Impact of the implementation of the Infarction Code strategy in patients with acute myocardial infarction diagnosis in the Hospital de Cardiología of the Centro Médico Nacional Siglo XXI / Impacto de la implementación de Código Infarto en pacientes con infarto agudo de miocardio con elevación del segmento ST en el Hospital de Cardiología del Centro Médico Nacional Siglo XXI.

Objective: To evaluate the impact of the implementation of the Infarction Code strategy in patients with acute myocardial infarction diagnosis. Methods: Consecutive patients with ST-elevation acute myocardial infarction ≤12 hours of evolution, were included in the infarction code strategy, before (Group I) and after (Group II). Times of medical attention and major cardiovascular events during hospitalization were analyzed. Results: 1227 patients were included, 919 men (75%) and 308 women (25%) with an average age of 62 ± 11 years. Among Group I and Group II, percutaneous coronary intervention reperfusion therapy changed (16.6% to 42.6%), fibrinolytic therapy (39.3% to 25%), and patients who did not receive any form of reperfusion therapy (44% to 32.6%; p < 0.0001). Times of medical attention decreased significantly (door-to-needle time decreased from 92 to 72 minutes, p = 0.004; door-to-balloon time decreased from 140 to 92 minutes, p < 0.0001). Kidney failure (24.6% vs. 17.9%; p = 0.006), major complications (35.3% to 29.3%), and death (21% vs. 12%; odds ratio: 0.52; 95% confidence interval: 0.38-0.71; p = 0.004). also decreased. Conclusion: The Infarction Code strategy improved treatment, times of medical attention and decreased complications and death in these patients.

[Obstruction of the right ventricular outflow tract on the obstructive hypertrophic cardiomyopathy. Case report and literature review]. / Obstrucción en la vía de salida del ventrículo derecho en la miocardiopatía hipertrófica obstructiva. Informe de un caso y revisión de la literatura.

OHC is a disorder with a broad spectrum of morphological, functional and genetics abnormalities. The Obstruction on the Right Ventricular Outflow (OHCRV) is not expected most of the time, that's way it is not usually detected and rarely mentioned in the cardiological literature. Its clinical presentation may include basically systemic venous hypertension symptoms that come with the hypertrophic cardyomiopathy manifestations. The manifestations of an apparent Right Ventricular Hypertrophic (RVH) in the ECG are probably due to the huge septal vector that activates the septum with a major thickness. The clinical confirmation of the obstruction on the OHCRV produced by a considerable asymmetric septal hypertrophic is easily shown with bidimensional an Doppler echocardiography.

[Calculated pulmonary vascular resistance, is definitively a worthless variable. Current methods for a better definition]. / La resistencia vascular pulmonar "calculada". Un parámetro incierto para la valoración de la circulación pulmonar. Los métodos actuales para determinarla.

The term pulmonary vascular resistance [PVR] describes, in part, the forces opposing the flow across the pulmonary vascular bed. The equation traditionally used is based on the assumption that the pulmonary capillaries, as well as some others vessels in series behave like a Poiseuille resistance. This assumption implies a laminar type of flow of a homogeneous Newtonian fluid, however blood is not a Newtonian fluid and flow is pulsatile in the pulmonary circulation. Neglecting these factors [which only slightly undermines the application of the equation] and others as well [like distension and recruitment of the vessels], will, however, not give us a true clinically practical solution for the calculation of PVR, because the concept of the equation is only true or partially true for part of the pulmonary circulation. In other parts of the lung, flow depends mainly on the behaviour of capillaries as a Starling resistor. If we considered always pulmonary venous pressure [measured clinically as left atrial pressure or pulmonary wedge pressure] as the effective downstream pressure for the calculation of PVR and we ignore or disregard the existence of a significant "critical closing pressure" [whatever the cause] in the lung it will lead to additional erroneous concept regarding PVR calculations and, in addition for the real hemodynamic conditions of the pulmonary vascular bed. Because, at least two different models of perfusion exist in the lung it is inadmissible from a theoretical point of view to calculate PVR, based on only in one of these models. According to the present knowledge of the pulmonary circulation hemodynamics, an improved definition for the PVR could be obtained: 1. by a multipoint pulmonary vascular pressure/flow plot at high flows and 2. with the use of the pulmonary artery occlusion pressure [PAOP] in addition to the determination of the pulmonary wedge pressure technique [PWP], in order to establish the estimated downstream pressure of the pulmonary circulation at zero flow. Therefore, pulmonary hemodynamic determinations of the PVR are better defined with the analysis of the pressure-flow relationships in addition to the information derived from the PAOP/PWP measurements. However, if none of the previous pressure-flow relationships [in order to obtain the slope = PVR at high flows] or the effective downstream pressure measurements [in order to estimate the critical closing pressure at zero flow] are applied for the analysis of the pulmonary circulation, a cautious interpretation of the measured variables [mean pulmonary artery pressure and cardiac output] is preferable to wrong conclusions made from a meaningless variable, the "calculated PVR".

La resistencia vascular pulmonar calculada. Un parámetro incierto para la valoración de lacirculación pulmonar. Los métodos actuales para determinarla / Calculated pulmonary vascular resistance, is definitively a worthless variable. Current methods for a better definition

The term pulmonary vascular resistance [PVR] describes, in part, the forces opposing the flow across the pulmonary vascular bed. The equation traditionally used is based on the assumption that the pulmonary capillaries, as well as some others vessels in series behave like a Poiseuille resistance. This assumption implies a laminar type of flow of a homogeneous Newtonian fluid, however blood is not a Newtonian fluid and flow is pulsatile in the pulmonary circulation. Neglecting these factors [which only slightly undermines the application of the equation] and others as well [like distension and recruitment of the vessels], will, however, not give us a true clinically practical solution for the calculation of PVR, because the concept of the equation is only true or partially true for part of the pulmonary circulation. In other parts of the lung, flow depends mainly on the behaviour of capillaries as a Starling resistor. If we considered always pulmonary venous pressure [measured clinically as left atrial pressure or pulmonary wedge pressure] as the effective downstream pressure for the calculation of PVR and we ignore or disregard the existence of a significant [quot ]critical closing pressure[quot ] [whatever the cause] in the lung it will lead to additional erroneous concept regarding PVR calculations and, in addition for the real hemodynamic conditions of the pulmonary vascular bed. Because, at least two different models of perfusion exist in the lung it is inadmissible from a theoretical point of view to calculate PVR, based on only in one of these models. According to the present knowledge of the pulmonary circulation hemodynamics, an improved definition for the PVR could be obtained: 1. by a multipoint pulmonary vascular pressure/flow plot at high flows and 2. with the use of the pulmonary artery occlusion pressure [PAOP] in addition to the determination of the pulmonary wedge pressure technique [PWP], in order to establish the estimated downstream pressure of the pulmonary circulation at zero flow. Therefore, pulmonary hemodynamic determinations of the PVR are better defined with the analysis of the pressure-flow relationships in addition to the information derived from the PAOP/PWP measurements. However, if none of the previous pressure-flow relationships [in order to obtain the slope = PVR at high flows] or the effective downstream pressure measurements [in order to estimate the critical closing pressure at zero flow] are applied for the analy.

Obstrucción en la vía de salida del ventrículo derecho en la miocardiopatía hipertrófica obstructiva. Informe de un caso y revisión de la literatura / Obstruction of the right ventricular outflow tract on the obstructive hypertrophic cardiomyopathy. Case report and literature review

OHC is a disorder with a broad spectrum of morphological, functional and genetics abnormalities. The Obstruction on the Right Ventricular Outflow (OHCRV) is not expected most of the time, that's way it is not usually detected and rarely mentioned in the cardiological literature. Its clinical presentation may include basically systemic venous hypertension symptoms that come with the hypertrophic cardyomiopathy manifestations. The manifestations of an apparent Right Ventricular Hypertrophic (RVH) in the ECG are probably due to the huge septal vector that activates the septum with a major thickness. The clinical confirmation of the obstruction on the OHCRV produced by a considerable asymmetric septal hypertrophic is easily shown with bidimensional an Doppler echocardiography.

Disminución de hemorragias totales con dosis reducidas de enoxaparina en angina inestable de alto riesgo / Estudio ENHNFAI. (ENoxaparina vs Heparina No Fraccionada en Angina inestable). Informe preliminar. Decrease of total hemorrhage with reduced doses of enoxaparin in high risk unstable angina. ENHNFAI study. (Enoxaparin vs non-fractionated heparin in unstable angina). Preliminary report

In this prospective, randomized and controlled study, we compare complications in 2 groups of patients: group 1, enoxaparin 0.8 mg/kg, subcutaneous every 12 hours during 5 days, and group 2, intravenous unfractionated heparin during 5 days, by infusion treated to activate partial tromboplastin time 1.5-2 the upper limit of normal. Blood samples were obtained at 4, 12, 24 hours and at day 5 of treatment, to measure anti-Xa levels, and also, evaluated end points at 30 days, between groups. Univariate and multivariate logistic regression analyses were performed with clinical and angiographic variables between groups, with p < 0.05. RESULTS: 203 consecutive patients, average age of 60.5 +/- 11.2 years, and 80 men, were included. There were no differences in clinical and angiographic characteristics. All patients with enoxaparin had therapeutic levels of anti-Xa, of 0.5 to 0.67 U/mL. There was increasing risk of total bleeding in group 2 (18.7) than in group 1 (5.6), with RR = 1.72 (95 CI 1.29, 2.29), p = .003. Also, there was 33.3 of MACE in group 2, and only 17.8 in group 1, with RR = 1.88 (CI 95 1.29, 2.29), p = .011. CONCLUSIONS: 1) Low doses of enoxaparine achieve therapeutic levels, since the first 4 hours of treatment. 2) A significant reduction of total bleeding occurred with the low doses of enoxaparin, with the same efficacy to reduce MACE during follow-up.

Hipertensión arterial en México: Resultados de la Encuesta Nacional de Salud (ENSA) 2000 / Arterial hypertension in Mexico: results of the National Health Survey 2000

AIMS: Hypertension remains as a major cause of cardiovascular morbidity in MÚxico. The Health National Survey 2000 of MÚxico was performed to analyze the current status of the prevalence of some risk factors such as diabetes, hypertension (HTA), obesity, smoking, and proteinuria. METHODS: A National Survey was carried out in MÚxico where 45,300 individuals between 20 to 69-y.o. were screened. The estimated sample size was calculated considering the total number of persons into the mentioned age; a minimal prevalence of 6 of the included risk factors, at a significance level of 0.05; a maximum relative error of 0.145, and a rate of response of at least 70. Diagnosis of HTA was accepted in: previous medical diagnosis with prescription of antihypertensive drugs, or high blood pressure (> or = 140/90 mmHg) detected during the interview. Data were adjusted for the national distribution of age-groups and gender (established in 2000, INEGI). RESULTS: 38,377 (98.8) individuals were correctly screened for blood pressure. The prevalence of hypertension in MÚxico was 30.05 (34.2 in men and 26.3 in women). The prevalence was directly related with age and gender. The percentage of mexicans with HTA after 50-y.o. is > 50. The prevalence was greater in women after 50-y.o. Among persons with hypertension, treatment was detected in 46 and approximately 20 of them were controlled (< 140/90 mmHg). The percentage of mexicans with HTA who were unaware that they have high blood pressure was 61. The total percentage of HTA controlled was 14.6. The North states had the greater prevalence (approximately 34) of HTA while South states had the lower prevalence (27). The odds ratio (age/sex-adjusted) for HTA were: for diabetes 1.54(CI95, 1.44-1.63); for obesity 2.3 (CI 95, 2.22-2.43); for smoking 1.26 (CI 95, 1.21-1.32). For proteinuria subjects, 40 had HTA. CONCLUSIONS: Around 15 millions of mexicans between 20 to 69-y.o. had hypertension, 60 of them are unaware. The prevalence of hypertension in MÚxico (30.05) has increased. Among persons with hypertension -15 are controlled. The North of MÚxico has the higher prevalence of hypertension. Diabetes, smoking, and obesity increase the risk of hypertension. The 2000 National Survey of Health shows the epidemiological trend in several important chronic diseases in MÚxico and declare an urgent need of new strategies for detection, control and treatment of hypertension.