We thank Dr Breithardt 1 for his interest in our paper reporting a case of discrete dissection of the ascending aorta 2. In the transoesophageal echocardiographic image published Dr Breithardt has interpreted the presence of a hazy horizontal line located approximately in the middle of the aortic lumen as an intimal flap dividing the aorta into an anterior false lumen and a posterior false lumen suggesting the presence of a “classic” aortic dissection (class 1 in the classification of the European Society of Cardiology 3), instead of a discrete aortic dissection (class 3 in the ESC classification). The structure indicated by Dr Breithardt as an intimal flap was just a linear artefact; it had fuzzy and indistinct borders, it was located twice as far from the transducer as the posterior aortic wall (type A artefact according to Evangelista et al 4), had a displacement parallel to the aortic walls, had a thickness > 2.5 mm 5 , and had a movement parallel to the posterior aortic wall: all features peculiar for linear artefacts. Last, but not least, no intimal flap was detected at surgical inspection. Finally, the arrow indicating the periaortic effusion points to a discrete separation of the pericardial layers representing a small amount of fluid around the ascending aorta; it had been therefore placed correctly.

With best regards,

Fabio Chirillo, Loris Salvador, and Francesco Bacchion

REFERENCES

1) Beithardt OA. Discrete dissection or overt intimal flap? Heart eLetter 6 August 2008. 2) Chirillo F, Salvador L, Bacchion F. Acute discrete dissection of the ascending aorta. Heart 2008; 94: 924. 3) Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection. Recommendations of the task force on aortic dissection of the European Society of Cardiology. Eur Heart J 2001; 22: 1642-1681. 4) Evangelista A, Garcia del Cavillo H, Gonzalez-Alujas T, et al. Diagnosis of ascending aortic dissection by transesophageal echocardiography: utility of M-mode in recognizing artifacts. J Am Coll Cardiol 1996; 27: 102-107. 5) Vignon P, Spencer KT, Rambaud G, et al. Differential transesophageal echocardiographic diagnosis between linear artifacts and intraluminal flap of aortic dissection or disruption. Chest 2001; 119: 1778-1790.

To the Editor,

In the April 2008 issue of the Journal, Aldous (1) reported the striking case of a young male with Libman-Sacks endocarditis due to primary antiphospholipid syndrome (PAS) A transesophageal echocardiogram performed on the patient revealed a 1.5 X 1.5cm aortic valve vegetation which had apparently embolized to his left lower extremity. A trial of anticoagulation failed to result regression of the lesion. The patient eventually underwent successful valve-sparing surgery and was again anticoagulated.

We differ with the author’s contention that long term anticoagulation in PAS will "usually proceed to regression of valve disease". While the effects of anticoagulation therapy on patients with PAS and cardiac involvement have not been extensively studied, several small recent studies have all shown that the cardiac lesions associated with the PAS may not respond to, or may even progress, despite, anticoagulation therapy. In the largest prospective study of which we are aware, Turiel et al (2) followed 47 patients with PAS over a 5 year period with serial transesophageal echocardiography. All patients received oral anticoagulants with or without anti-platelet therapy. Over the period of follow-up, cardiac involvement remained unchanged in 64% (30 subjects). Moreover, new cardiac abnormalities appeared in 36% (17 subjects). These findings reflect the findings of other smaller series (3,4). Hence, it would appear that anticoagulation therapy is ineffective in treating the cardiac lesions associated with PAS.

1.Aldous S. An interesting presentation of antiphospholipid syndrome Heart 2008; 94:421.

2.Turiel M, Sarzi-Putin P, Peretti R, Bonizzato S, Muzzupappa S, Atzeni F et al. Five year follow-up by transesophageal echocardiographic studies in primary antiphosphospholipid syndrome. Am J Cardiol 2005;96:574-9.

3.Espinola-Zavaleta N, Vargas-Barron J, Colmenares-Galvis,T, Cruz- Cruz F, Romero-Cardenas A, Keirns C et al. Echocardiographic evaluation of patients with primary antiphospholipid syndrome. Am Heart J 1998;137:974- 9.

4.Espinola-Zavaleta N, Montes RM, Soto ME, Vanzzini NA, Amigo MC. Primary antiphospholipid syndrome: a 5-year transesophageal echocardiographic follow-up study. J Rheumatol 2004;31:2402-7.

Competing interests: None

Correspondence to: jeffrey.silbiger@mssm.edu

Dear Editor,

We have read with interest the article of Mascherbauer et al.[1] recently published in Heart and we congratulate our colleagues for an honest effort on shedding some light on an important issue which is still generating some controversy. Nonetheless, based on the title and the conclusions of both the abstract and the paper, we are concerned that the paper may unfortunately convey the wrong message i.e. that moderate prosthesis-patient mismatch should never be a concern in patients undergoing aortic valve replacement. Moreover, from the introduction, justification for the study appears to be based on the perception that our previous papers were recommending “that even left ventricular outflow tract enlargement may be justified to prevent moderate PPM”. In fact, we have never made such an unqualified recommendation. Indeed, our findings as well as those of others [2] show that the impact of moderate PPM on outcomes is most significant in patients with LV dysfunction as compared to patients without dysfunction (e.g. early mortality = 16% vs 5%, p< 0.001) and our recommendation has always been that if PPM is anticipated, alternative options should be considered in light of the patient’s overall clinical condition and the risk to benefit ratio of doing such procedures.

Unfortunately, the number of patients with LV dysfunction in the present study is too small to do any analysis in this regard. Moreover, LV dysfunction might even be a confounding variable since it was significantly more prevalent (15.2% vs 5.6%, p = 0.003) in the patients without PPM and hence, it could explain the relatively high mortality observed in this group (5.5%). Indeed, operative mortality for AVR in patients without LV dysfunction is usually 1-4% and if such had been the case, the markedly higher operative mortality (10.2%) observed in the group with PPM might have become statistically significant.

Notwithstanding this consideration, the statistical power of the study is clearly limited. Indeed, the difference in short-term mortality (5.5% vs. 10.2%) between the 2 groups did not reach statistical significance (i.e. p=0.14 with Yates correction in the results section and in Table 4, or p=0.098 without Yates correction in the Table 3). However, considering the previous study of Blais et al. [3] for sample size estimation, the inclusion of 361 patients leads to a statistical power of only 43% for the analysis of operative mortality. Moreover, using the same percentage of operative mortality in the two groups, but with a sample size of 880 patients (i.e. corresponding to the number of patients which would have result in a 80% a priori statistical power), the p-value would have been of 0.009 (without Yates correction). Hence, had the same sample size been closer to that of previous series, the findings and conclusions of the paper could have been entirely different.

Furthermore, as opposed to the perception given in the article of Mascherbauer et al., aortic root enlargement is certainly not the only and/or first line option to avoid PPM. The preventive strategy should rather be focused primarily on the implantation of prosthesis models providing a better hemodynamic performance and thereby a larger EOA in relation to patient’s annulus size. And in this regard, several recent studies have demonstrated that PPM can successfully be avoided or its severity reduced with the use of such strategy. [4-6]

Given these limitations, the present paper provides little new information and the findings certainly do not justify the unqualified conclusion that moderate PPM has no impact on short or long term mortality which implies that it can almost be ignored. To the contrary, we reiterate that the projected indexed EOA should always be calculated at the time AVR and that the decision with regards to the prosthesis to be implanted should be made in light of the patient’s overall clinical condition.

Clearly and based on many concurring data in the literature, every effort should be made to avoid severe PPM in every patient undergoing aortic valve replacement and moderate PPM if LV dysfunction and/or severe LVH is present. Finally, it should be mentioned that the underestimation of EOA in bi-leaflet prosthesis is based on in vitro studies and that this has not been shown to be a consistent finding in vivo. Indeed, recent studies using either the indexed EOA measured at predischarge exam or the projected indexed EOA derived from in vivo reference values demonstrated that the same cut-off values for indexed EOA were valid to predict outcomes in their series of patients with bi-leaflet mechanical prosthesis. [7;8]

Moreover, in one of these studies, even a moderate PPM was shown to negatively impact long- term survival after adjustment for other risk factors. [8]

References

[1]. Mascherbauer J, Rosenhek R, Fuchs C, Pernicka E, Klaar U, Scholten C, Heger M, Wollenek G, Maurer G, Baumgartner H.
Moderate patient -prosthesis mismatch after valve replacement for severe aortic stenosis has no impact on s.
Heart. 2008.

[2]. Ruel M, Al-Faleh H, Kulik A, Chan K, Mesana TG, Burwash IG.
Prosthesis-patient mismatch after aortic valve replacement primarily affects patients with pre-existing left ventricular dysfunction: Impact on survival, freedom from heart failure, and left ventricular mass regression.
J Thorac Cardiovasc Surg. 2006;131:1036-1044.

[3]. Blais C, Dumesnil JG, Baillot R, Simard S, Doyle D, Pibarot P.
Impact of prosthesis-patient mismatch on short-term mortality after aortic valve replacement.
Circulation. 2003;108:983-988.

[4]. Bleiziffer S, Eichinger WB, Hettich I, Guenzinger R, Ruzicka D, Bauernschmitt R, Lange R.
Prediction of valve prosthesis-patient mismatch prior to aortic valve replacement: which is the best method?
Heart. 2007;93:615-620.

[5]. Dalmau MJ, Gonzalez-Santos JM, Lopez-Rodriguez J, Bueno M, Arribas A, Nieto F.
One year hemodynamic performance of the Perimount Magna pericardial xenograft and the Medtronic Mosaic bioprosthesis in the aortic position: a prospective randomized study.
ICVTS. 2007;6:345-349.

[6]. Kunadian B, Vijayalakshmi K, Thornley AR, de Belder MA, Hunter S, Kendall S, Graham R, Stewart M, Thambyrajah J, Dunning J.
Meta-analysis of valve hemodynamics and left ventricular mass regression for stentless versus stented aortic valves.
Ann Thorac Surg. 2007;84:73-78.

[7]. Mohty D, Malouf JF, Girard SE, Schaff HV, Grill DE, Enriquez- Sarano ME, Miller FA, Jr.
Impact of prosthesis-patient mismatch on long- term survival in patients with small St. Jude medical mechanical prostheses in the aortic position.
Circulation. 2006;113:420-426.

[8]. Kohsaka S, Mohan S, Virani S, Lee VV, Contreras A, Reul GJ, Coulter SA.
Prosthesis-patient mismatch affects long-term survival after mechanical valve replacement.
J Thorac Cardiovasc Surg. 2008,135:1076-80.