Key result
Diastolic vortex filling contribution is reduced to ~5% in HCM versus healthy controls.
Why the study?
The contribution of vortex structures to LV diastolic function had never been quantified in vivo, leaving the impact of intraventricular flow patterns on filling and diastolic dysfunction unclear.
Does the diastolic vortex ring contribute differently to left ventricular filling volume in patients with nonischemic dilated cardiomyopathy and hypertrophic cardiomyopathy compared to healthy controls?
Observational (n=60)
Does the diastolic vortex ring contribute differently to left ventricular filling volume in patients with nonischemic dilated cardiomyopathy and hypertrophic cardiomyopathy compared to healthy controls?
Absolute Event Rate: 5% vs 13%
p-value: p=< 0.0001
This study provides the first in vivo quantification showing that the diastolic vortex ring contributes significantly to left ventricular filling, with enhanced contribution in nonischemic dilated cardiomyopathy and severely impaired contribution in hypertrophic cardiomyopathy.
Background Intraventricular fluid dynamics can be assessed clinically using imaging. The contribution of vortex structures to left ventricular (LV) diastolic function has never been quantified in vivo. Objectives This study sought to understand the impact of intraventricular flow patterns on filling and to assess whether impaired fluid dynamics may be a source of diastolic dysfunction. Methods Two-dimensional flow velocity fields from color Doppler echocardiographic sequences were obtained in 20 patients with nonischemic dilated cardiomyopathy (NIDCM), 20 patients with hypertrophic cardiomyopathy (HCM), and 20 control healthy volunteers. Using a flow decomposition method, we isolated the rotational velocity generated by the vortex ring from the surrounding flow in the left ventricle. Results The vortex was responsible for entering 13 ± 6% of filling volume in the control group and 19 ± 8% in the NIDCM group (p = 0.004), but only 5 ± 5% in the HCM group (p < 0.0001 vs. controls). Favorable vortical effects on intraventricular pressure gradients were observed in the control and NIDCM groups but not in HCM patients. Differences in chamber sphericity explained variations in the vortex contribution to filling between groups (p < 0.005). Conclusions The diastolic vortex is responsible for entering a significant fraction of LV filling volume at no energetic or pressure cost. Thus, intraventricular fluid mechanics are an important determinant of global chamber LV operative stiffness. Reduced stiffness in NIDCM is partially related to enhanced vorticity. Conversely, impaired vortex generation is an unreported mechanism of diastolic dysfunction in HCM and probably other causes of concentric remodeling.
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Martínez‐Legazpi et al. (2014) conducted an observational in Nonischemic dilated cardiomyopathy and hypertrophic cardiomyopathy (n=60). Cardiomyopathy (NIDCM and HCM) vs. Healthy control volunteers was evaluated on Percentage of left ventricular filling volume entered by the diastolic vortex ring (p=< 0.0001). The diastolic vortex contributed to 19±8% of LV filling volume in NIDCM (p=0.004) and 5±5% in HCM (p<0.0001) compared with 13±6% in healthy controls.
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