Algorithm for identifying and separating beats from arterial pulse records

BACKGROUND: This project was designed as an epidemiological aid-selecting tool for a small country health center with the general objective of screening out possible coronary patients. Peripheral artery function can be non-invasively evaluated by impedance plethysmography. Changes in these vessels appear as good predictors of future coronary behavior. Impedance plethysmography detects volume variations after simple occlusive maneuvers that may show indicative modifications in arterial/venous responses. Averaging of a series of pulses is needed and this, in turn, requires proper determination of the beginning and end of each beat. Thus, the objective here is to describe an algorithm to identify and separate out beats from a plethysmographic record. A secondary objective was to compare the output given by human operators against the algorithm. METHODS: The identification algorithm detected the beat's onset and end on the basis of the maximum rising phase, the choice of possible ventricular systolic starting points considering cardiac frequency, and the adjustment of some tolerance values to optimize the behavior. Out of 800 patients in the study, 40 occlusive records (supradiastolic- subsystolic) were randomly selected without any preliminary diagnosis. Radial impedance plethysmographic pulse and standard ECG were recorded digitizing and storing the data. Cardiac frequency was estimated with the Power Density Function and, thereafter, the signal was derived twice, followed by binarization of the first derivative and rectification of the second derivative. The product of the two latter results led to a weighing signal from which the cycles' onsets and ends were established. Weighed and frequency filters are needed along with the pre-establishment of their respective tolerances. Out of the 40 records, 30 seconds strands were randomly chosen to be analyzed by the algorithm and by two operators. Sensitivity and accuracy were calculated by means of the true/false and positive/negative criteria. Synchronization ability was measured through the coefficient of variation and the median value of correlation for each patient. These parameters were assessed by means of Friedman's ANOVA and Kendall Concordance test. RESULTS: Sensitivity was 97% and 91% for the two operators, respectively, while accuracy was cero for both of them. The synchronism variability analysis was significant (p < 0.01) for the two statistics, showing that the algorithm produced the best result. CONCLUSION: The proposed algorithm showed good performance as expressed by its high sensitivity. The correlation analysis demonstrated that, from the synchronism point of view, the algorithm performed the best detection. Patients with marked arrhythmic processes are not good candidates for this kind of analysis. At most, they would be singled out by the algorithm and, thereafter, to be checked by an operator

Modulation of 11β-hydroxysteroid dehydrogenase as a strategy to reduce vascular inflammation

Atherosclerosis is a chronic inflammatory disease in which initial vascular damage leads to extensive macrophage and lymphocyte infiltration. Although acutely glucocorticoids suppress inflammation, chronic glucocorticoid excess worsens atherosclerosis, possibly by exacerbating systemic cardiovascular risk factors. However, glucocorticoid action within the lesion may reduce neointimal proliferation and inflammation. Glucocorticoid levels within cells do not necessarily reflect circulating levels due to pre-receptor metabolism by 11β-hydroxysteroid dehydrogenases (11β-HSDs). 11β-HSD2 converts active glucocorticoids into inert 11-keto forms. 11β-HSD1 catalyses the reverse reaction, regenerating active glucocorticoids. 11β-HSD2-deficiency/ inhibition causes hypertension, whereas deficiency/ inhibition of 11β-HSD1 generates a cardioprotective lipid profile and improves glycemic control. Importantly, 11β-HSD1-deficiency/ inhibition is atheroprotective, whereas 11β-HSD2-deficiency accelerates atherosclerosis. These effects are largely independent of systemic risk factors, reflecting modulation of glucocorticoid action and inflammation within the vasculature. Here, we consider whether evidence linking the 11β-HSDs to vascular inflammation suggests these isozymes are potential therapeutic targets in vascular injury and atherosclerosis

Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms

Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10(-8), in fixed-effects meta-analysis) from 15 genomic regions, including SNPs in or near genes involved in cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315). Correlation of these regions with cell-type-specific gene expression and plasma protein levels sheds light on potential disease mechanisms.J.D. is a British Heart Foundation Professor, European Research Council Senior Investigator and NIHR Senior Investigator. J.D.E. and A.D.J. were supported by NHLBI Intramural Research Program funds. N.F. is supported by R21HL123677-01 and R56 DK104806-01A1. N.S. is supported by the British Heart Foundation and is an NIHR Senior Investigator. T.L.A. is supported by NIH career development award K23DK088942. This work was funded by the UK Medical Research Council (G0800270), the British Heart Foundation (SP/09/002), the UK National Institute for Health Research Cambridge Biomedical Research Centre, the European Research Council (268834), European Commission Framework Programme 7 (HEALTH-F2-2012-279233) and Pfizer. The eQTL database construction was supported by NHLBI intramural funds

Factores de riesgo para la enfermedad coronaria temprana en mujeres

Introducción. La enfermedad coronaria es la causa principal de muerte en las mujeres; por esta razón, es prioritario el control del riesgo cardiovascular. Los estudios recientes sugieren una relación entre las alteraciones de la gestación y la enfermedad coronaria; sin embargo, esta hipótesis no ha sido evaluada en la población de mujeres latinoamericanas. Objetivo. Identificar la asociación de riesgo que existe entre la enfermedad coronaria prematura y las alteraciones de la gestación en una población de mujeres colombianas. Materiales y métodos. Es un estudio de casos y controles. Se consideraron casos a las mujeres menores de 55 años sometidas a nueva irrigación quirúrgica o percutánea, y los controles fueron mujeres menores de 55 años con diagnóstico de coronarias sanas por angiografía. Resultados. Se incluyeron 200 pacientes, 100 con coronarias sanas y 100 con enfermedad coronaria, con edad promedio de 46,5±4,3 y 49,5±3,7 años, respectivamente. El análisis univariado mostró asociación entre la enfermedad coronaria y los antecedentes de preeclampsia, partos prematuros, recién nacidos de bajo peso, diabetes mellitus, dislipidemia y tabaquismo. El análisis multivariado mostró persistencia de la asociación con partos pretérmino (OR=6,05; IC95% 2,3-15; p=0,00), dislipidemia (OR=4,09; IC95% 2,1-7,8; p=0,00) y tabaquismo (OR=1,7; IC95% 0,93-3,2; p=0,08). La práctica de actividad física regular se encontró como factor protector (OR=0,5; IC95% 0,27-0,97; p=0,04). Conclusiones. El presente estudio sugiere asociación entre la presencia de enfermedad coronaria prematura y el antecedente de alteraciones de la gestación