Effects of acetylstrophanthidin on baroreflex sensitivity in patients with acute myocardial infarction
Autor: | Valter Bianchi, Mario Petretta, Gianfranco Morgano, Assunta Carpinelli, Giuseppe Valva, Sakis Themistoclakis, Francesco Rotondi, Domenico Bonaduce |
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Přispěvatelé: | Bonaduce, Domenico, Petretta, Mario, Morgano, G, Bianchi, V, Themistoclakis, S, Rotondi, F, Valva, G, Carpinelli, A. |
Jazyk: | angličtina |
Rok vydání: | 1993 |
Předmět: |
Chronotropic
Adult Male medicine.medical_specialty Baroreceptor Time Factors Myocardial Infarction Hemodynamics Infarction Blood Pressure Strophanthidin Baroreflex Heart Rate Internal medicine Heart rate medicine Humans acetylstrophanthidin phenylephrine cardiovascular diseases Myocardial infarction Aged business.industry Stroke Volume Middle Aged medicine.disease Blood pressure acute heart infarction adult aged article clinical article clinical trial controlled study female human intravenous drug administration male pressoreceptor reflex priority journal receptor sensitivity Anesthesia cardiovascular system Cardiology Female Cardiology and Cardiovascular Medicine business Adult Aged Baroreflex Blood Pressure Female Heart Rate Human Male Middle Age Myocardial Infarction Stroke Volume Strophanthidin Time Factors circulatory and respiratory physiology |
Popis: | We evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocadial infarction. Baroreflex control of heart rate is frequently depressed after acute myocardial infarction and few data are available as to the effects of pharmacological intervention on this parameter. The reflex chronotropic response to arterial baroreceptor stimulation was assessed in 29 patients with uncomplicated acute myocardial infarction in control conditions (72-96 h after symptom onset) and 30 min after acetylstrophanthidin administration. To check for spontaneous baroreflex sensitivity variations, 24 patients with the same characteristics were evaluated at the same time intervals before and after a 10-cc bolus of saline placebo. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in RR intervals. Mean baseline baroreflex sensitivity value for the whole study population was 7.4 ± 4.5 ms/mmHg and was unchanged, 7.0 ± 4.5 ms/mmHg, after acetylstrophanthidin (P=NS). Mean baroreflex sensitivity values were also comparable dividing patients according to the site of infarction both before and after acetylstrophanthidin. Despite the lack of difference in mean baroreflex sensitivity values between the two studies, at a post hoc analysis an inverse relation was found in the total study population between baseline baroreflex sensitivity values and their changes after acetylstrophanthidin (r = -0.62; P < 0.005). The inverse relation was also evident separately in anterior (r = -0.57; P < 0.05) and in inferior (r =-0.70; P < 0.005) myocardial infarction patients. In the control group no difference was observed between mean baroreflex sensitivity values obtained in the two studies, nor was there any relationship between baseline baroreflex sensitivity values and their changes after placebo administration. These data demonstrate that after myocardial infarction acetylstrophanthidin administration had no effect on mean baroreflex sensitivity value. However, this drug seems to improve baroreflex sensitivity when it is depressed and to worsen it when normal or nearly normal. |
Databáze: | OpenAIRE |
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