Evaluation of responses to cardiac imaging questions by the artificial intelligence large language model ChatGPT.

PURPOSE: To assess ChatGPT's ability as a resource for educating patients on various aspects of cardiac imaging, including diagnosis, imaging modalities, indications, interpretation of radiology reports, and management. METHODS: 30 questions were posed to ChatGPT-3.5 and ChatGPT-4 three times in three separate chat sessions. Responses were scored as correct, incorrect, or clinically misleading categories by three observers-two board certified cardiologists and one board certified radiologist with cardiac imaging subspecialization. Consistency of responses across the three sessions was also evaluated. Final categorization was based on majority vote between at least two of the three observers. RESULTS: ChatGPT-3.5 answered seventeen of twenty eight questions correctly (61 %) by majority vote. Twenty one of twenty eight questions were answered correctly (75 %) by ChatGPT-4 by majority vote. Majority vote for correctness was not achieved for two questions. Twenty six of thirty questions were answered consistently by ChatGPT-3.5 (87 %). Twenty nine of thirty questions were answered consistently by ChatGPT-4 (97 %). ChatGPT-3.5 had both consistent and correct responses to seventeen of twenty eight questions (61 %). ChatGPT-4 had both consistent and correct responses to twenty of twenty eight questions (71 %). CONCLUSION: ChatGPT-4 had overall better performance than ChatGTP-3.5 when answering cardiac imaging questions with regard to correctness and consistency of responses. While both ChatGPT-3.5 and ChatGPT-4 answers over half of cardiac imaging questions correctly, inaccurate, clinically misleading and inconsistent responses suggest the need for further refinement before its application for educating patients about cardiac imaging.

Exploratory use of intraprocedural transesophageal echocardiography to guide implantation of the leadless pacemaker.

Background: Fluoroscopy is the standard tool for transvenous implantation of traditional and leadless pacemakers (LPs). LPs are used to avoid complications of conventional pacemakers, but there still is a 6.5% risk of major complications. Mid-right ventricular (RV) septal device implantation is suggested to decrease the risk, but helpful cardiac landmarks cannot be visualized under fluoroscopy. Transesophageal echocardiography (TEE) is an alternative intraprocedural imaging method. Objective: The purpose of this study was to explore the spatial relationship of the LP to cardiac landmarks via TEE and their correlations with electrocardiographic (ECG) parameters, and to outline an intraprocedural method to confirm mid-RV nonapical lead positioning. Methods: Fifty-six patients undergoing implantation of LP with TEE guidance were enrolled in the study. Device position was evaluated by fluoroscopy, ECG, and TEE. Distances between the device and cardiac landmarks were measured by TEE and analyzed with ECG parameters with and without RV pacing. Results: Mid-RV septal positioning was achieved in all patients. TEE transgastric view (0°-40°/90°-130°) was the optimal view for visualizing device position. Mean tricuspid valve-LP distance was 4.9 ± 0.9 cm, mean pulmonary valve-LP distance was 4.2 ± 1 cm, and calculated RV apex-LP distance was 2.9 ± 1 cm. Mean LP paced QRS width was 160.8 ± 28 ms and increased from 117.2 ± 34 ms at baseline. LP RV pacing resulted in left bundle branch block pattern on ECG and 37.8% QRS widening by 43.5 ± 29 ms. Conclusion: TEE may guide LP implantation in the nonapical mid-RV position. Further studies are required to establish whether this technique reduces implant complications compared with conventional fluoroscopy.

Blanching Defects at the Pressure Points: Observations from Dynamic Total-Body PET/CT Studies.

Total-body PET/CT allows simultaneous acquisition of all the body parts in a single bed position during the radiotracer uptake phase. Dynamic imaging protocols employing total-body PET could demonstrate findings that may not have been previously visualized or described using conventional PET/CT scanners. We examined the characteristics of blanching defects, areas of markedly reduced (partial defect) or absent (complete defect) radiotracer uptake seen at the skin/subcutaneous tissues opposite the bony prominences at pressure points. Methods: In this observational study, 77 participants underwent dynamic total-body PET/CT imaging using 18F-FDG (Group 1, N = 47, 60-min dynamic, arms-down, divided into 3 subgroups according to the injected dose) or 18F-fluciclovine (Group 2, N = 30, 25-min dynamic, arms above the head). 40 out of 47 participants in Group 1 were re-imaged at 90 min after being allowed off the scanning table. Blanching defects, partial or complete, were characterized opposite the bony prominences at 7 pressure points (the skull, scapula, and calcaneus bilaterally, as well as the sacrum). Association of the blanching defects with different clinical and technical characteristics were analyzed using uni- and multi-variate analyses. Results: A total of 124 blanching defects were seen in 68 out of 77 (88%) participants at one or more pressure points. Blanching defects were higher, on average, in Group 2 participants (3.5±1.7) compared to Group 1 (2.1±1.4; P <0.001), but it did not vary within Group 1 for different 18F-FDG dose subgroups. All defects resumed normal pattern on delayed static (90-min) images except for 14 partial defects. No complete blanching defects were seen on the 90-min images. By multivariate analysis, arm positioning above the head was associated with skull defects; scapular and sacral defects were significantly more encountered in men and with lower BMI, while calcaneal defects could not be associated to any factor. Conclusion: Blanching defects opposite the bony pressure points are common on dynamic total-body PET/CT images using different radiopharmaceuticals and injection doses. Their appearance should not be immediately interpreted as an abnormality. The current findings warrant further exploration in a prospective setting and may be utilized to study various mechano-pathologic conditions, such as pressure ulcers.

The Impact of Environmental Context on Intern Sign-Out Quality.

BACKGROUND: Resident duty-hour restrictions have led to more sign-out transitions, increasing the potential for preventable harm. An unfavorable environment is expected to exacerbate sign-out risks to patient safety. OBJECTIVE: The aim of the study was to evaluate the impact of noise, interruptions, long sign-outs, and sign-outs exceeding allotted time on sign-out quality. METHODS: Eight trained observers evaluated 620 evening patient sign-outs between interns for 40 weeknights between February and April 2015 at a large internal medicine training program. Quality of sign-out was measured three ways: information quality, scores from the Handoff CEX Tool, and peer evaluations. RESULTS: Noise had no impact on information quality. Interruptions negatively affected information quality (-0.10 < r < -0.15, P < 0.001) and Handoff CEX quality scores (-0.11 < r < -0.26, P < 0.001). Long sign-outs taking more than 1 hour negatively affected sign-out quality (-0.09 < r < -0.23, P < 0.05). Sign-outs exceeding allotted time negatively impacted peer evaluations (-0.11 < r < -0.22, P < 0.001). CONCLUSIONS: Interruptions, long sign-outs, and sign-outs exceeding allotted time were related to lower sign-out quality. Improving the environment to reduce interruptions and training interns to manage their time during sign-outs may improve sign-out quality.

Disconnect between Fibrotic Response and Right Ventricular Dysfunction.

Rationale: Remodeling and fibrosis of the right ventricle (RV) may cause RV dysfunction and poor survival in patients with pulmonary hypertension. Objectives: To investigate the consequences of RV fibrosis modulation and the accompanying cellular changes on RV function. Methods: Expression of fibrotic markers was assessed in the RV of patients with pulmonary hypertension, the murine pulmonary artery banding, and rat monocrotaline and Sugen5416/hypoxia models. Invasive hemodynamic and echocardiographic assessment was performed on galectin-3 knockout or inhibitor-treated mice. Measurements and Main Results: Established fibrosis was characterized by marked expression of galectin-3 and an enhanced number of proliferating RV fibroblasts. Galectin-3 genetic and pharmacologic inhibition or antifibrotic treatment with pirfenidone significantly diminished RV fibrosis progression in the pulmonary artery banding model, without improving RV functional parameters. RV fibrotic regions were populated with mesenchymal cells coexpressing vimentin and PDGFRα (platelet-derived growth factor receptor-α), but generally lacked αSMA (α-smooth muscle actin) positivity. Serum levels of galectin-3 were increased in patients with idiopathic pulmonary arterial hypertension but did not correlate with cardiac function. No changes of galectin-3 expression were observed in the lungs. Conclusions: We identified extrapulmonary galectin-3 as an important mediator that drives RV fibrosis in pulmonary hypertension through the expansion of PDGFRα/vimentin-expressing cardiac fibroblasts. However, interventions effectively targeting fibrosis lack significant beneficial effects on RV function.

A Randomized Cohort Controlled Trial to Compare Intern Sign-Out Training Interventions.

BACKGROUND: Although previous studies have investigated the efficacy of specific sign-out protocols (such as the illness severity, patient summary, action list, situation awareness and contingency planning, and synthesis by reviewer [I-PASS] bundle), the implementation of a bundle can be time consuming and costly. We compared 4 sign-out training pedagogies on sign-out quality. OBJECTIVE: To evaluate training interventions that best enhance multidimensional sign-out quality measured by information exchange, task accountability, and personal responsibility. INTERVENTION: Four general internal medicine firms were randomly assigned into 1 of the following 4 training interventions: didactics (control), I-PASS, policy mandate on task accountability, and Plan-Do-Study-Act (PDSA). SETTING: First-year interns at a large, Mid-Atlantic internal medicine residency program. MEASUREMENTS: Eight trained observers examined 10 days each in the pre- and postintervention periods for each firm using a standardized sign-out checklist. RESULTS: Pre- and postintervention differences showed significant improvements in the transfer of patient information, task accountability, and personal responsibility for the I-PASS, policy mandate, and PDSA groups, respectively, in line with their respective training foci. Compared to the control, I-PASS reported the best improvements in sign-out quality, although there was room to improve in task accountability and responsibility. CONCLUSIONS: Different training emphases improved different dimensions of sign-out quality. A combination of training pedagogies is likely to yield optimal results.

The vestigial enzyme D-dopachrome tautomerase protects the heart against ischemic injury.

The cellular response to stress involves the recruitment and coordination of molecular signaling pathways that prevent cell death. D-dopachrome tautomerase (DDT) is an enzyme that lacks physiologic substrates in mammalian cells, but shares partial sequence and structural homology with macrophage migration inhibitory factor (MIF). Here, we observed that DDT is highly expressed in murine cardiomyocytes and secreted by the heart after ischemic stress. Antibody-dependent neutralization of secreted DDT exacerbated both ischemia-induced cardiac contractile dysfunction and necrosis. We generated cardiomyocyte-specific DDT knockout mice (Myh6-Cre Ddtfl/fl), which demonstrated normal baseline cardiac size and function, but had an impaired physiologic response to ischemia-reperfusion. Hearts from Myh6-Cre Ddtfl/fl mice exhibited more necrosis and LV contractile dysfunction than control hearts after coronary artery ligation and reperfusion. Furthermore, treatment with DDT protected isolated hearts against injury and contractile dysfunction after ischemia-reperfusion. The protective effect of DDT required activation of the metabolic stress enzyme AMP-activated protein kinase (AMPK), which was mediated by a CD74/CaMKK2-dependent mechanism. Together, our data indicate that cardiomyocyte secretion of DDT has important autocrine/paracrine effects during ischemia-reperfusion that protect the heart against injury.

A small molecule AMPK activator protects the heart against ischemia-reperfusion injury.

AMP-activated protein kinase (AMPK) is a stress signaling enzyme that orchestrates the regulation of energy-generating and -consuming pathways. Intrinsic AMPK activation protects the heart against ischemic injury and apoptosis, but whether pharmacologic AMPK stimulation mitigates ischemia-reperfusion damage is unknown. The aims of this study were to determine whether direct stimulation of AMPK using a small molecule activator, A-769662, attenuates myocardial ischemia-reperfusion injury and to examine its cardioprotective mechanisms. Isolated mouse hearts pre-treated with A-769662 had better recovery of left ventricular contractile function (55% vs. 29% of baseline rate-pressure product; p=0.03) and less myocardial necrosis (56% reduction in infarct size; p<0.01) during post-ischemic reperfusion compared to control hearts. Pre-treatment with A-769662 in vivo attenuated infarct size in C57Bl/6 mice undergoing left coronary artery occlusion and reperfusion compared to vehicle (36% vs. 18%, p=0.025). Mouse hearts with genetically inactivated AMPK were not protected by A-769662, indicating the specificity of this compound. Pre-treatment with A-769662 increased the phosphorylation and inactivation of eukaryotic elongation factor 2 (eEF2), preserved energy charge during ischemia, delayed the development of ischemic contracture, and reduced myocardial apoptosis and necrosis. A-769662 also augmented endothelial nitric oxide synthase (eNOS) activation during ischemia, which partially attenuated myocardial stunning, but did not prevent necrosis. AMPK is a therapeutic target that can be stimulated by a direct-acting small molecule in order to prevent injury during ischemia-reperfusion. The use of AMPK activators may represent a novel strategy to protect the heart and other solid organs against ischemia.