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Midazolam and fentanyl together produce better sedation, analgesia and amnesia than do either drug alone, but the electrophysiologic effects of the combination are unknown. Twenty patients undergoing electrophysiologic studies for clinical reasons were studied. Blood pressure, heart rate, respiratory rate, oxygen saturation, and standard variables related to atrioventricular and ventriculoatrial conduction, dual pathways, accessory pathway conduction, sinus node function, and the inducibility of tachycardia were examined before and after intravenous injections of midazolam (0.07 [+ or -] 0.03 mg/kg) combined with fentanyl (0.8 [+ or -] 0.4 [Mu]g/kg). There were no significant changes in the electrophysiologic variables or ease of inducibility of tachycardia. The drugs were well tolerated; they produced minor and clinically unimportant reductions in mean blood pressure (99 [+ or -] 13 to 89 [+ or -] 16 mm Hg; p

Introduction:Bystander response including cardiopulmonary resuscitation (CPR) is critical to survival in out-of-hospital cardiac arrest (OHCA). Poorer outcomes have been reported in some immigrant communities but there has been less research about bystander response in these communities. Over a third of New South Wales (NSW) residents were born outside Australia.Hypothesis:Country of birth may explain variation in willingness to respond to OHCA.Methods:A survey was conducted between May 2021-May 2022. It employed multiple recruitment approaches including reaching out to 72 organisations and targeting multi-ethnic community organisations, advertising via social media, and leveraging local networks. Data were collected on demographic variables, CPR training, and attitudes towards responding to OHCA.Results:Of the 1267 respondents (average age 49.6 years, 52% female), 60% were born outside Australia; of which 44% (n=332) were from South Asia, 33% (n=246) from East Asia and the remaining 23% from a mix of other regions including north-west Europe, north Africa-middle east. Most immigrant respondents (73%) had lived in Australia for over ten years. Higher rates of previous CPR training were reported in Australian-born participants compared with South Asian-born and East Asian-born (76%, 35%, 47% respectively p<0.001) with current training rates i.e. in last 12 months (16%, 6%, 12% respectively, p=0.003). Higher rates of willingness to perform CPR on someone they did not know, was reported in Australian-born participants compared to South Asian-born and East Asian-born (74%, 63%, 56% respectively, p=<0.001. After adjusting for age, gender, education, employment status, self-reported general health, and previous CPR training, the odds of reporting willingness to perform CPR was OR:0.73 (95% CI: 0.51-1.04) among respondents born in South Asia and OR:0.58 (95% CI 0.41-0.83) among those from East Asian countries compared with Australian-born.Conclusions:Improving access to training and addressing barriers to response in multi-ethnic communities may improve willingness and consequently response to OHCA.

Inducible ventricular tachycardia (VT) is a strong predictor of spontaneous ventricular tachyarrhythmia following ST-segment–elevation myocardial infarction. Reduced left ventricular ejection fraction (EF) predisposes patients to inducible VT after ST-segment–elevation myocardial infarction. However, the role of right ventricular (RV) dysfunction in predisposing to inducible VT has not been described previously.

Cardiac and respiratory movements cause catheter instability. Lateral catheter sliding over target endocardial surface can lead to poor tissue contact and unpredictable lesion formation. We describe a novel method of overcoming the effects of lateral catheter sliding movements using an electrogram-gated pulsed power ablation.

Ventricular tachycardia (VT) is a significant complication of myocardial infarction. Radiofrequency ablation for postinfarct VT is reserved for drug refractory VT or VT storms. Our hypothesis is that radiofrequency ablation in the early postinfarct period could abolish or diminish late recurrences of VT.

Sudden arrhythmic death after myocardial infarction (MI) is most frequent in the first month. Early programmed ventricular stimulation (within 1 week) post-MI has been able to identify long-term ventricular tachycardia (VT) occurrence. We aimed to determine the timing of development and stabilization of VT circuits after MI and how the evolution of the underlying substrate differs with VT inducibility.

Electrophysiological study (EPS) after myocardial infarction may have a role in identifying patients at risk of sudden cardiac death. It has been shown previously that inducible very fast ventricular tachycardia (VT; cycle length CL, 200–230 ms) is predictive of arrhythmia recurrence; however, its significance early after reperfusion in ST-segment–elevation myocardial infarction is unknown.

In January 2005, Australia became the first country to introduce a publicly funded pneumococcal vaccination program for persons 65 years and older which is free at point of service, although the vaccine cost had previously been partially subsidised. Hospitalisation in this age group is an important indicator of risk of invasive pneumococcal disease but vaccine uptake has been suboptimal. To determine vaccination rates and predictors of vaccination in the elderly hospitalised patients before and after January 2005. We validated vaccination status against general practitioner (GP) records for patients aged ≥65 years admitted to a large teaching hospital in Sydney between 16th of May 2005 and the 20th of February 2006 and examined predictors of vaccinationCommencement of the new program resulted in a significant increase in vaccination uptake from 39% of inpatients prior to the free program to 73% in the same cohort of inpatients post January 2005. We found that patient recall of vaccination status was not reliable. Self-report of pneumococcal vaccination had a sensitivity of 0.53 and a specificity of 0.55, highlighting that validation of vaccination status is required. Age over 80 years and dementia significantly predicted under-vaccination.This highlights the importance of integrating free vaccine supply and delivery in primary care to achieve high vaccination coverage. However, demented patients and the very elderly remain under-vaccinated, despite being admitted to hospital for active management of acute conditions.

OBJECTIVES

G protein-gated inwardly rectifying potassium (GIRK) channels are a family of K+-selective ion channels that slow the firing rate of neurons and cardiac myocytes. GIRK channels are directly bound and activated by the G protein Gβγ subunit. As heterotetramers, they comprise the GIRK1 and the GIRK2, -3, or -4 subunits. Here we show that GIRK1 but not the GIRK4 subunit is phosphorylated when heterologously expressed. We found also that phosphatase PP2A dephosphorylation of a protein in the excised patch abrogates channel activation by Gβγ. Experiments with the truncated molecule demonstrated that the GIRK1 C-terminal is critical for both channel phosphorylation and channel regulation by protein phosphorylation, but the critical phosphorylation sites were not located on the C terminus. These data provide evidence for a novel switch mechanism in which protein phosphorylation enables Gβγ gating of the channel complex.

The article offers suggestions for keeping one's heart healthy. It states that one should exercise or indulge in some type of physical activity as it is beneficial for heart and overall health. It mentions that one should try to analyze why he is unable to sleep properly like feeling tired and anxious could be due to depression which can lead to a heart disease. It highlights that a test which measures calcium content in coronary arteries can help to predict risk of a heart disease.

There is emerging evidence that coronary catheterization can cause cerebrovascular embolization. We aimed to assess the proportion of cardiac patients with retinal emboli before coronary catheterization and the proportion with newly developed retinal embolism shortly after coronary catheterization.

Recombinant human platelet-derived growth factor-AB improves cardiac function and survival after myocardial infarction in a porcine model.

Background/Aims:New therapies to positively impact scar formation after myocardial infarction (MI) could prevent ensuing heart failure or death from ventricular arrhythmias. We have previously shown that recombinant human Platelet Derived Growth Factor-AB (rhPDGF-AB) improves cardiac function in a rodent model of MI. To progress clinical translation, we evaluated the effect of rhPDGF-AB treatment in a clinically relevant porcine model of ischemia-reperfusion.Methods:36 pigs underwent balloon occlusion of the left anterior descending coronary artery or sham procedure. Infarcted pigs were randomized to receive a 7-day intravenous infusion of rhPDGF-AB or vehicle alone.Results:At 1-month after MI, rhPDGF-AB (compared to vehicle) improved survival by 40% and cardiac magnetic resonance imaging showed improved left ventricular (LV) ejection fraction by 11.5%. Pressure volume loop analyses revealed improved myocardial contractility and energetics after rhPDGF-AB treatment with minimal effect on ventricular compliance. Interestingly, rhPDGF-AB enhanced vasculogenesis (Fig. a,b) and increased scar anisotropy (high fiber alignment) (Fig. c,d) without affecting overall scar size or stiffness. rhPDGF-AB decreased inducible ventricular tachycardia by attenuating heterogeneity of the ventricular scar, a substrate for re-entrant circuits (Fig. e,f).Conclusion:Here, we demonstrate that rhPDGF-AB promotes post-MI cardiac wound repair by altering infarct scar mechanics, resulting in robust cardiac functional improvement, decreased ventricular arrhythmias and improved survival. Our findings suggest a strong translational potential for rhPDGF-AB as an adjunct to current MI treatment.

We compared cardiac risk factors and the revised cardiac risk index (RCRI) as predictors of post-operative myocardial injury after non-cardiac surgery.

Background: Atrial tachycardia and fibrillation in humans may be partly consequent to vagal stimulation. Induction of fibrillation in the small heart is considered to be impossible due to lack of a critical mass of >100–200 mm2. Even with the recent progression of the technology of in vivo and in vitro mouse electrophysiological studies, few reports describe atrial tachycardia or fibrillation in mice. The purpose of this study was to attempt provocation of atrial tachyarrhythmia in mice using transvenous pacing following cholinergic stimulation. Methods and results: In vivo electrophysiology studies were performed in 14 normal mice. A six-lead ECG was recorded from surface limb leads, and an octapolar electrode catheter was inserted via jugular vein cutdown approach for simultaneous atrial and ventricular endocardial recording and pacing. Atrial tachycardia and fibrillation were inducible in one mouse at baseline electrophysiology study and eleven of fourteen mice after carbamyl choline injection. The mean duration of atrial tachycardia was 126±384 s. The longest episode lasted 35 min and only terminated after atropine injection. Reinduction of atrial tachycardia after administration of atropine was not possible. Conclusion: Despite the small mass of the normal mouse atria, sustained atrial tachycardia and fibrillation can be easily and reproducibly inducible with endocardial pacing after cholinergic agonist administration. This finding may contribute to our understanding of the classical theories of arrhythmogenesis and critical substrates necessary for sustaining microreentrant circuits. The techniques of transcatheter parasympathetic agonist-mediated atrial tachycardia induction may be valuable in further murine electrophysiological studies, especially mutant models with potential atrial arrhythmia phenotypes.