Introduction and objetives: The prolongation of ventricular M cell action potential lengthens QT, increases the supernormal phase and propitiates death by electrocution; however, it is not possible to identify the patient who is at risk. Because the descending branch of the T-wave in the area principally affected, the possibility of arrythmogenic risk could be identified by the relative duration of the T descending branch is worth considering. Material and methods: Electrocardiograms of patients in sinusal rhythm, with a cardiac frequency between 60 and 100 p/m, QRS lower than 0.100 s. and without myocardial infarction o medication affecting repolarization were analyzed. The R-R, QT, QRS and the descending branch of the T-wave (rdT) were measured. QRS was subtracted from QT (JT), rdT was divided by JT and multiplied by 100. QTc was calculated. Groups were separated according to QTc duration between 0.350 and 0.440 o greater (QTc N and QTc L). Histograms were made. Mean, standard deviation, median, mode and interquartile range were calculated. Data was analyzed using the Mann-Withney U test and the Z transformation of the normal curve. Result: There were 100 electrocardiograms of QTc L and 400 of QTc N. The curves were non-parametric with downward bias. There was significant difference (p = 0.002). The interquartile range was similar in 75% of the cases. Z transformation indicated abnormality in rdT/JT = 44. Conclusion: The descending branch of T bigger than 44% of JT is abnormal.

Introducción y objetivo: La prolongación del potencial de acción de las células M ventriculares alarga el QT, aumenta la fase supernormal y propicia la electrocución. Como afecta principalmente a la rama descendente de la onda T, preguntamos ¿difiere la duración relativa de la rama descendente de T en el síndrome de QTc largo? Definir ello aportará las herramientas accesibles al diagnóstico. Material y métodos: Electrocardiogramas en ritmo sinusal con frecuencia cardiaca entre 60 y 100 p/m, QRS menor de 0.100 s., sin infarto del miocardio ni efecto de medicamentos sobre la repolarización. Éstos se analizaron en sentido retrospectivo de efecto hacia factor de riesgo. Medimos el R-R, QT, QRS, y la rama descendente de T, desde la cima hasta la línea isoeléctrica (rdT). Restamos el QRS de QT (JT), dividimos rdT/JT y multiplicamos por 100; calculamos el QTc y separamos grupos según la duración del QTc entre 0.350 y 0.440 (QTc-N) o mayor (QTc-L). Hicimos histogramas y cálculos de la media y desviación estándar, la mediana, la moda y el recorrido intercuartílico. Analizamos con prueba U y transformación Z de la curva total para umbral de normalidad. Resultado: Hubo como resultado cien electrocardiogramas con QTc-L y 400 con QTc-N. Las curvas no fueron paramétricas con sesgo hacia abajo, pero diferentes con p = 0.002. El recorrido intercuartílico fue semejante en 75% y el umbral de normalidad se presentó en 44. Hubo valores de QTc-L a 5 desviaciones estándar. Conclusión: La rama descendente de la onda T igual o mayor a 44% del espacio JT fue anormal.

Purpose: To determine disproportion in thicknesses of the vascular wall and vasa vasorum in eight fragments of human aorta because of the irregular distribution of atherosclerosis in arterial walls. Method: The length and thickness of the wall and its layers were measured and the vasa vasorum were conted. Vascular density, considered as the number of vessels per square millimeter in healthy and diseased areas, was calculated along with mean value, variance, standard deviation and the confidence interval for values and null hypotesis. Variances were analyzed, and the comparative and paired "t" test was applied. Results: There were differences in thicknesses of the healthy (27 :m) and diseased (120.5 :m) intima (p < 0.001) and between the healthy (125.2 :m) and diseased (102.3 :m) media (P < 0.001). Vascular density was higher in healthy fragments (mean ± CI 99% = 4.40 ± 1.4 vs 2.20 ± 0.8, = < 0.001 for Ha; 0 ± 1.0775 for Ho; paired "t" 2.1 ± 1.1, P < 0.01), and higher compared to the healthy intima area (31.6 vs 5.1, P < 0.01). There were no differences compared to the media layer area. The relation between the number of vessels and the length of the vascular segments was greater in the healthy fragments (mean ± CI 95% = 4.9 ± 1.02 vs 3.5 ± 0.68; 1.4 difference, P < 0.05). Conclusion: Vascular density is lower in the atherosclerotic aortic wall than in the healthy aorta and this could initiate the pathologic process.

Antecedente: Por distribución irregular de aterosclerosis en paredes arteriales se buscó desproporción entre grosor de la pared vascular y vasa vasorum en ocho fragmentos de aorta humana. Método: Se midió longitud y grosor de pared y de sus capas y se contó vasa vasorum, se calculó densidad vascular como número de vasos por milímetro cuadrado en áreas sanas y enfermas, valor medio, varianza, desviación estándar e intervalo de confianza para valores y para hipótesis nula, se analizaron varianzas y se aplicó prueba "t" comparativa y pareada. Resultado: Hay diferencias de grosor entre íntima sana (27 micras) y enferma (120.5 micras), P < 0.001; y entre media sana (125.2 micras) y enferma (102.3 micras), P < 0.001. La densidad vascular es mayor en fragmentos sanos (media ± IC 99% = 4.4 ± 1.4 vs 2.2 ± 0.8, P < 0.001 para Ha; 0 ± 1.0775 para Ho; "t" pareada 2.1 ± 1.1, P < 0.01). Mayor ante íntima sana (31.6 vs 5.1, P < 0.01). No varía ante capa media. La relación entre número de vasos y longitud del segmento vascular es mayor en el fragmento sano (media ± IC 95% = 4.9 ± 1.02 vs 3.5 ± 0.68, diferencia 1.4, P < 0.05). Conclusión: La densidad vascular es menor en la pared de aorta aterosclerosa que en aorta sana lo que pudiera iniciar el proceso patógeno.

OBJECTIVE: To assess the prevalence of high blood pressure among young children. MATERIAL AND METHODS: This is a cross-sectional study, conducted in 1992 in Colima City, Mexico. Blood pressure readings were obtained from 400 children aged under 19. Statistical analysis consisted of calculation of means, variance, and Anova by group age. Association between age and blood pressure was assessed with correlation and determination coefficients. Comparisons by sex were made using Student's t, F, Mann-Whitney's U, and Z tests. Percentile 95th was used to define normal figures. RESULTS: A lineal correlation coefficient was found and confirmed by the determination coefficient. Groups where this association was statistically significant at p<0.01 were: a) children aged under 2; b) children from 2 to 13 years of age; and c) those over 13 years of age. High blood pressure figures for each group were: a) 92/50 mm/Hg; 110/70 mm/Hg; and 133/84 mm/Hg, respectively. CONCLUSIONS: The prevalence of high blood pressure in younger children may be 8% for systolic pressure and 9% for diastolic pressure.

OBJETIVO: Estimar la prevalencia de hipertensión arterial en menores de 19 años de Colima, Colima, México. MATERIAL Y MÉTODOS: Estudio transversal realizado en 1992 a partir de las mediciones de la tensión arterial (TA) de 400 menores, distribuidos por sexo y edad. Se calcularon: promedio, varianza y Anova por edad; coeficientes de correlación y determinación entre edad y TA; se compararon los grupos con pruebas t de Student, F y U de Mann-Whitney con Z para sexos seleccionados según la curva de distribución; asimismo, se calculó percentil 95 para definir cifras anormales. RESULTADOS: El coeficiente de correlación es lineal, el de determinación lo confirma, se distinguen con p<0.01 los grupos: a) menores de dos años; b) de 2 a 13 años, y c) mayores de 13 años. Cada grupo se califica como hipertenso con cifras correspondientes de: a) 92/50 mmHg; b) 110/70 mmHg, y c) 133/84 mmHg. CONCLUSIONES: La prevalencia de hipertensión arterial en menores pudiera ser: sistólica 8% y diastólica 9%. La hipertensión arterial resulta frecuente en los menores de edad en la ciudad de Colima y el diagnóstico es accesible.