Key result
Apparent drug-resistant hypertension was associated with significantly lower muscle sympathetic nerve traffic compared to true resistant hypertension (74.8 vs 89.2 bursts/100 hb, P<0.01).
Why the study?
It was unknown whether the marked neuroadrenergic activation and reflex alterations characterizing true drug-resistant hypertension are specific to that state or also shared by apparent drug-resistant hypertension.
Does apparent drug-resistant hypertension share the same neuroadrenergic activation and reflex alterations as true drug-resistant hypertension?
Cross-Sectional (n=114)
Does apparent drug-resistant hypertension share the same neuroadrenergic activation and reflex alterations as true drug-resistant hypertension?
Absolute Event Rate: 74.8% vs 89.2%
p-value: p=<0.01
Apparent drug-resistant hypertension does not exhibit the marked sympathetic activation and baroreflex dysfunction seen in true drug-resistant hypertension, but rather resembles controlled essential hypertension.
Sympathetic overactivity may distinguish true from apparent resistant hypertension; observational data leave open its diagnostic and therapeutic value.
True drug-resistant hypertension (RHT) is characterized by a marked neuroadrenergic activation and reflex alterations compared with the nonresistant hypertensive state. It is unknown however, whether this behavior is specific for the RHT state or is also shared by apparent RHT (ARHT). In 38 middle-age patients with RHT, 44 treated essential controlled hypertensives (HT) and 32 ARHT; we evaluated sphygmomanometric, beat-to-beat (Finapres) and 24-hour (Spacelabs) blood pressure, heart rate and muscle sympathetic nerve traffic (microneurography). Measurements included plasma aldosterone, plasma norepinephrine, homeostasis model assessment index, and spontaneous baroreflex-muscle sympathetic nerve traffic sensitivity. All the various above-mentioned blood pressure values were significantly greater in both RHT and ARHT as compared with HT, while 24-hour blood pressure was significantly lower in ARHT as compared with RHT. In ARHT, muscle sympathetic nerve traffic was significantly lower than RHT (74.8±5.2 versus 89.2±4.8 bursts/100 hb, P <0.01) and similar to HT (69.7±4.8 bursts/100 hb, P =NS). RHT showed, at variance from the other 2 groups, greater plasma aldosterone and homeostasis model assessment index values and an impaired baroreflex function. In RHT, but not in ARHT and HT, muscle sympathetic nerve traffic was significantly and inversely related to baroreflex function ( r =−0.40, P <0.02) and directly to plasma aldosterone and homeostasis model assessment index values ( r =0.34–0.36, P <0.05). Plasma norepinephrine and heart rate values were not significantly different in the 3 groups. These data provide evidence that the marked sympathetic activation and baroreflex dysfunction detected in RHT is not present in ARHT, which displays a sympathetic and baroreflex profile superimposable to that seen in HT. These differences in the neurogenic function may have important clinical and therapeutic implications.
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Dell’Oro et al. (2019) conducted a cross-sectional in Apparent drug-resistant hypertension (n=114). Apparent drug-resistant hypertension vs. True drug-resistant hypertension and controlled essential hypertension was evaluated on Muscle sympathetic nerve traffic (bursts/100 hb) (p=<0.01). Apparent drug-resistant hypertension was associated with significantly lower muscle sympathetic nerve traffic compared to true resistant hypertension (74.8 vs 89.2 bursts/100 hb, P<0.01).
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