Key result
Telmisartan reduced cardiac troponin I concentration and preserved left ventricular fractional shortening compared to control in a canine model of supraventricular tachyarrhythmia.
Why the study?
Maintaining good ventricular systolic function is important in long-term therapy for supraventricular tachyarrhythmia, prompting evaluation of the inhibitory effect of telmisartan on myocardial injury and ventricular systolic dysfunction.
Does telmisartan prevent myocardial injury and ventricular systolic dysfunction in a canine model of supraventricular tachyarrhythmia?
RCT (n=14)
Randomly assigned
No
Does telmisartan prevent myocardial injury and ventricular systolic dysfunction in a canine model of supraventricular tachyarrhythmia?
Telmisartan prevents myocardial injury and preserves ventricular systolic function in a canine model of supraventricular tachyarrhythmia.
Answers are grounded in this paper and cite their sources.
May support telmisartan in canine tachyarrhythmia models; hypothesis-generating for human arrhythmia-induced injury, needs prospective trials.
Maintaining a good ventricular systolic function is important in the long-term therapy of dogs with supraventricular tachyarrhythmia (SVTA). The objective of this study was to evaluate the inhibitory effect of telmisartan on myocardial injury and the resulting ventricular systolic dysfunction in a canine model of SVTA. A total of 14 dogs were randomly assigned to a Telmisartan (oral telmisartan, 1.0 mg/kg daily, n=7) or a Control (no drug administration, n=7) group; the duration of rapid atrial pacing (RAP) was 3 weeks for both groups. The cardiac troponin I (cTnI) concentration in the Control group was significantly increased after 3 weeks compared to that before RAP initiation (baseline), but no significant difference was observed in the Telmisartan group. Moreover, the cTnI concentration at 3 weeks was significantly lower in the Telmisartan group than in the Control group. The left ventricular fractional shortening was significantly decreased at 3 weeks compared to that at baseline in both groups. However, fractional shortening at 3 weeks was significantly higher in the Telmisartan group than in the Control group. The cardiac output values in the Control group were significantly decreased at 3 weeks compared with those at baseline, but no significant difference was observed in the Telmisartan group. This study demonstrates that telmisartan inhibits the reduction in ventricular systolic function and prevents myocardial injury in a canine model of SVTA. Therefore, telmisartan is suggested as a novel treatment for canine SVTA.
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KAWAGUCHI et al. (2019) conducted an RCT in Experimental supraventricular tachyarrhythmia (n=14). Telmisartan vs. No drug administration was evaluated on Cardiac troponin I (cTnI) concentration at 3 weeks (ng/ml) (p=<0.01). Telmisartan reduced cardiac troponin I concentration and preserved left ventricular fractional shortening compared to control in a canine model of supraventricular tachyarrhythmia.
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