Role of diastolic dyssynchrony in the delayed relaxation pattern of left ventricular filling
Malcolm I Burgess1, Zhi You Fang, Thomas H Marwick
1University of Queensland, Department of Medicine, Level 4, Princess Alexandra Hospital, Ipswich Rd, Brisbane, QLD 4120 Australia. mburgess@soms.uq.edu.au
Insights
Reduced myocardial lengthening, not diastolic dyssynchrony, is the primary cause of delayed left ventricular filling in diabetic patients. This finding impacts understanding of exercise capacity limitations in this population.
Area of Science:
- Cardiology
- Diabetology
- Physiology
Background:
- Diabetic cardiomyopathy is characterized by diastolic dysfunction.
- Delayed left ventricular relaxation impairs exercise capacity.
- The relative contributions of myocardial lengthening and diastolic dyssynchrony are unclear.
Purpose of the Study:
- To determine the extent to which diastolic dyssynchrony contributes to delayed left ventricular filling.
- To investigate the role of diastolic dyssynchrony in limiting exercise capacity in patients with diabetes.
Main Methods:
- 100 diabetic patients with preserved systolic function were studied.
- Measurements included early diastolic tissue lengthening and diastolic dyssynchrony.
- Patients were categorized based on transmitral flow patterns into normal filling and delayed relaxation groups.
Main Results:
- Patients with delayed relaxation showed reduced myocardial lengthening and increased diastolic dyssynchrony.
- Myocardial lengthening was the sole predictor of delayed relaxation.
- Lengthening indices correlated better with exercise capacity than diastolic dyssynchrony measures.
Conclusions:
- Reduced myocardial lengthening plays a more significant role in delayed relaxation than diastolic dyssynchrony in this patient group.
- These findings offer insights into diastolic dysfunction mechanisms in diabetes.
- Understanding these mechanisms can guide therapeutic strategies for improving exercise capacity.
Abstract:
We investigated the extent to which diastolic dyssynchrony contributes to the delayed relaxation pattern of left ventricular filling and limitation in exercise capacity. In 100 patients with diabetes, preserved left ventricular systolic function, normal filling pressure, and no coronary disease, we measured magnitude of early diastolic tissue lengthening (tissue velocity and strain rate) and diastolic dyssynchrony (SD in QRS to peak early diastolic tissue velocity interval across 4 basal myocardial segments). From transmitral flow patients were divided into those with normal filling (50 patients) and delayed relaxation (50 patients). Myocardial lengthening was reduced and SD in interval from QRS onset to peak early diastolic tissue velocity across all segments was higher in patients with delayed relaxation compared with control patients. Myocardial lengthening was the only predictor of delayed relaxation and correlation with exercise capacity was better for lengthening indices than SD in interval from QRS onset to peak early diastolic tissue velocity across all segments. Therefore, in this group a reduced rate of myocardial lengthening plays a more important role in delayed relaxation than diastolic dyssynchrony.
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