Is left ventricular diastolic dysfunction independent from presence of hypertension in metabolic syndrome? An
Sukru Aksoy1, Gündüz Durmuş1, Serhan Özcan1
1Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, Department of Cardiology, Istanbul, Turkey.
Insights
Left ventricular diastolic dysfunction (LVDD) can occur in metabolic syndrome (MetS) independently of hypertension. However, hypertension exacerbates LVDD in MetS patients, worsening diastolic function.
Area of Science:
- Cardiology
- Metabolic Disorders
- Echocardiography
Background:
- Metabolic syndrome (MetS) is associated with left ventricular diastolic dysfunction (LVDD).
- The role of hypertension in MetS-related LVDD requires further clarification.
- This study investigates whether LVDD in MetS is independent of hypertension.
Purpose of the Study:
- To determine if LVDD in patients with MetS is independent of hypertension.
- To assess the impact of hypertension on diastolic function in MetS.
Main Methods:
- 60 MetS patients (30 normotensive, 30 hypertensive) and 30 healthy controls were studied.
- Conventional echocardiography and tissue Doppler imaging were performed.
- Demographic and biochemical parameters were measured.
Main Results:
- MetS patients, both normotensive and hypertensive, showed impaired diastolic function compared to controls.
- Hypertensive MetS patients exhibited more severe diastolic dysfunction than normotensive MetS patients.
- Key echocardiographic parameters like E, E', and E/A ratio were significantly reduced in MetS groups.
Conclusions:
- LVDD can develop in MetS even without hypertension.
- Hypertension significantly worsens diastolic function in patients with MetS.
- These findings highlight the importance of managing blood pressure in MetS to preserve cardiac function.
Background:
It has been shown that left ventricular diastolic dysfunction (LVDD) develops in patients with metabolic syndrome (MetS). However, there is not sufficient evidence in the literature to determine whether this condition is due to increase in blood pressure, which is frequently encountered in MetS. The purpose of this study was to test the hypothesis whether LVDD in MetS is independent from the presence of hypertension.
Methods:
A total of 60 patients diagnosed with MetS and 30 healthy people, who were age- and gender-matched with the patient group, were included in the study as the control group. In the study group, 30 of the patients were normotensive whereas the other 30 had hypertension. Conventional echocardiographic examinations and tissue Doppler imaging were performed besides measurements of demographic and biochemical parameters.
Results:
In the hypertensive MetS group, early diastolic filling flow (E), early diastolic mitral annular velocity (E'), and E/A ratio were significantly lower compared to the control group. Late diastolic filling flow (A), deceleration time (DT), late diastolic mitral annular velocity (A'), and E/E' ratio were higher in the hypertensive MetS group than the control group. In the normotensive MetS group, E, E', and E/A ratio were also lower compared to the control group whereas DT, A', and E/E' ratio were higher.
Conclusion:
These findings support the idea that LVDD may develop in patients with MetS even in the absence of hypertension. In addition, co-existence of hypertension with MetS contributes to further worsening of diastolic functions.
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