| Myocardial remodeling is a central feature in the progression of myocardial failure. This process involves changes in the structure and function of the myocardium. Increased activities of the sympathetic nervous system and the renin-angiotensin system appear to contribute to progressive myocardial failure by acting directly on the myocardium to cause remodeling, which provides an explanation for the clinical success of agents inhibiting these pathways. The primary mechanism of action of ft -blocking agents in chronic heart failure is to prevent and reverse adrenergically mediated intrinsic myocardial dysfuction and remodeling. But this occurs via a time-dependent, biologic effect. Bisoprolol ,made in China, is second-generation fi-blocking agent, selectively blocking the fi \-receptor. It may prevent and reverse the process of heart failing, and what the highest tolerated doses are fitted for our Chinese.Methods There were 68 patients with chronic heart failure, divided into tow groups: the bisoprolol group and the controlled group. Blood samples were drawn from median cubital veins of all these patients at the beginning of the study and after 7 months follow-up. The plasma concentration of NE, Ang II and CGRP were detected by radioimmunoassay, and the static heart rate, blood pressure and left ventricular ejection fraction (EF%) were recorded to evaluate the effects of bisoprolol. Result:1. 7 months later, the plasma concentration of NE in bisoprolol group became significantly higher than at the beginning (P<0.05), and than that in controlled group (P<0.05).2. In bisoprolol group, the plasma concentrations of ET-1, Angll, CGRP were significantly less than after 7 months (all P<0.01). In controlled group, there is an decrease only in Angll (PO.05). Compared to the controlled group, the concentrations of these factors decreased significantly further in bisoprolol group (ET-1, CGRP: PO.01; Ang II: P<0.05).3. The values of EF% were higher in both groups after 7 months follow-up (all P<0.01). But 7 months later, there was significantly higher EF% among patients on bisoprolol than among those on controlled drugs.4. The static heart rate was significantly slower in bisoprolol group after 7 months (P<0.01), and than that in controlled group (P<0.01). Blood press doesn't significantly differ between both groups 7 months later, similar to the beginning. Conclusion:1. After a long time bisoprolol can decrease the plasma concentrations of NE and Ang II. That means it can depress the increased activities of sympathetic nervous system and of renal-angiotensin system, directly act on preventing the myocardial dysfuction and remodeling.2. With the decrease of the plasma concentrations of ET-1, CGRP and Ang II in bisoprolol group, it is referred that bisoprolol can make the active biological factor recovering the normal meditation, indirectly act on preventing the myocardial dysfuction and remodeling.3. From the higher EF% in the bisoprolol group, it is considered that bisoprolol can improve myocardial systolic function, which means bisoprolol can improve the myocardial function and prognosis of the patients with heart failure.4. Bisoprolol can slow the static heart rates, which can prevent some adrenergiclly mediated adverse myocardial effects and benefit for preventing the myocardial dysfuction and remodeling of the failing heart.5. For the highest tolerated dose of the bisoprolol, there are different between per day and per time. But the both highest tolerated doses are mainly S.Omg.
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