Ivabradine treatment prevents dobutamine-induced increase in HR and may be useful in reducing HR-related adverse effects of dobutamine.
A b s t r a c tBackground: Indirect evidences suggest that the I f blocker ivabradine may exert an antiarrhythmic effect in ventricular myocardium in heart failure (HF) patients by inhibiting spontaneous depolarisations, but the clinical relevance of this mechanism is not known. Dobutamine (DOB) has been known to increase heart rate and the incidence of cardiac arrhythmias. Aim:In this study, we evaluated the effects of ivabradine on DOB-induced ventricular arrhythmias and compared them with those of beta-blocker (BB) therapy. Methods:Patients with decompensated HF requiring inotropic support, left ventricular ejection fraction < 35%, and in sinus rhythm were included in the study (ivabradine group -29 patients, control group -29 patients, BB group -15 patients). All patients underwent Holter recording for 6 h before the initiation of DOB infusion. Following baseline recording, DOB was administered at incremental doses of 5, 10, and 15 µg/kg/min, with 6-h steps. Holter monitoring was continued during 18 h of DOB infusion and analysed for the median number of ventricular premature contractions (VPC), ventricular couplets, episodes of non-sustained ventricular tachycardia, and total ventricular arrhythmias in each step of the study protocol. Results:The positive chronotropic effect of incremental DOB doses was blunted by beta-blockade and was totally abolished by ivabradine. The median number of VPCs, ventricular couplets, and total ventricular arrhythmias significantly increased with incremental doses of DOB in the control group (p = 0.018) and, to a lesser extent, in the ivabradine group (p = 0.015). In the BB group the absolute VPCs numbers were smaller than in the control or the ivabradine group, with the on-ivabradine VPCs numbers falling between those seen in control and BB groups. A numeric increase in VPCs with incremental DOB doses occurred in the BB group but did not reach statistical significance (p > 0.05), consistent with a protective effect of beta-blockade. Ivabradine reduced VPCs by 43% at 5 µg/kg/min DOB and by 38% at 10 µg/kg/min DOB against the control group (VPCs median 256 vs. 147 and 251 vs. 158) in the absence of significant differences at 15 µg/kg/min DOB between the control and ivabradine groups (overall p > 0.05). Thus, ivabradine administered without background beta-blockade attenuated the arrhythmogenic effect of increasing doses of DOB in the low and moderate DOB dose but not in the high DOB dose. Conclusions:In patients with decompensated HF, ivabradine appears to reduce the incidence of VPCs in response to low and medium DOB dose. Whether the anti-arrhythmic effect of ivabradine is additive to the anti-arrhythmic effect of beta-blockade requires further investigation; this should also determine the clinical significance of ventricular arrhythmia attenuation with ivabradine.
The aim of the present study was to investigate the effect of intravascular ultrasound (IVUS)-guided stenting on angiographic results for drug eluting stent (DES) implantation. Material-Methods: For the present study, we included 30 patients who received DES with IVUS-guided stenting (Group A) and 30 patients receiving the DES without IVUS-guided stenting (Group B). The patients were evaluated for their ninth month control angiographies and were followed during two years for the development of relevant clinical events after the DES implantations. The angiographic and clinical results were compared between the groups. Results: After the percutaneous intervention, the minimal luminal diameter and net acute gain were significantly increased in Group A in respect to Group B (3.3AE0.34 vs. 2.8AE0.33, p <0.01). By contrast, stent restenosis rates were similar between the groups (p >0.3). Conclusions: The present results indicate that the use of IVUS for the implantation of DES can increase the success rate of the intervention. We think that the IVUS guidance during DES implantation can be complementary percutaneous intervention, in particularly by detecting the situations that need for post-dilatation.
Background/Objective: Levosimendan represents an alternative to other positive inotropic agents based on its different mechanisms of action and favorable electrophysiological properties. This study compared the effects of levosimendan and dobutamine on echocardiographic parameters in heart failure patients with acute decompensation necessitating positive inotropic support. Methods: Patients with acute decompensated heart failure were randomized to receive inotropic support with either levosimendan (n=25) or dobutamine (n=25). Treatment groups were compared in terms of echocardiography measurements including tissue Doppler examination findings, systolic time interval assessments and diastolic parameters. In addition, groups were compared for demographic features, clinical characteristics and laboratory findings. Results: Among tissue Doppler measurements, Sm-lateral and Sm-septal significantly increased after treatment in both groups. E/E' lateral and E/E' septal significantly decreased only in the levosimendan group. Among systolic time interval parameters, increasing in left ventricular ejection time and shortening in pre-ejection period are similar in both groups, however a significant decrease in QS2i was observed in the levosimendan group. Levosimendan treatment was associated with significant decreases in blood pressures along with a significant increase in ejection fraction. Dobutamine treatment on the other hand resulted in significant increases in blood pressure, heart rate and ejection fraction. Conclusions: Our findings suggest that levosimendan and dopamine treatments are associated with only marginal differences in echocardiographic parameters. This study suggests that both levosimendan and dobutamine are almost equally effective in systolic time intervals. However, levosimendan appears to have additional advantage over dobutamine in shortening QS2i, indicating a fairly strong positive inotropic effect.
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