Diagnosis
Differential diagnosis
Dressler syndrome needs to be differentiated from pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks. ischaemic heart disease. Treatment
Dressler syndrome is best treated with high dose aspirin. In some resistant cases, corticosteroids can be used but are not preferred (avoided) in first month due to the high frequency of impaired ventricular healing leading to increased rate of ventricular rupture. Other NSAIDs, though once used to treat Dressler syndrome, are less advocated and should be avoided in patients with ischemic heart disease. One NSAID in particular, indomethacin, can inhibit new collagen deposition, thus impairing the healing process for the infarcted region. Other NSAIDS should be used only in cases refractory to aspirin. Heparin should be avoided because it can lead to hemorrhage into the pericardial sac, leading to tamponade. The only time heparin could be used with pericarditis is with coexisting acute MI, in order to prevent further thrombus formation. References


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Uncertainties remain about whether vortioxetine is indeed a clinically multimodal antidepressant or whether it is effectively "[just] another selective serotonin reuptake inhibitor".Antagonism of the 5-HT3 receptor has been found to enhance the increase in brain serotonin levels produced by serotonin reuptake inhibition in animal studies. Whether or not the 5-HT3 receptor antagonism of vortioxetine likewise does this in humans or contributes to its clinical antidepressant efficacy is unclear. SSRIs and 5-HT1A receptor agonists often produce nausea as a side effect, whereas 5-HT3 receptor antagonists like ondansetron are antiemetics and have been found to be effective in treating SSRI-induced nausea. It was thought that the 5-HT3 receptor antagonism of vortioxetine would reduce the incidence of nausea relative to SSRIs. However, clinical trials found significant and dose-dependent rates of nausea with vortioxetine that appeared to be comparable to those found with the SNRI duloxetine. Pharmacokinetics
Vortioxetine is well-absorbed when taken orally and has an oral bioavailability of 75%. It is systemically detectable after a single oral dose by 0.781 hours. Peak levels of vortioxetine are reached within 7 to 11 hours post-dose with single or multiple doses. Steady-state levels of vortioxetine are generally reached within 2 weeks of administration, with 90% of individuals reaching 90% of steady state after 12 days of administration. Steady-state peak levels of vortioxetine with doses of 5, 10, and 20 mg/day were 9, 18, and 33 ng/mL, respectively. The accumulation index of vortioxetine (area-under-the-curve levels after a single dose versus at steady state) is 5 to 6.