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Published on: December 2, 2014
The relationship between aortic stiffness and left ventricular dyssynchrony in hypertensive patients with preserved
Mi-Na Kim1, Seong-Mi Park, Wan-Joo Shim
1Division of Cardiology, Korea University Cardiovascular Center, Korea University Anam Hospital, Seoul, Republic of Korea.
Insights
Arterial stiffness and increased left ventricular mass may cause diastolic dyssynchrony in hypertensive patients without heart failure. This study highlights the link between aortic stiffness and diastolic dysfunction in this population.
Area of Science:
- Cardiology
- Hypertension Research
- Echocardiography
Background:
- Left ventricular (LV) dyssynchrony is prevalent in hypertension, even without heart failure.
- Arterial stiffness is a known contributor to elevated blood pressure and impaired ventricular function.
Purpose of the Study:
- To investigate the association between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function.
Main Methods:
- Eighty hypertensive patients (LV ejection fraction > 50%) and 30 controls were assessed.
- LV systolic and diastolic dyssynchrony indices (Ts-SD, Te-SD, Ts-Max, Te-Max) were measured using echocardiography.
- Aortic stiffness index was calculated from aortic dimensions and blood pressure.
Main Results:
- No significant relationship was found between LV systolic and diastolic dyssynchrony indices.
- Aortic stiffness parameter correlated with LV mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony (Te-Max).
- Multiple regression revealed Te-Max was significantly related to aortic strain and aortic stiffness index; LVMI was related to aortic distensibility.
Conclusions:
- Increased LV mass and arterial stiffness are potential contributors to LV diastolic dyssynchronous changes in hypertensive patients.
- Findings suggest a link between arterial stiffness, LV remodeling, and diastolic dysfunction in hypertension.
Abstract:
Left ventricular (LV) dyssynchrony is often seen in patients with hypertension, even without heart failure. Arterial stiffness is well accepted as an important factor of increasing blood pressure and influencing ventricular function. The purpose of this study was to determine the relationship between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function. Eighty hypertensive patients with preserved LV systolic function (LV ejection fraction > 50%) and 30 controls were studied. The LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from onset of the QRS complex to peak myocardial systolic velocity (Ts-SD) and to early diastolic velocity (Te-SD) and the maximal differences in Ts (Ts-Max) and Te (Te-Max) in 12 LV segments. Aortic stiffness index was calculated from aortic diameters in the systolic and diastolic phases, as measured by echocardiography and blood pressure. No relationship was observed between LV systolic and diastolic dyssynchrony indices (r = 0.057, P = .61). In simple regression, aortic stiffness parameter was related to left ventricular mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony index. But using multiple linear regression, Te-Max remained as a single variable related to aortic strain and aortic stiffness index (r = -0.271, P = .008 and r = 0.269, P = .008). LVMI was related to aortic distensibility using multiple linear regression (r = -0.239, P = .02). Aortic stiffness index was related to LV diastolic dyssynchrony index and LVMI. These findings suggest that LV diastolic dyssynchronous changes may be caused by increased LV mass and arterial stiffness.
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