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Gepubliceerd in: Netherlands Heart Journal 5/2016

Open Access 09-02-2016 | Original Article - Design Study Article

Prevalence of blood type A and risk of vascular complications following transcatheter aortic valve implantation

Auteurs: M.-T. Rofe, Y. Shacham, A. Steinvi, L. Barak, M. Hareuveni, S. Banai, G. Keren, A. Finkelstein, H. Shmilovich

Gepubliceerd in: Netherlands Heart Journal | Uitgave 5/2016

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Abstract

Objectives

To assess the prevalence of blood type A among patients referred for transcatheter aortic valve implantation (TAVI) and whether it is related to vascular complications.

Backgrounds

Vascular complications following TAVI are associated with adverse outcomes. Various blood types, particularly type A, have been shown to be more prevalent in cardiovascular diseases and to be related to prognosis.

Methods

The prevalence of various blood types in a cohort of 491 consecutive patients who underwent TAVI was compared with a control group of 6500 consecutive hospitalised patients. The prevalence and predictors of vascular complications and bleeding events were evaluated in the blood type A group and were compared with non-type A patients.

Results

The mean age of TAVI patients was 83 ± 6 years, and 40 % were males. Patients were divided into two groups: blood type A (n = 220) and non-type A (n = 271). Type A was significantly more prevalent in the TAVI group than in the control group (45 vs. 38 %, p = 0.023). Compared with the non-type A group, patients with blood type A had more major and fatal bleeding (14.5 vs. 8.1 %, p = 0.027) and more vascular complications (any vascular complication: 24.5 vs. 15.9 % p = 0.016; major vascular complications: 12.3 vs. 7 % p = 0.047). In a multivariable analysis, blood type A emerged as a significant and independent predictor for vascular complications and bleeding events.

Conclusions

Blood type A is significantly more prevalent in TAVI patients than in the general population and is related to higher rates of vascular and bleeding complications.
Opmerkingen
M.-T. Rofe and Y. Shacham authors contributed equally

Introduction

Severe aortic stenosis is a major cause of morbidity and mortality in the elderly [1]. The risk of surgical aortic valve replacement rises dramatically in relation to comorbidities which can be evaluated using the Euroscore system [2, 3] thus deferring a large group of patients from surgery. In the last decade, transcatheter aortic valve implantation (TAVI) was shown to confer a lower risk of morbidity and mortality in this subset of patients with a high surgical risk and has now become common practice [46], but vascular complications after TAVI are associated with adverse short- and long-term outcomes [68].
Recent studies have confirmed that the ABO locus that encodes for the ABO blood type may be associated with myocardial infarction [9] and venous thromboembolism [10, 11]. Non-O blood types, mostly type A, were related to increased prevalence of morbidity and mortality in various cardiovascular diseases [1214] but this was not studied in patients undergoing TAVI.
We investigated the prevalence of blood type A in TAVI patients vs. its prevalence in the general population and whether it is related to periprocedural vascular complications as compared with non-type A patients who underwent TAVI.

Methods

Study population

The data for the present study were collected between the years 2009 and 2014 at a single tertiary-care facility [15]. The study was approved by the institutional ethics committee and written informed consent was obtained from each patient. Patients were recruited during their participation in the Tel-Aviv Angiography Prospective Study [16]. The diagnosis of severe symptomatic aortic stenosis was based on clinical, echocardiographic and haemodynamic criteria [17]. Suitability and eligibility for TAVI were determined by a joint team consisting of an interventional cardiologist, a cardiac surgeon, and an echocardiographer. The control group representing the general population consisted of 6500 consecutive patients who were hospitalised and underwent blood type sampling for other clinical reasons.

TAVI procedure

Two types of aortic valve prostheses were implanted: The CoreValve prosthesis (Medtronic, Minneapolis, MN, USA) and the Edwards Sapien or Sapien XT prosthesis (Edwards Lifesciences, Irvine, California). For all TAVI procedures, three senior interventional cardiologists performed the peripheral aspects of the TAVI procedures (introduction of the sheaths through the femoral artery, Prostar closure device deployment, and the suturing of the entry ports). Valve type and size were planned prior to the procedure according to preprocedural clinical, echocardiographic, angiographic and CT parameters and at the discretion of the senior interventional cardiologist. The available valve sizes for the Edwards Sapien XT prosthesis were 23 and 26 mm and the valve sizes for the CoreValve prosthesis were 26, 29, and 31 mm [15].

Definition of vascular complications

The original consensus report of the Valve Academic Research Consortium (VARC-1) standardised the endpoint definitions of TAVI procedures including the occurrence of vascular complications [18]. During 2012, these endpoints were updated – known as VARC-2 [19]. While the general definitions of vascular complications were unchanged following the update, VARC-2 incorporated a more rigorous approach to bleeding and haemoglobin decline following TAVI, stating that major bleeding definitions (a haemoglobin drop > 3 g/dl or transfusion of two or more packed red blood cell units) should also be considered to be major vascular complications, while in the former VARC-1 endpoints, only transfusion of ≥ 4 packed red blood cell units was considered a major vascular complication. Importantly, in both consensus documents, interventional or surgical repair for failed percutaneous closure during the initial procedure without other clinical consequences was considered a minor vascular complication [18, 19]. Accordingly, we classified vascular complications using VARC-2.

Statistical analysis

All data are displayed as mean (± standard deviation) for continuous variables, and as the number (percentage) of patients in each group for categorical variables. The Student’s t-test and χ 2 test were used to evaluate the statistical significance of differences between continuous and categorical variables, respectively.
Logistic regression models used any vascular complications, or the combined outcome variable of any vascular complication or major bleeding, as the dependant variables, and they were adjusted to age, gender, body mass index (BMI), diabetes mellitus, hypertension, estimated glomerular filtration rate, previous stroke, previous cardiac surgery, Society of Thoracic Surgeons risk model (STS) score, ejection fraction and anaemia. Cox proportional hazard models for all-cause mortality were adjusted separately for major vascular complications as well as to other predictors of mortality following TAVI [5, 20]: gender, age, BMI, systolic heart failure, prior coronary artery bypass graft, prior percutaneous coronary intervention, atrial fibrillation, pulmonary disease, STS score, preoperative mean gradient, and creatinine clearance test. Analyses were considered significant at a two-tailed p value of less than 0.05. SPSS statistical package was used to perform statistical evaluation (SPSS, Chicago, IL).

Results

The study population who underwent TAVI included 491 patients with a mean age of 83 ± 6 years (range 61–98), of whom 196 (40 %) were males. When comparing differences in blood type between TAVI patients and 6500 consecutive (non-TAVI) hospitalised patients, type A was significantly more prevalent in the TAVI group than in the above-mentioned control group (45 vs. 38 %, p = 0.023). All other blood types were distributed evenly between the TAVI and the control group.
We then divided our patients into two groups according to blood type: type A (n = 220) and non-type A (n = 271). Baseline demographic, clinical, and procedural characteristics for the two groups are presented in Table 1.
Table 1
Baseline study population characteristics
Units
Blood type A (n = 220)
Non-type A (n = 271)
p value
Age, years (mean ± SD)years
83 ± 6
83 ± 6
0.748
Male gender
86, 40%
127,47%
0.084
Diabetes mellitus
65, 29%
110, 40%
0.011
Dyslipidaemia
172, 78%
221, 81%
0.353
Hypertension
191, 87%
238, 88%
0.739
Smoking history
50, 23%
86, 32%
0.027
BMI (mean ± SD)kg/m2
27 ± 5
28 ± 5
0.110
CCT (mean ± SD)ml/min
63 ± 18
62 ± 20
0.770
PVD
10, 4.5%
23, 8.5%
0.083
Stroke
21, 9.5%
30, 11.1%
0.582
Systolic heart failure
36, 16%
47,17%
0.773
History of CAD
135, 61%
163, 60%
0.784
Prior MI
32, 14.5%
56, 21%
0.079
Prior CABG
39, 19%
53, 20%
0.605
Permanent pacemaker
16, 7.3%
40, 14.8%
0.009
AF (any type)
59, 27 %
88, 32%
0.174
EF % (mean ± SD)
56 ± 7.3
55 ± 7.7
0.253
STS score (mean ± SD)
4.2 ± 2.5
4.3 ± 3
0.510
Euroscore (mean ± SD)
25 ± 14
23 ± 14
0.259
AVA (mean ± SD)cm2
0.721 ± 0.19
0.714 ± 0.18
0.685
Dialysis
4, 2 %
6, 2 %
0.757
Frailty
36, 17 %
33, 12 %
0.164
PCI pre TAVI
117
141
0.800
Medications post TAVI
ASA
193
226
0.178
ADP
179
226
0.557
AC
45
58
0.798
ASA + ADP
164
188
0.207
(ASA or ADP) + AC
20
29
0.555
ASA + ADP + AC
23
24
0.550
Only AC
2
5
0.385
AC anticoagulation, ADP adenosine diphosphate inhibitors, AF atrial fibrillation, ASA aspirin, AVA aortic valve area, BMI body mass index, CABG coronary artery bypass grafting, CAD coronary artery disease, CAF chronic atrial fibrillation, CCT creatinine clearance test, COPD chronic obstructive pulmonary disease, EF ejection fraction, MI myocardial infarction, PCI percutaneous coronary intervention, PVD peripheral vascular disease, SD standard deviation, STS Society of Thoracic Surgeons risk model, TAVI transcatheter aortic valve implantation
The 30-day adverse events in the type A vs. the non-type A groups are presented in Table 2. Major and fatal bleeding were more prevalent in the type A group (14.5 vs. 8.2 %, p = 0.027). The rate of vascular complications was higher in the type A group including both major (12.3 vs. 7 %, p = 0.047), as well as major or minor vascular complications (24.5 vs. 15.9 %, p = 0.016). There was no difference in 30-day, 1-year, and all-time mortality.
Table 2
Thirty-day adverse events
Events/Patient numbers
Blood type A (n = 220)
Non-type A (n = 271)
p value
MI
0
0
NA
Cardiogenic shock
4 (1.8 %)
6 (2.2 %)
0.757
Respiratory failure
12 (5.5 %)
17 (6.3 %)
0.702
Ventricular tachycardia
0
0
NA
Ventricular fibrillation
1 (0.5 %)
0
0.267
New atrial fibrillation
13 (5.9 %)
17 (6.3 %)
0.867
Conduction defect
73 (33.2 %)
97 (35.8 %)
0.545
Stroke
2 (0.9 %)
5 (1.8 %)
0.384
New pacemaker
40 (18.2 %)
60 (22.1 %)
0.279
Bleeding- major/fatal
32 (14.5 %)
22 (8.1 %)
0.024
AKI during hospitalisation
33 (15 %)
51 (18.8 %)
0.264
VC-minor
27 (12.3 %)
24 (8.9 %)
0.218
VC-major
27 (12.3 %)
19 (7 %)
0.047
VC-minor or major
54 (24.5 %)
43(15.9 %)
0.016
Surgery for VC
7 (3.2 %)
4 (1.5 %)
0.204
Use of packed cells (1 or more)
81 (36.8 %)
86 (31.7 %)
0.237
Sepsis
6 (2.7 %)
5 (1.8 %)
0.511
Conversion to open surgery
1 (0.5 %)
1 (0.4 %)
0.882
Unplanned CPB during TAVI
0
0
NA
Coronary obstruction
1 (0.5 %)
1 (0.4 %)
0.882
Ventricular septal perforation
0
0
NA
Mitral valve damage
1 (0.5 %)
1 (0.4 %)
0.882
Tamponade
3 (1.4 %)
1 (0.4 %)
0.223
Endocarditis
0
0
NA
Valve thrombosis
0
0
NA
Valve migration
0
2 (0.7 %)
0.202
Valve embolisation
1 (0.5 %)
5 (1.8 %)
0.163
TAVI-in-TAVI
0
4 (1.5 %)
0.07
30 day mortality
8 (3.6 %)
6 (2.2 %)
0.346
AKI acute kidney injury, CPB cardiopulmonary bypass, MI myocardial infarction, TAVI transcatheter aortic valve implantation, VC vascular complication
In multivariable linear regression analysis, blood type A was significantly and independently associated with vascular complications (OR 1.64, 95 % CI 1.04–2.67, p = 0.033) and was marginally associated with vascular complications or major bleeding (OR 1.57, 95 % CI 0.99–2.2167, p = 0.056) (Table 3).
Table 3
Logistic regression models
Correlates:
Model 1a
Model 2b
 
p
OR
95 % CI
p
OR
95 % CI
Age
0.701
0.991
0.946–1.038
0.849
0.996
0.951–1.042
Gender
0.192
1.397
0.845–2.311
0.141
1.476
0.879–2.479
DM
0.058
0.597
0.350–1.018
0.017
0.521
0.305–0.890
Hypertension
0.198
1.694
0.760–3.777
0.510
1.287
0.607–2.726
eGFRc
0.830
0.999
0.985–1.012
0.331
1.007
0.993–1.021
STS score
0.183
1.070
0.968–1.183
0.036
1.117
1.008–1.239
Prior stroke
0.227
1.560
0.759–3.205
0.342
1.421
0.688–2.934
LVEF %
0.351
1.016
0.982–1.052
0.156
1.026
0.990–1.062
Blood type A
0.033
1.670
1.043–2.674
0.056
1.576
0.989–2.510
Anaemia
0.702
1.103
0.666–1.827
0.821
0.926
0.477–1.799
CI confidence interval, DM diabetes mellitus, LVEF left ventricular ejection fraction, eGFR estimated glomerular filtration rate, OR odds ratio, STS Society of Thoracic Surgeons risk model
aModel 1: dependant variable: Any vascular complication
bModel 2: dependant variable: Any vascular complication or major bleeding
ceGFR in ml/min/1.73 m2

Discussion

In the present study we demonstrated that among patients undergoing TAVI, blood type A was significantly more prevalent as compared with the general population, and that type A was independently and significantly associated with vascular complications.
Since 1901, when Landsteiner identified the ABO blood type system and its importance in transfusion and transplantation medicine, there has been debate regarding its usefulness as a predictor of diseases, in particular cardiovascular diseases. Carpeggiani et al. showed that non-O blood types are a predictor of increased mortality in patients with ischaemic heart disease and that it increases the risk of cardiac death amongst non-elderly patients [21]. In 1969, Jick et al. reported a deficit of patients with blood type O among those who received anticoagulants for venous thromboembolism [22]. A number of later studies elucidated that ABO blood types, particularly non-O blood types, are associated with major cardiovascular risk factors and/or increased rate of cardiovascular events [23, 24]. However, there is limited consensus regarding the magnitude and significance of the ABO effects at the population level and whether it relates to all disorders equally or predominantly modulates thrombotic pathways and disorders [25]. In addition, a genome-wide study showed an association between ABO blood types and myocardial infarction in the presence of coronary artery atherosclerosis [9]. Other reports, however, found no difference in the incidence of ABO blood type when patients with congenital and rheumatic valvular heart disease were compared with a control group [26]. Recently, various studies pointed to the association between blood type A and vascular diseases. One of them, a meta-analysis published by He et al., on 90,000 participants and more than 2 million person-years, showed that non-O blood types had a higher risk of coronary heart disease compared with blood type O [27].
Several mechanisms have been proposed to explain the possible relationship between blood types and vascular complications. ABO antigens are known to be carried by several platelet glycoproteins (GPs), for example, GPIb, GPIIb, GPIIIa, and platelet endothelial cell adhesion molecule (PECAM) [28], which play important roles in platelet function. GPIIb is an integral component of the GPIIb-GPIIIa fibrinogen receptor complex, which represents the critical final common pathway for platelet-driven thrombosis in homeostasis and pathological arterial thrombosis including acute myocardial infarction. Genetic variation in GPIIb that modulates fibrinogen binding has been associated with altered risk of thrombosis and myocardial infarction [29], so it is conceivable that ABO-driven carbohydrate modification of GPIIb might alter its functional interactions with fibrinogen and thus platelet-mediated thrombosis. However, this hypothesis has not been adequately addressed to date. Besides GPIIb and PECAM, blood type A antigen is also expressed on other uncharacterised platelet proteins. Thus these and other uncharacterised ABO-expressing platelet proteins may also act as potential functional modulators of the ABO associations with arterial thrombosis and cardiovascular events.
Previous data demonstrated that relative to non-type O, carriers of type O have significantly lower circulating plasma Von Willebrand factor (VWF) and factor VIII (FVIII) levels [30]. Although this clinically important effect of ABO type on plasma VWF-FVIII levels is well established, the mechanism through which it is mediated is not completely resolved. ABO appears to have direct functional effects on circulating VWF and indirectly (via influence of VWF levels) modulates FVIII levels. Whether VWF in platelets (a relatively abundant source) undergoes any modification by ABO remains controversial; such modification could alter platelet production and subsequent turnover of VWF, particularly locally during platelet-driven arterial thrombosis, although this remains to be established.
The limitation of this study is its relatively medium-sized study sample, a one-centre experience and the retrospective nature of the analyses. Further studies will elucidate the important questions as to whether patients with mild aortic stenosis and blood type A progress more rapidly to severe symptomatic aortic stenosis and the need for intervention and thus for a more rigorous follow-up, and whether patients with blood type A undergoing TAVI need a longer and more careful follow-up for vascular complications.
In conclusion, in this study we showed for the first time that patients referred for TAVI due to severe aortic stenosis have a higher prevalence of blood type A. We also showed that blood type A confers a higher risk of vascular complications, independent of other confounders. Future larger and multi-centre studies will assess whether blood type A is related to other aspects of diagnosis and prognosis in cardiovascular diseases and procedures.

Conflicts of interest

None declared.

Funding

None.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://​creativecommons.​org/​licenses/​by/​4.​0/​), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
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Literatuur
1.
go back to reference Osnabrugge RL, Mylotte D, Head SJ, et al. Aortic stenosis in the elderly: disease prevalence and number of candidates for transcatheter aortic valve replacement: a meta-analysis and modeling study. J Am Coll Cardiol. 2013;62:1002–12.CrossRefPubMed Osnabrugge RL, Mylotte D, Head SJ, et al. Aortic stenosis in the elderly: disease prevalence and number of candidates for transcatheter aortic valve replacement: a meta-analysis and modeling study. J Am Coll Cardiol. 2013;62:1002–12.CrossRefPubMed
2.
3.
go back to reference Roques F, Nashef SA, Michel P, et al. Risk factors and outcome in European cardiac surgery: analysis of the EuroSCORE multinational database of 19030 patients. Eur J Cardiothorac Surg. 1999;15:816–22, discussion 22–3.CrossRefPubMed Roques F, Nashef SA, Michel P, et al. Risk factors and outcome in European cardiac surgery: analysis of the EuroSCORE multinational database of 19030 patients. Eur J Cardiothorac Surg. 1999;15:816–22, discussion 22–3.CrossRefPubMed
4.
go back to reference Makkar RR, Fontana GP, Jilaihawi H, et al. Transcatheter aortic-valve replacement for inoperable severe aortic stenosis. N Engl J Med. 2012;366:1696–704.CrossRefPubMed Makkar RR, Fontana GP, Jilaihawi H, et al. Transcatheter aortic-valve replacement for inoperable severe aortic stenosis. N Engl J Med. 2012;366:1696–704.CrossRefPubMed
5.
go back to reference Kodali SK, Williams MR, Smith CR, et al. Two-year outcomes after transcatheter or surgical aortic-valve replacement. N Engl J Med. 2012;366:1686–95.CrossRefPubMed Kodali SK, Williams MR, Smith CR, et al. Two-year outcomes after transcatheter or surgical aortic-valve replacement. N Engl J Med. 2012;366:1686–95.CrossRefPubMed
6.
go back to reference Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. 2010;363:1597–607.CrossRefPubMed Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. 2010;363:1597–607.CrossRefPubMed
7.
go back to reference Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364:2187–98.CrossRefPubMed Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364:2187–98.CrossRefPubMed
8.
go back to reference Stepinska J, Czerwinska K, Witkowski A, et al. Risk factors for bleeding complications in patients undergoing transcatheter aortic valve implantation (TAVI). Cardiol J. 2013;20:125–33.CrossRefPubMed Stepinska J, Czerwinska K, Witkowski A, et al. Risk factors for bleeding complications in patients undergoing transcatheter aortic valve implantation (TAVI). Cardiol J. 2013;20:125–33.CrossRefPubMed
9.
go back to reference Reilly MP, Li M, He J, et al. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies. Lancet. 2011;377:383–92.CrossRefPubMedPubMedCentral Reilly MP, Li M, He J, et al. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies. Lancet. 2011;377:383–92.CrossRefPubMedPubMedCentral
10.
go back to reference Heit JA, Armasu SM, Asmann YW, et al. A genome-wide association study of venous thromboembolism identifies risk variants in chromosomes 1q24.2 and 9q. J Thromb Haemost. 2012;10:1521–31.CrossRefPubMedPubMedCentral Heit JA, Armasu SM, Asmann YW, et al. A genome-wide association study of venous thromboembolism identifies risk variants in chromosomes 1q24.2 and 9q. J Thromb Haemost. 2012;10:1521–31.CrossRefPubMedPubMedCentral
11.
go back to reference Terraube V, O’Donnell JS, Jenkins PV. Factor VIII and von Willebrand factor interaction: biological, clinical and therapeutic importance. Haemophilia. 2010;16:3–13.CrossRefPubMed Terraube V, O’Donnell JS, Jenkins PV. Factor VIII and von Willebrand factor interaction: biological, clinical and therapeutic importance. Haemophilia. 2010;16:3–13.CrossRefPubMed
12.
go back to reference Medalie JH, Levene C, Papier C, et al. Blood groups, myocardial infarction and angina pectoris among 10,000 adult males. N Engl J Med. 1971;285:1348–53.CrossRefPubMed Medalie JH, Levene C, Papier C, et al. Blood groups, myocardial infarction and angina pectoris among 10,000 adult males. N Engl J Med. 1971;285:1348–53.CrossRefPubMed
13.
go back to reference Cronenwett JL, Davis JT Jr, Garrett HE. ABO blood group and serum lipids in female atherosclerosis. J Cardiovasc Surg (Torino). 1983;24:658–61. Cronenwett JL, Davis JT Jr, Garrett HE. ABO blood group and serum lipids in female atherosclerosis. J Cardiovasc Surg (Torino). 1983;24:658–61.
14.
go back to reference Anvari MS, Boroumand MA, Shoar S, et al. Ascending aorta aneurysm and blood group A among Iranian patients. Thromb Res. 2013;131:e51–3.CrossRefPubMed Anvari MS, Boroumand MA, Shoar S, et al. Ascending aorta aneurysm and blood group A among Iranian patients. Thromb Res. 2013;131:e51–3.CrossRefPubMed
15.
go back to reference Finkelstein A, Birati EY, Abramowitz Y, et al. Transcatheter aortic valve implantation: a single-center experience of 300 cases. Isr Med Assoc J. 2013;15:613–6.PubMed Finkelstein A, Birati EY, Abramowitz Y, et al. Transcatheter aortic valve implantation: a single-center experience of 300 cases. Isr Med Assoc J. 2013;15:613–6.PubMed
16.
go back to reference Steinvil A, Sadeh B, Arbel Y, et al. Prevalence and predictors of concomitant carotid and coronary artery atherosclerotic disease. J Am Coll Cardiol. 2011;57:779–83.CrossRefPubMed Steinvil A, Sadeh B, Arbel Y, et al. Prevalence and predictors of concomitant carotid and coronary artery atherosclerotic disease. J Am Coll Cardiol. 2011;57:779–83.CrossRefPubMed
17.
go back to reference Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 Guidelines for the management of patients with valvular heart disease. Circulation. 2006;114:e84–231.CrossRefPubMed Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 Guidelines for the management of patients with valvular heart disease. Circulation. 2006;114:e84–231.CrossRefPubMed
18.
go back to reference Leon MB, Piazza N, Nikolsky E, et al. Standardized endpoint definitions for transcatheter aortic valve implantation clinical trials: a consensus report from the Valve Academic Research Consortium. Eur Heart J. 2011;32:205–17.CrossRefPubMedPubMedCentral Leon MB, Piazza N, Nikolsky E, et al. Standardized endpoint definitions for transcatheter aortic valve implantation clinical trials: a consensus report from the Valve Academic Research Consortium. Eur Heart J. 2011;32:205–17.CrossRefPubMedPubMedCentral
19.
go back to reference Kappetein AP, Head SJ, Genereux P, et al. Updated standardized endpoint definitions for transcatheter aortic valve implantation: the valve academic research consortium-2 consensus document. J Am Coll Cardiol. 2012;60:1438–54.CrossRefPubMed Kappetein AP, Head SJ, Genereux P, et al. Updated standardized endpoint definitions for transcatheter aortic valve implantation: the valve academic research consortium-2 consensus document. J Am Coll Cardiol. 2012;60:1438–54.CrossRefPubMed
20.
go back to reference Rodes-Cabau J, Webb JG, Cheung A, et al. Long-term outcomes after transcatheter aortic valve implantation: insights on prognostic factors and valve durability from the Canadian multicenter experience. J Am Coll Cardiol. 2012;60:1864–75.CrossRefPubMed Rodes-Cabau J, Webb JG, Cheung A, et al. Long-term outcomes after transcatheter aortic valve implantation: insights on prognostic factors and valve durability from the Canadian multicenter experience. J Am Coll Cardiol. 2012;60:1864–75.CrossRefPubMed
21.
go back to reference Carpeggiani C, Coceani M, Landi P, et al. ABO blood group alleles: a risk factor for coronary artery disease. An angiographic study. Atherosclerosis. 2010;211:461–6.CrossRefPubMed Carpeggiani C, Coceani M, Landi P, et al. ABO blood group alleles: a risk factor for coronary artery disease. An angiographic study. Atherosclerosis. 2010;211:461–6.CrossRefPubMed
22.
go back to reference Jick H, Slone D, Westerholm B, et al. Venous thromboembolic disease and ABO blood type. A cooperative study. Lancet. 1969;1:539–42.CrossRefPubMed Jick H, Slone D, Westerholm B, et al. Venous thromboembolic disease and ABO blood type. A cooperative study. Lancet. 1969;1:539–42.CrossRefPubMed
23.
go back to reference Medalie JH, Levene C, Papier C, et al. Blood groups, myocardial infarction and angina pectoris among 10,000 adult males. N Engl J Med. 1971,285:1348–53.CrossRefPubMed Medalie JH, Levene C, Papier C, et al. Blood groups, myocardial infarction and angina pectoris among 10,000 adult males. N Engl J Med. 1971,285:1348–53.CrossRefPubMed
24.
go back to reference Ketch TR, Turner SJ, Sacrinty MT, et al. ABO blood types: influence on infarct size, procedural characteristics and prognosis. Thromb Res. 2008;123:200–5.CrossRefPubMed Ketch TR, Turner SJ, Sacrinty MT, et al. ABO blood types: influence on infarct size, procedural characteristics and prognosis. Thromb Res. 2008;123:200–5.CrossRefPubMed
25.
go back to reference Oriol R, Mollicone R, Coullin P, et al. Genetic regulation of the expression of ABH and Lewis antigens in tissues. APMIS Suppl. 1992;27:28–38.PubMed Oriol R, Mollicone R, Coullin P, et al. Genetic regulation of the expression of ABH and Lewis antigens in tissues. APMIS Suppl. 1992;27:28–38.PubMed
26.
go back to reference Sartor V, Fraser RS. Abo blood groups in patients with congenital and rheumatic valvular heart disease. Can Med Assoc J. 1964;90:428–9.PubMedPubMedCentral Sartor V, Fraser RS. Abo blood groups in patients with congenital and rheumatic valvular heart disease. Can Med Assoc J. 1964;90:428–9.PubMedPubMedCentral
27.
go back to reference He M, Wolpin B, Rexrode K, et al. ABO blood group and risk of coronary heart disease in two prospective cohort studies. Arterioscler Thromb Vasc Biol. 2012;32:2314–20.CrossRefPubMedPubMedCentral He M, Wolpin B, Rexrode K, et al. ABO blood group and risk of coronary heart disease in two prospective cohort studies. Arterioscler Thromb Vasc Biol. 2012;32:2314–20.CrossRefPubMedPubMedCentral
28.
go back to reference Hou M, Stockelberg D, Rydberg L, et al. Blood group A antigen expression in platelets is prominently associated with glycoprotein Ib and IIb. Evidence for an A1/A2 difference. Transfus Med. 1996;6:51–9,CrossRefPubMed Hou M, Stockelberg D, Rydberg L, et al. Blood group A antigen expression in platelets is prominently associated with glycoprotein Ib and IIb. Evidence for an A1/A2 difference. Transfus Med. 1996;6:51–9,CrossRefPubMed
29.
go back to reference Cadroy Y, Sakariassen KS, Charlet JP, et al. Role of 4 platelet membrane glycoprotein polymorphisms on experimental arterial thrombus formation in men. Blood. 2001;98:3159–61.CrossRefPubMed Cadroy Y, Sakariassen KS, Charlet JP, et al. Role of 4 platelet membrane glycoprotein polymorphisms on experimental arterial thrombus formation in men. Blood. 2001;98:3159–61.CrossRefPubMed
30.
go back to reference Tirado I, Mateo J, Soria JM, et al. The ABO blood group genotype and factor VIII levels as independent risk factors for venous thromboembolism. Thromb Haemost. 2005;93:468–74.PubMed Tirado I, Mateo J, Soria JM, et al. The ABO blood group genotype and factor VIII levels as independent risk factors for venous thromboembolism. Thromb Haemost. 2005;93:468–74.PubMed
Metagegevens
Titel
Prevalence of blood type A and risk of vascular complications following transcatheter aortic valve implantation
Auteurs
M.-T. Rofe
Y. Shacham
A. Steinvi
L. Barak
M. Hareuveni
S. Banai
G. Keren
A. Finkelstein
H. Shmilovich
Publicatiedatum
09-02-2016
Uitgeverij
Bohn Stafleu van Loghum
Gepubliceerd in
Netherlands Heart Journal / Uitgave 5/2016
Print ISSN: 1568-5888
Elektronisch ISSN: 1876-6250
DOI
https://doi.org/10.1007/s12471-016-0804-z

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