Renal dysfunction and diastolic impairment among British ethnic minorities with hypertension: the Ethnic-Echocardiographic Heart of England Screening Study.

Renal dysfunction is frequently associated with left ventricular (LV) hypertrophy and diastolic dysfunction in hypertensive patients. Limited data exist on renal dysfunction and diastolic impairment among British ethnic minorities with hypertension. We studied associations between renal impairment and diastolic dysfunction in hypertensive subjects of African-Caribbean and South Asian origin. Five hundred and ten hypertensive subjects with ejection fraction ⩾55% and with no history of ischaemic heart disease/valve pathology were included from the original population of the Ethnic-Echocardiographic Heart of England Screening Study (E-ECHOES). Diastolic function and cardiac remodelling were measured by echocardiography. LV hypertrophy was common and present in 62% of patients with normal estimated glomerular filtration rate (eGFR, >90 ml min-1 per 1.73 m2), 73% in those with eGFR 60-89 ml min-1 per 1.73 m2 and 87% with eGFR <60 ml min-1 per 1.73 m2. On both univariate and multivariable linear regression, reduced eGFR was associated with higher LV mass index (LVMI, P=0.01 and P=0.039, respectively). On multivariable analyses, increased LVMI (but not eGFR) was an independent predictor of echocardiographic parameters of diastolic dysfunction. Higher LVMI was an independent predictor of all-cause or cardiovascular death on multivariable analyses (both P=0.002), but not eGFR. LV hypertrophy is common in minority ethnic groups with hypertension, especially in the presence of renal dysfunction. Increased LVMI rather than renal impairment per se is a major determinant of diastolic dysfunction and increased risk of cardiovascular or all-cause death among hypertensive patients without end-stage renal failure.

Monocyte-derived and CD34+/KDR+ endothelial progenitor cells in heart failure.

BACKGROUND: Endothelial progenitor cells (EPCs) are known to be altered in heart failure (HF), but monocyte-derived EPCs in HF have not been assessed. We aimed to characterize monocyte-derived EPCs in systolic HF. METHODS AND RESULTS: We recruited 128 subjects with systolic HF: 50 South Asian (SA), 50 white, and 28 African-Caribbean (AC), for interethnic comparisons. Additionally, SAs with HF were compared with 40 SAs with coronary artery disease (CAD) without HF (disease controls [DCs]) and 40 SA healthy controls (HCs). Counts of CD34(+) and kinase domain receptor (KDR)(+) monocytes attributed to specific monocyte subsets (CD14(++) /CD16(-) [Mon1], CD14(++)/CD16(+) [Mon2], and CD14(+)/CD16(++) [Mon3]) and monocyte expression of vascular endothelial growth factor (VEGF) receptor 1 were analyzed by flow cytometry. We also enumerated CD34(+)/KDR(+) EPCs derived from mononuclear cells ('classic' EPC definition). RESULTS: SAs with HF had significantly reduced counts of CD34(+) monocytes, attributed to the Mon1 and Mon2 subsets. KDR(+) Mon1 counts were 4.5-fold increased in DCs as compared with HCs, but significantly reduced in HF subjects vs. DCs. VEGF receptor type 1 expression on Mon1 and Mon2 cells was significantly reduced in HF patients as compared with DCs. Also, CD34(+)/KDR(+) EPC numbers were reduced in HF subjects. Whites had significantly fewer KDR(+) Mon3 cells than ACs, but significantly more CD34(+) Mon2 cells than SAs and ACs. VEGF receptor type 1 expression by Mon1 cells was predictive for left ventricular ejection fraction after adjustment for ethnicity (ß = - 0.25. P = 0.039). CD34(+) Mon2 counts correlated with measures of microvascular endothelial function, and were predictive of the future risk of hospital admission. CONCLUSIONS: Circulating counts of monocyte-derived EPCs are significantly altered in HF, with significant ethnic differences in the levels of monocyte-derived EPCs.