Letter by Dumesnil and Pibarot Regarding Article, “Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction”

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HomeCirculationVol. 124, No. 13Letter by Dumesnil and Pibarot Regarding Article, “Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Dumesnil and Pibarot Regarding Article, “Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction” Jean G. Dumesnil, MD, FRCP(C), FACC, FASE and Philippe Pibarot, DVM, PhD, FACC, FAHA, FASE, FESC Jean G. DumesnilJean G. Dumesnil Institut Universitaire de Cardiologie et de Pneumologie de Québec/Québec Heart & Lung Institute Department of Medicine Laval University Québec, Canada (Dumesnil, Pibarot) Search for more papers by this author and Philippe PibarotPhilippe Pibarot Institut Universitaire de Cardiologie et de Pneumologie de Québec/Québec Heart & Lung Institute Department of Medicine Laval University Québec, Canada (Dumesnil, Pibarot) Search for more papers by this author Originally published27 Sep 2011https://doi.org/10.1161/CIRCULATIONAHA.111.038497Circulation. 2011;124:e360To the Editor:We read with interest the paper by Jander et al1 reporting that patients with low-gradient severe aortic stenosis (LGSAS) and preserved ejection fraction have an outcome similar to that in patients with moderate aortic stenosis (AS). At first glance, this result is discordant with previous studies reporting the opposite,2–4 and in our opinion, further analysis is warranted. Indeed, the entity originally described as paradoxical low-flow or low-gradient AS2,3 is characterized by higher left ventricular (LV) global hemodynamic load, more severe LV concentric remodeling, smaller LV cavity size, and decreased LV midwall radius shortening, and the low gradient is deemed to be due to a lower LV stroke volume related to a restrictive physiology. The LGSAS patients reported by Jander et al1 do not, however, exhibit these features, and in our opinion, the finding of LGSAS in these cases could rather be due to 1 or more of the following2,3: (1) Small body size, (2) measurement errors, or (3) inconsistent grading due to intrinsic discrepancies in guidelines criteria. Body surface area was smaller in the LGSAS group, and some patients could thus have been misclassified as having severe rather than moderate aortic stenosis because the nonindexed rather than the indexed aortic valve area was used for classification. More noteworthy, however, is that recalculation of stroke volume in the LGSAS group by the 2-dimensional volumetric method (ie, LV end-diastolic volume times LV ejection fraction, using the results given in Table 2 in the article) yields much higher values for stroke volume and aortic valve areas (77 mL, 1.00 cm2, and 0.55 cm2/m2) than those reported in the same table (64 mL, 0.82 cm2, and 0.43 cm2/m2), and conversely, dividing the reported stroke volume by the reported LV end-diastolic volume yields a much lower value for ejection fraction than that reported (56% versus 67%). In our opinion, these discrepancies can likely be explained by measurement errors (underestimation) of stroke volume by Doppler and, in turn, could have resulted in overestimation of AS severity in many patients. This explanation is further buttressed by the results of a previous substudy5 from the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) trial whereby, in the same cohort of patients, Cramariuc et al identified only 100 low-flow patients rather than the 223 reported by Jander et al.1 Stroke volumes in the former study,1 however, were calculated with the Teicholz correction of the cube formula rather than by Doppler, and body surface area was taken into account when defining AS severity. Moreover, the low-flow patients also exhibited the restrictive features usually associated with this condition,2–5 and Cramariuc et al5 acknowledged that paradoxical low-flow AS indeed had important implications with regard to intrinsic LV myocardial function. Hence, we would submit that the report by Jander et al1 helps to advance the healthy debate about the assessment of AS severity, but that their results do not correspond to the entity described as paradoxical low-flow AS. Indeed, this condition should not be considered as benign, because it has repeatedly been shown that these patients are less frequently referred to surgery and have a higher mortality if treated medically rather than surgically.2–4Jean G. Dumesnil, MD, FRCP(C), FACC, FASEPhilippe Pibarot, DVM, PhD, FACC, FAHA, FASE, FESC Institut Universitaire de Cardiologie et de Pneumologie de Québec/Québec Heart & Lung Institute Department of Medicine Laval University Québec, CanadaDisclosuresNone.