Ambulatory Blood Pressure and Urinary Caffeine (page 691)
Intake of caffeinated beverages might be associated with reduced cardiovascular mortality, possibly via the lowering of blood pressure. Caffeine and caffeine metabolites (eg, paraxanthine, theobromine, and theophylline) are methylxanthines, a family of nonspecific adenosine receptor antagonists with several properties including diuretic and natriuretic properties. To date, studies on the association of caffeine and blood pressure have been limited by the use of reported caffeine intake instead of measured caffeine levels and the use of office blood pressure instead of ambulatory measurement. In this issue of Hypertension, results from the Swiss Kidney Project on Genes in Hypertension (SKIPOGH) indicate that ambulatory systolic blood pressure was inversely associated with urinary excretions of caffeine and caffeine metabolites. For each doubling of caffeine excretion, 24-hour and night-time systolic blood pressure was lower by 0.642 and 1.107 mm Hg, respectively. Similar inverse associations were observed for paraxanthine and theophylline. Night-time systolic blood pressures in the first (lowest), second, third, and fourth (highest) quartiles of caffeine urinary excretions were 110.2, 107.5, 106.0, and 106.2 mm Hg, respectively. These observational findings from 836 randomly recruited participants from the general adult population suggest a potential protective chronic effect of caffeine on blood pressure. Numerous beverages and food items contain caffeine, and the relationship of caffeine with blood pressure is often discussed in clinical practice. Yet, current hypertension guidelines either omit a specific guideline or include a recommendation to refrain from consuming caffeine-rich products.
Preterm Birth, Angiogenesis, and Blood Pressure (page 607)
By their mid-20s, systolic blood pressure is ≈8 mm Hg higher in those who were born preterm compared with those born at term. Improved survival of preterm babies during the past 2 decades means that the number who reach young adulthood has increased substantially. Understanding why they have higher blood pressure is therefore important to be able to understand whether this growing group would benefit from targeted treatment advice.
In this article, we demonstrate for the first time that young adults born preterm have higher levels of circulating antiangiogenic factors. The increase is proportional to their elevations in both clinic and ambulatory blood pressure. To build a more detailed picture of the pathway that links angiogenic factors with blood pressure, we studied a range of cardiac and vascular structural and functional measures known to vary in preterm offspring. We found reductions in both capillary density and ability to recruit capillaries known to be a key determinant of peripheral vascular resistance, and a characteristic finding in patients with primary hypertension was the main mediator of the association.
Together, these findings implicate abnormal angiogenesis and capillary rarefaction as a potential tractable pathway for future prevention strategies to treat, or delay the development of, hypertension in individuals born preterm.
Hyperuricemia Impairs Cardiac Diastolic Function (page 531)
Hyperuricemia is frequently observed in obese people and rising obesity rates parallel increased consumption of a western diet, high in fat and fructose. Both epidemiological and clinical data suggest that serum uric acid is positively associated with aortic stiffness, left ventricular hypertrophy, and cardiac diastolic dysfunction. In this issue of Hypertension, Jia et al report that increased production of uric acid with intake of a western diet promotes cardiomyocyte hypertrophy, inflammation, and oxidative stress that leads to myocardial fibrosis and associated impaired diastolic relaxation. Increased uric acid is accompanied by increases in cardiac tissue xanthine oxidase activity and thus results in the activation of both growth and profibrotic signaling pathways and macrophage proinflammatory. Blocking xanthine oxidase activity with allopurinol treatment inhibits these pathophysiological changes in the absence of any systemic effect on blood pressure, body weight, or systemic insulin sensitivity, suggesting that hyperuricemia independently induces heart failure with cardiac relaxation dysfunction. The results suggest that pharmacological inhibition of xanthine oxidase activity may prevent the development of obesity-associated diastolic relaxation by reduced uric acid and myocardial xanthine oxidase activity, oxidative stress, inflammation, and cardiac remodeling. This study extends the knowledge of the pathogenesis of heart failure with diastolic dysfunction, demonstrating that hyperuricemia is an instigator of cardiomyocyte hypertrophy, interstitial fibrosis, and obesity-related cardiomyopathy characterized by cardiac stiffness and impaired diastolic relaxation.
- © 2015 American Heart Association, Inc.