Effect of Transcatheter (via Femoral Artery) Aortic Valve Implantation on the Platelet Count and Its Consequences
2013; Elsevier BV; Volume: 111; Issue: 11 Linguagem: Inglês
10.1016/j.amjcard.2013.01.332
ISSN1879-1913
AutoresRomain Gallet, Aurélien Seemann, Masanori Yamamoto, Delphine Hayat, Gauthier Mouillet, Jean‐Luc Monin, Pascal Guéret, Jean-Paul Couëtil, Jean‐Luc Dubois‐Randé, Emmanuel Teíger, Pascal Lim,
Tópico(s)Venous Thromboembolism Diagnosis and Management
ResumoDecrease in blood platelet count has been described after percutaneous coronary intervention and surgical valve replacement, although no study has been performed in the setting of transcatheter aortic valve implantation (TAVI). The aim of this study was to address the incidence, mechanism, and impact of blood platelet count decrease after TAVI. One hundred forty-four consecutive patients (mean age 84 ± 7 years, 64 men) with severe symptomatic aortic stenosis who underwent TAVI from December 2007 to July 2011 were enrolled. Blood platelet count was recorded before and after aortic valve implantation. Decrease in blood platelet count was compared with in-hospital major adverse cardiovascular events (death, stroke, and major or life-threatening bleeding). Blood platelet count decreases occurred in all but 1 patient. The percentage of platelet count decrease averaged 34 ± 15% and was 24% greater than blood protein decrease. Decrease in platelet count was associated with a higher rate of prosthesis migration, longer x-ray and procedural times, and larger contrast amounts (230 ± 128 ml for the third tertile vs 170 ± 77 ml for the second and first tertiles, p = 0.0006), but no association was observed with regard to changes in bilirubin. In-hospital major adverse cardiovascular events (n = 50 [35%]) were observed more frequently in patients with severe platelet count decreases (21% for the first tertile, 35% for the second tertile, and 48% for the third tertile, p = 0.02). Finally, the percentage of blood platelet count decrease was the only predictor of in-hospital major adverse cardiovascular events (odds ratio 1.67, 95% confidence interval 1.05 to 2.67, p = 0.03). In conclusion, a decrease in platelet count is a common phenomenon after TAVI, and its severity is associated with poor outcomes. Decrease in blood platelet count has been described after percutaneous coronary intervention and surgical valve replacement, although no study has been performed in the setting of transcatheter aortic valve implantation (TAVI). The aim of this study was to address the incidence, mechanism, and impact of blood platelet count decrease after TAVI. One hundred forty-four consecutive patients (mean age 84 ± 7 years, 64 men) with severe symptomatic aortic stenosis who underwent TAVI from December 2007 to July 2011 were enrolled. Blood platelet count was recorded before and after aortic valve implantation. Decrease in blood platelet count was compared with in-hospital major adverse cardiovascular events (death, stroke, and major or life-threatening bleeding). Blood platelet count decreases occurred in all but 1 patient. The percentage of platelet count decrease averaged 34 ± 15% and was 24% greater than blood protein decrease. Decrease in platelet count was associated with a higher rate of prosthesis migration, longer x-ray and procedural times, and larger contrast amounts (230 ± 128 ml for the third tertile vs 170 ± 77 ml for the second and first tertiles, p = 0.0006), but no association was observed with regard to changes in bilirubin. In-hospital major adverse cardiovascular events (n = 50 [35%]) were observed more frequently in patients with severe platelet count decreases (21% for the first tertile, 35% for the second tertile, and 48% for the third tertile, p = 0.02). Finally, the percentage of blood platelet count decrease was the only predictor of in-hospital major adverse cardiovascular events (odds ratio 1.67, 95% confidence interval 1.05 to 2.67, p = 0.03). In conclusion, a decrease in platelet count is a common phenomenon after TAVI, and its severity is associated with poor outcomes. In recent years, transcatheter aortic valve implantation (TAVI) using stent-based prostheses has become an attractive alternative for high-risk elderly patients with symptomatic aortic stenosis.1Cribier A. Eltchaninoff H. Tron C. Bauer F. Agatiello C. Nercolini D. Tapiero S. Litzler P.Y. Bessou J.P. Babaliaros V. Treatment of calcific aortic stenosis with the percutaneous heart valve: mid-term follow-up from the initial feasibility studies: the French experience.J Am Coll Cardiol. 2006; 47: 1214-1223Abstract Full Text Full Text PDF PubMed Scopus (689) Google Scholar, 2Rodes-Cabau J. Webb J.G. Cheung A. Ye J. Dumont E. Feindel C.M. Osten M. Natarajan M.K. Velianou J.L. Martucci G. DeVarennes B. Chisholm R. Peterson M.D. Lichtenstein S.V. Nietlispach F. Doyle D. DeLarochelliere R. Teoh K. Chu V. Dancea A. Lachapelle K. Cheema A. Latter D. Horlick E. 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Clinical outcome and predictors for adverse events after transcatheter aortic valve implantation with the use of different devices and access routes.Am Heart J. 2011; 161: 1114-1124Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar Decreases in platelet counts have been observed after surgical aortic valve replacement13Hilker L. Wodny M. Ginesta M. Wollert H.G. Eckel L. Differences in the recovery of platelet counts after biological aortic valve replacement.Interact Cardiovasc Thorac Surg. 2009; 8: 70-73Crossref PubMed Scopus (42) Google Scholar, 14Repossini A. Bloch D. Muneretto C. Piccoli P. Bisleri G. Beholz S. Platelet reduction after stentless pericardial aortic valve replacement.Interact Cardiovasc Thorac Surg. 2012; 14: 434-438Crossref PubMed Scopus (20) Google Scholar, 15Steele P. Weily H. Davies H. Ppppas G. Genton E. Platelet survival time following aortic valve replacement.Circulation. 1975; 51: 358-362Crossref PubMed Scopus (30) Google Scholar and also occur after TAVI in clinical practice. However, a decrease in platelet count and its clinical impact on outcome after TAVI have never been studied. This study included 144 consecutive patients who underwent TAVI with self-expandable valves using the transfemoral approach from December 2007 to July 2011 at Henri Mondor University Hospital. The definition of severe aortic stenosis was determined by the echocardiographic findings of an aortic valve area 4.0 m/s, or a mean aortic valve gradient >40 mm Hg. All patients were screened before TAVI to determine whether they were considered unsuitable for surgical aortic valve replacement, according to a consensus between cardiac surgeons and cardiologists. Only patients with native aortic stenoses were included in the study. All patients provided written informed consent before enrollment in the registry. The TAVI procedure was previously reported in detail.2Rodes-Cabau J. Webb J.G. Cheung A. Ye J. Dumont E. Feindel C.M. Osten M. Natarajan M.K. Velianou J.L. Martucci G. DeVarennes B. Chisholm R. Peterson M.D. Lichtenstein S.V. Nietlispach F. Doyle D. DeLarochelliere R. Teoh K. Chu V. Dancea A. Lachapelle K. Cheema A. Latter D. Horlick E. Transcatheter aortic valve implantation for the treatment of severe symptomatic aortic stenosis in patients at very high or prohibitive surgical risk: acute and late outcomes of the multicenter Canadian experience.J Am Coll Cardiol. 2010; 55: 1080-1090Abstract Full Text Full Text PDF PubMed Scopus (879) Google Scholar, 16Yamamoto M. Meguro K. Mouillet G. Bergoend E. Monin J.L. Lim P. Dubois-Rande J.L. Teiger E. Comparison of effectiveness and safety of transcatheter aortic valve implantation in patients aged >/=90 years versus 250 seconds. Blood platelet count was measured before valve implantation (baseline) and every day after the procedure until discharge. Blood samples were drawn by venipuncture every morning. Baseline and nadir platelet count after TAVI was used to determine the maximum percentage of platelet count decrease. Blood was collected into ethylenediaminetetraacetic acid Vacuette tube (Greiner Bio-One, Kremsmünster, Austria) and processed for automatic platelet numeration (Beckman Coulter, Brea, California). The normal range of platelet count values for the automatic numeration is 150 × 109/L to 500 × 109/L, and the coefficient variation is <5%. The nadir of platelet count was defined as the minimum platelet count before any blood transfusion during the hospitalization period. Clinical follow-up was carried out through clinical visits or phone calls during the hospital stay and after 30 days. Major adverse cardiovascular events (MACEs) were prospectively collected during this period. The primary outcome was in-hospital MACEs, defined as all-cause death, life-threatening and major bleeding, and stroke during the hospitalization period as defined by the Valve Academic Research Consortium classification.20Leon M.B. Piazza N. Nikolsky E. Blackstone E.H. Cutlip D.E. Kappetein A.P. Krucoff M.W. Mack M. Mehran R. Miller C. Morel M.A. Petersen J. Popma J.J. Takkenberg J.J. Vahanian A. van Es G.A. Vranckx P. Webb J.G. Windecker S. Serruys P.W. Standardized endpoint definitions for transcatheter aortic valve implantation clinical trials: a consensus report from the Valve Academic Research Consortium.J Am Coll Cardiol. 2011; 57: 253-269Abstract Full Text Full Text PDF PubMed Scopus (707) Google Scholar Device success and 30-day combined safety data were evaluated according to the Valve Academic Research Consortium criteria. The combined safety end point was defined as follows: all-cause mortality, major stroke, life-threatening bleeding, stage 3 acute kidney injury, periprocedural myocardial infarction, major vascular complications, and a repeat procedure for valve-related dysfunction. Continuous variables with normal distributions are expressed as mean ± SD and nominal variables as percentages. To compare numerical data between groups, paired and unpaired Student's t tests were used as appropriate. Nominal variables were compared using chi-square tests. Kendall's correlation was used for trend testing. Multivariate analyses were performed using linear regression. Survival time-to-event analysis was performed using Kaplan-Meier curves. Two-tailed p values 140/90 mm Hg, previous diagnosis of hypertension, or use of antihypertensive medication.109 (76%)Dyslipidemia†Low-density lipoprotein >100 mg/dl or use of lipid-lowering medication.78 (54%)Previous myocardial infarction29 (13%)Previous vascular disease29 (20%)Previous cerebrovascular event17 (12%)Previous cardiac surgery20 (14%)Chronic obstructive pulmonary disease37 (26%)New York Heart Association class2.8 ± 0.6Creatinine (μmol/L)111 ± 38Estimated glomerular filtration rate (ml/min)55 ± 23Hemoglobin (g/dl)11.9 ± 1.7Platelet count (109/L)216 ± 67Data are expressed as mean ± SD or as number (percentage).∗ Blood pressure >140/90 mm Hg, previous diagnosis of hypertension, or use of antihypertensive medication.† Low-density lipoprotein >100 mg/dl or use of lipid-lowering medication. Open table in a new tab Data are expressed as mean ± SD or as number (percentage). Blood platelet count at baseline before TAVI averaged 216 × 109/L ± 67 × 109/L (range 77 × 109/L to 441 × 109/L). Decrease in platelet count after TAVI occurred in all but 1 patient. The minimum platelet count averaged 170 × 109/L ± 54 × 109/L (range 41 × 109/L to 336 × 109/L) and was observed 2.5 ± 1.1 days after TAVI (Figure 1). The decrease in platelet count averaged 34 ± 15% (18 ± 7% for the first tertile, 33 ± 4% for the second tertile, and 55 ± 10% for the third tertile). Overall, 90 patients had moderate thrombopenia (platelet count 50 × 109/L to 150 × 109/L), and only 3 had severe thrombopenia (platelet count <50 × 109/L). No patients received platelet transfusions, and dual-antiplatelet treatment was withdrawn in patients with severe thrombopenia, except for aspirin when recent stent implantation had been performed. Blood protein decrease was poorly correlated with the severity of platelet count decrease (r2 = 0.039, p = 0.02). In addition, decreases in hematocrit and blood proteins count averaged 11% and 15%, respectively, while the decrease in platelet count was systematically 24% greater than the plasmatic protein decrease (Figure 2). In addition, platelet change failed to correlate with change in hematocrit (r2 = 0.007, p = 0.30) and bilirubin (r2 = 0.004, p = 0.40). Patients with the most severe platelet count decreases (third tertile) had more complex procedures: 5 patients in the third tertile compared with none in the second and first tertiles had prosthesis displacement that required new prosthesis valve implantations in 3 patients (p = 0.04), resulting in lower procedural success in the third tertile. Moreover, patients in the third tertile had more prolonged procedural and x-ray times and larger contrast amounts (Table 2). The differences in procedural duration persisted even after excluding patients with prosthesis displacement (23 ± 13 min in the third tertile vs 17 ± 7 min in the second and first tertiles, p = 0.0008, for x-ray time, and 89 ± 32 vs 71 ± 21 min, respectively, p = 0.0001, for procedure time). Multivariate analysis demonstrated that procedural time (β = 0.23, p = 0.02) and prosthesis migration (β = 0.17, p = 0.03) were the 2 independent predictors of platelet count decrease.Figure 2Difference between changes in protein and platelet (y axis) according to changes in protein (x axis).View Large Image Figure ViewerDownload Hi-res image Download (PPT)Table 2Population characteristics and outcomes according to platelet decrease by tertileVariablePercentage of Platelet Count Decrease by Tertilep ValueFirstSecondThirdAge (yrs)84 ± 885 ± 783 ± 80.50Creatinine (μmol/L)113 ± 44107 ± 33112 ± 350.70Hemoglobin (g/L)11.4 ± 1.512.2 ± 1.512.1 ± 1.80.02Antithrombotic treatment Aspirin34 (70%)29 (60%)26 (54%)0.20 Clopidogrel35 (71%)32 (66%)29 (60%)0.60 Vitamin K antagonist14 (31%)18 (37%)10 (21%)0.20Procedural characteristics Postdilatation6 (13%)5 (10%)6 (13%)0.80 X-ray time (minutes)17 ± 718 ± 724 ± 130.002 Procedural time (minutes)70 ± 2072 ± 2292 ± 33 1 prosthesis0030.04 Prosthesis migration0050.005 Aortic regurgitation ≥25 (10%)10 (21%)11 (23%)0.30Biologic characteristics Platelet count at baseline (109/L)209 ± 66219 ± 63221 ± 720.60 Platelet count nadir (109/L)172 ± 55146 ± 42108 ± 38<0.0001 Platelet count decrease (%)18 ± 733 ± 450 ± 10<0.0001 Protein decrease (%)7 ± 1510 ± 814 ± 90.01 Hematocrit decrease (%)9 ± 1917 ± 1917 ± 100.02 Bilirubin increase (%)21 ± 4844 ± 7531 ± 740.30Valve Academic Research Consortium Procedural success48 (100%)47 (98%)42 (88%)0.009 30-day combined safety end point4 (8%)4 (8%)14 (29%)0.004 Stroke1 (2%)4 (8%)5 (10%)0.20 Major and life-threatening bleeding9 (19%)14 (29%)19 (40%)0.08 Major vascular complications4 (8%)5 (10%)10 (21%)0.20 Myocardial infarction0 (0%)2 (4%)1 (2%)0.40Other complications In-hospital mortality1 (2%)3 (6%)7 (15%)0.06 30-day mortality1 (2%)4 (8%)7 (15%)0.08 MACEs10 (21%)17 (35%)23 (48%)0.02 Hemoglobin loss (g/dl)1.6 ± 1.11.9 ± 1.22.8 ± 1.6<0.0001 Red blood cell transfusion5 (10%)5 (10%)17 (35%)0.001Data are expressed as mean ± SD or as number (percentage). Open table in a new tab Data are expressed as mean ± SD or as number (percentage). Kaplan-Meier curves for survival and MACE-free survival are shown in Figure 3. In-hospital and 30-day mortality were 7% (n = 11) and 8% (n = 12), respectively. Overall, MACEs occurred in 50 patients (35%) during the hospitalization period (11 deaths, 10 strokes and 42 episodes of major bleeding; Table 2, Figure 4). Blood transfusions were delivered in 27 patients, and 8 patients required surgical hemostatic intervention. Bleeding complications, stroke, and in-hospital death were correlated with the severity of platelet count decrease (Figure 4). MACEs were greater in patients with severe platelet count decreases (20% in the first tertile, 38% in the second tertile, and 46% in the third tertile, p = 0.02; Figure 4). MACEs were observed in 0 (0%), 35 (39%), and 14 (27%) patients with severe, moderate, and no thrombopenia, respectively. MACEs remained associated with the importance of platelet count decrease even after the exclusion of patients with procedural failure (p = 0.03; Figure 5). In addition, the relation between platelet count decrease and MACEs was more significant (p = 0.008) after exclusion of the 30 "learning curve" patients (Figure 4). Finally, blood platelet count decrease was the only predictor of in-hospital MACEs (odds ratio 1.67, 95% confidence interval 1.05 to 2.67, p = 0.03, on multivariate analysis; Table 3).Figure 4Stroke (A), major bleeding (B), in-hospital mortality (C), and 30-day mortality (D) according to the severity of platelet count decrease; p values are indicated for trend test. ‡p <0.05 versus first tertile.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 5In-hospital MACEs according to platelet tertiles in all patients (A), patients with procedural success only (B), and after exclusion of the 30 "learning curve" patients (C); p values are indicated for trend test. ‡p <0.05 versus first tertile.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Table 3Variables associated with major adverse cardiovascular eventsVariableAllMACEsp ValueYes (n = 50)No (n = 94)Age (yrs)84 ± 785 ± 684 ± 70.40European System for Cardiac Operative Risk Evaluation score (%)24 ± 1224 ± 1024 ± 130.90New York Heart Association class2.8 ± 0.62.8 ± 0.62.7 ± 0.70.80Creatinine (μmol/L)111 ± 38112 ± 32111 ± 410.80Hemoglobin (g/dl)11.9 ± 1.712.1 ± 1.711.8 ± 1.60.40Left ventricular ejection fraction (%)49 ± 1450 ± 1448 ± 140.50Maximal aortic velocity (m/s)4.3 ± 0.84.3 ± 0.84.3 ± 0.80.90Aortic valve area (cm2)0.7 ± 0.20.6 ± 0.20.7 ± 0.20.10Systolic pulmonary pressure (mm Hg)49 ± 1546 ± 1351 ± 160.10X-ray time (minutes)19 ± 1019 ± 919 ± 100.90Procedural time (minutes)78 ± 2784 ± 3175 ± 240.07Contrast amount (ml)189 ± 100197 ± 97186 ± 1010.50Prosthesis migration5140.50Procedural success9592970.20Aortic regurgitation ≥226 (18)17 (18)9 (18)0.90Platelet count at baseline (109/L)216 ± 67220 ± 65214 ± 680.60Platelet count nadir (109/L)140 ± 52137 ± 55144 ± 510.40Percentage decrease in platelet count34 ± 1538 ± 1432 ± 160.02Patients in tertile 333%44%27%0.03Patients in tertile 2 or 367%80%60%0.01Data are expressed as mean ± SD or as number (percentage). Open table in a new tab Data are expressed as mean ± SD or as number (percentage). Platelet count decrease has been reported after percutaneous coronary intervention21De Labriolle A. Bonello L. Lemesle G. Roy P. Steinberg D.H. Xue Z. Suddath W.O. Satler L.F. Kent K.M. Pichard A.D. Lindsay J. Waksman R. Decline in platelet count in patients treated by percutaneous coronary intervention: definition, incidence, prognostic importance, and predictive factors.Eur Heart J. 2010; 31: 1079-1087Crossref PubMed Scopus (41) Google Scholar and surgical aortic valve replacement.13Hilker L. Wodny M. Ginesta M. Wollert H.G. Eckel L. Differences in the recovery of platelet counts after biological aortic valve replacement.Interact Cardiovasc Thorac Surg. 2009; 8: 70-73Crossref PubMed Scopus (42) Google Scholar, 14Repossini A. Bloch D. Muneretto C. Piccoli P. Bisleri G. Beholz S. Platelet reduction after stentless pericardial aortic valve replacement.Interact Cardiovasc Thorac Surg. 2012; 14: 434-438Crossref PubMed Scopus (20) Google Scholar In the setting of TAVI, platelet count decrease was described in a first-in-humans study22Grube E. Laborde J.C. Gerckens U. Felderhoff T. Sauren B. Buellesfeld L. Mueller R. Menichelli M. Schmidt T. Zickmann B. Iversen S. Stone G.W. Percutaneous implantation of the CoreValve self-expanding valve prosthesis in high-risk patients with aortic valve disease: the Siegburg first-in-man study.Circulation. 2006; 114: 1616-1624Crossref PubMed Scopus (637) Google Scholar that enrolled very few patients, and to our knowledge, no other study has focused on platelet count decrease since that initial experience. Our study had 2 important results: (1) platelet count systematically decreased after TAVI, with an average decrease of 34 ± 15%, and (2) a decrease in platelet count strongly influenced patient outcome. A decrease in platelet count had been previously studied in percutaneous coronary intervention and had been shown to be associated with the use of low-osmolar contrast agents.21De Labriolle A. Bonello L. Lemesle G. Roy P. Steinberg D.H. Xue Z. Suddath W.O. Satler L.F. Kent K.M. Pichard A.D. Lindsay J. Waksman R. Decline in platelet count in patients treated by percutaneous coronary intervention: definition, incidence, prognostic importance, and predictive factors.Eur Heart J. 2010; 31: 1079-1087Crossref PubMed Scopus (41) Google Scholar In agreement with these studies, we also observed that patients with severe platelet count decreases after TAVI received more contrast agent. Hemolysis and hemodilution probably contribute little to platelet count decrease, as a poor correlation was observed between platelet count decrease and protein decrease, and no correlation was found with bilirubin. All patients received unfractionated heparin, so heparin probably does not take part in differences observed in platelet count decreases. Similarly, most patients were receiving antiplatelet treatment, and no association was observed between these treatments and decrease in platelet count. In percutaneous coronary intervention, no clear mechanism explains the association between low-osmolar contrast agents and the decrease in platelet count except a potential effect on platelet activation.23Parvez Z. Moncada R. Nonionic contrast medium: effects on blood coagulation and complement activation in vitro.Angiology. 1986; 37: 358-364Crossref PubMed Scopus (15) Google Scholar In the setting of TAVI procedures, comparison with surgical aortic valve replacement suggests that platelet activation may be involved in the mechanism of platelet count decrease. Indeed, except for extracorporeal circulation, several steps of surgical valve replacement that promote platelet activation15Steele P. Weily H. Davies H. Ppppas G. Genton E. Platelet survival time following aortic valve replacement.Circulation. 1975; 51: 358-362Crossref PubMed Scopus (30) Google Scholar, 24Badr Eslam R. Gremmel T. Schneller A. Stegfellner M. Kaider A. Mannhalter C. Lang I. Panzer S. High levels of platelet-monocyte aggregates after valve replacement for aortic stenosis: relation to soluble P-selectin and P-selectin glycoprotein ligand-1 genes.Thromb Res. 2011; 129: 453-458Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar, 25Goldsmith I.R. Blann A.D. Patel R.L. Lip G.Y. Plasma fibrinogen, soluble P-selectin, and von Willebrand factor in aortic valve disease: evidence for abnormal haemorheology, platelet activation, and endothelial dysfunction.Heart. 2000; 83: 577-578Crossref PubMed Scopus (12) Google Scholar, 26Goldsmith I.R. Blann A.D. Patel R.L. Lip G.Y. Effect of aortic valve replacement on plasma soluble P-selectin, von Willebrand factor, and fibrinogen.Am J Cardiol. 2001; 87: 107-110Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 27Leguyader A. Watanabe R. Berbe J. Boumediene A. Cogne M. Laskar M. Platelet activation after aortic prosthetic valve surgery.Interact Cardiovasc Thorac Surg. 2006; 5: 60-64Crossref PubMed Scopus (28) Google Scholar are present in the TAVI procedure: endothelial damage caused by prosthesis implantation, fibrinogen binding on metallic armatures, and shear stress modifications due to prosthesis implantation.28Nobili M. Sheriff J. Morbiducci U. Redaelli A. Bluestein D. Platelet activation due to hemodynamic shear stresses: damage accumulation model and comparison to in vitro measurements.ASAIO J. 2008; 54: 64-72Crossref PubMed Scopus (187) Google Scholar As suggested by the correlation between TAVI procedure complications (rate of prosthesis migration, contrast amount, and procedural time) and platelet count decrease, tissue injury during aortic valve implantation may play an important part in platelet activation. Platelet activation after surgical valve replacement has been shown to be predictive of worse outcomes.15Steele P. Weily H. Davies H. Ppppas G. Genton E. Platelet survival time following aortic valve replacement.Circulation. 1975; 51: 358-362Crossref PubMed Scopus (30) Google Scholar, 26Goldsmith I.R. Blann A.D. Patel R.L. Lip G.Y. Effect of aortic valve replacement on plasma soluble P-selectin, von Willebrand factor, and fibrinogen.Am J Cardiol. 2001; 87: 107-110Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar It is tempting to suggest that the association between patient outcomes and the severity of platelet count decreases is caused by severe platelet activation. Indeed, platelet activation may promote thrombosis and take part in the higher rate of stroke observed with higher platelet count decreases. In the first report of platelet count decrease after TAVI, by Grube et al,22Grube E. Laborde J.C. Gerckens U. Felderhoff T. Sauren B. Buellesfeld L. Mueller R. Menichelli M. Schmidt T. Zickmann B. Iversen S. Stone G.W. Percutaneous implantation of the CoreValve self-expanding valve prosthesis in high-risk patients with aortic valve disease: the Siegburg first-in-man study.Circulation. 2006; 114: 1616-1624Crossref PubMed Scopus (637) Google Scholar platelet count decrease was related to platelet activation. However, in that first-in-humans study, extracorporeal circulatory support, which is known to promote platelet activation and destruction, was routinely used. In our study, TAVI procedural complications were not predictive of outcomes, and platelet count decrease was the only predictor of MACEs. This may be explained by the small sample size of the population, which limits statistical power, or by the fact that platelet count decrease is a more sensitive marker of outcome because of its potential impact on bleeding and thrombotic complications. In addition, it supports the hypothesis that platelet count decrease severity reflects the intensity of platelet activation and inflammatory response induced by tissue injury related to prosthesis valve implantation. The deleterious impact of inflammation after TAVI procedure was recently reported by Sinning et al.29Sinning J.M. Scheer A.C. Adenauer V. Ghanem A. Hammerstingl C. Schueler R. Muller C. Vasa-Nicotera M. Grube E. Nickenig G. Werner N. Systemic inflammatory response syndrome predicts increased mortality in patients after transcatheter aortic valve implantation.Eur Heart J. 2012; 33: 1459-1468Crossref PubMed Scopus (119) Google Scholar In that study, the investigators reported a rate of systemic inflammation response in 40% of patients (61 of 151) after TAVI. They showed that systemic inflammation was associated with the amount of contrast used and postprocedural TAVI complications. However, they did not investigate platelet count in their study. Finally, our results underline the need to carefully monitor platelet count after TAVI, and future prospective studies are needed to better clarify the underlying mechanism and specific treatment to prevent platelet activation. The study design (retrospective and observational) carries all the limitations inherent to such an investigation, especially the lack of data that formally demonstrate the mechanism of platelet count decrease, as platelet activation parameters were not routinely recorded. Further prospective studies including platelet activity measurement are needed to confirm our hypotheses and to verify whether outcomes are related to platelet activation. The authors have no conflicts of interest to disclose.
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