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[Effect of left ventricular diastolic dysfunction on pathogenesis of angina decubitus]
1Cardiovascular Institute and Fu Wai Hospital, CAMS and PUMC, Beijing 100037, China.
Insights
Patients with angina decubitus exhibit left ventricular diastolic dysfunction. This condition, characterized by impaired heart relaxation, appears closely linked to the development of angina decubitus symptoms.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Context:
- Angina decubitus is a chest pain condition.
- Left ventricular diastolic dysfunction (LVDD) affects heart relaxation.
- The relationship between LVDD and angina decubitus requires further investigation.
Purpose:
- To investigate the role of left ventricular diastolic dysfunction in the pathogenesis of angina decubitus.
Summary:
- Patients with angina decubitus showed significantly lower LV first 1/3 filling fraction and higher LV late 1/3 filling fraction compared to control groups.
- Elevated left ventricular end-diastolic pressure (LVEDP) and left atrial contraction difference (LACD) were observed in angina decubitus patients, indicating diastolic dysfunction.
- These findings suggest LVDD is closely related to the pathogenesis of angina decubitus.
Impact:
- This study highlights the significance of diastolic function assessment in patients with angina decubitus.
- Understanding the role of LVDD can lead to improved diagnostic and therapeutic strategies for angina decubitus.
- The research provides insights into the pathophysiology of angina decubitus.
Objective:
To investigate the effect of left ventricular diastolic dysfunction on the pathogenesis of angina decubitus.
Methods:
The study population consisted of three groups: (1) group 1, 31 patients with angina decubitus who had ejection fraction > 50%; (2) group 2, 20 patients with coronary artery disease but without angina decubitus; group 2 and 1 were matched for age, EF and extent of coronary artery disease; (3) group 3, 20 patients without cardiovascular diseases.
Results:
Left ventriculography (LVG) showed that LV first 1/3 filling fraction (1/3 FF) and LV late 1/3 FF were 0.30 +/- 0.12, 0.41 +/- 0.12, 0.46 +/- 0.07 and 0.36 +/- 0.09, 0.31 +/- 0.08, 0.29 +/- 0.06 in groups 1 to 3 respectively. LV first 1/3 FF was significantly lower in group 1 than in group 2 and 3 (both P < 0.001), but LV late 1/3 FF was much higher in group 1 than in groups 2 and 3 (P < 0.05 and P < 0.01, respectively). Left ventricular end-diastolic pressure (LVEDP) was markedly increased before and after LVG in groups 1 and 2 as compared with group 3 (P < 0.001 and P < 0.05, respectively). The difference of LVEDP caused by left atrial contraction (LACD) was much higher before and after LVG in group 1 than in group 3 (P < 0.01 and P < 0.001, respectively). However, there were significant differences in LVEDP and LACD tested between before and after LVG in group 1 (both P < 0.01). No statistical differences were found in LVEDP and LACD tested between before and after LVG in both group 2 and group 3.
Conclusion:
Patients with angina decubitus have LV diastolic dysfunction, which may be closely related to the pathogenesis of angina decubitus.