Ventricular-Arterial Uncoupling and Hypertension Mediated Diastolic Dysfunction
Daniel Piskorz1, Luis Keller2, Luciano Citta2
1Cardiology Institute of the Rosario British Sanatorium, Jujuy 1540, floor 5th, 2000, Rosario, Argentina. danielpiskorz@ciudad.com.ar.
Insights
Ventricular-arterial uncoupling, a mismatch between the left ventricle and arteries, is common in hypertension. This study found that impaired ventricular-arterial coupling is linked to increased left ventricular hypertrophy and diastolic dysfunction.
Area of Science:
- Cardiology
- Physiology
- Hypertension Research
Background:
- Increased pulsatile afterload in hypertension can cause left ventricular (LV) afterload mismatch.
- Ventricular-arterial uncoupling is a suspected contributor to LV dysfunction in hypertensive patients.
Purpose of the Study:
- To determine the prevalence of ventricular-arterial uncoupling in hypertensive patients with preserved ejection fraction.
- To investigate the association between ventricular-arterial uncoupling, LV hypertrophy (LVH), and diastolic dysfunction (DD).
Main Methods:
- Observational study of 288 hypertensive patients with ejection fraction > 54%.
- Utilized 2D echocardiography and tissue Doppler to assess LV function.
- Measured end-systolic elastance (Ees), effective arterial elastance (Ea), and ventricular-arterial coupling (VAC) using the Chen single-beat method.
Main Results:
- Ventricular-arterial uncoupling (VAC) was frequently observed.
- Patients with the worst VAC showed significantly increased LV stroke volume and stroke work.
- Conversely, patients with the worst VAC had significantly reduced systolic stress and peripheral resistance index.
- The frequency of LVH or DD was significantly higher in patients with the worst VAC.
Conclusions:
- Ventricular-arterial uncoupling is prevalent in hypertension and associated with adverse LV remodeling.
- Impaired VAC is primarily driven by increased LV end-systolic elastance (Ees) rather than elevated arterial elastance (Ea).
- Ventricular-arterial uncoupling is a significant risk factor for developing LV hypertrophy and diastolic dysfunction in hypertensive individuals.
Introduction:
The increase in the pulsatile component of left ventricle afterload is suspected to cause a mismatch between the left ventricle (LV) and the vascular tree.
Aim:
To demonstrate that ventricular-arterial uncoupling is frequently present in the development of LV hypertrophy (H) and diastolic dysfunction (DD) in hypertension (HBP).
Methods:
Observational study, HBP patients with ejection fraction > 54%. Conventional 2D echocardiography and tissue Doppler performed following imaging guidelines. LV end systolic elastance (Ees), the effective arterial elastance (Ea), and ventricular-arterial coupling (VAC) measured by Chen single beat method.
Results:
288 patients, mean age 56.3 ± 12.5 years and 168 patients (58.3%) males. Mean LV mass index was 87.2 ± 20.4 grs/m2 and frequency of LVH 20.1% (58 patients). The mean VAC was 0.54 ± 9.23. LV Stroke volume, stroke work and systolic stress were 46.2 ± 10.3 cc/m2, 91.4 ± 22.2 g-min/m2, and 57 ± 14.6 dynes/cm2 in quartile 1, and 33.5 ± 6.6 cc/m2, 65.5 ± 15.2 g-min/m2, and 77.8 ± 17.1 dynes/cm2, in quartile 4, respectively (p < 0.001). Peripheral resistance index was 3349 ± 1072 and 4410 ± 1143 dynes*s/cm-5/m2 quartiles 1 vs. 4 (p < 0.005). The frequency of LVH was 31.9% in quartile 1 and 11.3% in quartile 4 (p < 0.005) and LVH or DD was 37.5% and 12.7%, respectively (p < 0.001).
Conclusions:
Stroke volume and stroke work were significantly increased while systolic stress and peripheral resistance index were significantly reduced in patients with worst VAC. Ventricular-arterial uncoupling is mostly caused by an increase in Ees rather than by an elevation of Ea. LVH or DD are more frequent in the worst cases of ventricular-arterial uncoupling.
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