Since its inception, the electrocardiogram (ECG) has been an essential tool in medicine. The ECG is more than a mere tracing of cardiac electrical activity; it can detect and diagnose various pathologies including arrhythmias, pericardial and myocardial disease, electrolyte disturbances, and pulmonary disease. The ECG is a simple, non-invasive, rapid, and cost-effective diagnostic tool in medicine; however, its clinical utility relies on the accuracy of its interpretation. Computer ECG analysis has become so widespread and relied upon that ECG literacy among clinicians is waning. With recent technological advances, the application of artificial intelligence-augmented ECG (AI-ECG) algorithms has demonstrated the potential to risk stratify, diagnose, and even interpret ECGs—all of which can have a tremendous impact on patient care and clinical workflow. In this review, we examine (i) the utility and importance of the ECG in clinical practice, (ii) the accuracy and limitations of current ECG interpretation methods, (iii) existing challenges in ECG education, and (iv) the potential use of AI-ECG algorithms for comprehensive ECG interpretation.

No abstract

No abstract

The medical complexity and high acuity of patients in the cardiac intensive care unit make for a unique patient population with high morbidity and mortality. While there are many tools for predictions of mortality in other settings, there is a lack of robust mortality prediction tools for cardiac intensive care unit patients. The ongoing advances in artificial intelligence and machine learning also pose a potential asset to the advancement of mortality prediction. Artificial intelligence algorithms have been developed for application of electrocardiogram interpretation with promising accuracy and clinical application. Additionally, artificial intelligence algorithms applied to electrocardiogram interpretation have been developed to predict various variables such as structural heart disease, left ventricular systolic dysfunction, and atrial fibrillation. These variables can be used and applied to new mortality prediction models that are dynamic with the changes in the patient's clinical course and may lead to more accurate and reliable mortality prediction. The application of artificial intelligence to mortality prediction will fill the gaps left by current mortality prediction tools.

No abstract

No abstract

OBJECTIVES/SPECIFIC AIMS: The objective of this study was to determine if trimethylamine N-oxide (TMAO) alone could acutely alter cardiac contractile function on a beat-to-beat basis. METHODS/STUDY POPULATION: CD1 adult mouse hearts were extracted, attached to a force transducer, oxygenated, and paced within an organ bath. Changes in contractility were measured after pipetting or reverse perfusing TMAO through the aorta via a modified Langendorff apparatus to facilitate TMAO delivery into the myocardium. To determine if our findings translated to the human heart, we performed contractility experiments using human right atrial appendage biopsy tissue retrieved during cardiopulmonary bypass procedures. To investigate whether TMAO alters contractile rate, in a separate series of experiments, the atria and sinoatrial node of isolated hearts were kept intact to allow for spontaneous beating without artificial pacing and were treated with TMAO or vehicle. In addition, intracellular calcium measurements were performed on spontaneously beating embryonic rat cardiomyocytes after TMAO or vehicle treatment. RESULTS/ANTICIPATED RESULTS: We found acute exposure to TMAO, diluted into the organ bath, increased average contraction amplitude 20% and 41% at 300 µM and 3000 µM, respectively (p<0.05, n=6). Langendorff reverse perfusion of mouse hearts ex vivo with 300 µM TMAO generated an even greater response than nonperfusion peripheral exposure and increased isometric force 32% (p<0.05, n=3). Consistent with what we observed in mouse hearts, incubation of human atrial muscle tissue with TMAO at 3000 µM increased isometric tension 31% compared with vehicle (p<0.05, n=4). TMAO treatment (3000 µM) also increased average beating frequency of ex vivo mouse hearts by 27% compared with vehicle (p<0.05, n=3) and increased the spontaneous beating frequency of primary rat cardiomyocytes by 13% compared with vehicle treatment (p<0.05, n=4). DISCUSSION/SIGNIFICANCE OF IMPACT: TMAO, at pathological concentrations, directly increases the force and rate of cardiac contractility. Initially, these inotropic and chronotropic effects may be adaptive during CKD; however, chronic increases in isometric tension and beating frequency can promote cardiac remodeling and heart failure. Further translational studies are needed to understand the intricate relationship between the microbiome, kidneys, and heart and to examine if TMAO represents a therapeutic target for reducing cardiovascular mortality in CKD patients.

BackgroundWhile it is understood that patients with chronic kidney disease (CKD) have an increased propensity for developing cardiovascular disease, the exact mechanisms remain unclear. Growing evidence suggests that the gut microbiome and its byproducts, such as TMAO, may be important contributors to this pathologic process. This uremic metabolite is cleared through renal excretion, which is compromised in CKD patients. Therefore, CKD patients often possess elevated plasma levels of this substance. In a previous study, we found that TMAO at pathological concentrations directly increases cardiac contractility in isolated, paced hearts. In this study, we sought to determine if TMAO also has chronotropic effects on isolated, spontaneously beating mouse hearts.MethodsWhole mouse hearts were extracted from anesthetized CD1 adult mice and subsequently connected to a force transducer and bubbled with oxygen inside an organ bath. The atria and sinoatrial node were kept intact to allow for spontaneous beating without artificial pacing. Changes in heart rate (in beats per minute) were measured after treatment with TMAO (3,000 μM) or vehicle (Ringer's solution). Additionally, calcium imaging was performed on cultured spontaneously beating embryonic rat cardiomyocytes. Intracellular Ca2+ responses in rat primary cardiomyocytes were measured with the fluorescent Ca2+ indicator Fura‐2 AM in response to vehicle and TMAO (3,000 uM).ResultsAverage beating frequency (in beats per minutes) of isolated hearts increased by 27% following treatment with 3,000 μM TMAO (P < 0.05, n =3) while there was no change with vehicle. Regarding isolated myocytes, TMAO was found to have a direct chronotropic effect as it increased beating frequency (as measured by calcium waves) by 13% compared to vehicle treatment (P < 0.05, n =4–5).ConclusionsIn addition to our previously described inotropic effects in the mouse heart, pathologic concentrations of TMAO also have a direct and positive chronotropic effect. The direct effects we have observed on the heart may increase cardiac output in early stages of CKD. However, cardiac remodeling as a result of increased beating frequency and contractility may have pathologic consequences in those with chronic disease. Further research is needed in order to elucidate the effect that TMAO has on cardiovascular function and pathology during CKD.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.