Initial systolic blood pressure associates with systemic inflammation, myocardial injury and outcomes in patients with acute coronary syndromes.

Winzap, Patric A; Kraler, Simon; Obeid, Slayman; Wenzl, Florian A; Templin, Christian; Klingenberg, Roland; von Eckardstein, Arnold; Roffi, Marco; Muller, Olivier; Räber, Lorenz; Lüscher, Thomas F (2023). Initial systolic blood pressure associates with systemic inflammation, myocardial injury and outcomes in patients with acute coronary syndromes. European heart journal. Acute cardiovascular care, 12(7), pp. 437-450. Oxford University Press 10.1093/ehjacc/zuad047

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BACKGROUND

Outcomes after acute coronary syndromes (ACS) are determined by baseline risk profiles, including initial systolic blood pressure (sBP). Herein, we aimed to characterize ACS patients stratified by initial sBP levels and study the relation to inflammation, myocardial injury and post-ACS outcomes.

METHODS

We analysed 4'724 prospectively recruited ACS patients according to invasively assessed sBP (<100, 100-139, and ≥140mmHg) at admission. Biomarkers of systemic inflammation (high-sensitivity C-reactive protein, hs-CRP) and myocardial injury (high-sensitivity cardiac troponin, hs-cTnT) were measured centrally. Major adverse cardiovascular events (MACE; non-fatal myocardial infarction (MI), non-fatal stroke and cardiovascular (CV) death) were externally adjudicated.

RESULTS

Leukocyte numbers, hs-CRP, hs-cTnT and creatine kinase (CK) levels decreased from low to high sBP strata (ptrend < 0.001). Expectedly, patients with sBP < 100mmHg developed more often cardiogenic shock (CS; p < 0.001), and had a 1.7- and 1.4-fold increased multi-variable-adjusted MACE risk at 30 days (HR 1.68, 95% CI 1.05-2.69, p = 0.031) and one year (HR 1.38, 95% CI 0.92-2.05, p = 0.117). Those with sBP < 100 mmHg and CS showed a higher leukocyte count (p < 0.001), an increased neutrophil-to-lymphocyte-ratio (p = 0.031), and higher hs-cTnT and CK levels relative to those without CS (p < 0.001 and p = 0.002, respectively), whereas hs-CRP levels did not differ. Patients who developed CS had a 3.6- and 2.9-fold increased MACE risk at 30 days (HR 3.58, 95% CI 1.77-7.24, p < 0.001) and at one year (HR 2.94 95% CI, 1.57-5.53, p < 0.001), which was attenuated after controlling for distinct inflammatory profiles.

CONCLUSIONS

In patients with ACS, proxies of systemic inflammation and myocardial injury are inversely associated with sBP, with highest levels in those <100mmHg. If linked to high levels of cellular inflammation, these patients are prone to develop CS and are at high MACE and mortality risk.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Department of Cardiovascular Disorders (DHGE) > Clinic of Cardiology
UniBE Contributor:	Räber, Lorenz
Subjects:	600 Technology > 610 Medicine & health
ISSN:	2048-8734
Publisher:	Oxford University Press
Language:	English
Submitter:	Pubmed Import
Date Deposited:	09 May 2023 13:02
Last Modified:	08 Jul 2023 00:14
Publisher DOI:	10.1093/ehjacc/zuad047
PubMed ID:	37155643
Uncontrolled Keywords:	Acute coronary syndromes C-reactive protein cardiogenic shock systemic inflammation systolic blood pressure
URI:	https://boris.unibe.ch/id/eprint/182395