Initial systolic blood pressure associates with systemic inflammation, myocardial injury and outcomes in patients with acute coronary syndromes.
Publisher DOI
PubMed ID
37155643
Abstract
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.
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.
Date Issued
2023-07-07
Publication Type
Article
Subject(s)
Subjects
Acute coronary syndromes C-reactive protein cardiogenic shock systemic inflammation systolic blood pressure
Language(s)
en
Author(s)
Winzap, Patric A | |
Kraler, Simon | |
Obeid, Slayman | |
Wenzl, Florian A | |
Templin, Christian | |
Klingenberg, Roland | |
von Eckardstein, Arnold | |
Roffi, Marco | |
Muller, Olivier | |
Lüscher, Thomas F |
Additional Credits
Journal
European heart journal. Acute cardiovascular care
Publisher
Oxford University Press
ISSN
2048-8734
Access(Rights)
metadata.only