Non-dipper hypertension was associated with a higher prevalence of hypertensive heart disease (72% vs 57%) and nephropathy (54% vs 23%) compared to dipper hypertension (p<0.001).
Observational (n=104)
Does left atrial phasic strain analysis predict cardiac and renal target organ damage in dipper and non-dipper hypertensive patients?
Left atrial phasic dysfunction, particularly reduced reservoir strain, is pronounced in non-dipper hypertensives and serves as a robust independent predictor of subclinical cardiac and renal target organ damage.
Absolute Event Rate: 72% vs 57%
p-value: p=<0.001
Abstract Background Non-dipper hypertension is increasingly recognized as a higher-risk phenotype, associated with disproportionate target organ involvement including hypertensive heart disease (HHD) and hypertensive nephropathy (HNP). The phasic mechanical behavior of the left atrium (LA)—including reservoir, conduit, and contraction phases—can now be quantified via speckle tracking echocardiography (STE). Despite this, the additive diagnostic and predictive value of LA phasic strain in dipper and non-dipper hypertensives remains underutilized in clinical stratification models. Purpose To assess alterations in LA phasic function across hypertensive subgroups and determine echocardiographic predictors of HHD and HNP using volumetric and deformation-based LA metrics. Methods A total of 104 individuals were enrolled: 30 normotensive controls, 35 dipper hypertensives, and 39 non-dipper hypertensives. All underwent comprehensive transthoracic echocardiography including 2D-STE. LA diameters, volumetric indices (LAVI), and phasic strain values (LASr: reservoir, LAScd: conduit, LASct: contraction) were measured. Cardiac target organ damage (HHD) was defined by concentric LV remodeling or LV hypertrophy, and renal involvement (HNP) was determined by elevated microalbuminuria (UACR 30 mg/g). Multivariate logistic regression models identified independent predictors of both endpoints. Results Compared to controls and dippers, non-dippers had significantly higher LA diameters (38.2 ± 3.9 mm), indexed volumes (31.5 ± 6.2 mL/m²), and microalbuminuria (87.4 ± 19.9 mg/g), all p 0.001. LA reservoir strain (LASr) was substantially lower in non-dippers (27.0 ± 3.1%) versus dippers (35.4 ± 4.9%) and controls (42.5 ± 6.6%). Similarly, LAScd and LASct followed a graded decrement. The prevalence of HHD and HNP was highest in non-dippers (72% and 54%, respectively), markedly exceeding dippers (57% and 23%, respectively; p 0.001 for both comparisons). Multivariate regression identified LASr (β = -0.127, 95% CI: 0.818–0.932, p 0.001), LA diameter (β = 0.091, 95% CI: 1.044–1.129, p 0.001), and LAVImax (β = 0.094, 95% CI: 1.041–1.121, p = 0.004) as independent predictors of HHD. In predicting HNP, LASr (β = -0.121, 95% CI: 0.832–0.936, p 0.001) and LA diameter (β = 0.087, 95% CI: 1.042–1.139, p 0.001) remained significant, while LAVImax and phasic conduit/contractile parameters did not enter the final model. Conclusion Our findings reveal that LA phasic dysfunction—especially reduced reservoir strain—is pronounced in non-dipper hypertensives and strongly associated with subclinical cardiac and renal involvement. Both LASr and LA diameter emerged as robust, independent predictors of target organ damage. These results underscore the clinical utility of integrating LA phasic strain analysis into standard hypertensive evaluations to better stratify risk and inform therapeutic decision-making in this vulnerable population.Clinical and LA Parameters Across Groups Predictors of HHD and Nephropathy
Seçkin et al. (Thu,) conducted a observational in Hypertension (dipper and non-dipper) (n=104). Non-dipper hypertension vs. Dipper hypertension and normotensive controls was evaluated on Hypertensive heart disease (HHD) (p=<0.001). Non-dipper hypertension was associated with a higher prevalence of hypertensive heart disease (72% vs 57%) and nephropathy (54% vs 23%) compared to dipper hypertension (p<0.001).