{"id":"9b42eda65771","type":"article","url":"https://hartvaat.nl/2025/08/01/sympathische-overactiviteit-bij-resistente-hypertensie-meta-analyse/","title":"Sympathische overactiviteit bij resistente hypertensie: meta-analyse","title_en":"Sympathetic Overactivation in the Resistant Hypertensive Phenotype: A Meta-Analysis of Published Studies.","category":"hypertensie","category_label":"Hypertensie","professions":["cardioloog","internist"],"tags":["aprocitentan","renale-denervatie","resistente-hypertensie","resistente-hypertensie-aldosteronremmers"],"journal":"Hypertension (Dallas, Tex. : 1979)","doi":"10.1161/HYPERTENSIONAHA.125.24749","source_url":"https://doi.org/10.1161/HYPERTENSIONAHA.125.24749","authors":["Guido Grassi","Fosca Quarti-Trevano","Cesare Cuspidi","Elias Sanidas","Giuseppe Mancia","Costas Thomopoulos"],"significance":5,"published":"2025-08-01","source_date":"2025-08-01","image":"","kennis":["https://hartvaat.nl/kennis/hypertensie/resistente-hypertensie/","https://hartvaat.nl/kennis/nierziekte/raas-blokkade-bij-nierziekte/"],"congress":"","summary_en":"A meta-analysis confirmed that sympathetic overactivation is a core pathophysiological mechanism in resistant hypertension. These findings support sympatholytic therapies such as renal denervation and baroreflex activation as targeted treatment options.","created":"2026-07-03T10:31:46Z","updated":"2026-07-03T18:39:17Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Meta-analyse bevestigde dat sympathische overactiviteit een kernmechanisme is bij resistente hypertensie. Dit ondersteunt sympatholytische therapieën (renale denervatie, baroreflexactivatie) als gerichte behandelopties.","abstract_original":"BACKGROUND: Indirect and direct approaches to assess sympathetic cardiovascular drive have shown that patients with essential hypertension responsive to the blood pressure-lowering effects of antihypertensive drugs are characterized by a pronounced adrenergic overactivity. Whether an emerging clinical hypertensive phenotype such as drug-resistant hypertension (RHT) is also characterized by sympathetic activation and whether its magnitude and underlying pathophysiological mechanisms differ from those of non-RHT is undefined. METHODS: Among the 54 studies identified providing information in RHT on muscle sympathetic nerve traffic (MSNA), 12 were eligible (508 patients) and meta-analyzed, grouping them based on clinically relevant questions: (1) Is MSNA increased in RHT? (2) Does the magnitude of the sympathetic activation differ from that observed in non-RHT? (3) Are heart rate and plasma norepinephrine valuable surrogate markers of MSNA in RHT? and (4) Is baroreflex-MSNA control impaired? RESULTS: MSNA was significantly greater in patients with RHT than in normotensive patients (73.2±6.6 versus 46.1±11.1 bursts/100 heartbeats, means±SD; P<0.0001) and this was the case also when data were compared with patients with non-RHT (59.8±8.4 bursts/100 heartbeats; P<0.001), despite the greater number of antihypertensive drugs. At variance from non-RHT, in RHT, elevated MSNA was unrelated to heart rate and plasma venous norepinephrine. Similar to non-RHT, MSNA in RHT was inversely related to the baroreflex function. CONCLUSIONS: RHT is characterized by a sustained sympathetic overdrive, significantly greater in magnitude than the 1 detected in non-RHT. Neither heart rate nor norepinephrine are capable of reflecting the marked adrenergic overdrive seen in this condition via MSNA recordings."}