset of AF.[2] In our study, the mean follow-up period was 4.36 (standard deviation, SD=3.41) and 5.35 (SD=3.19) years in traumatic ICH group and control group, respectively. Interestingly, the mean follow-up period of the onset of AF was 2.94 years (SD=2.64) in traumatic ICH group, which is significantly less than 3.57 (SD=2.67) years in control group (Table 1) (p<0.001). Although acute inflammation plays a role on the onset of AF,[3, 4] our study along with previous evidence indicate the chronic persistent inflammation, which occurs after traumatic brain injury (TBI), contributes the development of AF.[1, 5] This partly explains the results of AF occurrence on TBI patients in our study.
We agree that sepsis may contribute to the development of AF. In this study, after adjustment for age, sex, and comorbidities including sepsis and ventilator associated pneumonia, the adjusted HR (aHR) for developing AF was 1.24-fold higher (95% CI = 1.18-1.31) for patients with traumatic ICH compared with the control cohorts in multivariable cox regression models (Table 2). These results further support the association betwee...
We thank Dr. Launey Y et al for their constructive comments regarding our recent report.[1] We also greatly appreciate their shared interests in traumatic intra-cranial hemorrhage (ICH) and the subsequent incidence of atrial fibrillation (AF).
Dr Launey and colleagues concerned about the acute effects of inflammation on the onset of AF.[2] In our study, the mean follow-up period was 4.36 (standard deviation, SD=3.41) and 5.35 (SD=3.19) years in traumatic ICH group and control group, respectively. Interestingly, the mean follow-up period of the onset of AF was 2.94 years (SD=2.64) in traumatic ICH group, which is significantly less than 3.57 (SD=2.67) years in control group (Table 1) (p<0.001). Although acute inflammation plays a role on the onset of AF,[3, 4] our study along with previous evidence indicate the chronic persistent inflammation, which occurs after traumatic brain injury (TBI), contributes the development of AF.[1, 5] This partly explains the results of AF occurrence on TBI patients in our study.
We agree that sepsis may contribute to the development of AF. In this study, after adjustment for age, sex, and comorbidities including sepsis and ventilator associated pneumonia, the adjusted HR (aHR) for developing AF was 1.24-fold higher (95% CI = 1.18-1.31) for patients with traumatic ICH compared with the control cohorts in multivariable cox regression models (Table 2). These results further support the association between TBI and AF.
We acknowledge that our study had several limitations including no available data on the severity of TBI and AF occurrence, and the medication use in both traumatic ICH and control groups in the National Health Insurance Research Database. However, with the growing evidence suggesting the mechanisms linking inflammation, TBI, and AF, our studies provide critical clinical evidence supporting the important role of TBI on the development of AF.
References
1 Lin WS, Lin TC, Hung Y, et al. Traumatic intracranial haemorrhage is in association with an increased risk of subsequent atrial fibrillation. Heart 2017;103:1286-91.
2 Launey Y, Seguin, P. Is traumatic intracranial hemorrhage a specific risk factor of atrial fibrillation. Heart 2017;103.
3 Meierhenrich R, Steinhilber E, Eggermann C, et al. Incidence and prognostic impact of new-onset atrial fibrillation in patients with septic shock: a prospective observational study. Crit Care 2010;14:R108.
4 Chaikittisilpa N, Krishnamoorthy V, Lele AV, et al. Characterizing the relationship between systemic inflammatory response syndrome and early cardiac dysfunction in traumatic brain injury. J Neurosci Res 2017.
5 Mitrofanova LB, Orshanskaya V, Ho SY, et al. Histological evidence of inflammatory reaction associated with fibrosis in the atrial and ventricular walls in a case-control study of patients with history of atrial fibrillation. Europace 2016;18:iv156-iv62.
We thank dr. Katsouras for his response to our long-term EXPLORE manuscript (1). We agree that in the ST-segment elevation (STEMI) population the presence of collaterals to the concurrent chronic total occlusion (CTO) is of prognostic relevance. We previously reported in 413 consecutive STEMI patients with a CTO that the presence of well-developed collaterals to the CTO compared to poorly developed collaterals was associated with improved outcome. We also assessed the influence of the collateral origin on survival, as collaterals coming distally from the culprit lesion are (partially) blocked during the acute phase of STEMI. In 16% of the patients the collaterals originated directly or distal from the culprit lesion and these patients had a lower survival compared to the patients in whom the collaterals were not blocked during STEMI (2).
In the EXPLORE trial patients with well-developed collaterals to the CTO had a significantly better left ventricular (LV) function at 4 months follow-up. Nonetheless, we did not find a significant treatment effect of CTO-PCI on global LV function nor on clinical outcome in patients with poorly developed nor with well-developed collaterals (3). On a regional level we found that the recovery of segmental wall thickening of the dysfunctional CTO myocardium was better in patients with well-developed collaterals. However, no significant interaction of collateral quality on the effect of CTO PCI was found (4). In EXPLORE there were 34 p...
Show MoreI read with great interest the paper by Elias et al regarding the mid-term and long-term clinical outcome of the Evaluating Xience and left ventricular function in Percutaneous Coronary Interventions on occlusiOns afteR ST elevation myocardial infarction (EXPLORE) trial. [1] The authors are to be congratulated for this detailed analysis evaluating the effect of chronic total occlusions – percutaneous coronary intervention (CTO-PCI) compared with CTO-No PCI on clinical outcome, left ventricular function and angina status in patients with ST elevation myocardial infarction (STEMI) with a concurrent CTO. The message of their study is that early CTO-PCI in patients with STEMI presenting with a concurrent CTO during primary PCI should not be performed routinely.
Show MoreThe authors also analysed the study population combined and found higher long-term mortality in patients who were older (>60 years) (11% vs 3%; HR 3.74; 95% CI 1.37 to 10.21; P=0.01), who had diabetes (15% vs 6%; HR 2.94; 95% CI 1.19 to 7.30; P=0.02), had a higher left ventricular enddiastolic volume at baseline (12% vs 1%; HR 13.04; 95% CI 1.70 to 100.30; P=0.01) and who had a high SYNTAX score (10% vs 4%; HR 2.50; 95% CI 1.01 to 6.20; P=0.048). They also stated that cardiac death was more frequent in the CTO-PCI arm (6.0% vs 1.0%, P=0.02) with no difference in all-cause mortality. However, it is known that a major prognostic factor in STEMI patients with a concurrent CTO is the presence of collateral feeding...
I read with interest the bright review of stable coronary syndromes (1). In the formation of the fetal muscular part
of the interventricular septum (IVS), the expanding ventricles grow and their medial walls approach and fuse, forming
the septum. The inside corner between the septum and the right anterior ventricular wall exhibits the deep pits being
called interventricular sinuses (ISs). The IS passes through the right IVS formed from the medial wall of the expanding
fetal right ventricle (RV). The opening of the interventricular vessel (IV) (kuuselian vessel) is located in the IS between
the medial walls of the expanding fetal RV and fetal left ventricle (LV). The IV is not a canal or channel or blood
vessel, but a slit between the fibres of the muscle to the outer layer of the left central muscular part of the IVS and runs
at an angle of about 90 degrees through sphincter and the left IVS into the LV. The IV exhibits 2 to 3 oval 2x5 mm
openings in the left central muscular part of the IVS surrounded by the interventricular sphincter (ISP). The ISP and the
IV are feasible to be patent by relaxing and widening of the helical heart at the right atrial filling phase at the end of the
fetal diastole. The left to right communication do not result as the earliest left ventricular activation close the ISP. The
sinoatrial node initially activates the right atrium (RA), followed by activation...
Show MoreDear Editor,
Show MoreWith great interest, I read the article by Sainsbury and associates[1] and congratulate them for extensively reviewing the unsolved issue of refractory angina. How many suffer from this condition worldwide remains unclear. However, it is believed that hundreds of thousands of Americans are affected, and that this number increases annually. Likely, millions are affected worldwide. Diffuse coronary artery disease is the main reason for refractory angina, because such arteries are non-amenable to percutaneous interventions or bypass grafting. Comorbidities are a second reason, especially in our aging population. Yet history is a cycle; medicine’s history no exception. Old concept, experiments, and theories that have fallen by the wayside can sometimes be resurrected and re-explored, released from the technological constraints of their time. The coronary sinus reducer system is one good example, since the concept stems from studies on the effects of cardiac vein ligation performed in the 1930s by Canadian surgeon Mercier Fauteux[2]. Two additional concepts might be resurrected and adapted to modern technologies. One is the concept of internal mammary artery (IMA) occlusion which, at that time, was performed through a small bilateral incision between the second and third ribs. The belief was that localized hypertension superior to the obstruction increased perfusion pressure in channels leading to the heart, specifically through the peri-cardio-phrenic br...
We read with interest the excellent and timely article on increasingly detected cases of isolated tricuspid valve regurgitation (1) . The authors rightly note that there is an emerging population of adult patients without left-sided heart disease, pulmonary hypertension or congenital abnormalities who develop symptomatic isolated tricuspid regurgitation. While this is true, we believe that a proportion of these cases of isolated tricuspid regurgitation may well be congenital in origin.
Show MoreThe spectrum of congenital abnormalities of tricuspid valve abnormalities is large (2), and while Ebstein anomaly and tricuspid valve anomalies associated with atrioventricular septal defects and pulmonary atresia are the most commonly discussed, there is a group of patients with tricuspid valve dysplasia or congenitally abnormal tricuspid valves that are under-recognized. Said et al (3) and Dearani et al (4) from the authors’ institution have previously discussed the wide spectrum of congenital tricuspid valve anomalies. The importance of recognizing this group of cases as a separate entity is twofold. One that tricuspid valve dysplasia from failure of delamination of the tricuspid valve, like Ebstein anomaly can be associated with cardiomyopathy and arrhythmia and other congenital anomalies can be missed if focus if just on the valve. Secondly, surgical approach for tricuspid valve surgery, as authors suggest, should focus on the mechanisms of tricuspid regurgitation, which are uni...
We have read the interesting article from Bokma and colleagues [1] documenting the outcomes of pulmonary valve replacement (PVR) in patients with repaired tetralogy of Fallot (rTOF). In this large multi-centre rTOF cohort, PVR was not associated with a reduced rate of death at mid-term follow-up. Additionally, authors highlighted that there were more events after PVR compared with no PVR in subjects not meeting consensus criteria.
Show MoreCurrently, although the overall hemodynamic benefits of PVR are evident with broad consensus for surgery before clinical deterioration or symptoms develop, uncertainties remain about the optimal timing for PVR.
Haemodynamic assessment surrounding PVR has focused on assessment of the right ventricle (RV) size and function, with the goal of intervening in patient prior to the development of irreversible RV deterioration failure. However, although the concept of using RV volumes for decision-making for PVR is widely used, its evidence regarding its impact on long-term outcomes remains weak.
New information about optimal PVR timing has been continuously addressed. A cardiac magnetic resonance based study suggested that a preoperative RVESVi cutoff of ≤82 mL/m2 was equally sensitive and more specific for normalization of RV volumes compared with our preoperative RVEDVi threshold of ≤158 mL/m2, justifying the use of RVESVi for clinical timing for PVR [2]. In 2015, Bokma concluded that preoperative RVESVi < 80 mL/m2 was the best thr...
Title of E-letter: Intra coronary imaging to detect mal apposition: Are We Seeing Too Much!
Authors Name: Dr Yasir Parviz
Institution: Columbia University Medical Center
Intracoronary Imaging Heart 2017; 0: heartjnl-2015-307888v1
Link to the original paper: http://hwmaint.heart.bmj.com/cgi/content/full/heartjnl-2015-307888v1
Main Text:
We would like to congratulate Giavarini A et al on this comprehensive, educational article on intracoronary imaging. [1] Various modalities can be used to understand the mechanism of stent failure, and there is an ongoing debate on detection of stent mal-apposition, and whether this has any clinical impact. Acute stent mal-apposition on its own is not associated with adverse clinical events unless associated with under expansion or having inflow- outflow issues. Acute mal-apposition and its associated clinical events are possibly reduced due to negative remodelling.[2] The clinically events are non-significant may be due to the fact that newer generation of stents and stronger antiplatelets are performing very well. There is limited literature evidence to support that acute mal-apposition is associated with stent thrombosis. [3] Late acquired malaposition in combination with other contributing factors can be associated with stent failure. Most of the available literature looking into the mechanism of stent failure is from...
Show MoreWe thank Xue et al for their interest in our article (1). The KDIGO classification (2) comprises 3 criteria in the diagnosis of acute kidney injury (AKI), namely an increase in serum creatinine (SCr) by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or an increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or urine volume <0.5 ml/kg/h for 6 hours. In our study, we had collected serial blood samples for the first 72 hours and the second KDIGO criterion (an increase in SCr to ≥1.5 times baseline) was applied over the 72 hours period to assess for AKI. As for the impact of perioperative fluid balance, this is not currently part of the recommendation, and the available evidence quoted (3) was taken from a retrospective, single-center study using the AKIN classification for AKI. Unfortunately the perioperative fluid balance was not collected in our study and we could not take this into account.
Show MoreWe did look at the Receiver Operating Characteristic curve analysis using sNGAL as a continuous variable. The area under the curve (AUC) was 0.57 (95%CI 0.54-0.60), very similar to that of sNGAL tertiles reported in our paper.(1) The diagnostic performance of sNGAL alone was quite low and therefore we did not provide cut-off values/sensitivity/specificity and predictive values. Expressing sNGAL as quartiles is more practical from a clinical point of view and we showed that by adding clinical factors, the c-statistic improved...
The letter by Dr Al-Mohammad is welcomed by the study authors and highlights some of the important challenges with using single value cut-offs for diagnosis and in determining treatment options. This is particularly true for heart failure with preserved left ventricular ejection fraction (LVEF) (HFpEF) (and more recently mid-range ejection fraction [HFmrEF], 40-49%) where decisions on starting prognostic medications can be made based on subjective echocardiographic measurements, albeit with evidence of diastolic dysfunction (tissue Doppler, flow Doppler, and volumes). Clearly, additional patient-specific factors should be taken into account, including aetiology, co-morbidities, and underlying rhythm, which are nicely highlighted in the editorial piece accompanying our study[1 2].
Show MoreThe Study Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors With Heart Failure (SENIORS) trial investigated the effects of the beta-blocker nebivolol in the treatment of heart failure in patients aged 70 and over[3]. Patients were required to have a clinical diagnosis of heart failure with either hospitalisation for heart failure in the previous 12 months, or a documented LVEF ≤35%. Baseline LVEF was measured by transthoracic echocardiography in 94% of cases. While van Veldhuisen et al. used an LVEF cut-off of 35% to compare “reduced” with “preserved” ejection fraction, they also examined and reported on the effect of Nebivolol in 643 patients with an LVEF ≥40%....
To the Editor:
We thank Dr. Launey Y et al for their constructive comments regarding our recent report.[1] We also greatly appreciate their shared interests in traumatic intra-cranial hemorrhage (ICH) and the subsequent incidence of atrial fibrillation (AF).
Dr Launey and colleagues concerned about the acute effects of inflammation on the onset of AF.[2] In our study, the mean follow-up period was 4.36 (standard deviation, SD=3.41) and 5.35 (SD=3.19) years in traumatic ICH group and control group, respectively. Interestingly, the mean follow-up period of the onset of AF was 2.94 years (SD=2.64) in traumatic ICH group, which is significantly less than 3.57 (SD=2.67) years in control group (Table 1) (p<0.001). Although acute inflammation plays a role on the onset of AF,[3, 4] our study along with previous evidence indicate the chronic persistent inflammation, which occurs after traumatic brain injury (TBI), contributes the development of AF.[1, 5] This partly explains the results of AF occurrence on TBI patients in our study.
We agree that sepsis may contribute to the development of AF. In this study, after adjustment for age, sex, and comorbidities including sepsis and ventilator associated pneumonia, the adjusted HR (aHR) for developing AF was 1.24-fold higher (95% CI = 1.18-1.31) for patients with traumatic ICH compared with the control cohorts in multivariable cox regression models (Table 2). These results further support the association betwee...
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