scholarly journals Presence of myocardial fibrotic or fat change on cardiac CT influences the width of distribution range of J waves in survivors of ventricular fibrillation

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
N Funabashi ◽  
K Nakamura ◽  
T Sasaki ◽  
S Naito ◽  
Y Kobayashi
Keyword(s):  
Ventricular Fibrillation ◽  
Cardiac Ct ◽  
Cardiac Computed Tomography ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Distribution Range ◽  
Inferior Wall ◽  
Funding Sources ◽  
Relationship Of ◽  
The Relationship

Abstract Background The distribution of J waves may correlate with left ventricular (LV) myocardial damage in survivors of ventricular fibrillation (VF). Purpose To determine the relationship of the distribution of J waves with presence of myocardial damage such as fibrotic or fat change on cardiac computed tomography (CT) in survivors of VF. Methods We conducted a retrospective analysis of 21 survivors of VF (17 males; mean age, 61±14 years) that were implanted with a cardioverter defibrillator and underwent cardiac CT. Results On ECG, 4 patients had atrial fibrillation and 15 had J waves. On CT, 13 patients had organized LV myocardial fibrotic and/or fat change in myocardium. The mean corrected QT interval was 453±30 and 429±48 msec in patients with and without myocardial fibrotic and/or fat change, respectively (P=0.182). The distribution of J waves was as follows: 5 had J waves in II, III and aVF leads (one had myocardial fibrotic and/or fat change) and 2 had J waves in III lead (one had myocardial fibrotic and/or fat change). One patient each had J waves in V1 lead; V1,2 leads; II, III, aVF and V1–3 leads; I, III, aVF and V1 leads; II, III, aVF, aVL and V1–6 leads; II, III, aVF and V4,5 leads; II, III, aVF and V2–5 leads; and III and aVF leads. The first one did not have myocardial fibrotic and/or fat change and the remaining 6 had myocardial fibrotic and/or fat change (Figure). If the J waves reached to ≥1 of 3 LV inferior wall leads (II, III, aVF leads) (N=13), 10 (77%) had LV myocardial fibrotic and/or fat change. If not (N=8), 3 (38%) had LV myocardial fibrotic and/or fat change (P=0.071). If the J waves reached ≥2 of 3 LV inferior wall leads (N=11), 9 (82%) had LV myocardial fibrotic and/or fat change. If not (N=10), 4 (40%) had LV myocardial fibrotic and/or fat change (P=0.049). If the J waves reached all three LV inferior wall leads (N=10), 8 (80%) had LV myocardial fibrotic and/or fat change. If not (N=11), 5 (46%) had LV myocardial fibrotic and/or fat change (P=0.104). Conclusions In survivors of VF, organized LV myocardial fibrotic and/or fat changes on cardiac CT correlate with a wider distribution range of J waves (reached to LV inferior wall leads). The distribution of J waves and the presence of myocardial fibrotic and/or fat change on CT may be useful to predict the occurrence of VF. FUNDunding Acknowledgement Type of funding sources: None. CT fibrosis in VF survivors J waves and fibrotic and/or fat change

scholarly journals The Relationship of Left Ventricular Trabeculation to Ventricular Function and Structure Over a 9.5-Year Follow-Up

2014 ◽  
Vol 64 (19) ◽  
pp. 1971-1980 ◽  
Author(s):  
Filip Zemrak ◽  
Mark A. Ahlman ◽  
Gabriella Captur ◽  
Saidi A. Mohiddin ◽  
Nadine Kawel-Boehm ◽  
...  
Keyword(s):  
Ventricular Function ◽  
Left Ventricular ◽  
Relationship Of ◽  
The Relationship

scholarly journals Childhood and adult exposure to secondhand tobacco smoke and cardiac structure and function: results from Echo-SOL

Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000831 ◽  
Author(s):  
Melissa Suzanne Burroughs Peña ◽  
Katrina Swett ◽  
Robert C Kaplan ◽  
Krista Perreira ◽  
Martha Daviglus ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Structure And Function ◽  
Cardiac Structure ◽  
Isovolumic Relaxation Time ◽  
Shs Exposure ◽  
Cardiac Structure And Function ◽  
And Function ◽  
Relationship Of ◽  
The Relationship ◽  
Isovolumic Relaxation

ObjectiveTo describe the relationship of household secondhand smoke (SHS) exposure and cardiac structure and function.MethodsParticipants (n=1069; 68 % female; age 45–74 years) without history of tobacco use, coronary artery disease or severe valvular disease were included. Past childhood (starting at age <13 years), adolescent/adult and current exposure to household SHS was assessed. Survey linear regression analyses were used to model the relationship of SHS exposure and echocardiographic measures of cardiac structure and function, adjusting for covariates (age, sex, study site, alcohol use, physical activity and education).ResultsSHS exposure in childhood only was associated with reduced E/A velocity ratio (β=−0.06 (SE 0.02), p=0.008). SHS exposure in adolescence/adult only was associated with increased left ventricular ejection fraction (LVEF) (1.2 (0.6), p=0.04), left atrial volume index (1.7 (0.8), p=0.04) and decreased isovolumic relaxation time (−0.003 (0.002), p=0.03). SHS exposure in childhood and adolescence/adult was associated with worse left ventricular global longitudinal strain (LVGLS) (two-chamber) (0.8 (0.4), p= 0.049). Compared with individuals who do not live with a tobacco smoker, individuals who currently live with at least one tobacco smoker had reduced LVEF (−1.4 (0.6), p=0.02), LVGLS (average) (0.9 (0.40), p=0.03), medial E′ velocity (−0.5 (0.2), p=0.01), E/A ratio (−0.09 (0.03), p=0.003) and right ventricular fractional area change (−0.02 (0.01), p=0.01) with increased isovolumic relaxation time (0.006 (0.003), p=0.04).ConclusionsPast and current household exposure to SHS was associated with abnormalities in cardiac systolic and diastolic function. Reducing household SHS exposure may be an opportunity for cardiac dysfunction prevention to reduce the risk of future clinical heart failure.

2 THE RELATIONSHIP OF AGE AND LEFT VENTRICULAR DIASTOLIC FUNCTION.:

2006 ◽  
Vol 54 (2) ◽  
pp. S344.2-S344
Author(s):  
A. Maksoud ◽  
I. Porter ◽  
K. Schneider ◽  
R. Joseph ◽  
P. Lebourveau ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Ventricular Diastolic Function ◽  
Relationship Of ◽  
The Relationship

The Relationship of Left Ventricular Mass to Endothelium-Dependent Vasodilation of the Brachial Artery in Patients with Hypertension

Cardiology ◽  
2001 ◽  
Vol 96 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Takeshi Motoyama ◽  
Hiroaki Kawano ◽  
Nobutaka Hirai ◽  
Ryusuke Tsunoda ◽  
Yasushi Moriyama ◽  
...  
Keyword(s):  
Left Ventricular Mass ◽  
Brachial Artery ◽  
Left Ventricular ◽  
Ventricular Mass ◽  
Relationship Of ◽  
The Relationship

Readmissions after Acute Kidney Injury during Left Ventricular Assist Device Implantation Hospitalization

2020 ◽  
Vol 51 (3) ◽  
pp. 172-181 ◽  
Author(s):  
Carl P. Walther ◽  
Wolfgang C. Winkelmayer ◽  
Anita Deswal ◽  
Jingbo Niu ◽  
Sankar D. Navaneethan
Keyword(s):  
Acute Kidney Injury ◽  
Left Ventricular Assist Device ◽  
Kidney Injury ◽  
Left Ventricular ◽  
Assist Device ◽  
Ventricular Assist ◽  
Left Ventricular Assist ◽  
Relationship Of ◽  
The Relationship ◽  
Readmission Risk

Background: Acute kidney injury (AKI) frequently complicates hospitalizations for left ventricular assist device (LVAD) implantation. Little is known about the relationship of AKI with subsequent readmissions, and we investigated the relationship of AKI during LVAD implantation hospitalization with all-cause and cause-specific 30-day readmissions. Methods: We used a United States (US) nationwide all-payer administrative database, identifying patients who underwent implantable LVAD placement 2010–2015. Patients were classified into 3 mutually exclusive groups based on presence and severity of AKI during the LVAD placement hospitalization: no AKI, AKI, and AKI requiring dialysis (AKI-D). Outcomes were all-cause and cause-specific 30-day readmissions. Results: Within 30 days after discharge 25.4% of patients were readmitted. Of those without AKI, 23.9% were readmitted, compared to 25.5% of those with AKI and 42.2% of those with AKI-D. Compared to no AKI (adjusted for demographics, index hospitalization and chronic comorbidity factors, and year), odds of 30-day readmission were 2.18 (95% CI 1.37–3.49) times higher for those with AKI-D, whereas those with AKI not requiring dialysis had similar 30-day readmission risk (OR 1.03 [95% CI 0.89–1.20]). Those with AKI-D had higher risk of 30-day readmission for infection (OR 2.02 [95% CI 1.13–3.61]), gastrointestinal (GI) bleed (2.32 [95% CI 1.24–4.34]), and kidney disease (13.9 [95% CI 4.0–48]). There was no increased risk for stroke readmission with AKI or AKI-D. Conclusion: AKI-D was associated with highest ­30-day readmission risk, possibly related to negatively synergistic effects of LVAD, kidney dysfunction, and dialysis related factors on infection and GI bleeding risks. AKI alone was not associated with increased readmission risk.

3255Characterization of the arrhythmogenic substrate with multimodality imaging in ischemic patients undergoing VT ablation: relationship between cardiac computed tomography and magnetic resonance

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Zucchelli ◽  
D Soto Iglesias ◽  
B Jauregui ◽  
C Teres ◽  
D Penela ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Magnetic Resonance ◽  
Cardiac Ct ◽  
Low Voltage ◽  
Multimodality Imaging ◽  
Cardiac Computed Tomography ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Arrhythmogenic Substrate

Abstract Background Cardiac magnetic resonance (CMR)-aided ventricular tachycardia (VT) substrate ablation has shown to improve VT recurrence-free survival, through a better identification of the arrhythmogenic substrate. However, the access to CMR may be limited in certain centers or sometimes Its use can be contraindicated in patients with cardiac implantable electronic device. Cardiac computed tomography (CT) has shown to improve the results of substrate ablation, correlating with low-voltage areas and local abnormal ventricular activity, and identifying ridges of myocardial tissue (CT-channels) that may be appropriate target sites for ablation. Purpose To evaluate the correlation between CT and CMR imaging in identifying anatomical heterogeneous tissue channels (CMR-channels) or CT-channels in ischemic patients undergoing VT substrate ablation. Methods The study included 30 post-myocardial infarction (MI) patients (mean age 69±10; 94% male, left ventricular ejection fraction 35±10%), who underwent both CMR and cardiac CT before VT substrate ablation. Using a dedicated post-processing software, the myocardium was segmented in 10 layers from endocardium to epicardium both for the CMR and CT, characterizing the presence of CMR-channels and CT-channels, respectively, by two blinded operators, assigned either to CMR or CT analysis. CMR-channels were classified as endocardial (CMR-channels in layer <50%), epicardial (CMR-channels in layers ≥50%) or transmural (in both endo and epicardial layers). Presence and location of CT and CMR-channels were compared. Results In 26/30 patients (86.7%) 91 CT-channels (mean 3.0±1.9 per patient) were identified while 30/30 (100%) showed CMR-channels (n=76; mean 2.4±1.2 per patient). We found 190 CT-channel entrances (mean 6.3±4.1 per patient), and 275 CMR-channel entrances (mean 8.9±4.9 per patient) on cardiac CT and CMR, respectively. There were 47/91 (51.6%) true positive CT-channels. On the contrary, 44/91 (48.4%) CT-channels were considered false positives [19/91 (20.9%) identified out of CMR scar], and 29/76 (38.2%) CMR-channels could not be identified on CT. Thirty-six out of 76 (47.4%) CMR-channels were considered as non-endocardial (epi- or transmural). Twenty-nine out of 36 (80.5%) non-endocardial CMR-channels were coincident with CT-channels. CT and CMR Channels Conclusion CT shows a modest sensitivity in identifying CMR-channels and fails in ascertain their complexity, underestimating the number of entrances; however, channels location at CT fit well with CMR for those classified as transmural or epicardial.

Nature of [Ca2+]i transients during ventricular fibrillation and quinidine treatment in perfused rat hearts

1994 ◽  
Vol 266 (4) ◽  
pp. H1473-H1484
Author(s):  
S. Kojima ◽  
J. Wikman-Coffelt ◽  
S. T. Wu ◽  
W. W. Parmley
Keyword(s):  
Ventricular Fibrillation ◽  
Control Level ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Acetoxymethyl Ester ◽  
Ecg Signals ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Electrocardiogram Ecg ◽  
The Relationship

We studied intracellular Ca2+ concentration ([Ca2+]i) and the electrocardiographic signals during pacing-induced ventricular fibrillation (VF) and quinidine treatment (0.4 mg/min) using surface fluorometry in indo 1-acetoxymethyl ester (AM)-loaded perfused rat hearts. [Ca2+]i was evaluated as the indo 1 fluorescence ratio (F400/F510) and expressed as a percentage of the control amplitude of F400/F510 transients. F400/F510 increased to approximately 250% during 2- (n = 14) or 20-min (n = 9) VF. Quinidine significantly decreased F400/F510 by 60% after 2-min VF; however, this effect was blunted after 20-min VF. After 2-min VF, F400/F510 and left ventricular pressure recovered almost to the control level. However, recovery of F400/F510 and ventricular function was poor after 20-min VF. The relationship between [Ca2+]i and the electrocardiogram (ECG) during VF was evaluated by power spectrum analysis of F400/F510 and ECG signals. During VF (25 +/- 3 Hz) with high irregularity, there were no clear [Ca2+]i transients (n = 110). When the cardiac rhythm (22 +/- 3 Hz) was regular, including ventricular tachycardia, there were recognizable [Ca2+]i signals with dominant frequencies that were the same (n = 2), one-half (n = 12), or one-third (n = 1) of the ECG frequencies. The highest frequency of the [Ca2+]i transients was 19 Hz. During quinidine treatment, the VF rate decreased significantly, and clear [Ca2+]i transients were noted in all records responding to every one or two ECG signals. The conclusions were the following: 1) [Ca2+]i responds to electrical signals rapidly (up to 19 Hz) during VF. This fast [Ca2+]i response is a probable cause of high [Ca2+]i during VF. 2) Quinidine decreased [Ca2+]i after 2-min VF possibly in part by slowing the VF and [Ca2+]i transients rates. 3) 20-min VF caused [Ca2+]i overload and poor functional recovery after defibrillation.

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