Key result
Subclinical left ventricular systolic function (Sa) was independently and inversely associated with the presence of left ventricular systolic dyssynchrony (OR 0.67; 95% CI 0.48-0.93; P=0.018).
Cross-Sectional (n=266)
Subclinical left ventricular systolic function, rather than arterial stiffness or blood pressure parameters, is independently associated with the presence and degree of left ventricular systolic dyssynchrony in treatment-naive hypertensive patients.
Sa inversely associated with dyssynchrony in untreated hypertension; hypothesis-generating and should not yet change practice.
OBJECTIVE: Prevalence of left ventricular systolic dyssynchrony (LVSD) is over 40% in treatment-naive patients with hypertension and it improves after chronic antihypertensive treatment. These findings might support the hypothesis that blood pressure (BP), BP-derived parameters, central BP, or arterial stiffness would contribute to LVSD. Therefore, we aimed to investigate possible factors associated with LVSD in treatment-naive patients with hypertension. METHODS: The study groups consisted of 266 treatment-naive hypertensive patients who underwent anthropometric, clinical, laboratory, echocardiographic, arterial stiffness, central blood pressure, and 24-h ambulatory blood pressure monitoring evaluations. Echocardiographic measurement was recorded as follows: peak systolic velocity (Sa, subclinical left ventricular systolic function), peak early diastolic and late diastolic velocity at the mitral annulus (Ea and Aa, respectively), mitral E/Ea ratio (subclinical left ventricular diastolic function), standard deviation of time from ECG Q to systolic peak velocity of 12 left ventricular segments (Ts-SD12), and maximal difference between peak systolic velocities of any 2 of the 12 segments (Ts-Max). A Ts-SD12 at least 33 or Ts-Max at least 100 ms was regarded as presence of LVSD. RESULTS: Patients were divided into those without LVSD (group 1, n = 151, 56.8%) and those with LVSD (group 2, n = 115, 43.2%). Group 2 had higher E/Ea and high-density lipoprotein and lower Sa and triglyceride than group 1. On multivariate analysis, Sa was independently and inversely associated with the presence of LVSD [odds ratio (OR) 0.67, 95% confidence interval (CI) 0.48-0.93, P = 0.018]. The linear relationship between variables and degree of LVSD showed that serum potassium levels, E/Ea, and Sa remained significant after multivariate analysis (potassium, β = 0.199, P = 0.006; E/Ea, β = 0.211, P = 0.017; Sa, β = -0.301, P < 0.001 in Ts-SD12 and potassium, β=0.187, P = 0.010; E/Ea, β = 0.234, P = 0.008; Sa, β = -0.322, P < 0.001 in Ts-Max, respectively). CONCLUSION: Subclinical left ventricular systolic function is independently associated with both the presence and degree of LVSD in treatment-naive hypertensive patients. Subclinical left ventricular diastolic function and serum potassium levels are independently associated with the degree of LVSD. However, arterial stiffness and BP parameters are not determinants.
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Kwon et al. (2013) conducted a cross-sectional in Treatment-naive hypertension (n=266). Subclinical left ventricular systolic function (peak systolic velocity, Sa) was evaluated on Presence of left ventricular systolic dyssynchrony (LVSD) (OR 0.67, 95% CI 0.48-0.93, p=0.018). Subclinical left ventricular systolic function (Sa) was independently and inversely associated with the presence of left ventricular systolic dyssynchrony (OR 0.67; 95% CI 0.48-0.93; P=0.018).
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