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Quantifying Hemodynamic Cardiac Stress and Cardiomyocyte Injury in Normotensive and Hypertensive Acute Heart Failure
Nikola Kozhuharov1,2, Eleni Michou1, Desiree Wussler1
1Department of Cardiology and Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, University of Basel, Petersgraben 4, 4031 Basel, Switzerland.
Insights
Normotensive acute heart failure (AHF) patients exhibit greater cardiac stress and cardiomyocyte injury than hypertensive AHF patients. This biomarker difference in AHF is linked to increased mortality risk.
Area of Science:
- Cardiology
- Acute Heart Failure Pathophysiology
- Biomarker Analysis
Background:
- Understanding pathophysiological differences between normotensive and hypertensive acute heart failure (AHF) is crucial for personalized treatment strategies.
- Acute heart failure presents unique challenges in diagnosis and management based on blood pressure levels.
Purpose of the Study:
- To compare the extent of hemodynamic cardiac stress and cardiomyocyte injury in normotensive versus hypertensive AHF.
- To investigate the association between these pathophysiological markers and all-cause mortality in AHF patients.
Main Methods:
- Conducted a study on 1152 AHF patients, classifying them as normotensive (SBP 90-140 mmHg) or hypertensive (SBP > 140 mmHg).
- Quantified hemodynamic stress using B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) levels.
- Assessed cardiomyocyte injury via high-sensitivity cardiac troponin T (hs-cTnT) measurements.
- Validated findings in an independent cohort of 324 AHF patients.
Main Results:
- Normotensive AHF patients showed significantly higher BNP, NT-proBNP, and hs-cTnT levels compared to hypertensive AHF patients (p < 0.001 for all).
- All-cause mortality within 360 days was significantly higher in normotensive AHF patients (HR 1.66, p < 0.001).
- Elevated BNP, NT-proBNP, or hs-cTnT in normotensive AHF patients correlated with the highest mortality rates.
Conclusions:
- Biomarker profiling indicates greater hemodynamic stress and cardiomyocyte injury in normotensive AHF compared to hypertensive AHF.
- These findings highlight distinct pathophysiological profiles and prognostic implications for normotensive and hypertensive AHF.
Background:
The characterization of the different pathophysiological mechanisms involved in normotensive versus hypertensive acute heart failure (AHF) might help to develop individualized treatments.
Methods:
The extent of hemodynamic cardiac stress and cardiomyocyte injury was quantified by measuring the B-type natriuretic peptide (BNP), N-terminal proBNP (NT-proBNP), and high-sensitivity cardiac troponin T (hs-cTnT) concentrations in 1152 patients presenting with centrally adjudicated AHF to the emergency department (ED) (derivation cohort). AHF was classified as normotensive with a systolic blood pressure (SBP) of 90-140 mmHg and hypertensive with SBP > 140 mmHg at presentation to the ED. Findings were externally validated in an independent AHF cohort (n = 324).
Results:
In the derivation cohort, with a median age of 79 years, 43% being women, 667 (58%) patients had normotensive and 485 (42%) patients hypertensive AHF. Hemodynamic cardiac stress, as quantified by the BNP and NT-proBNP, was significantly higher in normotensive as compared to hypertensive AHF [1105 (611-1956) versus 827 (448-1419) pg/mL, and 5890 (2959-12,162) versus 4068 (1986-8118) pg/mL, both p < 0.001, respectively]. Similarly, the extent of cardiomyocyte injury, as quantified by hs-cTnT, was significantly higher in normotensive AHF as compared to hypertensive AHF [41 (24-71) versus 33 (19-59) ng/L, p < 0.001]. A total of 313 (28%) patients died during 360 days of follow-up. All-cause mortality was higher in patients with normotensive AHF vs. patients with hypertensive AHF (hazard ratio 1.66, 95%CI 1.31-2.10; p < 0.001). Normotensive patients with a high BNP, NT-proBNP, or hs-cTnT had the highest mortality. The findings were confirmed in the validation cohort.
Conclusion:
Biomarker profiling revealed a higher extent of hemodynamic stress and cardiomyocyte injury in patients with normotensive versus hypertensive AHF.
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