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Relationship between left ventricular geometry and left ventricular systolic and diastolic functions in patients with
Murat Cayli1, Mehmet Kanadaşi, Onur Akpinar
1Department of Cardiology, Faculty of Medicine, Cukurova University, Adana, Turkey. drcayli@yahoo.com
Insights
In chronic severe aortic regurgitation, the left ventricle
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Echocardiography
Background:
- Chronic aortic regurgitation (AR) causes left ventricle (LV) volume overload and dilatation.
- Disease progression involves myocardial fibrosis, apoptosis, and LV dysfunction.
- Understanding the relationship between LV geometry and function is crucial.
Purpose of the Study:
- To assess the relationship between left ventricle (LV) geometry and LV systolic and diastolic functions in patients with chronic severe aortic regurgitation (AR).
Main Methods:
- Eighty-eight patients with chronic severe AR and 42 controls underwent echocardiography.
- Left ventricle ejection fraction (LVEF), transmitral velocities, and annular velocities were measured.
- Diastolic function was classified into normal, impaired relaxation, pseudonormalization, and restrictive patterns.
Main Results:
- Left ventricle (LV) long- and short-axis diameters increased, while LV ejection fraction (LVEF) and annular systolic velocity (Sa) decreased progressively with worsening diastolic dysfunction.
- LV long-axis diastolic diameter was independently associated with LV systolic and diastolic functions.
- Patients with restrictive patterns showed significantly increased LV long-axis diastolic diameters and decreased LVEF and Sa velocity.
Conclusions:
- Left ventricle (LV) long-axis diastolic diameter is a key indicator closely related to LV systolic and diastolic functions in chronic severe aortic regurgitation (AR).
- This finding highlights the importance of LV geometry in assessing functional status in AR.
Background:
Chronic aortic regurgitation (AR) is a form of volume overload inducing left ventricle (LV) dilatation. Myocardial fibrosis, apoptosis, progressive LV dilatation, and eventually LV dysfunction are seen with the progression of disease. The aim of the study was to assess the relation between LV geometry and LV systolic and diastolic functions in patients with chronic severe AR.
Methods:
The study population consisted of 88 patients with chronic severe AR and 42 healthy controls. The LV ejection fraction (LVEF) was calculated. Subjects were divided as Group I (controls, n = 42), Group II (LVEF > 50%, n = 47), and Group III (LVEF < 50%, n = 41). Transmitral early and late diastolic velocities and deceleration time were measured. The annular systolic (Sa) and diastolic (Ea and Aa) velocities were recorded. Diastolic function was classified as normal, impaired relaxation (IR), pseudonormalization (PN), and restrictive pattern (RP).
Results:
The LVEF was similar in Group I and II, while significantly lower in Group III. Sa velocity was progressively decreasing, but LV long- and short-axis diameters were increasing from Group I to Group III. Forty-six, 31 and 11 patients had IR, PN, and RP, respectively. LV long-axis systolic and diastolic diameters were significantly increasing, while LVEF and Sa velocity were significantly decreasing from patients with IR to patients with RP. The LV long-axis diastolic diameter is independently associated with LV systolic and diastolic functions.
Conclusions:
The LV long-axis diastolic diameter is closely related with LV systolic and diastolic functions in patients with chronic severe AR.
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