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Published on: May 21, 2017
Late chronic hemolysis after valve replacement for aortic stenosis. Relation to residual hypertrophy and impaired
1Department of Thoracic and Cardiovascular Surgery, Skejby Sygehus, Aarhus University Hospital, Denmark.
Insights
Intravascular hemolysis after aortic valve replacement is linked to left ventricular dysfunction and specific prosthesis types. Left ventricular hypertrophy and certain valve types correlate with elevated hemolysis markers, suggesting turbulent flow impacts red blood cells.
Area of Science:
- Cardiology
- Biomedical Engineering
- Hematology
Background:
- Aortic valve replacement surgery can lead to intravascular hemolysis, a condition where red blood cells break down within blood vessels.
- Long-term effects of prosthetic aortic valves on patient health, particularly left ventricular function, require further investigation.
Purpose of the Study:
- To examine the relationship between intravascular hemolysis and patient status, including left ventricular (LV) function, in patients with aortic valve prostheses.
- To identify factors contributing to hemolysis in patients with aortic stenosis treated with valve replacement.
Main Methods:
- A cohort of 63 patients, 10-17 years post-aortic valve replacement for aortic stenosis, underwent assessment.
- Radionuclide cardiography was used to evaluate left ventricular function.
- Serum markers of hemolysis, including lactate dehydrogenase (LDH) and haptoglobin (HAPTO), were measured.
Main Results:
- Elevated serum LDH and reduced haptoglobin were observed in most patients, indicating significant hemolysis.
- Hemolysis markers (LDH) were higher in men, patients with ECG-defined left ventricular hypertrophy, advanced NYHA functional class, abnormal LV function, and those with Starr Edwards cloth-covered (SECC) prostheses.
- ECG hypertrophy score correlated with LDH and inversely with LV ejection fraction and filling rates.
Conclusions:
- Left ventricular hypertrophy and certain prosthetic valve types (SECC) are associated with increased intravascular hemolysis.
- Malfunctioning left ventricles may contribute to turbulent blood flow around aortic prostheses, exacerbating hemolysis.
- These findings highlight the interplay between cardiac structure, prosthesis type, and hemolysis in long-term aortic valve replacement outcomes.
Abstract:
The relationship between intravascular hemolysis induced by aortic valve prosteses and patient status/left ventricular (LV) function (radionuclide cardiography) was examined in 63 patients of 65 who were alive ten to seventeen years after valve replacement (1965-1973) for aortic stenosis. Serum-lactic dehydrogenase (LDH) exceeded upper reference limit in 62 patients and S-haptoglobin (HAPTO) was reduced in 62. One patient with normal LDH had reduced HAPTO and elevated plasma-hemoglobin. Anemia was noted in 4 patients (6%). S-LDH was higher in men than in women (p less than 0.05), in patients with increased ECG hypertrophy score than in those with a normal score (p less than 0.05), in patients with NYHA class II-III than in those with class I (p less than 0.05), in patients with abnormal LV function than in those with a normal radionuclide study (p less than 0.05), in patients with a pathologic Q wave in the ECG than in those without (p less than 0.05), and in patients with a Starr Edwards cloth-covered (SECC) prosthesis than in those with other types (p = 0.07). ECG hypertrophy score correlated directly with LDH (r = 0.33, p = 0.008) and inversely with LV ejection fraction (r = -0.57, p less than 0.0001), peak ejection rate (r = -0.47, p less than 0.0001), and peak filling rate (r = -0.41, p less than 0.001). Multiple linear regression analysis revealed that LDH was accounted for by ECG hypertrophy score (p = 0.001), SECC prosthesis (p = 0.04), and male gender (p = 0.05). Hypertrophic malfunctioning left ventricles may be responsible for higher degrees of turbulent flow characteristics in the vicinity of prosthetic valves in the aortic position and, by inference, explain the increased tendency toward hemolysis in these patients.
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