Metal-Free Dehomologative Oxidation of Arylacetic Acids for the Synthesis of Aryl Carboxylic Acids.

A novel I2-promoted direct conversion of arylacetic acids into aryl carboxylic acids under metal-free conditions has been described. This remarkable transformation involves decarboxylation followed by an oxidation reaction enabled just by using DMSO as the solvent as well as an oxidant. Notably, aryl carboxylic acids are isolated by simple filtration technique and obtained in good to excellent yields. This protocol is free from chromatographic purification, which makes it applicable for large-scale synthesis.

Right bundle branch block on alternate beats during acute pulmonary embolism.

The electrocardiogram of a patient with acute pulmonary embolism showed right bundle branch block (RBBB) on alternate beats; following thrombolysis, the pattern evolved to persistent RBBB and eventually to normal conduction. Analysis of serial tracings suggested that the mechanism of RBBB alternans was tachycardia-dependent bidirectional bundle branch block, caused by prolongation of both anterograde and retrograde refractory periods (RPs) of the right bundle branch (RBB). The sinus impulse found the RBB refractory, and was conducted over the left bundle branch only, depolarizing the left ventricle and then attempting to penetrate retrogradely the RBB; at that time, however, the RBB was still refractory. When a QRS complex had a RBBB configuration, therefore, the RBB was not depolarized; the ensuing sinus impulse found the RBB fully responsive as a consequence of the long period intervening between two successive depolarizations, and resulted in normal intraventricular conduction. With right ventricular afterload decrease, the recovery of RBB anterograde and retrograde excitability was asynchronous, since the retrograde RP became normal earlier than the anterograde one. In accordance with the relatively short retrograde RP, the RBB was retrogradely invaded by the transseptal impulse coming from the left ventricle; this "shifted to the right" the anterograde RP of the RBB. The RBB, thus, was still refractory to the next sinus impulse, and RBBB again occurred; the RBB, thus, was once more depolarized retrogradely, and this led to perpetuation of RBBB. Finally, intraventricular conduction became normal owing to full normalization of RBB anterograde and retrograde refractoriness.

S-metoprolol: the 2008 clinical review.

Metoprolol is a widely used cardioselective beta-blocker. However, like all other beta-blockers it is also a racemic mixture of R- and S- isomers. The beta 1 blocking activity (cardioselectivity) of metoprolol resides in S-isomer while R-isomer exhibits beta 2 blocking activity. As both these isomers have different pharmacological properties, racemic metoprolol can be considered a combination of two different drugs in a fixed 1:1 ratio. The needless administration of the non beta-blocking R-enantiomer that makes up 50% of racemate actually puts the patient at an increased risk of side-effects, drug interactions and loss of cardioselectivity with up-titration of dosing. Clinical experience with chirally pure S-metoprolol at half the dose of racemate has shown it to be as effective as racemate in the treatment of patients with hypertension and angina. S-metoprolol has been shown to be effective and well-tolerated in patients with coexisting diabetes, COPD, and hyperlipidaemia. This confirms higher cardioselectivity of S-metoprolol in clinical settings. Less interaction potential of S-metoprolol compared to R-isomer further makes it a sensible choice in patients taking CYP2D6 inhibitors or in patients with heart failure or hepatic insufficiency. This article reviews differing properties of two isomers of metoprolol with focus on clinical experience with S-metoprolol.

Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis.

The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications.