Use of a leadless pacemaker in the management of swallow syncope: A case report.

A 41-year-old male presented with syncope whilst eating and was subsequently demonstrated to have recurrent symptomatic sinus pauses whilst swallowing. Following the exclusion of structural heart disease, he was diagnosed with swallow syncope, an uncommon variant of neurocardiogenic syncope. To avoid long-term complications of a transvenous pacemaker, the case was managed with a leadless pacemaker which resulted in complete resolution of symptoms.

Electrocardiographic QRS duration is influenced by body mass index and sex.

Background: Electrocardiogram (ECG) measured QRS duration has been shown to influence cardiovascular outcomes. However, there is paucity of data on whether ECG QRS duration is influenced by obesity and sex in large populations.

Methods: All ECGs performed by a pathology provider over a 2-year period were included.

Pharmacological Therapy for Ventricular Arrhythmias: A State-of-the Art Review.

While implantable cardioverter defibrillators decrease mortality in high risk groups of patients who have ventricular arrhythmias, antiarrhythmic drugs are still required to reduce the burden of both benign and life-threatening arrhythmias. This review will address the available medical therapy for ventricular arrhythmias in Australia and their use in different clinical situations.

Stimulation of the cardiac myocyte Na+-K+ pump due to reversal of its constitutive oxidative inhibition.

Protein kinase C can activate NADPH oxidase and induce glutathionylation of the β1-Na(+)-K(+) pump subunit, inhibiting activity of the catalytic α-subunit. To examine if signaling of nitric oxide-induced soluble guanylyl cyclase (sGC)/cGMP/protein kinase G can cause Na(+)-K(+) pump stimulation by counteracting PKC/NADPH oxidase-dependent inhibition, cardiac myocytes were exposed to ANG II to activate NADPH oxidase and inhibit Na(+)-K(+) pump current (Ip). Coexposure to 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) to stimulate sGC prevented the decrease of Ip.

Redox-dependent regulation of the Na⁺-K⁺ pump: new twists to an old target for treatment of heart failure.

By the time it was appreciated that the positive inotropic effect of cardiac glycosides is due to inhibition of the membrane Na(+)-K(+) pump, glycosides had been used for treatment of heart failure on an empiric basis for ~200 years. The subsequent documentation of their lack of clinical efficacy and possible harmful effect largely coincided with the discovery that a raised Na(+) concentration in cardiac myocytes plays an important role in the electromechanical phenotype of heart failure syndromes. Consistent with this, efficacious pharmacological treatments for heart failure have been found to stimulate the Na(+)-K(+) pump, effectively the only export route for intracellular Na(+) in the heart failure.

β(3) adrenergic stimulation of the cardiac Na+-K+ pump by reversal of an inhibitory oxidative modification.

Background: inhibition of L-type Ca(2+) current contributes to negative inotropy of β(3) adrenergic receptor (β(3) AR) activation, but effects on other determinants of excitation-contraction coupling are not known. Of these, the Na(+)-K(+) pump is of particular interest because of adverse effects attributed to high cardiac myocyte Na(+) levels and upregulation of the β(3) AR in heart failure.

Methods And Results: we voltage clamped rabbit ventricular myocytes and identified electrogenic Na(+)-K(+) pump current (I(p)) as the shift in holding current induced by ouabain.

Frequency of late drug-eluting stent thrombosis with non-cardiac surgery.

Drug-eluting stents (DES) are highly effective in reducing restenosis but have a small but significant risk for late stent thrombosis (LAST). Cessation of antiplatelet drugs for noncardiac surgery has been implicated in precipitating LAST, prompting surgery to be done on antiplatelet therapy, with all the attendant bleeding risks, or deferred until 12 months after DES implantation, despite limited data defining the risk for LAST. Using billing data from 2 large health funds, members who had DES insertion (n = 9,321) with subsequent noncardiac surgery (n = 4,126) were mailed a questionnaire regarding their noncardiac procedures, antiplatelet use, and subsequent coronary events.

Activation of cAMP-dependent signaling induces oxidative modification of the cardiac Na+-K+ pump and inhibits its activity.

Cellular signaling can inhibit the membrane Na(+)-K(+) pump via protein kinase C (PKC)-dependent activation of NADPH oxidase and a downstream oxidative modification, glutathionylation, of the beta(1) subunit of the pump alpha/beta heterodimer. It is firmly established that cAMP-dependent signaling also regulates the pump, and we have now examined the hypothesis that such regulation can be mediated by glutathionylation. Exposure of rabbit cardiac myocytes to the adenylyl cyclase activator forskolin increased the co-immunoprecipitation of NADPH oxidase subunits p47(phox) and p22(phox), required for its activation, and increased superoxide-sensitive fluorescence.

Reversible oxidative modification: a key mechanism of Na+-K+ pump regulation.

Angiotensin II (Ang II) inhibits the cardiac sarcolemmal Na(+)-K(+) pump via protein kinase (PK)C-dependent activation of NADPH oxidase. We examined whether this is mediated by oxidative modification of the pump subunits. We detected glutathionylation of beta(1), but not alpha(1), subunits in rabbit ventricular myocytes at baseline.

Angiotensin II inhibits the Na+-K+ pump via PKC-dependent activation of NADPH oxidase.

The sarcolemmal Na(+)-K(+) pump, pivotal in cardiac myocyte function, is inhibited by angiotensin II (ANG II). Since ANG II activates NADPH oxidase, we tested the hypothesis that NADPH oxidase mediates the pump inhibition. Exposure to 100 nmol/l ANG II increased superoxide-sensitive fluorescence of isolated rabbit ventricular myocytes.

Viability of hypokinetic segments: influence of tethering from adjacent segments: influence of tethering from adjacent segments.

Hypokinetic myocardium is presumed to be reversibly dysfunctional. However, hypokinetic segments do not necessarily improve after revascularization since their outcome can be influenced by tethering effects of adjacent myocardium. To assess whether hypokinetic segments improve following revascularization, 24 patients underwent resting and dobutamine stress echocardiography (DSE), with a total of 420 (20 per patient) myocardial segments studied pre- and postrevascularization.