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OBJECTIVES: Late hypertension after coarctation repair is associated with high mortality, but its risk factors remain unclear. This study aims to determine early and late postoperative risk factors for late hypertension after coarctation repair. METHODS: A cross-sectional study including transthoracic echocardiogram and 24-h blood pressure (BP) monitoring was performed in 144 patients aged ≥10 years with previous coarctation repair. Median age at repair was 39 days (interquartile range 0-3 years). Early postoperative hypertension was evaluated by calculating the mean of BP measurements taken on the same day before hospital discharge or the need for antihypertensives prior to discharge. Multivariable analyses were performed to adjust for gender, surgical age, and followup age. RESULTS: After a mean follow-up period of 22 ± 7 years, 59% (84/142) of patients were hypertensive: 58% (82/142) on 24-h BP monitoring and 1% (2/142) on antihypertensives. Early postoperative hypertension was present in 58% (73/126): 39% (49/126) on BP measurements and 19% (24/126) on antihypertensives. Early and late arch reobstruction (transthoracic echocardiogram peak gradient ≥25 mmHg) was present in 37% (23/62) and 23% (33/144), respectively. On multivariable logistic analysis, early postoperative hypertension and maximum descending arch velocity on echocardiography were associated with late hypertension on 24-h BP monitoring (odds ratio 2.21, 95% confidence interval 1.05-4.66, P = 0.04; and odds ratio 2.28, 95% confidence interval 1.08-4.81, P = 0.03; respectively). CONCLUSIONS: There is a high prevalence of late hypertension after coarctation repair. Arch reobstruction may be a major determinant of late hypertension. Early postoperative hypertension may identify very early in life those at risk of developing late hypertension. [ABSTRACT FROM AUTHOR]

Background To (1) determine the prevalence of hypertension late after coarctation repair in patients with normal-sized transverse arches, and (2) evaluate the potential for end-organ damage related to hypertension after coarctation repair. There are no studies specifically investigating end-organ damage and hypertension after coarctation repair using noninvasive techniques. Methods Eighty-two patients aged 10 years or greater with a coarctation repair and a normal-sized arch operated on between 1978 and 2010, underwent a transthoracic echocardiogram, 24-hour blood pressure (BP) monitoring, and retinal imaging. Median age at repair was 1 year (interquartile range, 0 to 6); 45% (37 of 82) were operated in the first year of life. Results After a follow-up of 24 ± 7 years, 27% (22 of 82) and 50% (41 of 82) suffered resting hypertension and resting prehypertension, respectively. On 24-hour BP monitoring, 61% (49 of 80) and 21% (17 of 80) suffered hypertension and prehypertension, respectively. Arch reobstruction (echo gradient > 25 mm Hg) was present in only 15% (12 of 82), and in only 15% (7 of 47) with 24-hour hypertension. Resting hypertension was associated with a smaller central retinal artery equivalent (average width of arterioles) and central retinal vein equivalent (average width of venules) ( p = 0.0006 and p = 0.003, respectively). Left ventricular hypertrophy on echocardiography was present in 63% (31 of 49) with 24-hour hypertension compared with only 42% (13 of 31) with normal 24-hour BP ( p = 0.06). Conclusions There is a high rate of hypertension late after coarctation repair, even in patients with unobstructed arches. The presence of retinal imaging abnormalities and left ventricular hypertrophy signals the presence of end-organ damage in this young adult population. Regular follow-up with 24-hour BP monitoring is warranted. [ABSTRACT FROM AUTHOR]

Background Aortic intima-media thickness measured by transabdominal ultrasound (aIMT) is an intermediate phenotype of cardiovascular risk. We aimed to (1) investigate the reproducibility of aIMT in a population-derived cohort of infants; (2) establish the distribution of aIMT in early infancy; (3) compare measurement by edge-detection software to that by manual sonographic calipers; and (4) assess the effect of individual and environmental variables on image quality. Methods Participants were term infants recruited to a population-derived birth cohort study. Transabdominal ultrasound was performed at six weeks of age by one of two trained operators. Thirty participants had ultrasounds performed by both operators on the same day. Data were collected on environmental (infant sleeping, presence of a sibling, use of sucrose, timing during study visit) and individual (post-conception age, weight, gender) variables. Two readers assessed image quality and measured aIMT by edge-detection software and a subset by manual sonographic calipers. Measurements were repeated by the same reader and between readers to obtain intra-observer and inter-observer reliability. Results Aortic IMT was measured successfully using edge-detection in 814 infants, and 290 of these infants also had aIMT measured using manual sonographic calipers. The intra-reader intraclass correlation (ICC) (n = 20) was 0.90 (95%CI 0.76, 0.96), mean difference 1.5 μm (95%LOA -39, 59). The between reader ICC using edge-detection (n = 20) was 0.92 (95%CI 0.82, 0.97) mean difference 2 μm (95%LOA -45.0, 49.0) and with manual caliper measurement (n = 290) the ICC was 0.84 (95%CI 0.80, 0.87) mean difference 5 μm (95%LOA -51.8, 61.8). Edge-detection measurements were greater than those from manual sonographic calipers (mean aIMT 618 μm (50) versus mean aIMT 563 μm (49) respectively; p < 0.001, mean difference 44 μm, 95%LOA -54, 142). With the exception of infant crying (p = 0.001), no associations were observed between individual and environmental variables and image quality. Conclusion In a population-derived cohort of term infants, aIMT measurement has a high level of intra and inter-reader reproducibility. Measurement of aIMT using edge-detection software gives higher inter-reader ICC than manual sonographic calipers. Image quality is not substantially affected by individual and environmental factors. [ABSTRACT FROM AUTHOR]

Duchenne muscular dystrophy involves an absence of dystrophin, a cytoskeletal protein which supports cell structural integrity and scaffolding for signalling molecules in myocytes. Affected individuals experience progressive muscle degeneration that leads to irreversible loss of ambulation and respiratory diaphragm function. Although clinical management has greatly advanced, heart failure due to myocardial cell loss and fibrosis remains the major cause of death. We examined cardiac morphology and function in D2.B10-Dmd mdx /J (D2- mdx ) mice, a relatively new mouse model of muscular dystrophy, which we compared to their wild-type background DBA/2J mice (DBA/2). We also tested whether drug treatment with a specific blocker of mitochondrial permeability transition pore opening (Debio-025), or ACE inhibition (Perindopril), had any effect on dystrophy-related cardiomyopathy. D2- mdx mice were treated for six weeks with Vehicle control, Debio-025 (20 mg/kg/day), Perindopril (2 mg/kg/day), or a combination ( n = 8/group). At 18 weeks, compared to DBA/2, D2- mdx hearts displayed greater ventricular collagen, lower cell density, greater cell diameter, and greater protein expression levels of IL-6, TLR4, BAX/Bcl2, caspase-3, PGC-1 α , and notably monoamine oxidases A and B. Remarkably, these adaptations in D2- mdx mice were associated with preserved resting left ventricular function similar to DBA/2 mice. Compared to vehicle, although Perindopril partly attenuated the increase in heart weight and collagen at 18 weeks, the drug treatments had no marked impact on dystrophic cardiomyopathy., Competing Interests: All authors declare that they have no conflicts of financial interest., (Copyright © 2022 Holly M. Hayes et al.)