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Articles by T. G Yandle
Total Records ( 4 ) for T. G Yandle
  K. L Ellis , A. P Pilbrow , C. M Frampton , R. N Doughty , G. A Whalley , C. J Ellis , B. R Palmer , L Skelton , T. G Yandle , S. C Palmer , R. W Troughton , A. M Richards and V. A. Cameron

Chromosome 9p21.3 (chr9p21.3) recently was identified by several genome-wide association studies as the genomic region most strongly associated with the risk of coronary artery disease. Within the chr9p21.3 locus, the single-nucleotide polymorphism rs1333049 has been demonstrated to be most strongly associated with susceptibility to developing coronary artery disease. However, the effect of rs1333049 on clinical outcomes in patients with established coronary disease has yet to be determined.

Methods and Results—

Coronary Disease Cohort Study (CDCS) (n=1054) and Post-Myocardial Infarction (PMI) (n=816) study participants were genotyped for rs1333049. Clinical history, circulating lipids, neurohormones, cardiac function, and discharge medications were documented. All-cause mortality and cardiovascular hospital readmissions were recorded over a median follow-up period of 4.0 years for the CDCS cohort and 9.1 years for the PMI cohort. The CDCS patients homozygous for the high-risk C allele had an age of onset 2 to 5 years earlier for coronary disease (P=.005), angina (P=.025), myocardial infarction (P=.022), and percutaneous transluminal coronary angioplasty (P=.009). Patients with the CC genotype also had higher levels of total cholesterol (P=.033) and triglycerides (P=.003). The PMI participants with the CC genotype were 3 years younger on admission (P=.009). Cox proportional hazards analysis adjusting for established predictors of increased risk showed no significant association between rs1333049 genotype and mortality in either the CDCS (P=.214) or the PMI (P=.696) cohorts.


The chr9p21.3 polymorphism rs1333049 was associated with an earlier age of disease onset in 2 coronary disease cohorts but not with poorer clinical outcome in either cohort.

  S. P Wright , R. N Doughty , C. M Frampton , G. D Gamble , T. G Yandle and A. M. Richards

Background— The urocortins are emerging as potentially important contributors to neurohumoral regulation of the circulation with recent reports attributing a powerful array of hemodynamic, renal, and neurohumoral effects to the urocortins in cardiac failure. These peptides also seem to have cardioprotective effects in the setting of ischemia-reperfusion. Little is known concerning the plasma concentrations of the urocortins in health and disease. We have investigated plasma urocortin 1 as a potential diagnostic marker of heart failure and documented its relationships to symptoms, measures of cardiac function, and concurrent levels of other circulating neurohormones.

Methods and Results— In 299 patients with recent onset dyspnea or peripheral edema presenting to primary care, plasma urocortin 1 and other vasoactive hormones were assayed, and echocardiography was performed. Heart failure was present in 74 patients (25%) according to predefined diagnostic criteria. Urocortin 1 levels were increased in patients with heart failure and were related to functional class, clinical signs of heart failure, echocardiographic indicators of left ventricular dimensions and function, plasma creatinine, and concurrent circulating levels of plasma natriuretic peptides, adrenomedullin, and endothelin 1.

Conclusions— Plasma urocortin 1 is elevated in heart failure (in proportion to the degree of cardiac dysfunction) in concert with the generalized neurohormonal activation seen in this condition. Urocortin levels predict heart failure independent of age, history of previous myocardial infarction, diabetes, hypertension, fractional shortening, and N-terminal prohormone brain natriuretic peptide levels.

  Y. H Chen , T. G Yandle , A. M Richards and S. C. Palmer

Background: The sources of secretion and clearance of plasma urotensin II (UII) in the human circulation remain uncertain and may be relevant to understanding the role of UII in human physiology and cardiovascular disease.

Methods: In 94 subjects undergoing clinically indicated cardiac catheterization, we collected blood samples from arterial and multiple venous sites to measure transorgan gradients of plasma UII immunoreactivity.

Results: Net UII release occurred (in descending order of proportional transorgan gradient) across the heart, kidney, head and neck, liver, lower limb, and pulmonary circulations (P < 0.01). Although no specific clearance site was localized, the absence of an overall subdiaphragmatic aorto-caval peptide gradient indicated that there were lower body segment sites of UII clearance as well as secretion. The proportional increase in UII immunoreactivity was significantly correlated across all sites of net peptide release within an individual (P ≤ 0.05). In univariate analyses, mixed venous UII concentrations were correlated with diagnosis of acute coronary syndrome and femoral artery oxygen tension and inversely with systolic blood pressure and body mass index. Diagnosis of acute coronary syndrome and body mass index were independent predictors of mixed venous UII immunoreactivity in multivariate analysis. No correlates of net cardiac UII release were identified.

Conclusions: UII is secreted from the heart and multiple other tissues into the circulation. Related increments in UII immunoreactivity across multiple tissue sites suggest that peptide release occurs via a shared mechanism. Increased UII immunoreactivity is observed in subjects with acute coronary syndrome.

  S. C Palmer , T. G Yandle , C. M Frampton , R. W Troughton , M. G Nicholls and A. M. Richards

To determine whether combined renal and cardiac function after acute myocardial infarction (MI) predicts 10 year mortality and heart failure (HF).

Methods and results

Estimated glomerular filtration rate (eGFR), plasma amino terminal pro-brain natriuretic peptide (NT-proBNP), and radionuclide ventriculography were obtained in 1063 patients with MI between 24–96 h of symptom onset. Mortality and HF were documented over follow-up of 9.3 years. Estimated GFR, NT-proBNP, and left ventricular ejection fraction (LVEF) each independently predicted 10 year mortality. Reduced eGFR (below 60 mL/min/1.73 m2) combined with increased NT-proBNP (above 1000 pg/mL) was associated with higher mortality rate compared with preserved eGFR together with lower NT-proBNP (60 vs. 14%, P < 0.001). Similar results for mortality were identified for eGFR combined with LVEF (dichotomized about 50%) (58 vs. 17%, P < 0.001). Corresponding analysis combining eGFR and NT-proBNP to predict HF yielded rates of 34 and 7% for high- and low-risk groups, respectively (P < 0.001). Similar risk stratification for HF was observed when combining eGFR with LVEF (35 vs. 7%, P < 0.001).


Ten year rates of mortality and HF are 5–10 times higher when lower eGFR is present together with increased NT-proBNP or depressed LVEF.

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