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Decreased circulating endothelial progenitor cell levels and function in essential hypertensive patients with
Ching-Wei Lee1, Po-Hsun Huang, Shao-Sung Huang
1Division of Cardiology, Taipei Veterans General Hospital, Taipei, Taiwan.
Insights
Hypertensive patients with left ventricular hypertrophy (LVH) show reduced endothelial progenitor cells (EPCs) and impaired EPC function. These findings link LVH to endothelial injury in cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Hypertension Studies
- Endothelial Biology
Background:
- Essential hypertension is a major risk factor for cardiovascular disease.
- Left ventricular hypertrophy (LVH) is a common complication of hypertension.
- Endothelial dysfunction plays a critical role in the pathogenesis of hypertensive cardiovascular complications.
Purpose of the Study:
- To investigate the association between electrocardiographic left ventricular hypertrophy (LVH) and circulating endothelial progenitor cells (EPCs) in hypertensive patients.
- To evaluate the levels of endothelial apoptotic microparticles in hypertensive patients with and without LVH.
- To explore the role of EPCs and microparticles in the pathophysiology of hypertensive LVH.
Main Methods:
- Flow cytometry was used to quantify circulating EPC markers (CD34(+)CD133(+), CD34(+)KDR(+)) and endothelial apoptotic microparticles (CD31(+)/annexin V(+)).
- LVH was diagnosed using electrocardiogram (ECG) based on the Cornell voltage criteria.
- Peripheral blood samples were analyzed from 128 hypertensive patients (21 with LVH, 107 without LVH).
Main Results:
- Hypertensive patients with LVH exhibited significantly decreased circulating EPC numbers and impaired EPC adhesive function compared to those without LVH.
- While endothelial apoptotic microparticles were numerically higher in the LVH group, the difference was not statistically significant.
- Patients with LVH had a higher urine albumin excretion rate than those without LVH.
Conclusions:
- Electrocardiographic evidence of LVH in essential hypertension is associated with reduced circulating EPC numbers and function.
- These alterations in EPCs may contribute to the endothelial injury observed in hypertensive patients with LVH.
- The findings provide insights into the pathogenetic mechanisms linking hypertension, LVH, and cardiovascular disease.
Abstract:
The aim of this study was to explore the role of circulating endothelial progenitor cells (EPCs) and endothelial apoptotic microparticles in hypertensive patients with and without electrocardiographic left ventricular hypertrophy (LVH). Flow cytometry was used to assess endothelial cell apoptosis and circulating EPC level by quantification of circulating EPC markers (defined as CD34(+)CD133(+), CD34(+)KDR(+)) and endothelial apoptotic microparticles (defined as CD31(+)/annexin V(+)) in peripheral blood samples. The LVH was defined by ECG with the Cornell voltage criteria. In total, 128 hypertensive patients (83 men and 45 women, aged 59±14 years) were enrolled in this study, in which 107 patients (84%) showed no electrocardiographic evidence of LVH, and 21 patients (16%) fulfilled the LVH criteria by ECG. There were no significant differences in basic characteristics between the two groups, but hypertensive patients with LVH had a higher urine albumin excretion rate than those without LVH (P=0.027). Furthermore, hypertensive patients with LVH were shown to have decreased circulating EPC numbers (all P<0.05) and adhesive function compared with those without LVH (LVH vs. no LVH: 14±6 vs. 30±6 cells per high-power field, P<0.001). Increased numbers of endothelial apoptotic microparticles were noted in hypertensive patients with LVH (4.2±4.9 vs. 2.4±3.4%, P=0.115), although the difference was not significant. This study showed that essential hypertensive patients with electrocardiographic LVH evidence have decreased circulating EPC numbers and adhesive function compared with those without LVH. These findings may explain the pathogenetic processes that link hypertensive LVH and endothelial injury in cardiovascular disease.
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