Abstract
Background: We have recently demonstrated that muscle sympathetic nerve activity and normetanephrine levels are transiently increased for several days immediately after acute type B aortic dissection. We now report other markers of sympathetic activation, natriuresis and inflammation over the same time frame.
Methods: In 13 patients with known acute type B aortic dissection (median age 71 years, CI 29-89), we undertook serial measurements of catecholamine metabolites including: normetanephrine , metanephrine , and their second messenger cyclic adenosine monophosphate; renin and aldosterone; N terminal- pro-brain natriuretic peptide (NT-proBNP), and its second messenger cyclic guanosine monophosphate; C-type natriuretic peptide; the inflammatory growth differentiation factor GDF-15; the stress hormone copeptin; mid-regional- proadrenomedullin; and the marker of cardiac muscle damage Troponin T. Venous sampling times were: on admission; then 12 hours, 24 hours; one week and six weeks later. Serial measurements were also undertaken in 12 controls (median age 61 years CI 25-86) who presented with chest pain.
Results: During the first week after dissection, normetanephrine levels were increased: 617- 792 pmol/L versus 425-489 in controls (ANOVA p=0.01). There was also a simultaneous increase in NT-proBNP levels: 49-93 pmol/L versus 14-21 (ANOVA p=0.07) and GDF-15 levels 1507-2873 pg/ml versus 1146-1448 (ANOVA p=0.01) over the same period.
Conclusion: The increase in normetanephrine levels during the week after type B dissection confirms sympathetic nerve activity as a likely mechanism for hypertension in these patients. This surge of sympathetic activity may be partially antagonised by a simultaneous increase in NT-proBNP which is possibly triggered by acute inflammation and oxidative stress caused by the dissection.