RESUMEN
Increased QT dispersion (QT(d)) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QT(d). Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JT(d)), and QTc (QTc(d)) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QT(d) (115 +/- 31 vs. 49 +/- 15 ms), JT(d) (116 +/- 34 vs. 52 +/- 12 ms), and QTc(d) (141 +/- 40 vs. 58 +/- 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K(+) and seven on Mg(2+)-free diet followed by normal diet. Experimental hypokalemia significantly increased QT(d) (10 +/- 4 to 37 +/- 7 ms), and QTc(d) (32 +/- 6 to 79 +/- 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QT(d), 14 +/- 2; QTc(d), 34 +/- 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.
Asunto(s)
Arritmias Cardíacas/fisiopatología , Trastornos del Metabolismo del Calcio/fisiopatología , Hiperpotasemia/fisiopatología , Hipopotasemia/fisiopatología , Disfunción Ventricular/fisiopatología , Adulto , Anciano , Análisis de Varianza , Animales , Electrocardiografía , Femenino , Humanos , Hipercalcemia/fisiopatología , Hipocalcemia/fisiopatología , Masculino , Persona de Mediana Edad , Ratas , Disfunción Ventricular/sangreRESUMEN
Isolated rat left atria or right ventricular strips were electrically stimulated at a constant frequency. The amplitude of twitch contractions, thus elicited, rose as a function of stimulation intensity because of increases in the evoked release of sympathetic catecholamines. Bradykinin had no effect on contractile force in preparations paced at a minimal intensity (threshold). By contrast, bradykinin (1 nmol/L to 1 mumol/L) markedly increased twitch contractile force when the preparations were paced at a high intensity (two to three times threshold). The EC50 for the positive inotropic action of bradykinin averaged 42 nmol/L. Ramiprilat (1 mumol/L), an angiotensin I-converting enzyme/kinase II inhibitor, shifted the EC50 for bradykinin to approximately 2 nmol/L. Ramiprilat (1 mumol/L) per se also produced a modest positive inotropic effect. The effects of bradykinin and/or ramiprilate were inhibited by HOE 140 (300 nmol/L), a bradykinin B2-receptor antagonist. Propranolol (1 mumol/L), a beta-adrenoceptor blocker, abolished the effects of bradykinin. After the destruction of sympathetic nerve endings by use of 6-hydroxydopamine, bradykinin no longer exerted a positive inotropic action. Cocaine (10 micrograms/mL), an inhibitor of catecholamine reuptake, potentiated the effect of bradykinin. Bradykinin did not affect the positive inotropic response to tyramine (10 mumol/L), whereas cocaine blocked it. Furthermore, bradykinin did not modify the dose-response curves for added norepinephrine. omega-Conotoxin (100 nmol/L) inhibited the positive inotropic effect of intensified stimulation and bradykinin potentiation. Bradykinin is suggested to facilitate the evoked release of sympathetic catecholamines and thereby cause a positive inotropic effect.