The Impact of Simulation-Based Training in Cardiovascular Medicine: A Systematic Review.

Cardiovascular medicine and practice in recent times have evolved as complex procedures are performed to manage difficult cases. The majority of these interventions are done percutaneously in order to minimize patient risk. Additionally, training specialist in handling these interventions require a lot of exposure to them; as such, patients are at higher risk of errors and complications from trainees before attaining expertise. In order to avoid these possible risks to patients and ensure their safety, using simulation commonly in cardiovascular specialist education is a possible trend in the future. This article aims to review randomized controlled trials that were performed in cardiology and vascular medicine regarding the use of simulating models to transfer skills to trainees. This study is a systematic review that includes publications dated from 2010 from any country and only in English. The search involved several combinations of search terms from medical subject headings (MeSH). Keywords in the title, abstract, and text for the population, intervention, control, and outcomes were first done in a pilot search to establish the sensitivity of the search strategy. Studies were searched in PubMed, Medline, Cochrane Library, Embase, CINAHL, and Hirani. Data were presented in the PRISMA flowchart and tabular form. A total of 389 studies were obtained from five databases using the search strategies. Eighty-nine studies were excluded for duplication. The total number of studies that did not meet the inclusion criteria was 269, and they were excluded based on abstract and title screening. Another 18 studies were excluded based on full-text screening. In this study, 13 articles were selected ranging from 2011 to 2022. The majority of the outcomes of the study demonstrated that simulation tutoring complements traditional methods of training. Countries of publication were the United States of America, Canada, Italy, Korea, California, Ireland, Germany, Belgium, Switzerland, United Kingdom, Netherlands, and France. Procedures simulated include coronary angiography, transseptal catheterization, cardiopulmonary resuscitation, ultrasound-guided radial artery cannulation, diagnostic angiograms, coiled carotid terminus aneurysms in the setting of subarachnoid hemorrhage, middle cerebral artery embolectomies, renal artery angioplasty/stenting, endovascular aneurysm repair, transvenous pacing wire, intra-aortic balloon pump, and pericardiocentesis. Despite the accredited drawback of availability and cost noted with simulation-based education, there is evidence that it offers many advantages compared to traditional teaching methods. From this study, simulation-based teaching has been shown to effectively transfer skills to trainees especially when used as an adjunct to the apprenticeship method. As a result, we recommend that virtual reality education should be integrated with real-life teaching in modern cardiovascular modules as this will help ensure early skill transfer while maintaining patient safety.

Myocardial calcium signalling and arrhythmia pathogenesis.

Myocardial calcium signalling is a vital component of the normal physiological function of the heart. Key amongst the many roles calcium plays is its use as the primary signalling component of excitation-contraction coupling, the intracellular process that links cardiomyocyte depolarisation to contraction. Defective cellular calcium handling, due to abnormalities of the various components which mediate and control excitation-contraction coupling, is widely recognised as a significant patho-physiological event in the contractile dysfunction of the failing heart. In addition, similar defects also appear to be increasingly recognised as mediators of certain forms of cardiac arrhythmias. Such defects include single gene defects in excitation-contraction coupling components that lead to inherited sudden death arrhythmia syndromes. Alternatively, arrhythmogenesis occurring within the context of acquired cardiac disease, in particular heart failure, also appears to be highly dependent on abnormal calcium homeostasis. In this article we review the defects in cardiomyocyte calcium homeostasis that lead to particular pro-arrhythmogenic phenomena and discuss recent insights gained into a variety of inherited and acquired arrhythmia syndromes that appear to involve defective calcium signalling as a central component of their patho-physiology. Potential opportunities for new anti arrhythmic therapeutic strategies based on these recent insights are also discussed.

Ryanodine receptor regulation by intramolecular interaction between cytoplasmic and transmembrane domains.

Ryanodine receptors (RyR) function as Ca(2+) channels that regulate Ca(2+) release from intracellular stores to control a diverse array of cellular processes. The massive cytoplasmic domain of RyR is believed to be responsible for regulating channel function. We investigated interaction between the transmembrane Ca(2+)-releasing pore and a panel of cytoplasmic domains of the human cardiac RyR in living cells. Expression of eGFP-tagged RyR constructs encoding distinct transmembrane topological models profoundly altered intracellular Ca(2+) handling and was refractory to modulation by ryanodine, FKBP12.6 and caffeine. The impact of coexpressing dsRed-tagged cytoplasmic domains of RyR2 on intracellular Ca(2+) phenotype was assessed using confocal microscopy coupled with parallel determination of in situ protein: protein interaction using fluorescence resonance energy transfer (FRET). Dynamic interactions between RyR cytoplasmic and transmembrane domains were mediated by amino acids 3722-4610 (Interacting or "I"-domain) which critically modulated intracellular Ca(2+) handling and restored RyR sensitivity to caffeine activation. These results provide compelling evidence that specific interaction between cytoplasmic and transmembrane domains is an important mechanism in the intrinsic modulation of RyR Ca(2+) release channels.

The cardiac ryanodine receptor (calcium release channel): emerging role in heart failure and arrhythmia pathogenesis.

The cardiac sarcoplasmic reticulum calcium release channel, commonly referred to as the ryanodine receptor, is a key component in cardiac excitation-contraction coupling, where it is responsible for the release of calcium from the sarcoplasmic reticulum. As our knowledge of the ryanodine receptor has advanced an appreciation that this key E-C coupling component may have a role in the pathogenesis of human cardiac disease has emerged. Heart failure and arrhythmia generation are both pathophysiological states that can result from deranged excitation-contraction coupling. Evidence is now emerging that hyperphosphorylation of the cardiac ryanodine receptor is an important event in chronic heart failure, contributing to impaired contraction and the generation of triggered ventricular arrhythmias. Furthermore the therapeutic benefits of beta blockers in heart failure appear to be partly explained through a reversal of this phenomenon. Two rare inherited arrhythmogenic conditions, which can cause sudden death in children, have also been shown to result from mutations in the cardiac ryanodine receptor. These conditions, catecholaminergic polymorphic ventricular tachycardia and arrhythmogenic right ventricular cardiomyopathy (subtype 2), further implicate the ryanodine receptor as a potentially arrhythmogenic substrate and suggest that this channel may offer a new therapeutic target in the treatment of both cardiac arrhythmias and heart failure.