Key result
PAH linked to ~38% lower RV FAC and delayed systolic activation versus healthy controls.
Why the study?
Tissue Doppler imaging provides improved accuracy and reproducibility for quantifying RV function, but RV myocardial systolic activation in PAH patients was not well characterized.
Does Tissue Doppler imaging detect RV myocardial systolic activation delay in patients with pulmonary arterial hypertension compared to healthy volunteers?
Case-Control (n=60)
Does Tissue Doppler imaging detect RV myocardial systolic activation delay in patients with pulmonary arterial hypertension compared to healthy volunteers?
Absolute Event Rate: 35% vs 56%
p-value: p=<0.05
Tissue Doppler imaging reveals significant RV myocardial systolic activation delay in PAH patients, which correlates strongly with reduced RV fractional area change, offering a potential approach to predict RV dysfunction.
BACKGROUND: Tissue Doppler imaging (TDI) has provided an objective means to quantify global and regional left ventricular (LV) and right ventricular (RV) function with improved accuracy and greater reproducibility than conventional echocardiography. This study was conducted to assess RV myocardial systolic activation by TDI in subjects with pulmonary arterial hypertension (PAH). METHODS: A total of 30 patients with PAH and 30 healthy volunteers, all comparable in age and sex, underwent standard Doppler echo and TDI. Using pulsed Doppler echocardiography combined with TDI, the following regional parameters were evaluated in three different myocardial segments (RV basal lateral wall, basal septal, and LV basal lateral) on apical 4-chamber view: systolic (Sm), early- and late-diastolic (Em and Am) peak velocities. RV myocardial systolic activation delay was defined as the difference in time to peak TDI systolic velocities between the RV basal lateral wall and basal septal. In addition, RV end-diastolic and end-systolic areas were measured to calculate RV fractional area change from the same apical 4-chamber view. RESULTS: Compared with the control group, patients with PAH showed increased RA and RV end-diastolic diameter (RA: (4.5 +/- 1.2) cm vs (3.0 +/- 0.8) cm, P < 0.05 and RV: (4.8 +/- 1.9) cm vs (3.4 +/- 0.5) cm, P < 0.05) and reduced RV fractional area change; (35 +/- 14)% vs (56 +/- 9)%, P < 0.05. These PAH patients showed lower myocardial peak velocities and a significant activation delay compared with controls (P < 0.05). Moreover, a strong correlation between RV myocardial systolic activation delay and RV fractional area change was shown in patients with pulmonary arterial hypertension (r = -0.82). CONCLUSIONS: In PAH, RV myocardial systolic activation was markedly delayed, which was directly related to the RV fractional area change. RV myocardial systolic activation delay assessed by TDI could offer a unique approach to predict RV dysfunction.
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You et al. (2007) conducted a case-control in Pulmonary arterial hypertension (n=60). Pulmonary arterial hypertension vs. Healthy volunteers was evaluated on Right ventricular fractional area change (p=<0.05). Pulmonary arterial hypertension was associated with significantly reduced right ventricular fractional area change (35% vs 56%, P<0.05) and delayed myocardial systolic activation compared to controls.
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