106 research outputs found
A case report of acute inferior myocardial infarction in a patient with severe hemophilia A after recombinant factor VIII infusion
RATIONALE: The extent of protective effects of hemophilia against thrombotic events such as myocardial infarction (MI) and other acute coronary syndromes remains to be determined, as major risk factors for cardiovascular disease exist despite factor VIII (FVIII) deficiency. We present a case report of a 41-year-old male with severe hemophilia A and several cardiovascular risk factors. ----- PATIENT CONCERNS: This morbidly obese patient developed chest pressure, followed by chest pain and difficulty in breathing shortly after receiving on-demand treatment with intravenous recombinant FVIII (rFVIII) (turoctocog alfa) dosed per body weight. ----- DIAGNOSES: An electrocardiogram revealed a diagnosis of inferior ST-segment elevation MI. ----- INTERVENTIONS: The patient underwent an urgent coronary angiography using a radial artery approach. During the next 12 months, he received dual antiplatelet treatment, acetylsalicylic acid 100 mg, and clopidogrel 75 mg daily. His treatment for severe hemophilia A was changed to plasma-derived FVIII replacement therapy. -----OUTCOMES:
During this 12-month period, he experienced several small bleeds in his elbows. ----- CONCLUSIONS: The temporal relationship between rFVIII infusion and onset of the MI suggests a possible association; however, apart from obesity, the patient also had other major risk factors for arterial thrombosis, such as hypertension and smoking. Furthermore, atherosclerotic disease and underlying atherosclerotic changes could not be excluded with certainty. This case highlights the importance of studies assessing the impact of excess body weight on rFVIII dosing
A Meta-Analysis and Genome-Wide Association Study of Platelet Count and Mean Platelet Volume in African Americans
Several genetic variants associated with platelet count and mean platelet volume
(MPV) were recently reported in people of European ancestry. In this
meta-analysis of 7 genome-wide association studies (GWAS) enrolling African
Americans, our aim was to identify novel genetic variants associated with
platelet count and MPV. For all cohorts, GWAS analysis was performed using
additive models after adjusting for age, sex, and population stratification. For
both platelet phenotypes, meta-analyses were conducted using inverse-variance
weighted fixed-effect models. Platelet aggregation assays in whole blood were
performed in the participants of the GeneSTAR cohort. Genetic variants in ten
independent regions were associated with platelet count
(N = 16,388) with p<5×10−8 of
which 5 have not been associated with platelet count in previous GWAS. The novel
genetic variants associated with platelet count were in the following regions
(the most significant SNP, closest gene, and p-value): 6p22 (rs12526480,
LRRC16A, p = 9.1×10−9), 7q11
(rs13236689, CD36, p = 2.8×10−9),
10q21 (rs7896518, JMJD1C,
p = 2.3×10−12), 11q13 (rs477895,
BAD, p = 4.9×10−8), and 20q13
(rs151361, SLMO2, p = 9.4×10−9).
Three of these loci (10q21, 11q13, and 20q13) were replicated in European
Americans (N = 14,909) and one (11q13) in Hispanic
Americans (N = 3,462). For MPV
(N = 4,531), genetic variants in 3 regions were significant
at p<5×10−8, two of which were also associated with
platelet count. Previously reported regions that were also significant in this
study were 6p21, 6q23, 7q22, 12q24, and 19p13 for platelet count and 7q22,
17q11, and 19p13 for MPV. The most significant SNP in 1 region was also
associated with ADP-induced maximal platelet aggregation in whole blood (12q24).
Thus through a meta-analysis of GWAS enrolling African Americans, we have
identified 5 novel regions associated with platelet count of which 3 were
replicated in other ethnic groups. In addition, we also found one region
associated with platelet aggregation that may play a potential role in
atherothrombosis
Effects of HeartWare ventricular assist device on the von Willebrand factor: results of an academic Belgian center
Mechanical circulatory assist devices: a primer for critical care and emergency physicians
Obesity as a causal risk factor for deep venous thrombosis:a Mendelian randomization study
High platelet volume and increased risk of myocardial infarction: 39,531 participants from the general population
Development of Acquired von Willebrand Syndrome During Short-Term Micro Axial Pump Support
Elevated Fibrinogen Levels Associate with Risk of Pulmonary Embolism, but not with Deep Venous Thrombosis
Severely impaired von Willebrand factor-dependent platelet aggregation in patients with a continuous-flow left ventricular assist device (HeartMate II)
ObjectivesThis study investigated the influence of the mechanical blood pump HeartMate II (HMII) (Thoratec Corporation, Pleasanton, California) on blood coagulation and platelet function.BackgroundHMII is an implantable left ventricular assist device used for the treatment of heart failure. Patients treated with HMII have increased bleeding tendencies.MethodsWe measured agonist-induced platelet aggregation in 16 patients on HMII support.ResultsThe von Willebrand factor (vWF)-dependent ristocetin-induced platelet aggregation was impaired in 11 of the 16 patients, of which 12 had experienced at least 1 minor or major bleeding episode. The impaired ristocetin-induced platelet aggregation was associated both with decreased specific activity of plasma vWF, presumably due to lack of high molecular weight vWF multimers, as well as with attenuated function of the platelets themselves.ConclusionsThe results imply that HMII treatment is associated with impaired platelet aggregation, which may contribute to an increased tendency to bleed
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