Utility of a Deep-Learning Algorithm to Guide Novices to Acquire Echocardiograms for Limited Diagnostic Use

Original Investigation

Akhil Narang, MD1; Richard Bae, MD2; Ha Hong, PhD3; et al

JAMA Cardiol. 2021;6(6):624-632. doi:10.1001/jamacardio.2021.0185

Abstract

Importance  Artificial intelligence (AI) has been applied to analysis of medical imaging in recent years, but AI to guide the acquisition of ultrasonography images is a novel area of investigation. A novel deep-learning (DL) algorithm, trained on more than 5 million examples of the outcome of ultrasonographic probe movement on image quality, can provide real-time prescriptive guidance for novice operators to obtain limited diagnostic transthoracic echocardiographic images.

Objective  To test whether novice users could obtain 10-view transthoracic echocardiographic studies of diagnostic quality using this DL-based software.

Design, Setting, and Participants  This prospective, multicenter diagnostic study was conducted in 2 academic hospitals. A cohort of 8 nurses who had not previously conducted echocardiograms was recruited and trained with AI. Each nurse scanned 30 patients aged at least 18 years who were scheduled to undergo a clinically indicated echocardiogram at Northwestern Memorial Hospital or Minneapolis Heart Institute between March and May 2019. These scans were compared with those of sonographers using the same echocardiographic hardware but without AI guidance.

Interventions  Each patient underwent paired limited echocardiograms: one from a nurse without prior echocardiography experience using the DL algorithm and the other from a sonographer without the DL algorithm. Five level 3–trained echocardiographers independently and blindly evaluated each acquisition.

Main Outcomes and Measures  Four primary end points were sequentially assessed: qualitative judgement about left ventricular size and function, right ventricular size, and the presence of a pericardial effusion. Secondary end points included 6 other clinical parameters and comparison of scans by nurses vs sonographers.

Results  A total of 240 patients (mean [SD] age, 61 [16] years old; 139 men [57.9%]; 79 [32.9%] with body mass indexes >30) completed the study. Eight nurses each scanned 30 patients using the DL algorithm, producing studies judged to be of diagnostic quality for left ventricular size, function, and pericardial effusion in 237 of 240 cases (98.8%) and right ventricular size in 222 of 240 cases (92.5%). For the secondary end points, nurse and sonographer scans were not significantly different for most parameters.

Conclusions and Relevance  This DL algorithm allows novices without experience in ultrasonography to obtain diagnostic transthoracic echocardiographic studies for evaluation of left ventricular size and function, right ventricular size, and presence of a nontrivial pericardial effusion, expanding the reach of echocardiography to clinical settings in which immediate interrogation of anatomy and cardiac function is needed and settings with limited resources.

Echocardiography-Guided LQTS Risk Stratification

Sugrue, van Zyl M, Enger N, et al.

Echocardiography-Guided Risk Stratification for Long QT Syndrome. J Am Coll Cardiol 2020;76:2834-2843.

Study Questions:

Is it possible to identify a subset of patients at the highest risk for long QT syndrome (LQTS)–associated life-threatening cardiac events by examining the electromechanical window (EMW) negativity, as derived from continuous-wave Doppler echocardiography?

Methods:

There were 651 patients with LQTS (mean age, 26 years; 60% females; 158 symptomatic; 51% LQTS type 1; 33% LQTS type 2; 11% LQTS type 3) and 50 healthy controls. EMW was calculated as the difference between the interval from QRS onset to aortic valve closure midline, as derived for continuous-wave Doppler, and the electrocardiogram-derived QT interval for the same beat.

Results:

A negative EMW was found among nearly all patients with LQTS compared to controls, with more profound EMW negativity in patients with symptomatic LQTS compared to those with asymptomatic LQTS (-52 ± 38 ms vs. -18 ± 29 ms; p < 0.0001). Logistic regression identified EMW, corrected QT interval, female sex, and LQTS genotype as univariate predictors of symptomatic status. After multivariate analysis, EMW remained an independent predictor of symptomatic status (odds ratio for each 10-ms decrease in EMW, 1.37; 95% confidence interval, 1.27-1.48; p < 0.0001). EMW outperformed corrected QT interval in predicting symptomatic patients. EMW correlation across sonographers showed excellent reliability.

Conclusions:

In this validation study, patients with a history of LQTS-associated life-threatening cardiac events had a more profoundly negative EMW. EMW outperformed heart rate–corrected QT interval as a predictor of symptomatic status. EMW is now a clinically validated risk factor.

Perspective:

So far, efforts at risk prediction in LQTS have mainly focused on the electrical manifestations of this condition such as corrected QT interval and T-wave morphology. This fascinating manuscript ties together the abnormalities in electrical conduction with mechanical function abnormalities observable on echo with high interobserver reliability. In normal adults, the end of electrical systole occurs slightly before the end of mechanical systole, resulting in a positive EMW. A negative EMW occurs when there is a mismatch between the end of electrical and mechanical systole as a result of prolongation of electrical systole. The exact mechanism is speculative, and it is possible that EMW is a surrogate marker that highlights impaired relaxation and inhomogeneity across the ventricle as the substrate for arrhythmogenesis. EMW should be evaluated prospectively in the QTS population and potentially many other arrhythmogenic conditions.

Midlife Wealth Mobility and Long-term Cardiovascular Health

Original Investigation

June 30, 2021

Sara Machado, PhD1; Andrew Sumarsono, MD2,3; Muthiah Vaduganathan, MD, MPH4

1 Department of Health Policy, London School of Economics, London, United Kingdom
2 Department of Medicine, University of Texas Southwestern Medical Center, Dallas
3 Division of Hospital Medicine, Parkland Memorial Hospital, Dallas, Texas
4 Brigham and Women’s Hospital Heart & Vascular Center and Harvard Medical School, Boston, Massachusetts

JAMA Cardiol. Published online June 30, 2021. doi:10.1001/jamacardio.2021.2056

Abstract

Importance  The association of socioeconomic status and cardiovascular outcomes has been well described, but little is known about whether longitudinal changes in wealth are associated with cardiovascular health status.

Objective  To evaluate the association between midlife wealth mobility and risk of cardiovascular events.

Design, Setting, and Participants  This longitudinal, retrospective cohort study included US adults 50 years or older who participated in the Health and Retirement Study. Participants in the primary analysis had no history of cardiovascular disease and had observations in at least two of three 5-year age intervals (50-54, 55-59, and 60-64 years) and follow-up after 65 years of age. Data were collected from January 1, 1992, to December 31, 2016, and analyzed from November 10, 2020, to April 26, 2021.

Exposures  Quintiles of wealth (reflecting total nonhousing assets) were defined within each of 4 birth cohorts (1931-1935, 1936-1940, 1941-1945, and 1946-1950). Wealth mobility was defined as an increase or a decrease of 1 or more wealth quintiles and was compared with wealth stability (same quintile over time) using covariate-adjusted Cox proportional hazards regression models.

Main Outcomes and Measures  Composite outcome of nonfatal cardiovascular event (myocardial infarction, heart failure, cardiac arrhythmia, or stroke) or cardiovascular death.

Results  A total of 5579 participants were included in the primary analysis (mean [SD] age, 54.2 [2.6] years; 3078 women [55.2%]). During a mean (SD) follow-up of 16.9 (5.8) years, 1336 participants (24.0%) experienced a primary end point of nonfatal cardiovascular event or cardiovascular death (14.4 [95% CI, 13.6-15.2] per 1000 patient-years). Higher initial wealth (per quintile) was associated with lower cardiovascular risk (adjusted hazard ratio [aHR] per quintile, 0.89 [95% CI, 0.84-0.95]; P = .001). When compared with stable wealth, participants who experienced upward wealth mobility (by at least 1 quintile) had independently lower hazards of a subsequent nonfatal cardiovascular event or cardiovascular death (aHR, 0.84 [95% CI, 0.73-0.97]; P = .02), and participants who experienced downward wealth mobility had higher risks (aHR, 1.15 [95% CI, 1.00-1.32]; P = .046).

Conclusions and Relevance  These findings suggest that upward wealth mobility relative to peers in late middle age is associated with lower risks of cardiovascular events or death after 65 years of age.

Machine Learning of ECG Waveforms to Improve Selection for Testing for Asymptomatic Left Ventricular Dysfunction Prompt

Elizabeth L. Potter, MBBS, BSC, Carlos H.M. Rodrigues, BSC, David B. Ascher, PHD,
Walter P. Abhayaratna, MBBS, PHD, Partho P. Sengupta, MD, Thomas H. Marwick, MBBS, PHD, MPH

J Am Coll Cardiol Img. Jun 16, 2021.  Epublished DOI: 10.1016/j.jcmg.2021.04.020

ABSTRACT

OBJECTIVES To identify whether machine learning from processing of continuous wave transforms (CWTs) to provide an “energy waveform” electrocardiogram (ewECG) could be integrated with echocardiographic assessment of subclinical systolic and diastolic left ventricular dysfunction (LVD).

BACKGROUND Asymptomatic LVD has management implications, but routine echocardiography is not undertaken in subjects at risk of heart failure. Signal processing of the surface ECG with the use of CWT can identify abnormal myocardial relaxation.

METHODS EwECG and echocardiography were undertaken in 398 participants at risk of heart failure (HF). Reduced global longitudinal strain (GLS #16%)), diastolic abnormalities (E/e0 >15, left atrial enlargement with E/e0 >10 or impaired relaxation) or LV hypertrophy defined LVD. EwECG feature selection and supervised machine-learning by random forest (RF) classifier was undertaken with 643 CWT-derived features and the Atherosclerosis Risk in Communities (ARIC) heart failure risk score.

RESULTS The ARIC score and 18 CWT features were selected to build a RF predictive model for LVD in a training dataset (n ¼ 287; 60% female, median age 71 [interquartile range: 68 to 74] years). Model performance was tested in an in-dependent group (n ¼ 111; 49% female, median age 61 years [59 to 66 years]), demonstrating 85% sensitivity and 72%specificity (area under the receiver-operating characteristic curve [AUC]: 0.83; 95% confidence interval [CI]: 0.74 to 0.92). With ARIC score removed, sensitivity was 88% and specificity, 70% (AUC: 0.78; 95% CI: 0.70 to 0.86). RF models for reduced GLS and diastolic abnormalities including similar features had sensitivities that were unsuitable for screening. Conventional candidates for LVD screening (ARIC score, N-terminal pro–B-type natriuretic peptide, and standard auto-mated ECG analysis) had inferior discriminative ability. Integration of ewECG in screening of people at risk of HF would reduce need for echocardiography by 45% while missing 12% of LVD cases.

CONCLUSIONS Machine learning applied to ewECG is a sensitive screening test for LVD, and its integration into screening of patients at risk for HF would reduce the number of echocardiograms by almost one-half.

© 2021 by the American College of Cardiology Foundation.

Suicide prevention needs to go beyond the blue

From the Chair of Rural & Remote Mental Health – Genevieve Fraser

“Sunflowers” by Vincent Van Gogh

Visitors to Canberra during budget week were able to immerse themselves in more than the budget thanks to the National Gallery’s well timed “Masterpieces from the National Gallery, London”, featuring Vincent Van Gogh’s famous Sunflowers. $5 million dollars’ worth of refurbishments were undertaken last year to eliminate all dark corners of the Canberra exhibition space to shed equal light on each masterpiece. Despite these efforts the darkness of Van Gogh’s tragic story remains. In 1880, after the paint had dried on the petals of his celebrated flowers, Van Gogh walked into a nearby field in Auvers, France and shot himself in the stomach with a revolver.

Politicians who were able to take in Sunflowers over the past few months might spare a thought for those who equally lose hope in fields and homes across rural Australia 2021. Rural Australians suicide at two to three times the national average – a tragedy the 2020 Mental Health Productivity Commission asked our leaders to focus on in future funding decisions.

The report explained unambiguously who was dying, where, and why. The central recommendation for rural Australia was that half of those who suicide in Australia are NOT engaged with the medical system so future mental health spending needed to focus on community-based prevention.

Leaders were also told our suicide prevention model needs to change because suicide rates escalate the further someone lives from a capital city.  And this pattern is consistent across every state and Territory.  

Many of those who suicide in the country have no mental health history but are dealing with a trauma. It could be the loss of a child, a marriage, or a job, and they simply don’t have the tools to cope. They live a long way from mental health specialists, are not talking to their GP’s about their problems, and most of their friends and family don’t recognise the signs.

The families of Dolly Everett and Dr Andrew Bryant have both generously shared their experiences in recent times and both called for more community awareness because it is friends and families that need to know the signs to look for.

Rural Australians considering suicide are most likely to be saved by someone who already knows them or their community. Friends, family and work mates are the main line of defence.

Rural mental health charities like Rural & Remote Mental Health talk face to face with rural people and train locals in suicide prevention because it is the only way to save those not using our mental health services.

We don’t run million-dollar advertising campaigns on council buses and highways because the people we need to reach don’t have council buses or highways. Our work runs on cups of tea, biscuits, sandwiches, town halls and thousands of kilometres on country roads. Our trained presenters live and work across all states and territories. Most have other community-based roles – rural adversity nurses, indigenous elders, mine employees.

If people in these communities put their rural postcode into an online mental health directory it would often deliver the message  “there are no services in your area”. Clinics in neighbouring rural centres look promising until the fine print reveals it is visited once a month by a specialist from somewhere else.

The best way for us to save people is to visit more communities and more often. Without dedicated federal funding we can’t go where the risk is highest, only where there are funds ‘left over’ in local health network budget’s for prevention work. Communities support what we do and want us there. Since our funding stopped in June 2020 one community used the proceeds of a local pig race to fund us to come back. As grateful as we are, why are at-risk rural communities paying for a service that is funded via large charities in our more affluent cities? Rural Australians pay taxes too but are not receiving equitable investment in mental health.

That is why in 2020, charities like ours asked to be funded properly as part of the new mental health strategy.  Without the benefit of lobbyists or sophisticated marketing we provided honest hopeful submissions and genuinely expected that at least 5% of the billions being spent would be focused on the 29% of Australians who live in rural communities.

Our modest request for $2 million a year to reach at risk people across Australia was ignored and letters from politicians reminded us of the millions being spent on hospitals and resources in our cities and regional centres. Our charity is not alone. Many other rural mental health organisations lost some or all their funding and some folded or stopped going where they needed to go.

The responses we received from federal MP’s and ministers included:
“Your funding will not be renewed as the drought is over.”
“Apply to the rural Primary Health Network service – they might have funds left over”
“Doesn’t Beyond Blue/Lifeline/R U OK look after that?”

Many rural charities watched in despair during budget week. We had already received our “no’s” and we could only watch as hundreds of millions were allocated to the city based ‘national’ charities for core funding, project funding and special project funding – hundreds of millions of dollars allocated to a small number of very large organisations. Some of these organisations report over $50 million in cash reserves in their 2020 annual reports. The work they do is important and effective in the communities where they concentrate their efforts. But they don’t go where we go. We know it takes some digging to find those of us that work on the ground but we are there at the bottom of the pile of submissions on desks throughout Canberra.

Rather than give up, we are asking our leaders to allocate a fair percentage of our mental health prevention budget to charities serving the 29% of Australians who live in rural communities.

We need to reach places far from Canberra like the Kimberly where the suicide rate is four times the national average. Places like the Tablelands of Queensland where 55 people lost hope in 2020. Or Wangaratta (VIC) , Maryborough (QLD), West Tamar (TAS), Outback  North and the Outback Southern regions (QLD).

Places where the light of this mental health budget is not yet shining any light.

We need our politicians to see beyond the blue coastlines and cities and into high-risk red areas of our country. People need the tools to save themselves and others because some Australians will always be isolated from medical mental health facilities. Van Gogh’s brother Theo held him in his arms as he succumbed to the injuries inflicted in that rural paddock and lamented that he hadn’t recognised the signs of depression in time. We will keep sending our letters and visiting those paddocks and towns because we know this is our best line of defence.  But we need our leaders to recognise the signs and invest beyond the blue.

Outcomes of Patients With ST-Segment Elevation Myocardial Infarction Admitted During COVID-19 Pandemic Lockdown in Germany – Results of a Single Center Prospective Cohort Study

Manuel Rattka, Lina Stuhler, Claudia Winsauer, Jens Dreyhaupt, Kevin Thiessen, Michael Baumhardt, Sinisa Markovic, Wolfgang Rottbauer and Armin Imhof

1Clinic for Internal Medicine II, University Hospital Ulm – Medical Center, Ulm, Germany
2Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany

ORIGINAL RESEARCH article

Front. Cardiovasc. Med., 20 April 2021 | https://doi.org/10.3389/fcvm.2021.638954

Abstract

Objective: Since the outbreak of the COVID-19 pandemic, healthcare professionals reported declining numbers of patients admitted with ST-segment myocardial infarction (STEMI) associated with increased in-hospital morbidity and mortality. However, the effect of lockdown on outcomes of STEMI patients admitted during the COVID-19 crisis has not been prospectively evaluated.

Methods: A prospective, observational study on STEMI patients admitted to our tertiary care center during the COVID-19 pandemic was conducted. Outcomes of patients admitted during lockdown were compared to those patients admitted before and after pandemic-related lockdown.

Results: A total of 147 patients were enrolled in our study, including 57 patients in the pre-lockdown group (November 1, 2019 to March 20, 2020), 16 patients in the lockdown group (March 21 to April 19, 2020), and 74 patients in the post-lockdown group (April 20 to September 30, 2020). Patients admitted during lockdown had significantly longer time to first medical contact, longer door-to-needle-time, higher serum troponin T levels, worse left ventricular end-diastolic pressure, and higher need for circulatory support. After a median follow-up of 142 days, survival was significantly worse in STEMI patients of the lockdown group (log-rank: p = 0.0035).

Conclusions: This is the first prospective study on outcomes of STEMI patients admitted during public lockdown amid the COVID-19 pandemic. Our results suggest that lockdown might deteriorate outcomes of STEMI patients. Public health strategies to constrain spread of COVID-19, such as lockdown, have to be accompanied by distinct public instructions to ensure timely medical care in acute diseases such as STEMI.

Speech-Induced Atrial Tachycardia

André Zimerman, M.D., and Andre d’Avila, M.D., Ph.D.

Speech-Induced Atrial Tachycardia | NEJM

A 58-year-old man presented to the emergency department with a 1-month history of intermittent dizziness and palpitations that occurred when he spoke. Continuous electrocardiographic monitoring revealed atrial premature beats when he was speaking isolated words (Panel A) and sustained atrial tachycardia up to 167 beats per minute when he was speaking full sentences (Panel B). The arrhythmias promptly subsided when he stopped talking (Panel C). Arrhythmias were reproducibly triggered by any spoken syllable but not by soundless mouth movement, deep breathing, or an inspiratory breath hold. A transthoracic echocardiogram showed a structurally normal heart, and findings on computed tomography of the chest were unremarkable. Speech-induced atrial tachycardia may represent transient aberrant vagal stimulation from the recurrent laryngeal nerve to the atrial autonomic ganglia, resulting in abnormal automaticity or triggered activity. The patient’s symptoms resolved promptly with oral metoprolol treatment, which was continued for 3 months. The symptoms did not recur, and no catheter ablation was performed. At 3 years of follow-up, the patient remained asymptomatic.

May 29, 2021
DOI: 10.1056/NEJMicm2030596

Diastolic Dysfunction and Heart Failure With Preserved Ejection Fraction: Understanding Mechanisms by Using Noninvasive Methods

Masaru Obokata, Yogesh N.V. Reddy, and Barry A. Borlaug

J Am Coll Cardiol Img. 2020 Jan, 13 (1_Part_2) 245–257

Abstract

Research in the last decade has substantially advanced our understanding of the pathophysiology of heart failure with preserved ejection fraction (HFpEF). However, treatment options remain limited as clinical trials have largely failed to identify effective therapies. Part of this failure may be related to mechanistic heterogeneity. It is speculated that categorizing HFpEF patients based upon underlying pathophysiological phenotypes may represent the key next step in delivering the right therapies to the right patients. Echocardiography may provide valuable insight into both the pathophysiology and underlying phenotypes in HFpEF. Echocardiography also plays a key role in the evaluation of patients with unexplained dyspnea, where HFpEF is suspected but the diagnosis remains unknown. The combination of the E/e′ ratio and right ventricular systolic pressure has recently been shown to add independent value to the diagnostic evaluation of patients suspected of having HFpEF. Finally, echocardiography enables identification of the different causes that mimic HFpEF but are treated differently, such as valvular heart disease, pericardial constriction, and high-output heart failure or infiltrative myopathies such as cardiac amyloid. This review summarizes the current understanding of the pathophysiology and phenotyping of HFpEF with particular attention to the role of echocardiography in this context.

Highlights

HFpEF is a heterogeneous syndrome, and categorizing patients based upon pathophysiology may provide phenotype-specific therapies.
Echocardiography provides valuable information for assessing pathophysiological mechanisms, phenotyping, and diagnosis in cases of HFpEF.
Further study is needed to establish the HFpEF phenotype and roles of noninvasive imaging in it.

Introduction

Heart failure with preserved ejection fraction (HFpEF) is a common clinical syndrome that is increasing in prevalence. Rather than having an isolated abnormality in left ventricular (LV) diastolic function, patients with HFpEF display multifaceted limitations in cardiac, vascular, and peripheral functions (1). Phenotyping based upon pathophysiology, comorbidities, or some combination may provide targeted therapies for the specific HFpEF subpopulations that are positioned to derive the greatest benefit (2).

Cardiovascular imaging plays a key role in the diagnosis and evaluation of HFpEF, particularly echocardiography, which allows for assessment of cardiac structure, function, and hemodynamics (3). This review summarizes the current understanding of the pathophysiology and phenotypes of HFpEF, with a focus on the essential role of imaging for the evaluation and care of patients with HFpEF.

Pathophysiology of HFpEF: Beyond Diastolic Dysfunction

LV diastolic dysfunction plays a fundamental, overarching role in the pathophysiology of HFpEF (1). LV diastolic dysfunction is defined by an impairment in relaxation, an increase in viscoelastic chamber stiffness, or some combination of the 2 (4,5) and leads to symptomatic HF by causing elevated filling pressures at rest or with exertion (6). Elevated filling pressures promote symptoms of dyspnea (7), impair exercise capacity (7,8), increase risk for HF hospitalization (9), and decrease survival in HFpEF (10). The importance and assessment of LV diastolic dysfunction in HFpEF are reviewed in detail in other articles in this issue.

Although diastolic dysfunction is central to HFpEF, it is also important to acknowledge that there are declines in LV relaxation and compliance with normal aging or with cardiometabolic comorbidities such as obesity, insulin resistance, and hypertension (11–13). Not all patients with diastolic dysfunction have or will develop clinical HFpEF (14,15). Research in the past decade has demonstrated that, in addition to LV diastolic dysfunction, multiple nondiastolic abnormalities in cardiovascular system contribute to the syndrome of HFpEF. These abnormalities include subtle LV systolic dysfunction, left atrial (LA) impairment, relative pericardial restraint, abnormal right ventricular-pulmonary artery coupling, pulmonary vascular disease, systemic vascular stiffening, coronary and peripheral microvascular dysfunction, and chronotropic incompetence…

Association of Echocardiographic Left Ventricular End-Systolic Volume and Volume-Derived Ejection Fraction With Outcome in Asymptomatic Chronic Aortic Regurgitation

Li-Tan Yang, MD1,2Vidhu Anand, MBBS1Elena I. Zambito, RDCS1Patricia A. Pellikka, MD1Christopher G. Scott, MS3Prabin Thapa, MS3Ratnasari Padang, MBBS, PhD1Masaaki Takeuchi, MD4Rick A. Nishimura, MD1Maurice Enriquez-Sarano, MD1Hector I. Michelena, MD1

JAMA Cardiol. 2021;6(2):189-198. doi:10.1001/jamacardio.2020.5268

Key Points

Question  Are disk-summation method–derived left ventricular (LV) end-systolic volume index and LV ejection fraction (LVEF) associated with mortality in asymptomatic patients with hemodynamically significant chronic aortic regurgitation?

Findings  In this cohort study of 492 asymptomatic patients with moderately severe to severe aortic regurgitation, besides conventional linear LVEF and LV end-systolic dimension index, LV end-systolic volume index and volume-derived LVEF were robust independent factors associated with mortality. Thresholds of increased mortality risk for linear LVEF and volume-derived LVEF were 60%, and for LV end-systolic dimension index and volume index, 21 to 22 mm/m2 and 40 to 45 mL/m2, respectively; previously reported LV end-systolic volume index threshold of 45 mL/m2 was a robust marker of increased risk of death.

Meaning  In asymptomatic low-risk patients with aortic regurgitation, LV end-systolic volume index and volume-derived LVEF provided similar risk-stratifying power as conventional linear LVEF and LV end-systolic dimension index.

Abstract

Importance  Volumetric measurements by transthoracic echocardiogram may better reflect left ventricular (LV) remodeling than conventional linear LV dimensions. However, the association of LV volumes with mortality in patients with chronic hemodynamically significant aortic regurgitation (AR) is unknown.

Objective  To assess whether LV volumes and volume-derived LV ejection fraction (Vol-LVEF) are determinants of mortality in AR.

Design, Setting, and Participants  This cohort study included consecutive asymptomatic patients with chronic moderately severe to severe AR from a tertiary referral center (January 2004 through April 2019).

Exposures  Clinical and echocardiographic data were analyzed retrospectively. Aortic regurgitation severity was graded by comprehensive integrated approach. De novo disk-summation method was used to derive LV volumes and Vol-LVEF.

Main Outcome and Measures  Associations between all-cause mortality under medical surveillance and the following LV indexes: linear LV end-systolic dimension index (LVESDi), linear LVEF, LV end-systolic volume index (LVESVi), and Vol-LVEF.

Results  Of 492 asymptomatic patients (mean [SD] age, 60 [17] years; 425 men [86%]), ischemic heart disease prevalence was low (41 [9%]), and 453 (92.1%) had preserved linear LVEF (≥50%) with mean (SD) LVESVi of 41 (15) mL/m2. At a median (interquartile range) of 5.4 (2.5-10.1) years, 66 patients (13.4%) died under medical surveillance; overall survival was not different than the age- and sex-matched general population (P = .55). Separate multivariate models, adjusted for age, sex, Charlson Comorbidity Index, and AR severity, demonstrated that in addition to linear LVEF and LVESDi, LVESVi and Vol-LVEF were independently associated with mortality under surveillance (all P < .046) with similar C statistics (range, 0.83-0.84). Spline curves showed that continuous risks of death started to rise for both linear LVEF and Vol-LVEF less than 60%, LVESVi more than 40 to 45 mL/m2, and LVESDi above 21 to 22 mm/m2. As dichotomized variables, patients with LVESVi more than 45 mL/m2 exhibited increased relative death risk (hazard ratio, 1.93; 95% CI, 1.10-3.38; P = .02) while LVESDi more than 20 mm/m2 did not (P = .32). LVESVi more than 45 mL/m2 showed a decreased survival trend compared with expected population survival.

Conclusions and Relevance  In this large asymptomatic cohort of patients with hemodynamically significant AR, LVESVi and Vol-LVEF worked equally as well as LVESDi and linear LVEF in risk discriminating patients with excess mortality. A LVESVi threshold of 45 mL/m2 or greater was significantly associated with an increased mortality risk.

Long Working Hours and Risk of Recurrent Coronary Events

Xavier Trudel PhD; Chantal Brisson PhD; Denis Talbot PhD; Mahée Gilbert-Ouimet PhD; Alain Milot MD

Journal of the American College of Cardiology
Volume 77, Issue 13, 6 April 2021, Pages 1616-1625 https://doi.org/10.1016/j.jacc.2021.02.012

Abstract

Background

Evidence from prospective studies has suggested that long working hours are associated with incident coronary heart disease (CHD) events. However, no previous study has examined whether long working hours are associated with an increased risk of recurrent CHD events among patients returning to work after a first myocardial infarction (MI).

Objectives

The purpose of this study was to examine the effect of long working hours on the risk of recurrent CHD events.

Methods

This is a prospective cohort study of 967 men and women age 35 to 59 years who returned to work after a first MI. Patients were recruited from 30 hospitals across the province of Quebec, Canada. The mean follow-up duration was 5.9 years. Long working hours were assessed on average 6 weeks after their return to work. Incident CHD events (fatal or nonfatal MI and unstable angina) occurring during follow-up were determined using patients’ medical files. Hazard ratios were estimated using Cox proportional hazard regression models. Splines and fractional polynomial regressions were used for flexible exposure and time modeling.

Results

Recurrent CHD events occurred among 205 patients. Participants working long hours (≥55 h/week) had a higher risk of recurrent CHD events after controlling for sociodemographics, lifestyle-related risk factors, clinical risk factors, work environment factors, and personality factors (hazard ratio vs. 35 to 40 h/week: 1.67; 95% confidence interval: 1.10 to 2.53). These results showed a linear risk increase after 40 h/week and a stronger effect after the first 4 years of follow-up and when long working hours are combined with job strain.

Conclusions

Among patients returning to work after a first MI, longer working hours per week is associated with an increased risk of recurrent CHD events. Secondary prevention interventions aiming to reduce the number of working hours among these patients may lower the risk of CHD recurrence.