RESUMEN
BACKGROUND: Recent studies have emphasized the importance of perioperative fluid restriction. However, fluid restriction regimens may increase the likelihood of insufficient perioperative fluid administration or may result in excess intravascular crystalloid replacement. We postulate that the use of transesophageal echocardiography may reduce the amount of crystalloid administered during open and laparoscopic colorectal surgery. METHODS: Fifteen ASA I and II patients scheduled for open colorectal surgery, and 15 patients scheduled for laparoscopic surgery were studied. Lactated Ringer's solution was infused during the procedures. Left ventricular end diastolic volume index (LVEDVI) and cardiac index were assessed throughout surgery and used to guide the rate of lactated Ringer's solution administration. Statistical analysis was performed with Student's t-test for unpaired samples. RESULTS: The rate of crystalloid administration required to maintain baseline LVEDVI and cardiac index was 5.9 +/- 2 mL x kg(-1) x h(-1) for open surgery and 3.4 +/- 0.8 mL x kg(-1) x h(-1) for laparoscopic surgery (P < 0.01). This slower rate for laparoscopic surgery was offset by the longer surgical duration. CONCLUSION: The rate of crystalloid solution to maintain baseline LVEDVI and cardiac index was greater in open surgery than laparoscopic surgery, and lower than commonly recommended for colorectal surgery.
Asunto(s)
Volumen Sanguíneo/fisiología , Gasto Cardíaco/efectos de los fármacos , Procedimientos Quirúrgicos del Sistema Digestivo , Fluidoterapia , Soluciones Isotónicas/administración & dosificación , Laparoscopía , Sustitutos del Plasma/administración & dosificación , Anciano , Volumen Cardíaco/efectos de los fármacos , Volumen Cardíaco/fisiología , Colon/cirugía , Soluciones Cristaloides , Ecocardiografía Transesofágica , Efedrina/efectos adversos , Efedrina/uso terapéutico , Femenino , Humanos , Hipovolemia/prevención & control , Soluciones Isotónicas/uso terapéutico , Masculino , Persona de Mediana Edad , Monitoreo Intraoperatorio , Atención Perioperativa , Lactato de Ringer , Vasoconstrictores/administración & dosificación , Vasoconstrictores/uso terapéutico , Función Ventricular Izquierda/fisiologíaRESUMEN
The aim of this study was to analyze by echocardiogram, the action of two Na+/H+ exchange, inhibitors, HOE 642 (HOE) and BIIB 723 (BIIB) on left ventricular (LV) mass and LV systolic function. We studied 16 spontaneously hypertensive rats (SHR), 8 treated with HOE 30 mg/kg/day, 8 with 30 mg/kg/day of BIIB during 30 days and 4 SHR as controls during those 30 days. Results are expressed as mean values +/- SEM. The systolic blood pressure and the echocardiograpic parameters examined did not evidence changes during that period in the controls rats. Even though HOE determined a slight decrease in blood pressure (HOE C: 184 +/- 1.75 mm Hg; HOE 30d: 176.20 +/- 2.60 mm Hg - p < 0.01) which was not detected with BIIB, both drugs provoked an increase of peak systolic stress (HOE C: 166 +/- 29 kdynes/cm2; HOE 30d: 204 +/- 34 kdynes/cm2, p < 0.04; BIIB C: 164 +/- 25.90 kdynes/ cm2; BIIB 30d: 234 +/- 29.30 kdynes/cm2, p < 0.02). HOE and BIIB reduced LV mass after 30 days of administration (HOE C: 612.50 +/- 50 mg; 30d: 452 +/- 37 mg, p < 0.01. BIIB C: 544 +/- 16mg; 30d: 374 +/- 25 mg, p < 0.01). LV endocardial shortening was similar independently of the NHE inhibitors used (HOE C: 62.30 +/- 2.75%; 30d: 65.50 +/- 2.40%, ns. BIIB C: 63.20 +/- 2,39%; 30d 67,20 +/- 1.62%, ns). These data demonstrate that long-treatment with HOE or BIIB produced similar LV mass regression without changes in endocardial fractional shortening in spite of the increase of peak systolic stress. This finding could represent an increased inotropism previously depressed by the development of hypertrophy.
Asunto(s)
Guanidinas/farmacología , Guanidinas/uso terapéutico , Corazón/efectos de los fármacos , Hipertrofia Ventricular Izquierda/diagnóstico por imagen , Intercambiadores de Sodio-Hidrógeno/antagonistas & inhibidores , Sulfonas/uso terapéutico , Función Ventricular Izquierda/efectos de los fármacos , Administración Oral , Animales , Antiarrítmicos/uso terapéutico , Volumen Cardíaco/efectos de los fármacos , Volumen Cardíaco/fisiología , Modelos Animales de Enfermedad , Ventrículos Cardíacos/diagnóstico por imagen , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/fisiopatología , Hipertrofia Ventricular Izquierda/inducido químicamente , Masculino , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Ratas , Ratas Endogámicas SHR , Estimulación Química , Ultrasonografía , Función Ventricular Izquierda/fisiologíaRESUMEN
El presente estudio fue proyectado para analizar mediante ecocardiograma los efectos del HOE 642 (cariporide) (HOE) y del BIIB 723 (BIIB) sobre la estructura y función sistólica del ventrículo izquierdo en ratas espontáneamente hipertensas (SHR)- 8 con 30 mg/kg/día de HOE, 8 con 30 mg/kg/día de BIIB durante 30 días y 4 sin tratamiento (grupo control) durante esos 30 días. Los distintos parámetros analizados no mostraron cambios durante ese período en las ratas controles. Si bien el HOE determinó un leve descenso de la presión arterial (C: 184 ± 1.75 mm Hg; 30d:176.20 ± 2.60 mm Hg, p <0.01), no detectada con BIIB,ambas drogas provocaron un aumento del estrés sistólico pico (HOE C:166 ± 29 kdinas/cm2; 30d: 204 ± 34kdinas/cm2, p <0.04. BIIB C: 164 ± 25.90 kdinas/cm2; 30d: 234 ± 29.30 kdinas/cm2, p<0.02).Tanto HOE comoBIIB redujeron significativamente la masa ventricular izquierda (MVI) (HOE C: 612.50±50 mg; 30d:452 ± 37 mg,p <0.01; BIIB C: 544 ± 16mg; 30 d: 374 ± 25 mg, p<0.01). El porcentaje de acortamiento endocárdico no semodificó luego del tratamiento con HOE (C: 62.30 ± 2.75; 30d 65.50 ± 2.40%, ns) y BIIB (C: 63.20 ± 2.39%;30d 67.20 ± 1.62%, ns). Los resultados analizados permiten concluir que ambos inhibidores determinaron similarreducción de la MVI. Esa reducción se acompañó de mejoría en los índices de evaluación de la función sistólica ventricular izquierda, pese al incremento del estrés sistólico pico. Estas evidencias sugieren que independientemente del inhibidor utilizado se encuentra un aumento del inotropismo, previamente comprometidodurante el desarrollo de la hipertrofia (AU)
The aim of this study was to analyze by echocardiogram, the action of two Na+/H+ exchange, inhibitors, HOE 642 (HOE) and BIIB 723 (BIIB) on left ventricular (LV) mass and LV systolic function. We studied 16 spontaneously hypertensive rats (SHR), 8 treated with HOE 30 mg/kg/day, 8 with 30 mg/kg/day of BIIB during 30 days and 4 SHR as controls during those 30 days. Results are expressed as mean values ± SEM. The systolic blood pressure and theechocardiograpic parameters examined did not evidence changes during that period in the controls rats. Eventhough HOE determined a slight decrease in blood pressure (HOE C: 184 ± 1.75 mm Hg; HOE 30d: 176.20 ±2.60 mm Hg - p <0.01) which was not detected with BIIB, both drugs provoked an increase of peak systolic stress (HOE C: 166 ± 29 kdynes/cm2; HOE 30d: 204 ± 34 kdynes/cm2, p <0.04; BIIB C: 164 ± 25.90 kdynes/cm2; BIIB 30d: 234 ± 29.30 kdynes/cm2, p <0.02). HOE and BIIB reduced LV mass after 30 days of administration (HOE C: 612.50 ± 50 mg; 30d: 452 ± 37 mg, p <0.01. BIIB C: 544 ± 16mg; 30d: 374 ± 25 mg, p <0.01). LV endocardial shortening was similar independently of the NHE inhibitors used (HOE C: 62.30 ± 2.75%; 30d: 65.50 ± 2.40%, ns. BIIB C: 63.20 ± 2,39%; 30d 67,20 ± 1.62%, ns). These data demonstrate that long-treatment with HOE or BIIB produced similar LV mass regression without changes in endocardial fractional shortening in spite of the increase of peak systolic stress. This finding could represent an increased inotropism previously depressed by the development of hypertrophy (AU)
Asunto(s)
Animales , Masculino , Ratas , Guanidinas/uso terapéutico , Sulfonas/uso terapéutico , Hipertrofia Ventricular Izquierda/diagnóstico por imagen , Ventrículos Cardíacos/diagnóstico por imagen , Intercambiadores de Sodio-Hidrógeno/antagonistas & inhibidores , Función Ventricular Izquierda/efectos de los fármacos , Administración Oral , Antiarrítmicos/farmacología , Antiarrítmicos/uso terapéutico , Guanidinas/farmacología , Volumen Cardíaco/efectos de los fármacos , Volumen Cardíaco/fisiología , Modelos Animales de Enfermedad , Sulfonas/farmacología , Hipertrofia Ventricular Izquierda/inducido químicamente , Hipertrofia Ventricular Izquierda/fisiopatología , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/fisiopatología , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Ratas Endogámicas SHR , Intercambiadores de Sodio-Hidrógeno/farmacología , Intercambiadores de Sodio-Hidrógeno/uso terapéutico , Estimulación Química , Función Ventricular Izquierda/fisiologíaRESUMEN
El presente estudio fue proyectado para analizar mediante ecocardiograma los efectos del HOE 642 (cariporide) (HOE) y del BIIB 723 (BIIB) sobre la estructura y función sistólica del ventrículo izquierdo en ratas espontáneamente hipertensas (SHR)- 8 con 30 mg/kg/día de HOE, 8 con 30 mg/kg/día de BIIB durante 30 días y 4 sin tratamiento (grupo control) durante esos 30 días. Los distintos parámetros analizados no mostraron cambios durante ese período en las ratas controles. Si bien el HOE determinó un leve descenso de la presión arterial (C: 184 ± 1.75 mm Hg; 30d:176.20 ± 2.60 mm Hg, p <0.01), no detectada con BIIB,ambas drogas provocaron un aumento del estrés sistólico pico (HOE C:166 ± 29 kdinas/cm2; 30d: 204 ± 34kdinas/cm2, p <0.04. BIIB C: 164 ± 25.90 kdinas/cm2; 30d: 234 ± 29.30 kdinas/cm2, p<0.02).Tanto HOE comoBIIB redujeron significativamente la masa ventricular izquierda (MVI) (HOE C: 612.50±50 mg; 30d:452 ± 37 mg,p <0.01; BIIB C: 544 ± 16mg; 30 d: 374 ± 25 mg, p<0.01). El porcentaje de acortamiento endocárdico no semodificó luego del tratamiento con HOE (C: 62.30 ± 2.75; 30d 65.50 ± 2.40%, ns) y BIIB (C: 63.20 ± 2.39%;30d 67.20 ± 1.62%, ns). Los resultados analizados permiten concluir que ambos inhibidores determinaron similarreducción de la MVI. Esa reducción se acompañó de mejoría en los índices de evaluación de la función sistólica ventricular izquierda, pese al incremento del estrés sistólico pico. Estas evidencias sugieren que independientemente del inhibidor utilizado se encuentra un aumento del inotropismo, previamente comprometidodurante el desarrollo de la hipertrofia
The aim of this study was to analyze by echocardiogram, the action of two Na+/H+ exchange, inhibitors, HOE 642 (HOE) and BIIB 723 (BIIB) on left ventricular (LV) mass and LV systolic function. We studied 16 spontaneously hypertensive rats (SHR), 8 treated with HOE 30 mg/kg/day, 8 with 30 mg/kg/day of BIIB during 30 days and 4 SHR as controls during those 30 days. Results are expressed as mean values ± SEM. The systolic blood pressure and theechocardiograpic parameters examined did not evidence changes during that period in the controls rats. Eventhough HOE determined a slight decrease in blood pressure (HOE C: 184 ± 1.75 mm Hg; HOE 30d: 176.20 ±2.60 mm Hg - p <0.01) which was not detected with BIIB, both drugs provoked an increase of peak systolic stress (HOE C: 166 ± 29 kdynes/cm2; HOE 30d: 204 ± 34 kdynes/cm2, p <0.04; BIIB C: 164 ± 25.90 kdynes/cm2; BIIB 30d: 234 ± 29.30 kdynes/cm2, p <0.02). HOE and BIIB reduced LV mass after 30 days of administration (HOE C: 612.50 ± 50 mg; 30d: 452 ± 37 mg, p <0.01. BIIB C: 544 ± 16mg; 30d: 374 ± 25 mg, p <0.01). LV endocardial shortening was similar independently of the NHE inhibitors used (HOE C: 62.30 ± 2.75%; 30d: 65.50 ± 2.40%, ns. BIIB C: 63.20 ± 2,39%; 30d 67,20 ± 1.62%, ns). These data demonstrate that long-treatment with HOE or BIIB produced similar LV mass regression without changes in endocardial fractional shortening in spite of the increase of peak systolic stress. This finding could represent an increased inotropism previously depressed by the development of hypertrophy
Asunto(s)
Animales , Masculino , Ratas , Guanidinas/uso terapéutico , Ventrículos Cardíacos , Hipertrofia Ventricular Izquierda , Intercambiadores de Sodio-Hidrógeno/antagonistas & inhibidores , Sulfonas/uso terapéutico , Función Ventricular Izquierda/efectos de los fármacos , Administración Oral , Antiarrítmicos/farmacología , Antiarrítmicos/uso terapéutico , Volumen Cardíaco/efectos de los fármacos , Volumen Cardíaco/fisiología , Modelos Animales de Enfermedad , Guanidinas/farmacología , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/fisiopatología , Hipertrofia Ventricular Izquierda/inducido químicamente , Hipertrofia Ventricular Izquierda/fisiopatología , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Ratas Endogámicas SHR , Estimulación Química , Intercambiadores de Sodio-Hidrógeno/farmacología , Intercambiadores de Sodio-Hidrógeno/uso terapéutico , Sulfonas/farmacología , Función Ventricular Izquierda/fisiologíaRESUMEN
El presente estudio fue proyectado para analizar mediante ecocardiograma los efectos del HOE 642 (cariporide) (HOE) y del BIIB 723 (BIIB) sobre la estructura y función sistólica del ventrículo izquierdo en ratas espontáneamente hipertensas (SHR)- 8 con 30 mg/kg/día de HOE, 8 con 30 mg/kg/día de BIIB durante 30 días y 4 sin tratamiento (grupo control) durante esos 30 días. Los distintos parámetros analizados no mostraron cambios durante ese período en las ratas controles. Si bien el HOE determinó un leve descenso de la presión arterial (C: 184 ± 1.75 mm Hg; 30d:176.20 ± 2.60 mm Hg, p <0.01), no detectada con BIIB,ambas drogas provocaron un aumento del estrés sistólico pico (HOE C:166 ± 29 kdinas/cm2; 30d: 204 ± 34kdinas/cm2, p <0.04. BIIB C: 164 ± 25.90 kdinas/cm2; 30d: 234 ± 29.30 kdinas/cm2, p<0.02).Tanto HOE comoBIIB redujeron significativamente la masa ventricular izquierda (MVI) (HOE C: 612.50±50 mg; 30d:452 ± 37 mg,p <0.01; BIIB C: 544 ± 16mg; 30 d: 374 ± 25 mg, p<0.01). El porcentaje de acortamiento endocárdico no semodificó luego del tratamiento con HOE (C: 62.30 ± 2.75; 30d 65.50 ± 2.40%, ns) y BIIB (C: 63.20 ± 2.39%;30d 67.20 ± 1.62%, ns). Los resultados analizados permiten concluir que ambos inhibidores determinaron similarreducción de la MVI. Esa reducción se acompañó de mejoría en los índices de evaluación de la función sistólica ventricular izquierda, pese al incremento del estrés sistólico pico. Estas evidencias sugieren que independientemente del inhibidor utilizado se encuentra un aumento del inotropismo, previamente comprometidodurante el desarrollo de la hipertrofia (AU)
The aim of this study was to analyze by echocardiogram, the action of two Na+/H+ exchange, inhibitors, HOE 642 (HOE) and BIIB 723 (BIIB) on left ventricular (LV) mass and LV systolic function. We studied 16 spontaneously hypertensive rats (SHR), 8 treated with HOE 30 mg/kg/day, 8 with 30 mg/kg/day of BIIB during 30 days and 4 SHR as controls during those 30 days. Results are expressed as mean values ± SEM. The systolic blood pressure and theechocardiograpic parameters examined did not evidence changes during that period in the controls rats. Eventhough HOE determined a slight decrease in blood pressure (HOE C: 184 ± 1.75 mm Hg; HOE 30d: 176.20 ±2.60 mm Hg - p <0.01) which was not detected with BIIB, both drugs provoked an increase of peak systolic stress (HOE C: 166 ± 29 kdynes/cm2; HOE 30d: 204 ± 34 kdynes/cm2, p <0.04; BIIB C: 164 ± 25.90 kdynes/cm2; BIIB 30d: 234 ± 29.30 kdynes/cm2, p <0.02). HOE and BIIB reduced LV mass after 30 days of administration (HOE C: 612.50 ± 50 mg; 30d: 452 ± 37 mg, p <0.01. BIIB C: 544 ± 16mg; 30d: 374 ± 25 mg, p <0.01). LV endocardial shortening was similar independently of the NHE inhibitors used (HOE C: 62.30 ± 2.75%; 30d: 65.50 ± 2.40%, ns. BIIB C: 63.20 ± 2,39%; 30d 67,20 ± 1.62%, ns). These data demonstrate that long-treatment with HOE or BIIB produced similar LV mass regression without changes in endocardial fractional shortening in spite of the increase of peak systolic stress. This finding could represent an increased inotropism previously depressed by the development of hypertrophy (AU)
Asunto(s)
Animales , Masculino , Ratas , Guanidinas/uso terapéutico , Sulfonas/uso terapéutico , Hipertrofia Ventricular Izquierda/diagnóstico por imagen , Ventrículos Cardíacos/diagnóstico por imagen , Intercambiadores de Sodio-Hidrógeno/antagonistas & inhibidores , Función Ventricular Izquierda/efectos de los fármacos , Administración Oral , Antiarrítmicos/farmacología , Antiarrítmicos/uso terapéutico , Guanidinas/farmacología , Volumen Cardíaco/efectos de los fármacos , Volumen Cardíaco/fisiología , Modelos Animales de Enfermedad , Sulfonas/farmacología , Hipertrofia Ventricular Izquierda/inducido químicamente , Hipertrofia Ventricular Izquierda/fisiopatología , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/fisiopatología , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Ratas Endogámicas SHR , Intercambiadores de Sodio-Hidrógeno/farmacología , Intercambiadores de Sodio-Hidrógeno/uso terapéutico , Estimulación Química , Función Ventricular Izquierda/fisiologíaRESUMEN
The neurotransmitter substance P acts also as a potent vasodilator. Its participation in the pathogenesis of deoxycorticosterone acetate (DOCA)-salt hypertension was evaluated by an acute infusion of a newly synthesized, potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt rats but only small, transient, and nonsignificant rises in blood pressure of sham-treated control rats. The rise in blood pressure was not accompanied by changes in heart rate. Maximal blood pressure increase in DOCA-salt rats was 31.7 +/- 14.8 mm Hg. In a second series of experiments, the hemodynamic effects of this antagonist were evaluated under anesthesia in both DOCA-salt and sham-treated control rats by the thermodilution method. During CP 96,345 infusion, sustained increases in cardiac index and stroke volume and decreases in total peripheral resistance were observed in both DOCA-salt and control rats. In DOCA-salt rats, cardiac index rose by 79.4%, while total peripheral resistance fell by 27.9% of the baseline values. In control rats, the changes were smaller (+27.2% and -22.5%, respectively). Stroke volume changed in parallel to cardiac output in both groups. The data suggest that acute blockade of NK-1 receptors increases blood pressure in DOCA-salt rats mainly by an increase in cardiac output. We conclude that endogenous substance P tends to counteract the DOCA-salt-induced elevation of blood pressure by modulating both cardiac output and peripheral resistance.
Asunto(s)
Compuestos de Bifenilo/farmacología , Desoxicorticosterona , Hemodinámica/efectos de los fármacos , Hipertensión/fisiopatología , Hipnóticos y Sedantes/farmacología , Antagonistas del Receptor de Neuroquinina-1 , Sustancia P/fisiología , Animales , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Volumen Cardíaco/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Hipertensión/inducido químicamente , Masculino , Ratas , Ratas Wistar , Cloruro de Sodio , Resistencia Vascular/efectos de los fármacosRESUMEN
Ejection fraction (EF), the ratio between stroke volume (SV) and end-diastolic volume (EDV), is a valuable contractility indicator. Unlike SV, the Frank-Starling effect is automatically compensated in the calculation of EF. It was the aim of this study to evaluate the physiological behavior of impedance derived measurements of relative right ventricular (RV) volumes and EF, obtained with standard pacing leads. Seven patients were evaluated at the time of pacemaker implant or replacement. Since no absolute standard of comparison was available for RV volumes, the value of the measurements was assessed by observing their behavior under cardio-circulatory challenges. A 2.5-kHz carrier was fed to the ring and tip electrodes of standard bipolar pacing leads and the resulting voltage was digitized and stored. The peak-to-peak voltage (PPV) of the carrier at the time of QRS was used as EDV, and the largest PPV as end-systolic volume (ESV). Relative SV was the difference between EDV and ESV, and EF = SV/EDV x 100. Pacing was used to reduce EDV, and the effect of contractility was tested with isometric hand grip, recumbent leg exercise, or isoproterenol drip. Only minimal changes in EF were noted during incremental pacing; relative SV and EDV decreased as expected; and EF increased significantly during contractility challenges. A high correlation coefficient was observed between EDV and SV changes induced by incremental pacing at rest (r values from 0.62 to 0.98, P from < 0.01 to 0.001). The study revealed that impedance volumetry, utilizing conventional bipolar pacing leads, yields useful hemodynamic data related to EDV, ESV, and EF. Given the simplicity of the method, it is reasonable to conclude on the feasibility of using said impedance derived hemodynamic parameters in implantable rhythm control devices.
Asunto(s)
Volumen Cardíaco/fisiología , Marcapaso Artificial , Volumen Sistólico/fisiología , Función Ventricular Derecha/fisiología , Adulto , Anciano , Gasto Cardíaco/efectos de los fármacos , Gasto Cardíaco/fisiología , Volumen Cardíaco/efectos de los fármacos , Diástole/fisiología , Impedancia Eléctrica , Diseño de Equipo , Estudios de Factibilidad , Femenino , Humanos , Contracción Isométrica/fisiología , Isoproterenol/farmacología , Contracción Isotónica/fisiología , Masculino , Persona de Mediana Edad , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Esfuerzo Físico/fisiología , Volumen Sistólico/efectos de los fármacos , Función Ventricular Derecha/efectos de los fármacosRESUMEN
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system and its beneficial modification with the use of angiotensin-converting enzyme inhibin after inferior wall myocardial infarction (MI) was evaluated. Fifty patients with acute inferior MI were randomly assigned to receive 5 mg per day of either enalapril or placebo after admission. Blood tests for neurohormone levels and echocardiograms were performed at initial examination and 4 weeks later. Baseline characteristics were similar in the two groups. Four weeks after randomization, patients treated with enalapril had lower end-diastolic volume (146 +/- 29 vs 167 +/- 15 ml; p = 0.04), end-systolic volume (56 +/- 18 vs 107 +/- 17 ml; p = 0.03), serum norepinephrine levels (320 +/- 93 vs 465 +/- 77 pg/ml; p < 0.01), angiotensin II levels (18 +/- 6 vs 54 +/- 11 pg/ml; p < 0.01), and atrial natriuretic polypeptide levels (106 +/- 9 vs 122 +/- 17 pg/ml; p = 0.05) than patients given placebo. The incidence of heart failure after MI was also lower in this group (4% vs 16%; p = 0.009). Results show that there is early neurohumoral activation in the course of acute inferior wall MI. Enalapril reduces neurohumoral levels and preserves ventricular volumes. These effects were associated with a reduction in the incidence of heart failure 4 weeks after MI in these patients.
Asunto(s)
Volumen Cardíaco/efectos de los fármacos , Enalapril/uso terapéutico , Infarto del Miocardio/tratamiento farmacológico , Función Ventricular Izquierda/efectos de los fármacos , Anciano , Aldosterona/sangre , Angiotensina II/sangre , Método Doble Ciego , Femenino , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/sangre , Infarto del Miocardio/fisiopatología , Norepinefrina/sangreRESUMEN
Thirty patients (18 male), mean age 49.5 +/- 6.3 years, were treated with lisinopril 10-40 mg once daily for 16 weeks. The effect of treatment on left ventricular mass and improvement in left ventricular diastolic function (measured by echo-Doppler) was assessed. Blood pressure changes were measured conventionally in the clinic and by ambulatory blood pressure monitoring. Clinic blood pressure decreased from 168.3 +/- 13.8/105.5 +/- 5.4 mm Hg to 137.5 +/- 4.1/88.8 +/- 4.1 mm Hg (p < 0.005 for both systolic and diastolic blood pressures), and the heart rate from 75.2 +/- 3.7 to 74.4 +/- 7.6 beats per minute (NS). The frequency of ambulatory systolic blood pressure values > 140 mm Hg decreased in percentage from 63.3 +/- 12.8 to 29.9 +/- 9.1% (p < 0.005) and the frequency of ambulatory diastolic blood pressure values > 90 mm Hg decreased in percentage from 61.1 +/- 12.8 to 28.6 +/- 7.5% (p < 0.005). Septal and left ventricular posterior wall thickness decreased from 11.2 +/- 0.9 to 10.3 +/- 0.6 mm and from 10.9 +/- 0.9 to 10.1 +/- 0.6 mm, respectively (both p < 0.005). Left ventricular diastolic diameter and the shortening fraction did not change significantly. Left ventricular mass, calculated from left ventricular wall thickness and diastolic diameter, decreased from 132.6 +/- 11.5 to 119.9 +/- 6.3 g/m2 (p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Volumen Cardíaco/efectos de los fármacos , Diástole/efectos de los fármacos , Hipertensión/tratamiento farmacológico , Hipertrofia Ventricular Izquierda/tratamiento farmacológico , Lisinopril/uso terapéutico , Función Ventricular Izquierda/efectos de los fármacos , Adulto , Monitores de Presión Sanguínea , Volumen Cardíaco/fisiología , Diástole/fisiología , Relación Dosis-Respuesta a Droga , Ecocardiografía Doppler/efectos de los fármacos , Femenino , Hemodinámica/efectos de los fármacos , Hemodinámica/fisiología , Humanos , Hipertensión/diagnóstico por imagen , Hipertensión/fisiopatología , Hipertrofia Ventricular Izquierda/diagnóstico por imagen , Hipertrofia Ventricular Izquierda/fisiopatología , Masculino , Persona de Mediana Edad , Función Ventricular Izquierda/fisiologíaAsunto(s)
Insuficiencia de la Válvula Aórtica/tratamiento farmacológico , Hemodinámica/efectos de los fármacos , Hidralazina/uso terapéutico , Adulto , Insuficiencia de la Válvula Aórtica/fisiopatología , Volumen Cardíaco/efectos de los fármacos , Ecocardiografía , Prueba de Esfuerzo , Ventrículos Cardíacos/fisiopatología , Humanos , Hidralazina/farmacología , Masculino , Persona de Mediana EdadRESUMEN
Two homogeneous groups of patients with acute myocardial infarction were observed within the first six hours from the coronary attack. On admittance and for ten days, 105 patients were treated with C3: the mortality rate resulted in 13.3%. The control group of 108 patients showed a mortality of 18.5%. Strict criteria of randomization were followed in allocating patients to the two groups. Although the difference is not statistically significant it is however interesting since it confirms a previous research. Statistically significant differences between the two groups were observed in all surviving patients in the injury signs regression time and in the cardiac volume in favour of the group treated with C3.