Comparison of the number of contrast exposures according to the presence of hypotension.

<p>*p<0.05.</p

Anaphylactic reactions and total number of RCM use in every year of the study period.

<p>Anaphylactic reactions and total number of RCM use in every year of the study period.</p

Clinical characteristics according to the development of hypotension.

<p>Continuous variables are expressed as mean ± standard deviation.</p><p>*P<0.05, ^†P<0.01. ^‡Among the total 104 subjects, radiocontrast media involved in anaphylaxis could not be identified in seven patients who had experienced anaphylaxis prior to the introduction of electronic medical recording system.</p

Sensitivity and false negative rate on skin test.

<p>*Five patients in whom causal contrast media could not be identified were excluded from this analysis among 51 patients with skin test results.</p><p>Iopromide, iopamidol, iomeprol, iohexol, and iobitridol are low-osmolar contrast media. Iodixanol is an iso-osmolar contrast media.</p

Gender Difference in Ventricular Response to Aortic Stenosis: Insight from Cardiovascular Magnetic Resonance

<div><p>Background</p><p>Although left ventricular hypertrophy (LVH) and remodeling is associated with cardiac mortality and morbidity, little is known about the impact of gender on the ventricular response in aortic stenosis (AS) patients. This study aimed to analyze the differential effect of gender on ventricular remodeling in moderate to severe AS patients.</p><p>Methods and Results</p><p>A total of 118 consecutive patients (67±9 years; 63 males) with moderate or severe AS (severe 81.4%) underwent transthoracic echocardiography and cardiovascular magnetic resonance (CMR) within a 1-month period in this two-center prospective registry. The pattern of LV remodeling was assessed using the LV mass index (LVMI) and LV remodeling index (LVRI; LV mass/LV end-diastolic volume) by CMR. Although there were no differences in AS severity parameters nor baseline characteristics between genders, males showed a significantly higher LVMI (102.6±29.1g/m² vs. 86.1±29.2g/m², p=0.003) and LVRI (1.1±0.2 vs. 1.0±0.3, p=0.018), regardless of AS severity. The LVMI was significantly associated with aortic valve area (AVA) index and valvuloarterial impedance in females, whereas it was not in males, resulting in significant interaction between genders (PInteraction=0.007/0.014 for AVA index/valvuloarterial impedance, respectively). Similarly, the LVRI also showed a significantly different association between male and female subjects with the change in AS severity parameters (PInteraction=0.033/<0.001/0.029 for AVA index/transaortic mean pressure gradient/valvuloarterial impedance, respectively).</p><p>Conclusion</p><p>Males are associated with greater degree of LVH and higher LVRI compared to females at moderate to severe AS. However, females showed a more exaggerated LV remodeling response, with increased severity of AS and hemodynamic loads, than males.</p></div

Baseline clinical characteristics of the study participants.

<p>The data are presented as mean (SD) or number (percentage).</p><p>Abbreviations: ACEI/ARB, angiotensin converting enzyme inhibitor/angiotensin receptor blocker; BMI, body mass index; HTN, hypertension; NYHA, New York Heart Association.</p><p>Baseline clinical characteristics of the study participants.</p

The association between left ventricular remodeling index and the severity of aortic stenosis or valvuloarterial impedance.

<p>Males consistently showed relatively higher left ventricular remodeling index in (A) larger aortic valve area index, (B) lower mean transaortic pressure gradient, or (C) lower valvuloarterial impedance, compared with females. However, there were significant differences between the two genders in the degree of correlation between the left ventricular remodeling index and the above three parameters. The univariate linear regression coefficient and the interaction p value across the gender are shown. Abbreviations: AV, aortic valve; AVA, aortic valve area; CMR, cardiovascular magnetic resonance; PG, pressure gradient.</p

Echocardiographic and cardiovascular magnetic resonance (CMR) parameters of the study participants.

<p>The data are presented as mean (SD), except adjusted mean (SE) in the body mass index adjusted LV mass.</p><p>^†When quantifying the LV mass, the trabeculations and the papillary muscles were excluded.</p><p>Abbreviations: AR, aortic regurgitation; AS, aortic stenosis; AVA, aortic valve area; BMI, body mass index; BSA, body surface area; E, early diastolic velocity at the mitral valve tip; e’, early mitral annular velocity at the septal annulus; IVST, interventricular septal thickness; LV, left ventricle; PG, pressure gradient; PWT, posterior wall thickness; Vmax, maximal transaortic velocity; Z_VA, valvuloarterial impedance.</p><p>Echocardiographic and cardiovascular magnetic resonance (CMR) parameters of the study participants.</p

Vascular Calcifying Progenitor Cells Possess Bidirectional Differentiation Potentials

<div><p>Vascular calcification is an advanced feature of atherosclerosis for which no effective therapy is available. To investigate the modulation or reversal of calcification, we identified calcifying progenitor cells and investigated their calcifying/decalcifying potentials. Cells from the aortas of mice were sorted into four groups using Sca-1 and PDGFRα markers. Sca-1⁺ (Sca-1⁺/PDGFRα⁺ and Sca-1⁺/PDGFRα⁻) progenitor cells exhibited greater osteoblastic differentiation potentials than Sca-1⁻ (Sca-1⁻/PDGFRα⁺ and Sca-1⁻/PDGFRα⁻) progenitor cells. Among Sca-1⁺ progenitor populations, Sca-1⁺/PDGFRα⁻ cells possessed bidirectional differentiation potentials towards both osteoblastic and osteoclastic lineages, whereas Sca-1⁺/PDGFRα⁺ cells differentiated into an osteoblastic lineage unidirectionally. When treated with a peroxisome proliferator activated receptor γ (PPARγ) agonist, Sca-1⁺/PDGFRα⁻ cells preferentially differentiated into osteoclast-like cells. Sca-1⁺ progenitor cells in the artery originated from the bone marrow (BM) and could be clonally expanded. Vessel-resident BM-derived Sca-1⁺ calcifying progenitor cells displayed nonhematopoietic, mesenchymal characteristics. To evaluate the modulation of in vivo calcification, we established models of ectopic and atherosclerotic calcification. Computed tomography indicated that Sca-1⁺ progenitor cells increased the volume and calcium scores of ectopic calcification. However, Sca-1⁺/PDGFRα⁻ cells treated with a PPARγ agonist decreased bone formation 2-fold compared with untreated cells. Systemic infusion of Sca-1⁺/PDGFRα⁻ cells into Apoe^−/− mice increased the severity of calcified atherosclerotic plaques. However, Sca-1⁺/PDGFRα⁻ cells in which PPARγ was activated displayed markedly decreased plaque severity. Immunofluorescent staining indicated that Sca-1⁺/PDGFRα⁻ cells mainly expressed osteocalcin; however, activation of PPARγ triggered receptor activator for nuclear factor-κB (RANK) expression, indicating their bidirectional fate in vivo. These findings suggest that a subtype of BM-derived and vessel-resident progenitor cells offer a therapeutic target for the prevention of vascular calcification and that PPARγ activation may be an option to reverse calcification.</p> </div

Clonal expansion of calcifying progenitor cells.

<p>(A) Schematic of the clonal expansion assay. (B) Giemsa staining to detect a single-cell colony. Bars: 1 mm. (C) For statistical analysis, colony-forming cells were counted among 96 wells per group. Experiments were performed in triplicate. Colonies formed by Sca-1⁺ cells were much more compact and abundant than Sca-1⁻ cells. *<i>P</i><0.001 versus Sca-1⁻/PDGFRα⁺ cells. ‡<i>P</i><0.005 versus Sca-1⁺/PDGFRα⁺ cells. (D) Schematic depicting osteoblastic and osteoclastic differentiation of clonally expanded cells. (E) Alizarin Red S and osteocalcin staining to detect osteoblast differentiation from single-colony cells after 14 d of differentiation. Bars: black = 1 mm; white = 20 µm. (F) TRAP and cathepsin K staining to detect osteoclast differentiation from single-colony cells after 14 d of differentiation. Bars: black = 100 µm; white = 20 µm.</p