Majority of the studies have defined peripheral arterial disease as ankle brachial index (which is a ratio of absolute systolic ankle blood pressures and absolute systolic brachial blood pressures) of <0.9. Peripheral arterial disease ought to be defined by both low ankle brachial index and high ankle brachial index as both low and high ankle brachial index are predictors of cardiovascular disease and mortality in Europeans. The prevalence of hypertension and its association with cardiovascular disease in South Asians do not significantly differ from that of Europeans. The prevalence of ankle brachial index <0.9 in South-Asians is less than in Europeans both in subjects with or without diabetes. However, absolute systolic ankle blood pressures increase with diabetes in young South Asians and these increases are greater in South-Asians compared to Europeans (Kain K, Heart 2013; 99:614-619). Therefore, in South Asians peripheral arterial disease ought to be defined by high ankle brachial index rather than low ankle brachial index and the paradox of lower prevalence of peripheral arterial disease even though South Asians have increased prevalence of ischemic heart disease and ischemic stroke will disappear.

Conflict of Interest:

None declared

INVASIVE VERSUS CONSERVATIVE STRATEGY FOR THE MANAGEMENT OF SPONTANEOUS CORONARY ARTERY DISSECTION: WHICH IS BETTER ?

Kenan YALTA, MD

Mustafa YILMAZTEPE, MD

Flora OZKALAYCI, MD

Nasir SIVRI, MD

Bilal GEYIK, MD

Trakya ?niversity, Cardiology Department, Edirne, Turkey

Corresponding Author: Kenan Yalta , e-mail: kyalta@gmail.com

To the Editor,

In the recent years, spontaneous coronary artery dissection (SCAD) has been a point of debate with regard to its management strategies. In their recently published article (1), Taleyratne JD et al described a case of spontaneous coronary artery dissection (SCAD) in a middle-aged woman presenting with acute coronary syndrome (ACS) (1). As far as we understand, the case was exclusively managed with a conservative strategy (with aspirin, ticagrelor, glycoprotein IIb/IIIa inhibitors and heparin) after coronary angiography (CAG) and intravascular ultrasound (IVUS). If that was the case, we strongly oppose the exclusive use of a non-interventional approach in this patient due to reasons described below.

Regarding the single- vessel SCAD, conservative strategy is only warranted in asymptomatic cases in which the degree of stenosis due to SCAD is < 50% along with a distal perfusion of TIMI 3 in the affected vessel (2). In other terms, where applicable, PCI is strongly recommended in the setting of a high-risk SCAD associated with a severe luminal narrowing (70-99%) and/or a poor distal vessel perfusion (TIMI 0- 1) and presenting with an unstable condition (2) (as in the case reported by Taleyratne JD (1)). Surgical management might also be performed in a more selected portion of cases including those with left main coronary artery (LMCA) or multivessel involvement in which there is no SCAD extension to the distal segments of the affected vessel (2).

There exists a strong rationale behind these therapeutic recommendations : SCADs treated conservatively might not always demonstrate a resolution or spontaneous healing, and might even worsen in some situations in the short and long terms (2,3). On follow-up, unfavorable results might be encountered in as high as 60% of SCADs managed with a conservative strategy alone (2,4). Among these long-term complications , late recurrences (2, 5) and aneurysm formation (3) in the affected vessel might be quite troublesome, and might be regarded as major therapeutic challenges in the conservatively treated patients with a SCAD. More importantly, witholding an early invasive strategy in the acute phase might be associated with acute life-threatening consequences including refractory arrhythmic events, retrograde propagation of the dissection towards the LMCA, etc. Interestingly, propagation of SCAD is more likely to occur in normal vessels in comparison to atherosclerotic ones (2) . On the other hand, PCI was previously suggested as the primary therapeutic option in the setting of SCAD (6). However, when the final decision is PCI, it should be done by expert hands: the operator should avoid advancing guide-wire into the false lumen to prevent SCAD extension (2). Direct stenting without stent oversizing should be the preferred strategy (2). Unfortunately, despite meticulous care, additional stents might be required in a portion of cases due to the propagation of SCAD after initial stenting (2,5). Nevertheless, PCI when combined with endovascular imaging techniques (IVUS, etc) seems to be a more promising therapeutic approach in the setting of SCAD particularly with high-risk features.

In summary; conservative management might pose a significant risk to patients with SCAD (2-4) particularly to those with high- risk features both in the short and long terms. On the other hand, invasive strategy including PCI, when performed by experienced operators and with the assistance of endovascular imaging techniques, seems to be a radical and efficient alternative in these patients (2,6). We wonder why Taleyratne JD et al (1) preferred a 'wait and see' approach rather than performing an IVUS-guided urgent PCI in their high-risk patient. Furthermore, as SCAD might be regarded as a continuum of evolving vascular pathology with an unpredictable course even after healing, their patient (1) needs to be monitored closely for potential late complications including recurrence , aneurysm formation, etc. Accordingly, the authors (1) may want to make clear their future strategies (follow-up, medication, repeat CAG or non-invasive imaging ?, etc.) regarding their patient in a more comprehensive manner. However, future studies are still warranted to establish furher risk prediction models that might help determine the initial therapeutic strategy, and more importantly, might allow timely diagnosis and management of acute and chronic complications in patients with SCAD.

REFERENCES: 1- Taleyratne JD, Fernandez JP. Anterior ST elevation myocardial infarction in a 40-year-old woman. Heart. 2014 Jun 27. pii: heartjnl-2014- 305985. doi: 10.1136/heartjnl-2014-305985. [Epub ahead of print. 2- Giacoppo D, Capodanno D, Dangas G, Tamburino C. Spontaneous coronary artery dissection. Int J Cardiol. 2014; 175(1): 8-20. 3- Furuichi, S. , Montorfano, M., Godino, C., Murino, M., Sangiorgi, G.M., Colombo, A. How should I treat a long and huge coronary pseudoaneurysm after spontaneous coronary artery dissection? EuroIntervention. 2011; 6: 1131-1136. 4- Shamloo BK, Chintala RS, Nasur A, Ghazvini M, Shariat P, Diggs JA, Singh SN. Spontaneous coronary artery dissection: aggressive vs. conservative therapy. J Invasive Cardiol. 2010; 22(5): 222-8. 5- Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, Gersh BJ, Khambatta S, Best PJ, Rihal CS, Gulati R. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012; 126(5) :579-88. 6- Butler R, Webster MW, Davies G, Kerr A, Bass N, Armstrong G, Stewart JT, Ruygrok P, Ormiston J. Spontaneous dissection of native coronary arteries. Heart. 2005; 91(2) :223-4.

Conflict of Interest:

None declared

Firstly, looking at the study design the selected age range of HCM subjects (mean age of 56 years) may at least in part account for the high percentage of myocardial fibrosis at baseline (66 %) as in addition to the fibrosis likely being a pathological consequence of HCM itself, this age group of participants may harbour occult or sub-clinical coronary artery disease and a prior association between cardiac ischemia and myocardial fibrosis has been reported in the literature (1).

While these findings theoretically justify the use of routine cardiac MRI at the time of HCM diagnosis in conjunction with echocardiography (enabling the detection of two predictive variables of sudden cardiac death, fibrosis and left ventricular ejection fraction, respectively) as a comprehensive diagnostic work-up, this consideration needs to be carefully balanced against the economic burden of widely implementing such sophisticated imaging and the realisation that such techniques do not exist widely in all centres for effective risk stratification to take place on a national level (2).

Finally, the question remains as to what represents an appropriate time interval for monitoring the progression of myocardial fibrosis once already detected and how this will be determined? This may be of particular importance as you have established that the extent of myocardial fibrosis (if we place this irreversible process along a continuum) was a statistically significant predictor of sudden cardiac death. Thus, if the fibrotic process wasn't monitored linearly over time in these patients, and the myocardial fibrosis was detected once already 'extensive', the risk of sudden cardiac death in this subset of HCM subjects may remain high despite any prevailing medical or surgical intervention.

References:-

1) Wilson JM, Villareal RP, Hariharan R, Massumi A, Muthupillai R, Flamm SD. Magnetic Resonance Imaging of Myocardial Fibrosis in Hypertrophic Cardiomyopathy (2002). Tex Heart Inst J.29:176-180.

2) To ACY, Dhillon A, Desai MY. Cardiac Magnetic Resonance in Hypertrophic Cardiomyopathy (2011). J Am Coll Cardiol Img. 4(10):1123- 1137.

Conflict of Interest:

None declared

We read with great interest the article by Di Maria et al. [1], describing the importance of right ventricular (RV) performance, especially RV stroke work (RVSW) in children with pulmonary arterial hypertension (PAH). The authors investigated the relation between echocardiographic measurements of RV function and the "gold standard" of right heart catheterization in children and found that the RVSW strongly correlates with non-invasive data of RV function [1]. The authors concluded that RVSW correlates with outcome parameters, e.g. abnormal WHO class, and mortality, in children with PAH. We completely agree with the findings of Di Maria et al. [1] and want to emphasize the importance of echocardiographic evaluation, e.g. tricuspid annular peak systolic excursion (TAPSE) for longitudinal management of pediatric patients with PAH. Di Maria et al. compared data of patients with adverse outcomes to patients with WHO class I-III, of different age groups: median 16.9 versus 11.8 years (table 1) and found no statistically significant difference of TAPSE (mean values 1.3 versus 1.5 cm, respectively) between those groups [1]. In our opinion their data would have been more promising and statistically significant, if the authors would have compared their TAPSE data with already existing normative data of TAPSE [2] (comparing 1.5 to 2.14 cm for 12 years of age, and 1.3 cm to 2.45 cm for 17 years of age). This might highlight the importance of their data for future pediatric PAH follow ups. We want to encourage the prospective use of echocardiography for routine assessment of RV systolic function in pediatric PAH patients.

References 1.) Di Maria MV, Younoszai AK, Mertens L, Landeck BF 2nd, Ivy DD, Hunter KS, Friedberg MK. RV stroke work in children with pulmonary arterial hypertension: estimation based on invasive haemodynamic assessment and correlation with outcomes. Heart 2014 Apr 29. doi: 10.1136/heartjnl-2013- 305298 [Epub ahead of print].

2.) Koestenberger M, Nagel B, Ravekes W, Avian A, Heinzl B, Fandl A, et al. Tricuspid annular peak systolic velocity (S') in children and young adults with pulmonary artery hypertension secondary to congenital heart diseases, and in those with repaired tetralogy of Fallot: echocardiography and MRI data. J Am Soc Echocardiogr 2012; 25: 1041-9.

Conflict of Interest:

None declared