Evaluation of vardenafil and sildenafil on cardiac repolarization

Morganroth, Joel; Ilson, Bernard E.; Shaddinger, Bonnie C.; Dabiri, Guissou A; Patel, B. J.; Boyle, Duane A.; Sethuraman, Venkat; Montague, Timothy H.

doi:10.1016/j.amjcard.2004.02.034

Cited by 69 publications

(50 citation statements)

References 6 publications

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“…The effects of single oral therapeutic and supratherapeutic doses of sildenafil (50 and 400 mg) and vardenafil (10 and 80 mg) on the Q-T interval corrected for heart rate (QTc) have been examined in a well-designed study in healthy males [68]. Placebo-corrected mean changes in QTc were calculated by two methods.…”

Section: Clinical Pharmacology Of Selective Pde5 Inhibitorsmentioning

confidence: 99%

Phosphodiesterase inhibitors for the treatment of pulmonary hypertension

Wilkins¹,

Wharton²,

Grimminger³

et al. 2008

Eur Respir J

131

106

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The pulmonary vascular bed is both a source of and target for a number of vasoactive factors. Among the most important for pulmonary vascular homeostasis are factors that utilise cyclic guanosine monophosphate (cGMP) as an intracellular second messenger. These include nitric oxide and the natriuretic peptide family (atrial, brain and C-type natriuretic peptides). In the search for therapeutic strategies that engage the cGMP signalling pathway for the treatment of pulmonary arterial hypertension (PAH), inhibition of cGMP metabolism by phosphodiesterase type 5 (PDE5)-targeted compounds has proven most successful to date. One PDE5 inhibitor, sildenafil, has been shown to improve pulmonary haemodynamics and exercise capacity in patients with PAH and is now an approved treatment. Others are under investigation.An interesting, although still tentative, observation is the potential of sildenafil to reduce pulmonary vascular resistance without adversely affecting ventilation-perfusion matching. Another is the expression of phosphodiesterase type 5 in the hypertrophied right ventricle. These data suggest that phosphodiesterase type 5 inhibitors may have effects that distinguish them from other treatments for pulmonary hypertension and merit further study.

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Section: Clinical Pharmacology Of Selective Pde5 Inhibitorsmentioning

confidence: 99%

Phosphodiesterase inhibitors for the treatment of pulmonary hypertension

Wilkins¹,

Wharton²,

Grimminger³

et al. 2008

Eur Respir J

131

106

View full text Add to dashboard Cite

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“…These results are in agreement with previous studies in which levofloxacin has been shown to be more likely to lower blood glucose levels than moxifloxacin. 8,[18][19][20]26,[35][36][37] Since, in the present study, the insulin levels of diabetic rats remained low even after 14 days of treatment, the hypoglycaemic action of levofloxacin is very likely not due to an insulinotropic effect of the drug. Instead, downstream insulin-independent mechanisms (such as enhanced activity of glucose transporters) must be involved.…”

Section: Effects Of Levofloxacin and Moxifloxacin On Glucose Levelsmentioning

confidence: 91%

The effect of levofloxacin and moxifloxacin on cardiovascular functions of rats with streptozotocin-induced diabetes

Absi

Ghareeb

Khalil

et al. 2012

Diabetes and Vascular Disease Research

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Fluoroquinolone antibiotics cause rare, but clinically important, adverse events including hyperglycaemia and hypoglycaemia. The present study focuses on the possible effect of levofloxacin and moxifloxacin on the cardiovascular functions of rats with type I diabetes. Both antibiotics caused bradycardia. Levofloxacin but not moxifloxacin caused hypoglycaemia in diabetic rats and an increase in amplitude of the ST segment revealed by electrocardiogram (ECG) analysis of isolated hearts. In pressurized mesenteric arteries, levofloxacin did not affect the endothelium-derived hyperpolarising factor (EDHF) pathway or its main components, the small-conductance Ca 2+ activated potassium (SK Ca ) and intermediateconductance Ca 2+ activated potassium (IK Ca ) channels. In moxifloxacin-treated rats, an increase in the EDHF response was observed, which was largely attributed to SK Ca -activation. In conclusion, levofloxacin and moxifloxacin use appeared to vary but with no evidence of impairment of the cardiovascular function. However, it is still possible that these antibiotics may produce different effects if there are co-morbidities and therefore their use must be with care.

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“…3 Sildenafil and vardenafil reportedly did not increase absolute QT, and each minimally increased corrected QT (by 4 to 8 ms). 63 The clinical implications of this small effect are unknown, and no cases of torsade de pointes are known to date. 3,63 …”

Section: Miscellaneousmentioning

confidence: 99%

“…63 The clinical implications of this small effect are unknown, and no cases of torsade de pointes are known to date. 3,63 …”

Section: Miscellaneousmentioning

confidence: 99%