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OBJECTIVE. Hypertension is common in the pediatric population. There is increasing evidence for early hypertensive target organ damage that may lead to substantial long-term morbidity. Because a critical aspect of [...]

Background: Childhood hypertension is increasingly common and likely contributes to the premature development of cardiovascular and renal disease. Early detection of hypertensive cardiac damage may allow for prompt therapy and reduce the risk of late morbidity and mortality. While left ventricular mass index (LVMI) has been used as a surrogate of hypertensive cardiac damage in children, its prognostic and diagnostic value is not completely understood in this population.Objective: To test the hypothesis that strain assessment using automated function imaging (AFI) detects cardiac changes in hypertensive children earlier than standard 2D echocardiographic techniques.METHODS: A cross-sectional study of hypertensive children < 19 years old between October 2010 and May 2012 was performed. Any patient who was newly diagnosed with hypertension and underwent echocardiographic examination including standard 2D, Doppler, and automated function imaging (AFI) modalities was included. Global peak longitudinal systolic strain (GLPSS) was measured using a 17 segment model of the left ventricle. All echocardiographic measures were compared to normative reference values for age.Results: Twenty four patients (mean age 14.6 ± 2.7 years, 67% male) were identified. Mean systolic and diastolic blood pressure index was 1.1 ± 0.1 and 0.9 ± 0.1, respectively. Mean LVMI did not significantly differ from 95th-percentile normative values (41.6 ± 11.2 g/m2.7 vs. 39.3 ± 1.5 g/m2.7, p = 0.328). Mean GLPSS was significantly lower than 5th-percentile normative values (-17.6 ± 2.5 vs. -19.5 ± 0.42, p = 0.001) and were decreased across all myocardial segments. Left atrial volume was significantly higher than reported normal values in children (27.6 ± 7.3 ml/m2 vs. 22.0 ± 6.0 ml/m2, p = 0.002). No patient exhibited abnormal shortening or ejection fraction, mitral E-wave to A-wave ratio, or lateral mitral E-wave to e’-wave ratio.Conclusions: A population of unselected, newly diagnosed hypertensive adolescents had atypically low GLPSS and increased left atrial volume. The use of GLPSS measured by AFI may be a more sensitive marker of early myocardial remodeling in hypertensive children and routine measurement of GLPSS should be considered. [ABSTRACT FROM AUTHOR]

The article reviews the study on perinatal programming relative to later development of hypertension in adult. It states that researchers' observation that children with a history of delivery at low birth weight have increased serum uric acid, and even at age three years have a slightly higher blood pressure, suggests a novel mechanism for higher blood pressure and increased cardiovascular risk.

Purpose of Review: Studies have shown an association between hyperuricemia and essential hypertension in children, presenting the possibility for serum uric acid level to serve as a biomarker for diagnosis and potential treatment target., Recent Findings: The proposed mechanism of uric acid-induced hypertension is biphasic, with a reversible early phase, implying added significance for new-onset hypertension. Current evidence shows a strong correlation between uric acid level and essential hypertension, supporting its use in diagnosis. Small studies have shown that the use of uric acid-lowering agents allopurinol and probenecid can lower blood pressure in adolescents. These medications require further study in large populations and careful consideration of their side-effect profiles prior to clinical use as antihypertensive agents. Recent studies have also linked dietary fructose intake to hyperuricemia and hypertension, but the clinical effect of fructose reduction on blood pressure has not been confirmed., Summary: Current evidence supports use of serum uric acid level as a biomarker for diagnosis of essential hypertension in children. More research is needed to evaluate the utility of pharmacologic and nonpharmacologic means of serum uric acid reduction prior to clinical use as a therapy for hypertension.

Serum uric acid was first noted to be associated with increased BP by Frederick Mohamed in the 1870s. Although the link was rediscovered periodically over the years, it generally was dismissed as a surrogate marker for decreased renal function that led to increased uric acid and increased risk for hypertension and cardiovascular (CV) disease. Recently, however, several lines of evidence suggest that increased serum uric acid may be a significant modifiable risk factor. Increased serum uric acid is associated with increased risk for future hypertension in several large longitudinal clinical trials as well as an independent risk factor for poor CV prognosis. Animal model experiments demonstrate that increased serum uric acid causes increased BP that initially is reversible but becomes irreversible, salt sensitive, and uric acid independent over time. The mechanisms include the direct action of uric acid on smooth muscle and vascular endothelial cells. Finally, in adolescents with new-onset essential hypertension, the prevalence of elevated serum uric acid is >90%, and preliminary clinical trial evidence suggests that agents that lower serum uric acid may lower BP in this select population. Although the investigations are still preliminary, serum uric acid represents a possible new and intriguing target for the reduction of morbidity and mortality associated with hypertension and CV disease.