Search

BackgroundThe detection of dyskalemias—hypokalemia and hyperkalemia—currently depends on laboratory tests. Since cardiac tissue is very sensitive to dyskalemia, electrocardiography (ECG) may be able to uncover clinically important dyskalemias before laboratory results. ObjectiveOur study aimed to develop a deep-learning model, ECG12Net, to detect dyskalemias based on ECG presentations and to evaluate the logic and performance of this model. MethodsSpanning from May 2011 to December 2016, 66,321 ECG records with corresponding serum potassium (K+) concentrations were obtained from 40,180 patients admitted to the emergency department. ECG12Net is an 82-layer convolutional neural network that estimates serum K+ concentration. Six clinicians—three emergency physicians and three cardiologists—participated in human-machine competition. Sensitivity, specificity, and balance accuracy were used to evaluate the performance of ECG12Net with that of these physicians. ResultsIn a human-machine competition including 300 ECGs of different serum K+ concentrations, the area under the curve for detecting hypokalemia and hyperkalemia with ECG12Net was 0.926 and 0.958, respectively, which was significantly better than that of our best clinicians. Moreover, in detecting hypokalemia and hyperkalemia, the sensitivities were 96.7% and 83.3%, respectively, and the specificities were 93.3% and 97.8%, respectively. In a test set including 13,222 ECGs, ECG12Net had a similar performance in terms of sensitivity for severe hypokalemia (95.6%) and severe hyperkalemia (84.5%), with a mean absolute error of 0.531. The specificities for detecting hypokalemia and hyperkalemia were 81.6% and 96.0%, respectively. ConclusionsA deep-learning model based on a 12-lead ECG may help physicians promptly recognize severe dyskalemias and thereby potentially reduce cardiac events.

BackgroundHypertension is a major cause of mortality in cardiac, vascular, and renal disease. Effective control of elevated blood pressure has been shown to reduce target organ damage. A Web-based self-titration program may empower patients to control their own disease, share decisions about antihypertensive dose titration, and improve self-management, ultimately improving health-related quality of life. ObjectiveOur primary aim was to evaluate the effects of a Web-based self-titration program for improving blood pressure control in patients with primary hypertension. Our secondary aim was to evaluate the effects of that program on improving health-related quality of life. MethodsThis was a parallel-group, double-blind, randomized controlled trial with assessments at baseline, 3 months, and 6 months. We included patients with primary hypertension (blood pressure>130/80 mm Hg) from a cardiology outpatient department in northern Taiwan and divided them randomly into intervention and control groups. The intervention group received the Web-based self-titration program, while the control group received usual care. The random allocation was concealed from participants and outcome evaluators. Health-related quality of life was measured by the EuroQol five-dimension self-report questionnaire. We used generalized estimating equations to evaluate the effects of the intervention. ResultsWe included 222 patients and divided them equally into intervention (n=111) and control (n=111) groups. Patients receiving the Web-based self-titration program showed significantly greater improvement in the systolic and diastolic blood pressure control than those who did not receive this program, at 3 months (–21.4 mm Hg and –5.4 mm Hg, respectively; P

Takotsubo cardiomyopathy (TCM), also known as stress cardiomyopathy, is a type of nonischemic cardiomyopathy, in which there is a sudden temporary weakening of the muscular portion of the heart. It is usually the result of severe emotional or physical stress, such as a sudden illness, the loss of a loved one, or a serious accident. The most commonly discussed possible mechanism is stress-induced catecholamine release, with toxicity to and subsequent stunning of the myocardium. We describe a rare case of TCM in a young woman after receiving cosmetic facial mole removal under local laser therapy. She denied history of systemic disease. The patient had chest pain, shortness of breath, elevated cardiac enzymes, and ST-segment elevations in V1–V4. There is absence of significant coronary artery disease in emergent cardiac catheterization. Left ventriculography revealed apical ballooning akinesis with basal hyperkinesis during systole. Takotsubo cardiomyopathy was impressed under above findings. The patient was successfully treated with medical conservative treatment without complication.

Background: Ceramide is involved in regulating metabolism and energy expenditure, and its abnormal myocardial accumulation may contribute to heart injury or lipotoxic cardiomyopathy. Whether ceramide can modulate the electrophysiology of pulmonary veins (PVs) remains unknown. Materials and methods: We used conventional microelectrodes to measure the electrical activity of isolated rabbit PV tissue preparations before and after treatment with various concentrations of ceramide with or without H2O2 (2 mM), MitoQ, wortmannin or 740 YP. A whole‐cell patch clamp and fluorescence imaging were used to record the ionic currents, calcium (Ca2+) transients, and intracellular reactive oxygen species (ROS) and sodium (Na+) in isolated single PV cardiomyocytes before and after ceramide (1 μM) treatment. Results: Ceramide (0.1, 0.3, 1 and 3 μM) reduced the beating rate of PV tissues. Furthermore, ceramide (1 μM) suppressed the 2 mM H2O2‐induced faster PV beating rate, triggered activities and burst firings, which were further reduced by MitoQ. In the presence of wortmannin, ceramide did not change the PV beating rate. The H2O2‐induced faster PV beating rate could be counteracted by MitoQ or wortmannin with no additive effect from the ceramide. Ceramide inhibited pPI3K. Ceramide reduced Ca2+ transients, sarcoplasmic reticulum Ca2+ contents, L‐type Ca2+ currents, Na+ currents, late Na+ currents, Na+‐hydrogen exchange currents, and intracellular ROS and Na+ in PV cardiomyocytes, but did not change Na+‐Ca2+ exchange currents. Conclusion: C2 ceramide may exert the distinctive electrophysiological effect of modulating PV activities, which may be affected by PI3K pathway–mediated oxidative stress, and might play a role in the pathogenesis of PV arrhythmogenesis. [ABSTRACT FROM AUTHOR]