This meta-analysis provides new evidence supporting the conclusion that the JAK2 46/1 haplotype enrichment is significantly associated with the development of MPNs and SVT in these patients.
Recent research has demonstrated in patients with MPN the existence of factors increasing the risk of SVT such as the presence of the JAK2V617F mutation and its 46/1 haplotype.
In addition, our findings in JAK2(V617F)-negative SVT patients indicate an important role for the 46/1 haplotype in the etiology and diagnosis of SVT-related MPNs, independent of JAK2(V617F), that requires further exploration.
Anticoagulation is the treatment of choice for all SVT and proper treatment of the MPD is recommended in patients with SVT associated with the JAK2(V617F) mutation.
Anticoagulation therapy combined with low-dose aspirin and proper treatment of the MPD is recommended in patients with SVT associated with the JAK2(V617F) mutation.
The pooled proportion of CALR mutations was 1.21%, 1.41%, and 1.59% in SVT, BCS, and PVT patients, respectively; 1.52%, 1.03%, and 1.82% in these patients without JAK2V617F mutation, respectively; 3.71%, 2.79%, and 7.87% in these patients with MPN, respectively; and 15.16%, 17.22%, and 31.44% in these patients with MPN but without JAK2V617F mutation, respectively.
Criteria to identify patients at high risk of CALR mutations in this test cohort was used and evaluated in a validation cohort that included 209 patients with SVT.
Rare genetic variants in TNNI3K encoding troponin-I interacting kinase have been linked to a distinct syndrome consisting primarily of supraventricular tachycardias and variably expressed conduction disturbance and dilated cardiomyopathy in 2 families.
To synthesize the prevalence of CALR mutations according to the different types (i.e., Budd-Chiari syndrome [BCS] and portal vein thrombosis [PVT]) and characteristics (i.e., with and without myeloproliferative neoplasms [MPNs] and JAK2V617F mutation) of SVT patients.
Serious adverse events occurred in 7 patients (6.5%) in the interferon beta-1a group and included infection (in 2 patients) and supraventricular tachycardia (in 1 patient).
To synthesize the prevalence of CALR mutations according to the different types (i.e., Budd-Chiari syndrome [BCS] and portal vein thrombosis [PVT]) and characteristics (i.e., with and without myeloproliferative neoplasms [MPNs] and JAK2V617F mutation) of SVT patients.
The summed difference score between MIBG and MPI images, which evaluated the extent of denervated but viable myocardium, was significantly higher in SVT group (20.0 ± 8.0) as compared with the control group (2.0 ± 5.0, P < .0001) and with the NSVT group (11.0 ± 8.0, P < .05).
We determined serum levels of YKL-40, C-reactive protein (CRP) and IL-6 in 70 patients with AFib, atrial flutter, atrioventricular node reentry tachycardia or other supraventricular tachycardias before, immediately after therapy and 1 week after therapy; 20 healthy patients served as controls.
We determined serum levels of YKL-40, C-reactive protein (CRP) and IL-6 in 70 patients with AFib, atrial flutter, atrioventricular node reentry tachycardia or other supraventricular tachycardias before, immediately after therapy and 1 week after therapy; 20 healthy patients served as controls.