852 e-Letters

  • Hospitalization for Heart Failure as a Promising Risk Stratification Tool for Pulmonary Hypertension Related to Congenital Heart Disease

    To the Editor, we read with great interest the article by Ntiloudi et al[1], describing hospitalization for heart failure (HF) as a powerful predictor of mortality among adults with pulmonary hypertension related to congenital heart disease (PH-ACHD). Although pulmonary arterial hypertension (PAH) targeted therapy has improved their survival, long-term complications such as HF hospitalization commonly occurred, and dismal prognosis with a mortality rate of 18.5% deeply broke our heart, thus requiring earlier diagnosis, risk stratification and therapeutic intervention.
    Hospitalization for HF, a sign of clinical worsening, is associated with poor outcomes and generally used as one of composite endpoints in PAH[2], Ntiloudi et al stated nearly one-quarter of patients were hospitalized for HF, and they encountered a ninefold increased mortality risk compared to those not-hospitalized, since NYHA functional class III/IV raised a tenfold risk of death, its combination with HF hospitalization may better predict outcomes. A previous study[3] reported 29% patients with idiopathic and associated PAH were hospitalized for acute right heart failure at least once during a 39.1-month follow up, and those with hospitalizations had worse NYHA functional class, inferior right ventricle function, lower six minute walk test (6MWT) distance and worse outcomes defined by death/transplant (67% vs 33%). These two findings indicated a potential role of HF hospitalization for identifying...

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  • Hyponatramia may be drug side effect.

    There was significantly higher usage of both loop diuretics and aldosterone antagonist in the group with persistent hyponatraemia. Is it possible that one of the clinical manifestation of RV dysfunction, i.e peripheral oedema, led to an increased use of diuretic in this group and hence hyponatraemia as a complication of this treatment? Over diuresis in this scenario leads to activation of the RAAS which in turn worsens pulmonary hypertension and tricuspid regurgitation. The consequence of this is worsening peripheral oedema and the tendency to increase the diuretic dose.Hyponatraemia therefore may not be an independent predictor of outcome as stated.

  • We must continue to EXPLORE the benefits of CTO PCI

    We read with great interest the article by Elias et al (1) regarding the longer term clinical outcomes from the EXPLORE trial. The authors are to be congratulated for conducting this important study to address the optimal management of patients presenting with a concurrent CTO in a non-infarct related artery (non-IRA) during a STEMI. The results at 1 year are similar to those in the initial 4 month outcome (2), with no difference in the primary endpoints of cardiac MRI determined LVEF or LVEDV in either CTO-PCI and CTO-No PCI groups. At a median of 3.9 years, there was no difference in long term MACE, although an apparent increase in cardiovascular mortality (6% vs 1%, p=0.02).

    Whilst this important study adds to the much needed literature on randomised studies related to PCI of CTOs, the results should be interpreted with caution. Firstly, large scale contemporaneous studies in CTO PCI have had procedural success rates in the region of 90% (3), whilst in EXPLORE (2) this rate was considerably lower, at 73% by core laboratory. This suggests either a more anatomically complex subset of patients, or else attempts by non-dedicated CTO PCI operators, both of which affect the interpretation of the intention to treat population.

    Furthermore, the mortality data should be reviewed with care. At 12 months, there were 4 cardiovascular deaths (2.7%) in the CTO PCI group, with no deaths in the CTO-No PCI groups. These rates are significantly lower compared with other t...

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  • 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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