Key result
Initial systolic blood pressure < 100 mmHg in ACS patients was associated with an increased risk of MACE at 30 days (HR 1.68; 95% CI 1.05-2.69; P=0.031).
Why the study?
Outcomes after ACS are determined by baseline risk profiles, including initial systolic blood pressure levels, but their relationship to inflammation, myocardial injury, and post-ACS outcomes required characterization.
Does initial systolic blood pressure associate with systemic inflammation, myocardial injury, and outcomes in patients with acute coronary syndromes?
Cohort (n=4,724)
Does initial systolic blood pressure associate with systemic inflammation, myocardial injury, and outcomes in patients with acute coronary syndromes?
In patients with acute coronary syndromes, an initial systolic blood pressure <100 mmHg is associated with greater systemic inflammation, myocardial injury, and an increased short-term risk of major adverse cardiovascular events.
Low admission sBP signals higher early MACE risk in ACS; hypothesis-generating for inflammation-targeted interventions in hypotensive patients.
AIMS: Outcomes after acute coronary syndromes (ACS) are determined by baseline risk profiles, including initial systolic blood pressure (sBP) levels. Herein, we aimed to characterize ACS patients stratified by initial sBP levels and study their relation to inflammation, myocardial injury and post-ACS outcomes. METHODS AND RESULTS: We analysed 4724 prospectively recruited ACS patients according to invasively assessed sBP (<100, 100-139, and ≥140 mmHg) at admission. Biomarkers of systemic inflammation [high-sensitivity C-reactive protein (hs-CRP)] and myocardial injury [high-sensitivity cardiac troponin T (hs-cTnT)] were measured centrally. Major adverse cardiovascular events (MACE; composite measure of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death) were externally adjudicated. Leukocyte counts, hs-CRP, hs-cTnT, and creatine kinase (CK) levels decreased from low to high sBP strata (ptrend < 0.001). Patients with sBP < 100 mmHg developed more often cardiogenic shock (CS; P < 0.001), and had a 1.7-fold increased multivariable-adjusted MACE risk at 30 days (HR 1.68, 95% CI 1.05-2.69, P = 0.031) which did not persist at 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 intriguingely attenuated after controlling for distinct inflammatory profiles. CONCLUSION: In patients with ACS, proxies of systemic inflammation and myocardial injury are inversely associated with initial sBP levels, with highest biomarker levels observed in those <100 mmHg. If linked to high levels of cellular inflammation, these patients are prone to develop CS and are at high MACE and mortality risk.
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Winzap et al. (2023) conducted a cohort in Acute coronary syndromes (n=4,724). Initial systolic blood pressure < 100 mmHg vs. Initial systolic blood pressure ≥ 100 mmHg was evaluated on Major adverse cardiovascular events (MACE) at 30 days (HR 1.68, 95% CI 1.05-2.69, p=0.031). Initial systolic blood pressure < 100 mmHg in ACS patients was associated with an increased risk of MACE at 30 days (HR 1.68; 95% CI 1.05-2.69; P=0.031).
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