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Articles by P Elliott
Total Records ( 5 ) for P Elliott
  J Stamler , I. J Brown , M. L Daviglus , Q Chan , H Kesteloot , H Ueshima , L Zhao , P Elliott and for the INTERMAP Research Group

Background— Data are available that indicate an independent inverse relationship of dietary vegetable protein to the blood pressure (BP) of individuals. Here, we assess whether BP is associated with glutamic acid intake (the predominant dietary amino acid, especially in vegetable protein) and with each of 4 other amino acids that are relatively higher in vegetable than animal protein (proline, phenylalanine, serine, and cystine).

Methods and Results— This was a cross-sectional epidemiological study with 4680 persons 40 to 59 years of age from 17 random population samples in China, Japan, the United Kingdom, and the United States. BP was measured 8 times at 4 visits; dietary data (83 nutrients, 18 amino acids) were obtained from 4 standardized, multipass, 24-hour dietary recalls and 2 timed 24-hour urine collections. Dietary glutamic acid (percentage of total protein intake) was inversely related to BP. Across multivariate regression models (model 1, which controlled for age, gender, and sample, through model 5, which controlled for 16 possible nonnutrient and nutrient confounders), estimated average BP differences associated with a glutamic acid intake that was higher by 4.72% of total dietary protein (2 SD) were –1.5 to –3.0 mm Hg systolic and –1.0 to –1.6 mm Hg diastolic (z scores –2.15 to –5.11). Results were similar for the glutamic acid–BP relationship with each of the other amino acids also in the model; eg, with control for 15 variables plus proline, systolic/diastolic pressure differences were –2.7/–2.0 mm Hg (z scores –2.51, –2.82). In these 2–amino acid models, higher intake (by 2 SD) of each of the other amino acids was associated with small BP differences and z scores.

Conclusions— Dietary glutamic acid may have independent BP-lowering effects, which may contribute to the inverse relation of vegetable protein to BP.

  K Abozguia , P Elliott , W McKenna , T. T Phan , G Nallur Shivu , I Ahmed , A. R Maher , K Kaur , J Taylor , A Henning , H Ashrafian , H Watkins and M. Frenneaux

Hypertrophic cardiomyopathy patients exhibit myocardial energetic impairment, but a causative role for this energy deficiency in the pathophysiology of hypertrophic cardiomyopathy remains unproven. We hypothesized that the metabolic modulator perhexiline would ameliorate myocardial energy deficiency and thereby improve diastolic function and exercise capacity.

Methods and Results—

Forty-six consecutive patients with symptomatic exercise limitation (peak Vo2 <75% of predicted) caused by nonobstructive hypertrophic cardiomyopathy (mean age, 55±0.26 years) were randomized to perhexiline 100 mg (n=24) or placebo (n=22). Myocardial ratio of phosphocreatine to adenosine triphosphate, an established marker of cardiac energetic status, as measured by 31P magnetic resonance spectroscopy, left ventricular diastolic filling (heart rate normalized time to peak filling) at rest and during exercise using radionuclide ventriculography, peak Vo2, symptoms, quality of life, and serum metabolites were assessed at baseline and study end (4.6±1.8 months). Perhexiline improved myocardial ratios of phosphocreatine to adenosine triphosphate (from 1.27±0.02 to 1.73±0.02 versus 1.29±0.01 to 1.23±0.01; P=0.003) and normalized the abnormal prolongation of heart rate normalized time to peak filling between rest and exercise (0.11±0.008 to –0.01±0.005 versus 0.15±0.007 to 0.11±0.008 second; P=0.03). These changes were accompanied by an improvement in primary end point (peak Vo2) (22.2±0.2 to 24.3±0.2 versus 23.6±0.3 to 22.3±0.2 mL · kg–1 · min–1; P=0.003) and New York Heart Association class (P<0.001) (all P values ANCOVA, perhexiline versus placebo).


In symptomatic hypertrophic cardiomyopathy, perhexiline, a modulator of substrate metabolism, ameliorates cardiac energetic impairment, corrects diastolic dysfunction, and increases exercise capacity. This study supports the hypothesis that energy deficiency contributes to the pathophysiology and provides a rationale for further consideration of metabolic therapies in hypertrophic cardiomyopathy.

Clinical Trial Registration—

URL: Unique identifier: NCT00500552.

  P Elliott , C O'Mahony , P Syrris , A Evans , C Rivera Sorensen , M. N Sheppard , G Carr White , A Pantazis and W. J. McKenna

Idiopathic dilated cardiomyopathy is a familial disorder in 25% to 50% of patients, but the genetic basis in the majority of cases remains unknown. Genes encoding desmosomal proteins, currently regarded as synonymous with another disorder, arrhythmogenic right ventricular cardiomyopathy, are known to cause left ventricular dysfunction, but their importance in unselected patients with unequivocal dilated cardiomyopathy is unknown. The objective of this study was to determine the prevalence of mutations in 5 desmosomal protein genes in patients with dilated cardiomyopathy.

Methods and Results—

We studied 100 unrelated patients with idiopathic dilated cardiomyopathy consecutively referred to a dedicated cardiomyopathy unit. Patients underwent clinical evaluation, ECG, echocardiography, exercise testing, 24-hour ambulatory ECG monitoring, and mutation screening of 5 genes implicated in arrhythmogenic right ventricular cardiomyopathy: plakoglobin, desmoplakin, plakophilin-2, desmoglein-2, and desmocollin-2. Of the 100 patients (mean age at evaluation, 46.8±13.8 years; range, 17.0 to 72.8 years; male sex, 63%), 5 were found to carry pathogenic desmosomal protein gene mutations. An additional 13 patients had sequence variants of uncertain pathogenic significance and were excluded from further comparative analysis. Patients harboring desmosomal gene mutations had a phenotype indistinguishable from the 82 noncarriers, with the exception of exercise-induced ventricular ectopy, which was more frequent in the desmosomal mutation carriers (P=0.033). None of the 5 carriers of desmosomal mutations fulfilled current diagnostic criteria for arrhythmogenic right ventricular cardiomyopathy, but 1 had fibrofatty change in the left ventricle at autopsy.


Heart failure caused by a dilated, poorly contracting left ventricle and arrhythmogenic right ventricular cardiomyopathy have been considered distinct clinicopathologic entities. This study suggests that both clinical presentations can be caused by mutations in desmosomal protein genes.

  R. M Freathy , A. J Bennett , S. M Ring , B Shields , C. J Groves , N. J Timpson , M. N Weedon , E Zeggini , C. M Lindgren , H Lango , J. R.B Perry , A Pouta , A Ruokonen , E Hypponen , C Power , P Elliott , D. P Strachan , M. R Jarvelin , G. D Smith , M. I McCarthy , T. M Frayling and A. T. Hattersley

Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight.


We genotyped single-nucleotide polymorphisms (SNPs) at five recently identified type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC30A8) in 7,986 mothers and 19,200 offspring from four studies of white Europeans. We tested the association between maternal or fetal genotype at each locus and birth weight of the offspring.


We found that type 2 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when inherited by the fetus (21 g [95% CI 11–31], P = 2 x 10–5, and 14 g [4–23], P = 0.004, lower birth weight per risk allele, respectively). The 4% of offspring carrying four risk alleles at these two loci were 80 g (95% CI 39–120) lighter at birth than the 8% carrying none (Ptrend = 5 x 10–7). There were no associations between birth weight and fetal genotypes at the three other loci or maternal genotypes at any locus.


Our results are in keeping with the fetal insulin hypothesis and provide robust evidence that common disease-associated variants can alter size at birth directly through the fetal genotype.

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