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Aims: Hypertensive patients of African ancestry (Afr-a) have higher incidences of heart failure and worse clinical outcomes than hypertensive patients of European ancestry (Eu-a), yet the underlying mechanisms remain misunderstood. This study investigated right (RV) and left (LV) ventricular remodelling alongside myocardial tissue derangements between Afr-a and Eu-a hypertensives., Methods and Results: 63 Afr-a and 47 Eu-a hypertensives underwent multi-parametric cardiovascular magnetic resonance. Biventricular volumes, mass, function, mass/end-diastolic volume (M/V) ratios, T2 and pre-/post-contrast T1 relaxation times, synthetic extracellular volume, and myocardial fibrosis (MF) were measured. 3D shape modelling was implemented to delineate ventricular geometry. LV and RV mass (indexed to body-surface-area) and M/V ratio were significantly greater in Afr-a than Eu-a hypertensives (67.1 ± 21.7 vs. 58.3 ± 16.7 g/m2, 12.6 ± 3.48 vs. 10.7 ± 2.71 g/m2, 0.79 ± 0.21 vs. 0.70 ± 0.14 g/mL, and 0.16 ± 0.04 vs. 0.13 ± 0.03 g/mL, respectively; P < 0.03). Afr-a patients showed greater basal interventricular septum thickness than Eu-a patients, influencing LV hypertrophy and RV cavity changes. This biventricular remodelling was associated with prolonged T2 relaxation time (47.0 ± 2.2 vs. 45.7 ± 2.2 ms, P = 0.005) and higher prevalence (23% vs. 4%, P = 0.001) and extent of MF [2.3 (0.6-14.3) vs. 1.6 (0.9-2.5) % LV mass, P = 0.008] in Afr-a patients. Multivariable linear regression showed that modifiable cardiovascular risk factors and greater end-diastolic volume, but not ethnicity, were independently associated with greater LV mass., Conclusion: Afr-a hypertensives had distinctive biventricular remodelling, including increased RV mass, septal thickening and myocardial tissue abnormalities compared with Eu-a hypertensives. From this study, modifiable cardiovascular risk factors and ventricular geometry, but not ethnicity, were independently associated with greater LV myocardial mass., Competing Interests: Conflict of interest: P.-G.M. is a consultant at Perspectum Diagnostics Ltd (Oxford, UK), (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Objectives: Sympathetic activation has a role in the development of left ventricular hypertrophy (LVH). The presynaptic α(2C)-adrenoceptor inhibits the release of norepinephrine from sympathetic nerve terminals in the heart. A deletion polymorphism in the α(2C)-adrenoceptor (α(2C)Del322-325) generates a hypofunctional α(2C)-adrenoceptor, which may result in chronic adrenergic signalling. This study aimed to investigate whether the α(2C)Del322-325 polymorphism was associated with an increased prevalence of LVH in patients with systemic hypertension., Methods: Left ventricular mass was measured in 205 patients with systemic hypertension and 60 normal volunteers using a 1.5-T Philips MRI system. Genotyping was performed using a restriction fragment length polymorphism assay., Results: No significant difference was observed between the distribution of the α(2C)Del322-325 genotypes in hypertensive patients with LVH compared with those without LVH. Adjusting for confounding variables the odds ratio (OR) of being ins/del for the α(2C)Del322-325 and having LVH was 0.49 (95% CI 0.14-1.69, p = 0.256)., Conclusions: These observations suggest that there is little evidence for an association between α(2C)Del322-325 polymorphism and an increased prevalence of LVH in patients with systemic hypertension.

LVH [LV (left ventricular) hypertrophy] is an independent risk factor for CHD (coronary heart disease). During LVH, the preferred cardiac energy substrate switches from FAs (fatty acids) to glucose. LPL (lipoprotein lipase) is the key enzyme in triacylglycerol (triglyceride) hydrolysis and supplies FAs to the heart. To investigate whether substrate utilization influences cardiac growth and CHD risk, we examined the association between the functional LPL S447X (rs328) variant and hypertension-induced LV growth and CHD risk. LPL-X447 has been shown to be more hydrolytically efficient and would therefore release more free FAs than LPL-S477. In a cohort of 190 hypertensive subjects, LPL X447 was associated with a greater LV mass index [85.2 (1.7) in S/S compared with 91.1 (3.4) in S/X+X/X; P=0.01], but no such association was seen in normotensive controls (n=60). X447 allele frequency was higher in hypertensives with than those without LVH {0.14 [95% CI (confidence interval), 0.08-0.19] compared with 0.07 (95% CI, 0.05-0.10) respectively; odds ratio, 2.52 (95% CI, 1.17-5.40), P=0.02}. The association of LPL S447X with CHD risk was then examined in a prospective study of healthy middle-aged U.K. men (n=2716). In normotensive individuals, compared with S447 homozygotes, X447 carriers were protected from CHD risk [HR (hazard ratio), 0.48 (95% CI, 0.23-1.00); P=0.05], whereas, in the hypertensives, X447 carriers had increased risk [HR, 1.54 (95% CI, 1.13-2.09) for S/S (P=0.006) and 2.30 (95% CI, 1.53-3.45) for X447+ (P<0.0001)] and had a significant interaction with hypertension in CHD risk determination (P=0.007). In conclusion, hypertensive LPL X447 carriers have increased risk of LVH and CHD, suggesting that altered FA delivery constitutes a mechanism through which LVH and CHD are associated in hypertensive subjects.

The presence of left ventricular hypertrophy (LVH) in hypertension, as detected by the electrocardiogram or echocardiography, is associated with an increased risk of mortality and morbidity several times above and beyond the risk of hypertension alone. The LIFE (Losartan Intervention For Endpoint reduction in hypertension) study confirmed that pharmacological agents, which reduce LVH, confer further reduction in morbidity and mortality. This makes the identification of patients with LVH all the more important. In this article we describe the various methods available to diagnose the presence of LVH in patients with hypertension, and consider their strengths and their place in clinical practice and in research.

Purpose: To compare left ventricular mass (LVM) as measured by two-dimensional (2D) echocardiography using two different calculation methods: truncated ellipse (TE) and area length (AL), in both fundamental and tissue harmonic imaging frequencies, to LVM as measured by, the current gold standard, cardiac magnetic resonance imaging (MRI). Turbo gradient echo (TGE) pulse sequence was utilized for MRI., Materials and Methods: Thirty-two subjects with history of hypertension were recruited. The images were acquired, contours were traced and the LVM was calculated for all four different echocardiography methods as well as for the cardiac MRI method. The intra-observer variabilities were calculated. The four different echocardiography methods were compared to cardiac MRI using the method described by Bland and Altman., Results: Twenty-five subjects had adequate paired data sets. The mean LVM as measured by cardiac MRI was 162+/-55 g and for the four different echocardiography methods were: fundamental AL 165+/-55 g, harmonic AL 168+/-53 g, fundamental TE 148+/-50 g, harmonic TE 149+/-45 g. The intra-observer variability for cardiac MRI method, expressed as bias +/- 1 standard deviation of the difference (S.D.D.), was 2.3+/-9.2 g and for the four different echocardiography methods were: fundamental TE 0.4+/-26.8 g, fundamental AL 0.6+/-27.0 g, harmonic TE 6.7+/-21.8 g, harmonic AL 6.4+/-22.9 g. The mean LVM for the AL method was closest to the cardiac MRI technique, while TE underestimated LVM. The 95% limits of agreement were consistently wide for all the 2D echocardiography modalities when compared with the cardiac MRI technique., Conclusion: The intra-observer variability in measurements of 2D echocardiographic LVM, together with the wide limits of agreement when compared to the gold standard (cardiac MRI) are sufficiently large to make serial estimates of LVM, of single patients or small groups of subjects, by 2D echocardiography, unreliable.

A common intronic polymorphism, (-1332 G/A) of the angiotensin type-2 receptor gene, located on the X-chromosome, has been reported to be functional. The aim of our study was to evaluate this polymorphism for an association with left ventricular hypertrophy. Left ventricle (LV) mass was measured in 197 patients with systemic hypertension and 60 normal volunteers using a 1.5-Tesla Philips MRI system. Genotyping was performed using a restriction enzyme digestion of an initial 310-bp polymerase chain reaction product that included the angiotensin type-2 (-1332 G/A) locus. The mean LV mass index for the male patients was 94.3+/-19.6 g/m2 (n=125) and for the female patients was 71.2+/-12.0 g/m2 (n=72). Seventy-three (37.1%) of all patients had an elevated LV mass index, defined as the mean LV mass index for normal volunteers plus 2 SD (males 77.8+/-9.1 g/m2, n=30; females 61.5+/-7.5 g/m2, n=30). Comparison of LV mass index of the A&#95;/AA genotype (mean LV mass index=82.4+/-21.1 g/m2; n=123) against that of the G&#95;/GG genotype (mean LV mass index=88.1+/-19.0 g/m2; n=89) as a continuous variable was significant by ANOVA (P=0.044). chi2 Comparison between subjects with and subjects without left ventricular hypertrophy revealed an excess of the G&#95;/GG genotype among the group with LV hypertrophy (P=0.031). We observed an association between the angiotensin type-2 receptor (-1332 G) allele and the presence of left ventricular hypertrophy in hypertensive subjects.