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Dasatinib, a tyrosine kinase inhibitor (TKI), induces pulmonary hypertension (PH) in patients with chronic myeloid leukemia (CML). However, information on other TKIs is limited. We retrospectively analyzed PH prevalence by reviewing transthoracic echocardiography (TTE) findings in a population of Korean CML patients treated with TKI at a single hospital between 2003 and 2020. PH was defined as a high PH probability according to the European Society of Cardiology/European Respiratory Society (ESC/ERS) guidelines. Of the 189 patients treated with TKI(s) during the study period, 112 (59.3%) underwent TTE. Among the 112 patients treated with a TKI for a median of 40.4 months (range: 1.1–167.2 months), PH was found in 12 (10.7%), most frequently in those treated with dasatinib (ie, in 3 [7.5%] of 40 of those treated with imatinib, 1 [3.1%] of 32 of those treated with nilotinib, and 8 [21.6%] of 37 of those treated with dasatinib). PH resolved in 4 (50.0%) of the 8 dasatinib-treated patients after discontinuation of the agent. One nilotinib-treated and all three imatinib-treated patients recovered from PH. In multivariate analyses, age >60 years, dasatinib treatment, and positive cardiopulmonary symptoms/signs at the time of transthoracic echocardiography were statistically significant risk factors for developing PH. These results show that PH is induced not only by dasatinib, but also by imatinib and nilotinib. Careful screening for PH during any TKI treatment may thus be warranted in patients with CML.

Background: Recently introduced dichotomous phenotypic classification of bicuspid aortic valve (BAV) showed potential association between BAV phenotype and patterns of valvulopathy or aortopathy. However its potential advantage needs to be compared with the conventional BAV classification in a large patient population. Methods: In 486 consecutive patients (309 male, 58±14 years) who underwent aortic valve (AV) surgery (n=483) or aortic surgery (n=146), BAV phenotype was classified using echocardiography. Dichotomous classification was based on the orientation of coronary arteries: AP (both coronary arteries originating from the anterior cusp) and RL (each coronary artery originating from each cusp). Conventional classification (type 1 - 4) was based on the fused cusp (Figure). We analyzed the associations between the BAV phenotype and 1) indication of AV surgery (aortic stenosis [AS] vs. regurgitation [AR]), and 2) implementation of aortic surgery. Results: BAV-AP (n=271, 56%) was more common than BAV-RL (n=215, 44%). Using conventional classification, fused cusps were indistinguishable in 15% (type 4). Indications of AV surgery included dominant AS (n=352), AR (n=96), and infective endocarditis (IE; n=35). Aortic surgeries were performed for aortic aneurysm (n=135), IE with abscess (n=9), dissection (n=1), and coarctation (n=1). Patients with BAV-RL type presented lower frequency of male (55% vs. 70%, P=0.001), AV surgery for dominant AS (82% vs. 66%, P Conclusions: New classification can overcome the ambiguity of the conventional classification and shows better association with type of valvulopathy and combined aortopathy.

Background: Although aortic stenosis (AS) is a prototype of left ventricular hypertrophy (LVH) due to pressure overloading, patterns of LV geometric changes in patients with tight AS and their potential impact remain to be established. Methods: LV mass index (LVMI), LV end-diastolic volume (LVEDV) and regional LV wall thickness in 16 segments were measured in 147 patients with tight AS (indexed aortic valve area [AVA] < 0.6 cm 2 /m 2 ) using multi-detector computed tomography and compared with those of 32 normal controls. LVH was defined as LVMI >95 th percentile of normal controls and LV remodeling as increased LVM/LVEDV with normal range of LVMI. Asymmetric remodeling or hypertrophy were used for patients with septal wall thickness >1.5 fold compared to the opposite segment. Patients with increased LVMI but normal range of LVM/LVEDV were classified to have eccentric LVH and those with eccentric LVH and decreased LV systolic function were defined to have de-compensation. Results: AS patients with mean indexed AVA of 0.36 ± 0.08 cm 2 /m 2 showed 7 different patterns of LV geometry including normal LV geometry (n=44), remodeling (n=7), asymmetric remodeling (n=7), concentric hypertrophy (n=16), asymmetric hypertrophy (n=23), eccentric hypertrophy (n=38), and de-compensation (n=12). Peak transaortic velocity (r=0.31, p2 , p=0.005). Conclusions: Various remodeling patterns of LV geometry were observed in tight AS and individual variation in LVH severity under similar LV pressure overloading could explain different severity of diastolic dysfunction.

Introduction: Mitral annulus (MA) is generally enlarged in patients with mitral valve prolapse (MVP), which may raise MV closing force acting to shift the MV and its adjacent basal left ventricular (LV) wall toward left atrium. Hypothesis: MA dilatation with augmented MV closing force may disturb basal LV wall systolic contraction in patients with MVP. Methods: In 11 healthy controls and 34 patients with MVP, 3 apical views were obtained to assess longitudinal strain of basal- and mid-LV segments by speckle tracking analysis. The ratio of basal- to mid-LV strain value was then calculated. MA area was calculated by annulus diameters in apical 4- and 2- chamber views. MV closing force was calculated as MA area х (systolic blood pressure - 10). Results: Patients with MVP showed significantly larger MA area (5.3±1.0 vs 3.8±0.7 cm2/m2) and MV closing force (638±192 vs 431±66 mmHg•cm2/m2), and reduced basal-LV strain (-18±3 vs -21±2%) than controls (all p Conclusions: In patients with MVP, an increase in MV closing force corresponding to MA dilatation, as opposed to the severity of mitral regurgitation, was related to attenuated basal LV wall contraction, which can be restored by MV plasty with annular size reduction.