New-onset Left Ventricular Dysfunction Research Articles

New-Onset Left Ventricular Dysfunction After Left Bundle Branch Pacing.

Left bundle branch pacing (LBBP) provides stable pacing parameters and has been suggested as an alternative for right ventricular pacing and cardiac resynchronization therapy. The aim of the study was to assess the incidence and etiology of new-onset left ventricular dysfunction (NOLVD) following LBBP in patients with baseline normal left ventricular (LV) function and cardiomyopathy patients with normalized LV function. Patients undergoing successful LBBP for symptomatic bradyarrhythmia or as an alternative to cardiac resynchronization therapy were included. Normalization of LV function was defined as improvement in LV ejection fraction to≥50%. Patients with baseline normal LV function and those with recovered LV function after LBBP constituted the study group. Loss of conduction system capture (LOCSC) was defined as complete or partial loss of right bundle branch delay pattern along with inability to demonstrate capture transition during threshold assessment. A total of 426 patients were included; 59% (n=250) had baseline normal LV function (group I) and 41% (n=176) had recovered LV function after LBBP (group II). Mean follow-up duration of 28.3 ± 16.7months. NOLVD was noted in 3.75% (n=16; group I=5 and group II=11) of patients. The etiologies for NOLVD were LOCSC in 62.5% (n=10), suboptimal atrioventricular (AV) delay in 18.7% (n=3), atrial fibrillation in 6.3% (n=1), and idiopathic in 12.5% (n=2). LOCSC occurred at a mean interval of 9.2 ± 6.4months after the initial implantation. Reinterventions (n=6) including lead repositioning, AV delay optimization, and AV junction ablation resulted in renormalization of LV function in all 6 patients. Periodic assessment in device clinic is required because NOLVD from reversible causes can occur duringfollow-up in patients after LBBP.

Bacterial Pneumonia Is Associated With Myocardial Fibrosis and New-Onset Left Ventricular Dysfunction

Bacterial Pneumonia Is Associated With Myocardial Fibrosis and New-Onset Left Ventricular Dysfunction

Artificial Intelligence-Enabled Electrocardiogram Predicted Left Ventricle Diameter as an Independent Risk Factor of Long-Term Cardiovascular Outcome in Patients With Normal Ejection Fraction.

BackgroundHeart failure (HF) is a global disease with increasing prevalence in an aging society. However, the survival rate is poor despite the patient receiving standard treatment. Early identification of patients with a high risk of HF is important but challenging. Left ventricular end-diastolic diameter (LV-D) increase was an independent risk factor of HF and adverse cardiovascular (CV) outcomes. In this study, we aimed to develop an artificial intelligence (AI) enabled electrocardiogram (ECG) system to detect LV-D increase early.ObjectiveWe developed a deep learning model (DLM) to predict left ventricular end-diastolic and end-systolic diameter (LV-D and LV-S) with internal and external validations and investigated the relationship between ECG-LV-D and echocardiographic LV-D and explored the contributions of ECG-LV-D on future CV outcomes.MethodsElectrocardiograms and corresponding echocardiography data within 7 days were collected and paired for DLM training with 99,692 ECGs in the development set and 20,197 ECGs in the tuning set. The other 7,551 and 11,644 ECGs were collected from two different hospitals to validate the DLM performance in internal and external validation sets. We analyzed the association and prediction ability of ECG-LVD for CV outcomes, including left ventricular (LV) dysfunction, CV mortality, acute myocardial infarction (AMI), and coronary artery disease (CAD).ResultsThe mean absolute errors (MAE) of ECG-LV-D were 5.25/5.29, and the area under the receiver operating characteristic (ROC) curves (AUCs) were 0.8297/0.8072 and 0.9295/0.9148 for the detection of mild (56 ≦ LV-D < 65 mm) and severe (LV-D ≧ 65 mm) LV-D dilation in internal/external validation sets, respectively. Patients with normal ejection fraction (EF) who were identified as high ECHO-LV-D had the higher hazard ratios (HRs) of developing new onset LV dysfunction [HR: 2.34, 95% conference interval (CI): 1.78–3.08], CV mortality (HR 2.30, 95% CI 1.05–5.05), new-onset AMI (HR 2.12, 95% CI 1.36–3.29), and CAD (HR 1.59, 95% CI 1.26–2.00) in the internal validation set. In addition, the ECG-LV-D presents a 1.88-fold risk (95% CI 1.47–2.39) on new-onset LV dysfunction in the external validation set.ConclusionThe ECG-LV-D not only identifies high-risk patients with normal EF but also serves as an independent risk factor of long-term CV outcomes.

Artificial intelligence-enabled electrocardiogram screens low left ventricular ejection fraction with a degree of confidence.

Artificial intelligence-enabled electrocardiogram has become a substitute tool for echocardiography in left ventricular ejection fraction estimation. However, the direct use of artificial intelligence-enabled electrocardiogram may be not trustable due to the uncertainty of the prediction. The study aimed to establish an artificial intelligence-enabled electrocardiogram with a degree of confidence to identify left ventricular dysfunction. The study collected 76,081 and 11,771 electrocardiograms from an academic medical center and a community hospital to establish and validate the deep learning model, respectively. The proposed deep learning model provided the point estimation of the actual ejection fraction and its standard deviation derived from the maximum probability density function of a normal distribution. The primary analysis focused on the accuracy of identifying patients with left ventricular dysfunction (ejection fraction ≤ 40%). Since the standard deviation was an uncertainty indicator in a normal distribution, we used it as a degree of confidence in the artificial intelligence-enabled electrocardiogram. We further explored the clinical application of estimated standard deviation and followed up on the new-onset left ventricular dysfunction in patients with initially normal ejection fraction. The area under receiver operating characteristic curves (AUC) of detecting left ventricular dysfunction were 0.9549 and 0.9365 in internal and external validation sets. After excluding the cases with a lower degree of confidence, the artificial intelligence-enabled electrocardiogram performed better in the remaining cases in internal (AUC = 0.9759) and external (AUC = 0.9653) validation sets. For the application of future left ventricular dysfunction risk stratification in patients with initially normal ejection fraction, a 4.57-fold risk of future left ventricular dysfunction when the artificial intelligence-enabled electrocardiogram is positive in the internal validation set. The hazard ratio was increased to 8.67 after excluding the cases with a lower degree of confidence. This trend was also validated in the external validation set. The deep learning model with a degree of confidence can provide advanced improvements in identifying left ventricular dysfunction and serve as a decision support and management-guided screening tool for prognosis.

495 New-onset left ventricular dysfunction and critical coronary artery disease: an MRI can help—a clinical case

Abstract Aims Understanding the aetiology of heart failure is crucial for treatment. Gadolinium cardiac magnetic resonance (CMR) is a powerful technique to distinguish dilated cardiomyopathy (DCM) from left ventricular (LV) dysfunction related to coronary artery disease (CAD). Methods and results Clinical case: a 61 years old Caucasian woman with a history of hypertension and dyslipidaemia presented to the emergency department of our hospital with pulmonary oedema and hypertensive crisis, requiring non-invasive ventilatory support. She complained about shortness of breath and exertional angina for almost one year. On admission, the echocardiography showed severe LV systolic dysfunction and severe functional mitral regurgitation (FMR). Troponin levels were slightly increased, and NT-proBNP was 2809 pg/ml. Once obtained clinical stability, anti-remodelling cardiac therapy was introduced and up titrated. Due to the history of angina and the new-onset severe LV systolic dysfunction, coronary angiography was performed, showing critical stenosis of the left main (LM) and of the proximal tract of the left anterior descending artery (LAD). In deciding the best treatment pathway for the patient evaluate myocardial viability and characterize myocardial tissue was of paramount importance. Subsequently, a CMR confirmed severe LV systolic dysfunction and severe functional mitral regurgitation but demonstrated myocardial viability, with no late gadolinium enhancement. Therefore the patient underwent surgical myocardial revascularization with triple coronary artery bypass grafts (left internal mammary artery-LAD, saphenous vein graft-obtuse marginal artery, saphenous vein graft-diagonal branch of LAD) and mitral valve repair (annuloplasty). The patient underwent a period of cardiac rehabilitation asymptomatic and in good clinical status. Three months later, echocardiography demonstrated an initial recovery of LV systolic dysfunction with signs of reverse cardiac remodelling and a good result of mitral valve repair. The patient is now on optimal medical therapy, free of symptoms and in good clinical and functional condition. Conclusions Cardiovascular magnetic resonance (CMR) is an excellent diagnostic tool in heart failure. This clinical case can be formative, confirming once again the importance of an accurate and complete diagnostic workup and a subsequent therapy of aetiology in heart failure.

HIV, hepatitis C virus and risk of new-onset left ventricular dysfunction in women.

HIV and HCV have each been linked with cardiac dysfunction. Studies of HIV have often lacked appropriate controls and primarily involved men, whereas data for HCV are sparse. We performed repeat echocardiography over a median interval of 12 years in participants from the Women's Interagency HIV Study in order to evaluate the relationships of HIV and HCV with incident left ventricular (LV) dysfunction (systolic or diastolic). Of the 311 women included (age 39 ± 9), 70% were HIV-positive and 20% HCV-positive. Forty three participants (13.8%) developed LV dysfunction, of which 79.1% was diastolic. Compared with participants with neither infection, the group with HIV--HCV coinfection showed a significantly increased risk of incident LV dysfunction after adjustment for risk factors [RR = 2.96 (95% CI = 1.05-8.31)], but associations for the HCV monoinfected and HIV monoinfected groups were not statistically significant [RR = 2.54 (0.83-7.73) and RR = 1.66 (0.65-4.25), respectively]. Comparison of HCV-positive and HCV-negative women showed a significantly increased risk independent of covariates [RR = 1.96 (1.02-3.77)] but this was not the case for HIV-positive vs. HIV-negative women [RR = 1.43 (0.76-2.69)]. There was no evidence of HCV-by-HIV interaction. A more restrictive definition of LV diastolic dysfunction led to fewer incident cases, but a similar, though nonsignificant, risk estimate for HCV. Among mostly middle-aged women, HCV but not HIV infection was associated with a pronounced risk of incident LV dysfunction. Although the influence of residual confounding cannot be excluded, these findings bolster the potential benefits that could be realized by adopting recent recommendations for expanding HCV screening and treatment.

P798Clinical and electrocardiographic characteristics for prediction of new-onset left ventricular dysfunction in patients with frequent idiopathic ventricular premature complex &gt;10%

P798Clinical and electrocardiographic characteristics for prediction of new-onset left ventricular dysfunction in patients with frequent idiopathic ventricular premature complex &gt;10%

Impact of New-Onset Left Ventricular Dysfunction on Outcomes in Mechanically Ventilated Patients With Severe Sepsis and Septic Shock.

Left ventricular systolic dysfunction (LVSD) and LV diastolic dysfunction (LVDD) are commonly seen in severe sepsis and septic shock; however, their role in patients with concurrent invasive mechanical ventilation (IMV) is less well defined. This was a prospective observational study on all patients admitted to all the intensive care units (ICUs) at Mayo Clinic, Rochester from August 2007 to January 2009. All adult patients with severe sepsis and septic shock and concurrent IMV without prior heart failure underwent transthoracic echocardiography within 24 hours. Patients with active pregnancy, prior congenital or valvular heart disease, and prosthetic cardiac valves were excluded. Left ventricular systolic dysfunction was defined as LV ejection fraction (LVEF) <50% and LVDD as E/e' >15. Primary outcome was hospital mortality, and secondary outcomes included IMV duration, ICU length of stay (LOS), and total LOS. Two-tailed P value of <.05 was considered statistically significant. In a total of 106 patients, 58 (54.7%) met our inclusion criteria, with 17 (29.3%), 11 (19.0%), and 5 (8.6%) having LVSD, LVDD, and both, respectively. The cohorts with and without LVSD and LVDD did not differ significantly in their baseline characteristics and laboratory and ventilatory parameters. Compared to those without LVSD, patients with LVSD had higher LV end-systolic diameters but were not different in their left atrial diameters or E/e' ratio. Patients with LVDD had a higher E velocity and E/e' ratio compared to those without LVDD. Hospital mortality was not different in patients with and without LVSD (8 [47%] vs 21 [51%], P = 1.00) and LVDD (8 [73%] vs 21 [45%], P = .18). Secondary outcomes were not different between the 2 groups. Left ventricular systolic or diastolic dysfunction did not influence in-hospital outcomes in patients with severe sepsis and septic shock and concurrent IMV.

Circulating Histones Are Major Mediators of Cardiac Injury in Patients With Sepsis.

To investigate the impact of circulating histones on cardiac injury and dysfunction in a murine model and patients with sepsis. Prospective, observational clinical study with in vivo and ex vivo translational laboratory investigations. General ICU and university research laboratory. Sixty-five septic patients and 27 healthy volunteers. Twelve-week-old male C57BL/6N mice. Serial blood samples from 65 patients with sepsis were analyzed, and left ventricular function was assessed by echocardiography. Patients' sera were incubated with cultured cardiomyocytes in the presence or absence of antihistone antibody, and cellular viability was assessed. Murine sepsis was initiated by intraperitoneal Escherichia coli injection (10(8) colony-forming unit/mouse) in 12-week-old male C57BL/6N mice, and the effect of antihistone antibody (10 mg/kg) was studied. Murine blood samples were collected serially, and left ventricular function was assessed by intraventricular catheters and electrocardiography. Circulating histones and cardiac troponins in human and murine plasma were quantified. In 65 patients with sepsis, circulating histones were significantly elevated compared with healthy controls (n = 27) and linearly correlated with cardiac troponin T levels (rs = 0.650; p < 0.001), noradrenaline doses required to achieve hemodynamic stability (rs = 0.608; p < 0.001), Sequential Organ Failure Assessment scores (p = 0.028), and mortality (p = 0.008). In a subset of 36 septic patients without prior cardiac disease, high histone levels were significantly associated with new-onset left ventricular dysfunction (p = 0.001) and arrhythmias (p = 0.01). Left ventricular dysfunction only predicted adverse outcomes when combined with elevated histones or cardiac troponin levels. Furthermore, patients' sera directly induced histone-specific cardiomyocyte death ex vivo, which was abrogated by antihistone antibodies. In vivo studies on septic mice confirmed the cause-effect relationship between circulating histones and the development of cardiac injury, arrhythmias, and left ventricular dysfunction. Circulating histones are novel and important mediators of septic cardiomyopathy, which can potentially be utilized for prognostic and therapeutic purposes.

Cardiac Magnetic Resonance and Cardiac Magnetic Field Mapping in a Patient with Stress‐Induced Cardiomyopathy (Tako‐Tsubo)

We encountered a 65-year-old woman with typical electrocardiogram (ECG) changes and new-onset left ventricular dysfunction with apical ballooning that exhibited typical changes of tako-tsubo-like cardiomyopathy. We used cardiac magnetic resonance (CMR) and cardiac magnetic field mapping (CMFM) to detect changes in structural, mechanical, and electrophysiological myocardial properties during follow-up. CMR displayed an acute myocardial injury, but neither fibrosis nor necrosis. CMFM exhibited severely disturbed repolarization with an inhomogeneous magnetic field. These pathological findings persisted much longer than the abnormalities detected by CMR and the ECG.

Medical management of significant coronary angiographic stenoses: outcome of 60 patients observed for 433 patient years.

Percutaneous transluminal coronary angioplasty (PTCA) has become routine in the management of patients with stable angina pectoris and significant coronary stenoses, while medical management of such patients has declined. The purpose of the present study was to evaluate the outcome of 60 patients at the Virginia Heart Institute with stable angina pectoris, observed between 1976 and 1997, who had documented evidence of severe angiographic disease but were elected to be monitored and managed in an outpatient pharmacologic rehabilitation program. Sixty patients with significant stenoses by coronary angiography (21 with single-vessel, 26 with double-vessel, and 13 with triple-vessel) without impaired ventricular function, exercise-induced ischemia or hypotension, limited exercise performance, malignant arrhythmias, or drug intolerance were enrolled in a program of pharmacologic rehabilitation and observed for an average of 7.2 years. Among the 60 patients, there were 6 deaths at a mean interval of 8.3 years. Two deaths were in patients ineligible for revascularization. Another patient who died had refused revascularization after new-onset left ventricular dysfunction, and another died intraoperatively during abdominal aortic aneurysm repair. Two patients died while exercising. Thirteen patients underwent follow-up catheterization for worsening angina; 11 of 13 showed progression, predominantly from new lesions. Four of 11 were referred for revascularization; 7 of 11 continued medical treatment; 49 patients were stable on medical therapy throughout the period of observation. Medical management of selected patients with significant coronary stenoses is safe and effective.

Effect of exercise training on heart rate variability in patients with new-onset left ventricular dysfunction after myocardial infarction

Background Cardiac rehabilitation with exercise training alters sympathovagal control of heart rate variability (HRV) toward parasympathetic dominance in patients after acute myocardial infarction (MI). However, its effects on HRV in patients after MI with new-onset left ventricular dysfunction are yet unknown. We aimed to investigate the effects of 8 weeks of supervised, high-intensity exercise training on time- and frequency-domain measures of HRV in this selected patient population. Methods and Results Twenty-five men with an acute MI and a low ejection fraction were randomly assigned to enter or not to enter a training program in a regional rehabilitation center. HRV was evaluated before and after 1 and 2 months of training and at 12 months. Maximal exercise testing with respiratory gas exchange was performed at baseline and after training. Resting heart rate decreased (P <.01) and the percentage of R-R intervals differing >50 ms from the preceding one (pNN50) increased (P <.05) after training. The standard deviation of R-R intervals (SDRR) tended to increase, but frequency-domain indexes remained unchanged. There was a significant decrease in SDRR (P <.05) and high-frequency power (P <.01) at 12 months in untrained patients. Exercise time increased by 38% and maximal oxygen uptake increased by 29% in the training group (P <.01). Conclusions Despite beneficial effects on clinical variables, exercise training did not markedly alter HRV indexes. A significant decrease in SDRR and high-frequency power in the control group suggests an ongoing process of sympathovagal imbalance in favor of sympathetic dominance in untrained patients after MI with new-onset left ventricular dysfunction. (Am Heart J 2000;140:157-61.)