Abstract
Objective: Sacubitril/valsartan is a first-in-class, novel-acting, angiotensin receptor neprilysin inhibitor (ARNI) that provides inhibition of neprilysin and the angiotensin (AT1) receptor. Effects of Sacubitril/valsartan on carotid arterial IMT and elastic modulus, baPWV in hypertensive patients with heart failure Methods: Thirty-three hypertensive patients with chronic heart failure (mean age 79 years, male 15) were assigned to receive Sacubitril/valsartan (gradual increase depending on the condition) of Sacubitril/valsartan added to existing drug therapies (average number of antihypertensive agents 3) or switched from ARB or ACE inhibitor for 6 months. Changes in home BP, BNP, NT-proBNP, hANP, estimated glomerular filtration rate (eGFR), baPWV and central blood pressure (cSBP) were evaluated. EΘ was obtained by the phased-tracking method (Kanai, Circulation 2003). At four locations of bilateral common carotid arteries, IMT and Etheta; were measured simultaneously. Results: The basal values before Sacubitril/valsartan administration of Body weight(BW), BNP, NT-proBNP, hANP, EF, serum K, eGFR, home early morning blood pressure, home early morning heart rate, baPWV, cSBP, IMT, EΘ were 63 ± 16 kg and 310 ± 237 pg /,mL, 1981 ± 237 pg / mL, 475 ± 514 pg / mL, 51 ± 14%, 4.2 ± 0.4 mEq / L, 46 ± 14 ml / min / 1.73 m2, 141 ± 8/75 ± 11 mmHg, 76 ± 14 bpm, 1526 ± 245 cm / sec, 137 ± 13 mmHg, 0.84 ± 0.12 mm, and 301 ± 141 kPa respectively. ARNI s reduced BW (-4%), BNP (-32%), NT-proBNP (-38%), home early morning blood pressure-17 / -10mmHg, and baPWV (-4%) significantly (p < 0.05). In addition, EF (+ 5%) and hANP were significantly increased, and serum K and eGFR were unchanged. On the other hand, IMT (-5%) in carotid echo decreased, and EΘ decreased significantly. Conclusions: Sacubitril/valsartan was effective for BP control improved cardiac function and arterial stiffness in hypertensive patients with chronic heart failure. EΘ is a good surrogate marker for the early detection of vascular remodeling such as improvement of endothelial dysfunction prior to changes in IMT.
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