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<t>ECG</t> processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: <t>electrocardiogram.</t>
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<t>ECG</t> processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: <t>electrocardiogram.</t>
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ADInstruments ecg signals
<t>ECG</t> processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: <t>electrocardiogram.</t>
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<t>ECG</t> processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: <t>electrocardiogram.</t>
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<t>ECG</t> processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: <t>electrocardiogram.</t>
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<t>ECG</t> processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: <t>electrocardiogram.</t>
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a. Schematic overview of the IMPC data gathering. In total, 705 candidate genes with ≥ 1 significant parameter (q-value <0.05) in <t>electrocardiography</t> <t>(ECG)</t> or transthoracic <t>echocardiography</t> (TTE) derivates: <t>ECG</t> n = 424, TTE n = 243, TTE & ECG n = 38 target genes. b: Comprehensive representation of phenotype distribution across 705 genes. Genotype < >phenotype represented by chord graphs. Strength indicated by line thickness (thin lines - low phenotype count). Number of significant phenotypes (called ‘hits’) per gene (q-value <0.05). ECG - left, TTE – middle, both ECG and ECHO - right. Most genes with 1-2 hits, few with ≥ 3 hits. In gene knockouts with abnormal ECG, we observed an abnormal heart rate and inversely correlated RR interval duration in 29% (123/424) of mutant lines. A total of 24% of gene knockouts had QT alterations (102/424), 17% (72/424) in QRS, and 16% (68/424) in ST interval length. In the 243 knockouts with abnormal TTE data, we identified altered fractional shortening and ejection fraction associated with left ventricular dysfunction in 23% (56/243) of gene knockouts. Morphological differences in left ventricular interior diameter (LVID) or left ventricular posterior wall (LVPW) or anterior wall (LVAW) thickness observed in 20% (49/243) of the abnormal TTE knockouts. Half of the gene knockouts with abnormal cardiac phenotypes had a single abnormal phenotype; 49% (207/424) with ECG only and 57% (139/243) with TTE only compared to control animals.
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ECG processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: electrocardiogram.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: ECG processing methodology. Column (A) illustrates processing steps for a healthy human volunteer ECG recorded at 0.55T isocenter and column (B) illustrates the processing steps for a porcine subject ECG recorded at 3T isocenter. Step (1) A threshold was manually adjusted (dashed red line) to pass through QRS complexes while excluding the T wave. Detected QRS complexes are marked below the ECG tracing (red arrows and tick marks). Blue arrows highlight that at 0.55T low amplitude features, such as P waves, can be discerned before additional processing steps. Step (2) Examples of each different QRS morphology in the ECG recording are manually selected as QRS “templates.” In the 0.55T example, the smaller amplitude QRS complex was selected as one template and the larger amplitude QRS complex was selected as another template. The remaining QRS complexes are assigned to the template with the greatest cross-correlation. Step (3) Heartbeats matching the most frequent “normal sinus beat” QRS template are averaged after alignment of the QRS complexes to maximize cross-correlation. The ECGs used for averaging are plotted in gray and the resulting averaged ECG plotted in blue. One standard deviation bounds are show in green and red. The blue arrow illustrates that at 3T low amplitude features, such as the P wave, can fall within beat-to-beat ECG variation making detection more difficult. Steps (4) and (5) illustrate the methodology for evaluating error (red tracing) of the ECG tracing at isocenter (blue tracing) relative to the ECG outside the scanner room (green tracing). The PR, QRS, and ST, and T intervals are manually marked to assess error in different portions of the ECG. Step (4) shows simple subtraction results in overcalled “error” during the QRS complex that does not correspond to clinically significant differences in QRS morphology. Step (5) illustrates the effect of the alignment processing described in the for suppressing sub-clinical QRS error while preserving error in other portions of the ECG. The solid blue arrow highlights at 3T low amplitude features, such as the P wave, can be obscured by ECG error. The dashed blue arrow highlights the shape of the higher amplitude QRS complex is better preserved at 3T, but error can be seen in later portions of the QRS complex. ECG: electrocardiogram.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Standard Deviation, Preserving

Illustration of 12-lead ECG distortion at different MRI scanner field strengths. For reference, the PR, QRS, ST, and T wave intervals are labeled for each lead. The top trace for each lead is the baseline ECG outside the scanner room (labeled REF). ECGs at MRI scanner isocenter are shown for 0.55T (second trace), 1.5T (third trace), and 3T (fourth trace). The black line for each trace is the average ECG over a 2-minute ECG recording. The colored bounds indicate the one standard deviation bound for each ECG time point. Increased ST segment and T wave distortion are seen at increasing scanner field strength. At 3T, distortion can also be seen toward the end of the QRS complex. Standard deviation bounds are wider at higher field strength but relatively uniform across different ECG intervals. All ECGs are from the same porcine subject with the same ECG lead positions. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Illustration of 12-lead ECG distortion at different MRI scanner field strengths. For reference, the PR, QRS, ST, and T wave intervals are labeled for each lead. The top trace for each lead is the baseline ECG outside the scanner room (labeled REF). ECGs at MRI scanner isocenter are shown for 0.55T (second trace), 1.5T (third trace), and 3T (fourth trace). The black line for each trace is the average ECG over a 2-minute ECG recording. The colored bounds indicate the one standard deviation bound for each ECG time point. Increased ST segment and T wave distortion are seen at increasing scanner field strength. At 3T, distortion can also be seen toward the end of the QRS complex. Standard deviation bounds are wider at higher field strength but relatively uniform across different ECG intervals. All ECGs are from the same porcine subject with the same ECG lead positions. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Labeling, Standard Deviation, Magnetic Resonance Imaging

Illustration of beat-to-beat ECG variation over 2-minute recordings at different MRI scanner field strengths. The gray color scale indicates the difference of each heartbeat ECG from the 2-minute averaged ECG. Periodic variation in ECG distortion is most prominent at the respiration rate. Variation is least noticeable at 0.55T (top plot), and more conspicuous at 1.5T (middle plot), and 3T (bottom plot). ECGs are from the same porcine subject as with the same ECG lead position. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Illustration of beat-to-beat ECG variation over 2-minute recordings at different MRI scanner field strengths. The gray color scale indicates the difference of each heartbeat ECG from the 2-minute averaged ECG. Periodic variation in ECG distortion is most prominent at the respiration rate. Variation is least noticeable at 0.55T (top plot), and more conspicuous at 1.5T (middle plot), and 3T (bottom plot). ECGs are from the same porcine subject as with the same ECG lead position. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

ECG error in 0.55T, 1.5T, and 3T MRI scanners. (A) ECG error increased at each field strength when moving from scanner home position to isocenter. ECG error was lower at 0.55T compared to 1.5T and 3T both at scanner isocenter and at home position. (B) Compares ECG error between different ECG intervals at scanner isocenter. At 1.5T and 3T, ST segment error was higher than P wave error. Increasing ECG error with increasing scanner field strength reached more consistent statistical significance for the ST segment than the PR and QRS intervals. These findings are consistent with maximum MHD effect occurring during the ST segment. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: ECG error in 0.55T, 1.5T, and 3T MRI scanners. (A) ECG error increased at each field strength when moving from scanner home position to isocenter. ECG error was lower at 0.55T compared to 1.5T and 3T both at scanner isocenter and at home position. (B) Compares ECG error between different ECG intervals at scanner isocenter. At 1.5T and 3T, ST segment error was higher than P wave error. Increasing ECG error with increasing scanner field strength reached more consistent statistical significance for the ST segment than the PR and QRS intervals. These findings are consistent with maximum MHD effect occurring during the ST segment. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

ECG variation in 0.55T, 1.5T, and 3T MRI scanners. (A) Shows ECG variation increased at each field strength when moving from scanner home position to isocenter. At isocenter, ECG variation was significantly lower for 0.55T compared to 1.5T and 3T scanners. (B) Compares ECG variation between different ECG intervals at scanner isocenter. ECG variation was significantly lower at 0.55T compared to 1.5T and 3T for all intervals. However, in contrast to ECG error , ECG variation was not significantly different between the PR, QRS, and ST intervals. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: ECG variation in 0.55T, 1.5T, and 3T MRI scanners. (A) Shows ECG variation increased at each field strength when moving from scanner home position to isocenter. At isocenter, ECG variation was significantly lower for 0.55T compared to 1.5T and 3T scanners. (B) Compares ECG variation between different ECG intervals at scanner isocenter. ECG variation was significantly lower at 0.55T compared to 1.5T and 3T for all intervals. However, in contrast to ECG error , ECG variation was not significantly different between the PR, QRS, and ST intervals. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

Illustration of reduced ECG variation after cinching together ECG lead wires. The top trace for each lead is the baseline ECG outside the scanner room (labeled REF). ECGs at MRI scanner isocenter are shown for 0.55T (second trace), 1.5T (third trace), and 3T (fourth trace). The black line for each trace is the average ECG value for each heartbeat time point over a 2-minute ECG recording. The colored bounds indicated the one standard deviation bound for each ECG time point. Standard deviation bounds are narrower for this ECG, with cinching together ECG leads, compared to the ECG in , without cinching of ECG leads. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Illustration of reduced ECG variation after cinching together ECG lead wires. The top trace for each lead is the baseline ECG outside the scanner room (labeled REF). ECGs at MRI scanner isocenter are shown for 0.55T (second trace), 1.5T (third trace), and 3T (fourth trace). The black line for each trace is the average ECG value for each heartbeat time point over a 2-minute ECG recording. The colored bounds indicated the one standard deviation bound for each ECG time point. Standard deviation bounds are narrower for this ECG, with cinching together ECG leads, compared to the ECG in , without cinching of ECG leads. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Labeling, Standard Deviation, Magnetic Resonance Imaging

Effect of cinching together ECG lead wires on ECG distortion. (A1–3) ECG standard deviation measurements and (B1–3) ECG error measurements before lead wires were cinched together (study 1, 2) compared to after leads were cinched together (study 3–7). ECG variation improved after lead cinching for all MRI scanner field strengths. However, ECG error was not affected by lead cinching. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Effect of cinching together ECG lead wires on ECG distortion. (A1–3) ECG standard deviation measurements and (B1–3) ECG error measurements before lead wires were cinched together (study 1, 2) compared to after leads were cinched together (study 3–7). ECG variation improved after lead cinching for all MRI scanner field strengths. However, ECG error was not affected by lead cinching. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Standard Deviation, Magnetic Resonance Imaging

Error for detecting ischemic ST changes in 0.55T, 1.5T, and 3T MRI scanners. J point error, the primary time point used to detect ischemic ECG changes, was lower than overall ST error at all field strengths both at scanner table home position (A) and at isocenter (B). J point error and overall ST error were significantly lower at 0.55T compared to 1.5T and 3T scanners. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Error for detecting ischemic ST changes in 0.55T, 1.5T, and 3T MRI scanners. J point error, the primary time point used to detect ischemic ECG changes, was lower than overall ST error at all field strengths both at scanner table home position (A) and at isocenter (B). J point error and overall ST error were significantly lower at 0.55T compared to 1.5T and 3T scanners. Figure data are from porcine subjects. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

Illustration of ischemic ECG changes before and after porcine coronary artery occlusion in a 0.55T scanner. (A) Shows the baseline 12-lead ECG prior to coronary artery occlusion outside the MRI scanner (green line), at scanner home position (blue line), and at isocenter (red line). The ECG at scanner home position closely approximates the ECG outside the MRI. Some deviation of the ECG at scanner isocenter is noted within the ST segment and T wave intervals compared to the ECG outside the scanner. (B) Shows marked ST segment deviation is seen in several ECG leads after coronary artery occlusion. Changes in the QRS complex shape are also seen. Good agreement of gross ST segment and QRS changes is noted outside the scanner room (green line) compared to scanner home position (blue line) and scanner isocenter (red line). More subtle deviations between the ECG outside the scanner room and inside the MRI scanner are within the range noted for the repeat ECG outside the MRI scanner (dashed yellow line). ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Illustration of ischemic ECG changes before and after porcine coronary artery occlusion in a 0.55T scanner. (A) Shows the baseline 12-lead ECG prior to coronary artery occlusion outside the MRI scanner (green line), at scanner home position (blue line), and at isocenter (red line). The ECG at scanner home position closely approximates the ECG outside the MRI. Some deviation of the ECG at scanner isocenter is noted within the ST segment and T wave intervals compared to the ECG outside the scanner. (B) Shows marked ST segment deviation is seen in several ECG leads after coronary artery occlusion. Changes in the QRS complex shape are also seen. Good agreement of gross ST segment and QRS changes is noted outside the scanner room (green line) compared to scanner home position (blue line) and scanner isocenter (red line). More subtle deviations between the ECG outside the scanner room and inside the MRI scanner are within the range noted for the repeat ECG outside the MRI scanner (dashed yellow line). ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

Correlation of ischemic ST assessment inside vs. outside the 0.55T MRI scanner following porcine coronary artery occlusion. J point measurements including all 12 leads from 7 subjects are shown. There was good correlation of the J point measurement outside the MRI scanner compared to the J point measurement (A) at scanner home position (r 2 = 0.97) and (B) at isocenter (r 2 = 0.92). J point correlation inside the scanner was within the range of (C) repeat measurements outside the scanner room (r 2 = 0.90). J point changes between repeat ECGs outside the scanner room reflect true variations in the ST segment during coronary artery occlusion. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Correlation of ischemic ST assessment inside vs. outside the 0.55T MRI scanner following porcine coronary artery occlusion. J point measurements including all 12 leads from 7 subjects are shown. There was good correlation of the J point measurement outside the MRI scanner compared to the J point measurement (A) at scanner home position (r 2 = 0.97) and (B) at isocenter (r 2 = 0.92). J point correlation inside the scanner was within the range of (C) repeat measurements outside the scanner room (r 2 = 0.90). J point changes between repeat ECGs outside the scanner room reflect true variations in the ST segment during coronary artery occlusion. ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

Illustration of ST interpretation for human volunteers in a 0.55T MRI scanner. (A) A volunteer with ST segment and T wave distortion at scanner isocenter (red ECG trace) compared to outside the scanner room (green ECG trace). Though the ST segment is distorted in several leads, interpretation of ST segment deviation at the J point (at the start of the ST segment) appears preserved. (B) A volunteer with preserved ECG morphology at scanner isocenter compared to outside the MRI (overlapping green and red ECG traces). ECG: electrocardiogram, MRI: magnetic resonance imaging.

Journal: Journal of Cardiovascular Magnetic Resonance

Article Title: Evaluation of 12-lead electrocardiogram at 0.55T for improved cardiac monitoring in magnetic resonance imaging

doi: 10.1016/j.jocmr.2024.101009

Figure Lengend Snippet: Illustration of ST interpretation for human volunteers in a 0.55T MRI scanner. (A) A volunteer with ST segment and T wave distortion at scanner isocenter (red ECG trace) compared to outside the scanner room (green ECG trace). Though the ST segment is distorted in several leads, interpretation of ST segment deviation at the J point (at the start of the ST segment) appears preserved. (B) A volunteer with preserved ECG morphology at scanner isocenter compared to outside the MRI (overlapping green and red ECG traces). ECG: electrocardiogram, MRI: magnetic resonance imaging.

Article Snippet: ECG signal processing and statistical analysis were performed using MATLAB (MathWorks, Natick, Massachusetts).

Techniques: Magnetic Resonance Imaging

a. Schematic overview of the IMPC data gathering. In total, 705 candidate genes with ≥ 1 significant parameter (q-value <0.05) in electrocardiography (ECG) or transthoracic echocardiography (TTE) derivates: ECG n = 424, TTE n = 243, TTE & ECG n = 38 target genes. b: Comprehensive representation of phenotype distribution across 705 genes. Genotype < >phenotype represented by chord graphs. Strength indicated by line thickness (thin lines - low phenotype count). Number of significant phenotypes (called ‘hits’) per gene (q-value <0.05). ECG - left, TTE – middle, both ECG and ECHO - right. Most genes with 1-2 hits, few with ≥ 3 hits. In gene knockouts with abnormal ECG, we observed an abnormal heart rate and inversely correlated RR interval duration in 29% (123/424) of mutant lines. A total of 24% of gene knockouts had QT alterations (102/424), 17% (72/424) in QRS, and 16% (68/424) in ST interval length. In the 243 knockouts with abnormal TTE data, we identified altered fractional shortening and ejection fraction associated with left ventricular dysfunction in 23% (56/243) of gene knockouts. Morphological differences in left ventricular interior diameter (LVID) or left ventricular posterior wall (LVPW) or anterior wall (LVAW) thickness observed in 20% (49/243) of the abnormal TTE knockouts. Half of the gene knockouts with abnormal cardiac phenotypes had a single abnormal phenotype; 49% (207/424) with ECG only and 57% (139/243) with TTE only compared to control animals.

Journal: Nature Cardiovascular Research

Article Title: Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy

doi: 10.1038/s44161-022-00018-8

Figure Lengend Snippet: a. Schematic overview of the IMPC data gathering. In total, 705 candidate genes with ≥ 1 significant parameter (q-value <0.05) in electrocardiography (ECG) or transthoracic echocardiography (TTE) derivates: ECG n = 424, TTE n = 243, TTE & ECG n = 38 target genes. b: Comprehensive representation of phenotype distribution across 705 genes. Genotype < >phenotype represented by chord graphs. Strength indicated by line thickness (thin lines - low phenotype count). Number of significant phenotypes (called ‘hits’) per gene (q-value <0.05). ECG - left, TTE – middle, both ECG and ECHO - right. Most genes with 1-2 hits, few with ≥ 3 hits. In gene knockouts with abnormal ECG, we observed an abnormal heart rate and inversely correlated RR interval duration in 29% (123/424) of mutant lines. A total of 24% of gene knockouts had QT alterations (102/424), 17% (72/424) in QRS, and 16% (68/424) in ST interval length. In the 243 knockouts with abnormal TTE data, we identified altered fractional shortening and ejection fraction associated with left ventricular dysfunction in 23% (56/243) of gene knockouts. Morphological differences in left ventricular interior diameter (LVID) or left ventricular posterior wall (LVPW) or anterior wall (LVAW) thickness observed in 20% (49/243) of the abnormal TTE knockouts. Half of the gene knockouts with abnormal cardiac phenotypes had a single abnormal phenotype; 49% (207/424) with ECG only and 57% (139/243) with TTE only compared to control animals.

Article Snippet: Data were analyzed using standard protocols for ECG signal analysis by eMouse (Mouse Specifics).

Techniques: Mutagenesis, Control

Representative electrocardiograms from conscious mutant and control mice with indication of ECG parameters and interval durations. a , Gatm loss ( Gatm −/− ) caused lower heart rate with prolonged QRS width and QTc and ST interval lengths. b , Pla2g10 loss ( Pla2g10 −/− ) lowered heart rate and prolonged PR, PQ and QTc intervals in female null mice. c , Cap2 depletion ( Cap2 −/+ ) induced lower heart rate and lengthy QTc and ST durations in male null mice compared with C57BL/6N controls. Data are presented by Mouse Specifics software. Interval durations are given in milliseconds. M-mode recordings are through a short-axis view tangential to the papillary muscle from representative mutant and control mice. Images show the LVID throughout diastole and systole. d , Leprotl1 depletion ( Leprotl1 −/− ) reduced LV diameters (LVIDs and LVIDd) and increased myocardial wall thickness (LVAWs, LVAWd and LVPWs) with decreased systolic function compared with C57BL/6N controls. e , Alpk3 depletion ( Alpk3 −/− ) increased LV diameters (LVIDs and LVIDd) and decreased systolic function via reduced fractional shortening and ejection fraction, suggesting dilated left ventricle or even dilated cardiomyopathy. The y axis represents the distance (in mm) from the transducer (Vevo 2100); time (in ms) is on the x axis. f , Ap4e1 loss ( Ap4e1 −/− ) caused an impairment of LVIDd and LVIDs and consequently lowered stroke volume. The y axis represents the distance (in mm) from the transducer (Vevo 2100); time (in ms) is on the x axis. g , Representative electrocardiograms from conscious Ap4e1 -mutant and C57BL/6N control mice with indication of ECG parameters and interval durations. Ap4e1 loss lowered heart rate and concurrently increased RR interval duration. Data are presented by Mouse Specifics software.

Journal: Nature Cardiovascular Research

Article Title: Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy

doi: 10.1038/s44161-022-00018-8

Figure Lengend Snippet: Representative electrocardiograms from conscious mutant and control mice with indication of ECG parameters and interval durations. a , Gatm loss ( Gatm −/− ) caused lower heart rate with prolonged QRS width and QTc and ST interval lengths. b , Pla2g10 loss ( Pla2g10 −/− ) lowered heart rate and prolonged PR, PQ and QTc intervals in female null mice. c , Cap2 depletion ( Cap2 −/+ ) induced lower heart rate and lengthy QTc and ST durations in male null mice compared with C57BL/6N controls. Data are presented by Mouse Specifics software. Interval durations are given in milliseconds. M-mode recordings are through a short-axis view tangential to the papillary muscle from representative mutant and control mice. Images show the LVID throughout diastole and systole. d , Leprotl1 depletion ( Leprotl1 −/− ) reduced LV diameters (LVIDs and LVIDd) and increased myocardial wall thickness (LVAWs, LVAWd and LVPWs) with decreased systolic function compared with C57BL/6N controls. e , Alpk3 depletion ( Alpk3 −/− ) increased LV diameters (LVIDs and LVIDd) and decreased systolic function via reduced fractional shortening and ejection fraction, suggesting dilated left ventricle or even dilated cardiomyopathy. The y axis represents the distance (in mm) from the transducer (Vevo 2100); time (in ms) is on the x axis. f , Ap4e1 loss ( Ap4e1 −/− ) caused an impairment of LVIDd and LVIDs and consequently lowered stroke volume. The y axis represents the distance (in mm) from the transducer (Vevo 2100); time (in ms) is on the x axis. g , Representative electrocardiograms from conscious Ap4e1 -mutant and C57BL/6N control mice with indication of ECG parameters and interval durations. Ap4e1 loss lowered heart rate and concurrently increased RR interval duration. Data are presented by Mouse Specifics software.

Article Snippet: Data were analyzed using standard protocols for ECG signal analysis by eMouse (Mouse Specifics).

Techniques: Mutagenesis, Control, Software

Ex situ imaging of the embryo heart in homozygous lethal or homozygous subviable single-gene-knockout mice used to identify structural heart defects, such as VSD. Of the mouse lines studied here, 65% were homozygous knockouts (corresponding to LOF in human) and 35% were heterozygous knockouts. This dataset included 248 of 705 lines (35%). Lines were confirmed to be lethal or subviable; we assessed cardiac development by analyzing three-dimensional micro-CT data obtained from iodine contrast-enhanced micro-CT that provides high spatial resolution of up to 3–14 μm per voxel from embryonic day (E)9.5–E18.5 embryos ( http://www.mousephenotype.org/data/embryo ). No embryo imaging was performed on viable knockout lines. Embryo data were available for only a small subset of the total knockout genes used for this study. The VSD network included nine genes ( Sirt1 , Stambp , Casz1 , Wfdc2 , Tmem161b , Nxn , Dnajc18 , Gnao1 and Slc25a ) that, when LOF was induced, caused early mortality due to structural heart changes but most notably VSDs in the null mutant mice, experimentally shown by computed tomography microscopy. Five more genes ( Zpf503 (human ZNF503 ), Ubr4 , Furin , Shox2 and Smo ) were associated with cardiac abnormalities after gene depletion, confirmed by gross morphology data. An additional 45 genes were integrated using their association with cardiac malformations and development of a VSD. Only in vivo ECG and TTE data from young adult mice are available because these mutant lines tested positive for viability; therefore, no embryo screening was performed. The network analysis also identified 13 non-IMPC interacting genes. Two transcription factors, NKX2-5 ( Furin , Bmp10 , Shox2 , Sirt1 and Sspn ) and TBX20 ( Bmp4 , Bmp10 , Tfap2b and Casz1 ), known to be important for early cardiac development, were strongly represented. Furthermore, BMP10, a critical regulator of cardiac growth and chamber maturation, chromatin-modifying ( Hdac1 and Smarcb1 ) genes and genes regulated by processes essential for cardiogenesis, for example, smoothened and WNT signaling ( Gnao1 , Emilin2 , Aldoa , Nxn , Smo , Sufu and Ift81 ), were strongly represented in the network. Compelling evidence of experimental human or rodent data is from relevant publications, primarily peer-reviewed ‘small-scale experiment’ literature used in the network analysis. ECHO, transthoracic echocardiography; ECG, electrocardiography; NONE, genes not analyzed so far in the IMPC; ER, endoplasmic reticulum.

Journal: Nature Cardiovascular Research

Article Title: Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy

doi: 10.1038/s44161-022-00018-8

Figure Lengend Snippet: Ex situ imaging of the embryo heart in homozygous lethal or homozygous subviable single-gene-knockout mice used to identify structural heart defects, such as VSD. Of the mouse lines studied here, 65% were homozygous knockouts (corresponding to LOF in human) and 35% were heterozygous knockouts. This dataset included 248 of 705 lines (35%). Lines were confirmed to be lethal or subviable; we assessed cardiac development by analyzing three-dimensional micro-CT data obtained from iodine contrast-enhanced micro-CT that provides high spatial resolution of up to 3–14 μm per voxel from embryonic day (E)9.5–E18.5 embryos ( http://www.mousephenotype.org/data/embryo ). No embryo imaging was performed on viable knockout lines. Embryo data were available for only a small subset of the total knockout genes used for this study. The VSD network included nine genes ( Sirt1 , Stambp , Casz1 , Wfdc2 , Tmem161b , Nxn , Dnajc18 , Gnao1 and Slc25a ) that, when LOF was induced, caused early mortality due to structural heart changes but most notably VSDs in the null mutant mice, experimentally shown by computed tomography microscopy. Five more genes ( Zpf503 (human ZNF503 ), Ubr4 , Furin , Shox2 and Smo ) were associated with cardiac abnormalities after gene depletion, confirmed by gross morphology data. An additional 45 genes were integrated using their association with cardiac malformations and development of a VSD. Only in vivo ECG and TTE data from young adult mice are available because these mutant lines tested positive for viability; therefore, no embryo screening was performed. The network analysis also identified 13 non-IMPC interacting genes. Two transcription factors, NKX2-5 ( Furin , Bmp10 , Shox2 , Sirt1 and Sspn ) and TBX20 ( Bmp4 , Bmp10 , Tfap2b and Casz1 ), known to be important for early cardiac development, were strongly represented. Furthermore, BMP10, a critical regulator of cardiac growth and chamber maturation, chromatin-modifying ( Hdac1 and Smarcb1 ) genes and genes regulated by processes essential for cardiogenesis, for example, smoothened and WNT signaling ( Gnao1 , Emilin2 , Aldoa , Nxn , Smo , Sufu and Ift81 ), were strongly represented in the network. Compelling evidence of experimental human or rodent data is from relevant publications, primarily peer-reviewed ‘small-scale experiment’ literature used in the network analysis. ECHO, transthoracic echocardiography; ECG, electrocardiography; NONE, genes not analyzed so far in the IMPC; ER, endoplasmic reticulum.

Article Snippet: Data were analyzed using standard protocols for ECG signal analysis by eMouse (Mouse Specifics).

Techniques: Ex Situ, Imaging, Gene Knockout, Micro-CT, Knock-Out, Mutagenesis, Computed Tomography, Microscopy, In Vivo

Gene based expression levels in mouse and human heart tissues performed to evaluate the impact of the size difference between positive and negative gene groups. Expression levels in known CHD genes added at all three stages for reference. Known CHD genes, however, showed significantly increased expression levels compared with positive mouse genes at all three stages. This analysis was further expanded to human heart tissue for genes with a mouse-human orthologue and presented a similar picture. Mean expression levels per groups compared using a Wilcoxon rank-sum test. X-axis denotes the gene groups evaluated; y-axis denotes the log-transformed mean expression in heart. The analysis was stratified by procedure (ECG and TTE) and developmental stages (development, maturation and postnatal). Data shown as mean, minimum, maximum and lower/upper quartiles. a . Expression analysis in mouse heart for ECG genes; b . Expression analysis in mouse heart for TTE genes. Note: RPKM, Reads per kilobase of transcript per Million mapped reads. c . Expression analysis in human heart for ECG genes; d . Expression analysis in human heart for TTE genes. Distribution of the mean expression in mouse heart differences between P and N genes. The negative gene group (higher number of genes) randomly down sampled to generate equal-size subgroups compared to the positive group. P-values denote the probability of observing by chance higher averaged expression level in negative group compared to positive group, in 50,000 permutations. The analysis stratified by procedure ( e . ECG and f . TTE) and developmental stages (development, maturation and postnatal. Distribution of the mean expression in human heart differences between P and N genes. g . ECG and h . TTE and developmental stages (development, maturation and postnatal.

Journal: Nature Cardiovascular Research

Article Title: Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy

doi: 10.1038/s44161-022-00018-8

Figure Lengend Snippet: Gene based expression levels in mouse and human heart tissues performed to evaluate the impact of the size difference between positive and negative gene groups. Expression levels in known CHD genes added at all three stages for reference. Known CHD genes, however, showed significantly increased expression levels compared with positive mouse genes at all three stages. This analysis was further expanded to human heart tissue for genes with a mouse-human orthologue and presented a similar picture. Mean expression levels per groups compared using a Wilcoxon rank-sum test. X-axis denotes the gene groups evaluated; y-axis denotes the log-transformed mean expression in heart. The analysis was stratified by procedure (ECG and TTE) and developmental stages (development, maturation and postnatal). Data shown as mean, minimum, maximum and lower/upper quartiles. a . Expression analysis in mouse heart for ECG genes; b . Expression analysis in mouse heart for TTE genes. Note: RPKM, Reads per kilobase of transcript per Million mapped reads. c . Expression analysis in human heart for ECG genes; d . Expression analysis in human heart for TTE genes. Distribution of the mean expression in mouse heart differences between P and N genes. The negative gene group (higher number of genes) randomly down sampled to generate equal-size subgroups compared to the positive group. P-values denote the probability of observing by chance higher averaged expression level in negative group compared to positive group, in 50,000 permutations. The analysis stratified by procedure ( e . ECG and f . TTE) and developmental stages (development, maturation and postnatal. Distribution of the mean expression in human heart differences between P and N genes. g . ECG and h . TTE and developmental stages (development, maturation and postnatal.

Article Snippet: Data were analyzed using standard protocols for ECG signal analysis by eMouse (Mouse Specifics).

Techniques: Gene Expression, Expressing, Transformation Assay

In-depth characteristics of 14 genes included in the VSD network

Journal: Nature Cardiovascular Research

Article Title: Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy

doi: 10.1038/s44161-022-00018-8

Figure Lengend Snippet: In-depth characteristics of 14 genes included in the VSD network

Article Snippet: Data were analyzed using standard protocols for ECG signal analysis by eMouse (Mouse Specifics).

Techniques: Micro-CT, Dispersion