eLetters

779 e-Letters

  • The prognostic role of collaterals should be explored.

    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...

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  • More data are needed to explore the impact of chronic total occlusion recanalisation on the prognosis of patients with ST elevation myocardial infarction.

    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...

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  • Interventricular vessel of the heart

    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...

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  • Endovascular occlusion and intra-myocardial tunnelization of the internal mammary arteries:

    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...

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  • Congenital Tricuspid Valve Disease Can Masquerade as Primary Idiopathic Tricuspid Regurgitation

    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...

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  • Considerations in Pursuing the Optimal Timing for Pulmonary Valve Replacement in Repaired Tetralogy of Fallot

    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...

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  • Intra coronary imaging to detect mal apposition:Are We Seeing Too Much!

    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...

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  • Reply to e-letter by Xue et al - Use of preoperative neutrophil gelatinase-associated lipocalin to predicts acute kidney injury and mortality after cardiac surgery

    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...

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  • Targeting beta blocker therapy to individual heart failure with preserved ejection fraction phenotypes

    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%....

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  • Is traumatic intracranial hemorrhage a specific risk factor of atrial fibrillation: Reply

    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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