The first description of sudden cardiac death was made by Hippocrates in the 4‘th century BC1. Such cases of sudden collapse and death has intrigued both the public and medical science for centuries and a practical definition is that sudden cardiac death is the unexpected and natural death from a cardiac cause within a short period of time, usually less than 1 hour from the onset of symptoms, in a person without any known prior condition1,2. Sudden cardiac death (SCD) is clearly the end-result of a wide variety of cardiac conditions—both congenital and acquired. However, the most common mechanism for the event of SCD is ventricular fibrillation1. However this is an evolving field of study and the recent study published by Stojanovic et al3 is of great importance as it links two well known risk factors for SCD—left ventricular hypertrophy (LVH) and QT-dispersion4. The finding by Stojanovic et al3 that septal thickness in both athletes and sedentary men are associated with increased QTd is concerning and future studies need to clarify if we need to keep the septum thin at all costs with more exercise for some and less for others.

Hao et al analyzed echocardiographic data from 80 patients with atrial fibrillation (AF) who underwent radiofrequency ablation. Comparing the 21% of the patients who developed recurrent AF to those who did not, they found that left atrial appendage (LAA) emptying velocities (eV) of <34.5 cm/s and LAA strain (LAAS) < 11.6% were independent predictors of recurrent AF; indeed, combining these 2 values predicted AF recurrence with an area under the curve (AUC) of 0.978, sensitivity of 94.1% and specificity of 93.7%. Left atrial measurements differed significantly between those with and without recurrent AF but did not independently affect the recurrence of AF. Is there something unique about the LAA that provides an insight into the cause and recurrence of AF beyond the left atrium (LA) per se?

Cardiovascular imaging, a fundamental component in the diagnosis and management of cardiovascular diseases, has a great potential for evolution with the advent of technologies such as artificial intelligence (AI), virtual reality (VR), and the metaverse. 1,2 These innovations promise to enhance diagnostic accuracy, streamline workflows, and transform patient-clinician interactions. However, their true impact on clinical practice remains a topic of debate. 3 While AI’s potential to automate image analysis is actively being explored, the roles of VR and the metaverse are less clear, often appearing more aspirational than immediately practical. 4 This article presents an opinion challenging established thinking about these technologies, focusing on whether they will truly revolutionize cardiovascular imaging or simply augment current approaches without fundamentally changing the landscape.

This is a commentary on the manuscript authored by Stadter P, Keller K. Atrial Adaptations in Athletes Heart. Echocardiography. Sep 2024;41(9):e15931. doi:10.1111/echo.15931

High risk PFO-associated stroke: Proposed algorithm for better risk stratificationPetronela Cristina Chiriac1†, PhD, Anca Dumitrescu Bordianu2†, MD, Mariana Floria 1,3, MD, PhD1 Internal Medicine Clinic, ”Sf. Spiridon” Emergency Clinical Hospital Iasi, 700111, Romania.2 Vascular Surgery Clinic, ”Sf. Spiridon” Emergency Clinical Hospital Iași, 700111, Iasi, Romania.3 Faculty of Medicine, Department of Internal Medicine, University of Medicine and Pharmacy ”Grigore T. Popa”, 700111 Iasi, Romania.† Both authors contributed equally.Running title: PFO-associated strokePetronela Cristina Chiriac: [email protected];Anca Dumitrescu Bordianu: [email protected];Mariana Floria: [email protected]; https://orcid.org/0000-0002-9465-1503Correspondence : Floria Mariana, Internal Medicine Department, Grigore T. Popa” University of Medicine and Pharmacy, 16th University Iași, 700115, Romania. E-mail: [email protected]; [email protected]

Mihos and coworkers present an interesting report on the impact of apical aneurysm in patients with apical hypertrophic cardiomyopathy (ApHCM). They reference the literature that shows it occurs in 10-15% of patients with ApHCM and that its presence confers a 3-fold increase in HCM-related death or life-saving aborted HCM-related events, and that it is considered a marker of increased risk of sudden death1-2. Their study shows differences in myocardial work efficiency and global wasted work between patients with and without aneurysms. The question is whether the aneurysm caused the differences or are the aneurysms caused by the differences?

Thanks to impressive advances in the field of oncology over the last thirty years, there has been a dramatic rise in cancer survivors. Nowadays, the risk of dying from cardiovascular disease exceeds cancer-related mortality in this population. Coronary artery disease (CAD) is a major problem due to shared risk factors, an ageing population and in many cases induced and/or accelerated by antitumoral treatment during and even decades after the end of cancer therapy. On the other hand, the presence of CAD at the timepoint of cancer diagnosis largely increases the risk of any cancer therapy related cardiovascular toxicity (CTR-CVT). It is therefore of outermost importance to detect CAD before, during, and after certain types of chemo-, molecular-, and radiotherapy. Multimodality cardiovascular imaging plays a central role in this fragile population where individual risk stratification and multidisciplinary decision making is critical.

Cardiovascular magnetic resonance imaging (MRI) in patients with cardiac implants, such as pacemakers and defibrillators, has gained importance in recent years with the development of modern cardiac implantable electronic devices. The increasing clinical need to perform MRI examinations in patients with cardiac implants has driven the development of new advanced MRI sequences to mitigate image artifacts associated with cardiac implants. More specifically, advances in imaging techniques, such as wideband late gadolinium enhancement imaging, wideband T1 mapping, and wideband perfusion, have been designed to improve image quality and examinations in patients with cardiac implants, enabling a comprehensive and more reliable diagnosis, which was previously unattainable in these patients. This review article explores recent developments and applications of wideband techniques in the field of cardiovascular MRI, offering insights into their transformative potential. Clinical applications of wideband cardiovascular MRI are highlighted, particularly in assessing myocardial viability, guiding ventricular tachycardia ablation, and characterizing myocardial tissue.

Objective This study aimed to assess alterations in right ventricular (RV) function following percutaneous coronary intervention (PCI) in patients with non–acute coronary syndrome angina utilizing three-dimensional speckle tracking echocardiography (3D-STE). Methods A prospective study was conducted involving 136 patients diagnosed with non–acute coronary syndrome angina undergoing PCI, constituting the study group, alongside 110 age and gender-matched healthy volunteers serving as the control group. Echocardiographic evaluations, including both conventional and three-dimensional assessments, were performed on all study participants at 1 week, 6 months, and 12 months post-PCI. Parameters such as tricuspid annular plane systolic excursion (TAPSE) were derived from conventional echocardiography, while tricuspid lateral annular systolic velocity (S’) was measured via tissue Doppler imaging. Three-dimensional speckle tracking echocardiography (3D-STE) was utilized to quantify metrics including right ventricular fractional area change (RVFAC), right ventricular free wall longitudinal strain (RVFWLS), right ventricular global longitudinal strain (RVGLS), right ventricular stroke volume (RVSV), and right ventricular ejection fraction (RVEF). Results TAPSE, S’, RVFAC, RVFWLS, RVGLS, RVSV and RVEF exhibited significant increases from 1 week to 6 months post-PCI ( P < 0.05). However, from 6 to 12 months post-PCI, RVFAC, RVGLS, RVSV and RVEF demonstrated no notable changes ( P > 0.05). Meanwhile, TAPSE, S’, and RVFWLS sustained significant elevations: TAPSE (19.63±3.253% to 22.603±2.885%, P < 0.001); S’ (10.57±2.643 cm/s to 12.61±2.189 cm/s, P < 0.001); RVFWLS (18.64±2.745% to 19.926±3.291%, P = 0.002).By the 12-month mark post-PCI, S’, RVFAC, RVFWLS, RVGLS and RVEF were notably lower compared to those in the healthy control group: S’ (12.61±2.189 cm/s vs. 13.20±1.946 cm/s, P < 0.001), RVFAC (48.469±2.402% vs. 49.20±3.222%, P < 0.001), RVFWLS (19.926±3.291% vs. 22.10±1.994%, P < 0.001), RVEF (49.191±5.801% vs. 50.15±4.844%, P < 0.001). Conclusion Following PCI, right ventricular systolic function in patients with non–acute coronary syndrome angina improves significantly over time. However, even at the 12-month post-PCI mark, the right ventricular systolic function remains inferior to that of the control group. Notably, 3D-STE emerges as a non-invasive method for quantifying right ventricular systolic function post-PCI in non–acute coronary syndrome angina patients.

Abstract: Background: The transesophageal echocardiogram (TEE) is the standard imaging modality for confirming the presence or absence of patent foramen ovale. There is a causal association between PFO and unexplained stroke. It seems that 3D-TEE can present a high-risk PFO morphological feature, which seems to show more than just being easier to open. Methods: In total 134 consecutive patients with cryptogenic stroke or migraine who had suspected PFO and underwent c-TCD, TTE, and c-TEE were included in this study. TEE confirmed the PFO. The right-to-left shunt (RLS) grade of PFO at rest and abdominal compression Valsalva maneuver was detected by c-TEE. Results: The long diameter of FO (1.74±0.3 vs. 1.60±0.4, P=0.039), the short diameter of FO (1.12±0.3 vs. 1.00±0.3, P=0.036), perimeter of FO (4.62±0.7 vs. 4.22±1.0, P=0.026) and area (1.80±0.8 vs. 1.35±0.8, P=0.05) of the FO were significantly larger in the larger RLS group. The cut-off value calculated by ROC for the diagnosis of high-risk PFO was that the length of the PFO tunnel was 12 mm and Left funnelform combined with multiple exits of left atrial (sensitivity was 92%, specificity was 90%). Conclusions: A larger oval fossa can be more easily activated and cause a large right-to-left shunt. The left funnelform, a longer length of the PFO tunnel, and multiple exits of the tunnel of LA increase the risk of CS in anatomical of PFO respect. TEE can precisely visualize the specific morphological characteristics of PFO. These features on TEE have a strong correlation with CS.

Infective endocarditis (IE) continues to have high rates of adverse outcomes, despite recent advances in diagnosis and management. Although the use of computer tomography and nuclear imaging appears to be increasing, echocardiography, widely available in most centers, is the recommended initial modality of choice to diagnose and consequently guide the management of IE in a timely-dependent fashion. Echocardiographic imaging should be performed as soon as the IE diagnosis is suspected. Several factors may delay diagnosis, for example echocardiography findings may be negative early in the disease course. Thus, repeated echocardiography is recommended in patients with negative initial echocardiography if high suspicion for IE persists, in patients at high risk. However systematic echocardiographic screening should not be utilized as a common tool for fever, but only in the presence of a reasonable clinical suspicion of IE. It may increase the risk of false positive rates of patients requiring IE therapy or may exacerbate diagnostic uncertainty about subtle findings. Considering the complexity of the disease, the echocardiographic proper use should be increasingly time-efficient and focused on the correct identification of IE lesions and associated complications. The path to identify patients who need surgery passes through an echocardiographic skill ensuring the identification of the cardiac anatomical structures and their involvement on the destructive infective extension. We pointed out the role of echocardiography focused on the correct identification of IE distinctive lesions and the associated complications, as part of a diagnostic strategy, within an integrated multimodality imaging, managed by an “endocarditis team”.

Title: Papillary muscle free strain- promising parameter to predict sudden cardiac death in hypertrophic cardiomyopathy?Author:Dr Aslannif Roslan (MBBS, MRCP)Institut Jantung Negara,50400 Kuala Lumpur,MalaysiaE-mail: [email protected] author:Dr Aslannif Roslan (MBBS, MRCP)Institut Jantung Negara,50400 Kuala Lumpur,MalaysiaE-mail:[email protected] Cardiomyopathy (HCM) generally have a good prognosis. In the long follow-up study over 5 decades annual overall HCM-related mortality was 1.3%/y (0.7% first decade to 1.8% in second and third decades). The sudden cardiac death (SCD) mortality rate was also low (0.1%/y first decade to 0.44% in second and third decades)1. SCD is the most feared HCM complication and the only effective treatment for this is Implantable Cardioverter Defibrillator (ICD) that is responsible for >10-fold decrease in HCM related mortality2. In 2014,the European Society of Cardiology (ESC) come out with risk score comprising 7 variables but this risk score have low sensitivity3,4. This led to the search for additional risk factors such as percentage of late gadolinium enhancement (LGE) in the left ventricle, presence of apical aneurysm and left ventricle ejection fraction <50% .The American Society of Cardiology/American Heart Association (ACC/AHA) incorporate this for their guidelines in 20205.Eventhough this guidelines have high sensitivity, it have low ability to identify low risk patients which can lead to inappropriate ICD implantation4. The ongoing challenge is to identify the small yet significant group of patients who are at risk of sudden cardiac death, heart failure, and death resulting from heart failure.Neither the 2014 nor the 2020 SCD risk calculators/predictors, nor even the latest 2022 ESC guidelines, have incorporated the relatively new echocardiography technique of speckle-tracking strain measurements. This technique is non-doppler oriented, angle independent and have been shown to be highly reproducible with high sensitivity and specificity6. These techniques can measure Global longitudinal strain (GLS), left atrial reservoir (LArS), conduit (LAcS) and booster (LAbS) strain and right ventricle global (RVGLS) and free wall strain (RVFWS). The most studied of these is Global Longitudinal Strain (GLS) and a recent study showed GLS have the highest accuracy to predict fatal arrhythmia and accurate ICD indication compare to all the other echocardiographic parameters that was previously considered important like diastolic left atrial (LA) diameter, left ventricular wall thickness and ejection fraction7.This is consistent with another study of large cohort of 427 HCM patients showing independent association between GLS and all cause mortality, heart transplantation, aborted SCD, and appropriate ICD therapy8. Furthermore, the latest meta-analysis of 13 studies with 2441 HCM patients showed significant correlation between impaired GLS and major adverse cardiovascular outcomes (MACE). The same correlation was also found with LA strain. A recent meta-analysis in 2023 shows significant association between all aspect of LA strain (reservoir, conduit and booster) with MACE as well as development of new atrial fibrillation (AF)9. This is not only true with echocardiography derived strain. In a Cardiac MRI (CMR) strain study published in 2024, the combination of left ventricle circumferential strain and left atrial reservoir strain model shows high diagnostic value of SCD with staggeringly high area under the curve (AUC) of 0.9510. All of these studies show how powerful is strain study in HCM SCD prognosis and it is natural to then look at papillary muscle (PM) strain as this structure is frequently abnormal in HCM11.It is widely known that papillary muscle abnormalities are part of HCM phenotypes, in addition to elongated mitral valve leaflets and hypertrophied muscle with excessive contractility (the sine qua non of HCM)11. Abnormal papillary muscle morphology is independently associated with increase left ventricular outflow tract (LVOT) obstruction with anteroapically displaced PM and double bifid PM patients having higher resting LVOT gradients than control independent of septal thickness, use of rate control medications and resting heart rate12. The variations of papillary muscle abnormalities are anterior and apical displacement of the PM usually involving ALPM, bifid PM characterized by the presence of more than one muscle head (If both PM involved it is called double bifid morphology), accessory PM that extend from the LV apex and inserted to basal myocardium without insertion into the mitral leaflets and anomalous insertion of the PM itself12,13,14.In HCM, the PM are frequently hypertrophied, with a mass measuring roughly twice the healthy controls. HCM patients also tend to have larger number of PM (2.5 muscles vs 2.1 in control) with half of the patients demonstrating multiple (3 or 4) PM15.In this issue of Echocardiography Atilla Koyuncu et al look at 79 patients with HCM that were divided into low/intermediate-risk (n=57, ESC risk score <6 points) and high risk (n=22, ESC risk score ≥6 points) groups based on the ESC risk calculator. Their mean follow-up duration is 6.2 years. They specifically look for PM abnormalities and measured anterolateral papillary muscle (ALPM) and posteromedial papillary muscle (PMPM) free strain in addition to other conventional 2-dimensional echocardiographic parameters and GLS. They enrolled all HCM phenotypic groups with or without obstruction and they exclude patients with hypertension, valvular heart diseases, hepatic/renal failure or inflammatory diseases. Of note, they did not perform left atrium (LA) or right ventricle (RV) strain. Papillary muscle strain is a relatively new tool and the measurements of ALPM strain is done in apical 4 chamber view and measurement for PMPM strain is done in apical 3 chamber view. The majority of patients have sigmoid or reverse curvature phenotype (70.9%). Interestingly 5 patients (6.3%) had anteriorly displaced papillary muscles, 7(8.8%) had bifid ALPM, 5(6.3%) had bifid PMPM and 2 patients have both bifid ALPM and PMPM (double bifid morphology).They found that the high SCD-risk group had greater wall thickness, interventricular septum thickness, posterior wall thickness and left ventricle mass index and lower GLS, ALPM (-16.88 ± 4.41% vs. -14.34 ± 3.68%, p = .028) and PMPM (-18.48 ± 6.31% vs. -15.28 ± 6.88%, p = .042) free strain. Furthermore, the SCD risk score was positively correlated with GLS, ALPM (r=0.658, p<0.001) and PMPM (r=0.600, p<0.001) strain. Also important is the fact that patient who have papillary muscle abnormalities had significantly worse ALPM and PMPM free strain. Finally, in multivariate analysis, LVMI, presence of syncope, worse GLS and ALPM-free strain were predictors of death. In terms of PM free strain value in normal healthy populations, one study done in 2016 shows between -32.5% to -48% for ALPM and -34.5% to -39.5% for PMPM but for the moment at least there are no guidelines for normal values16.What is the relevance of this paper for our understanding of HCM? It introduces an additional parameter that is easy to measure and reproducible alongside GLS and LA strain, aiding in the prediction of SCD. Although the technique is new and the sample size is limited, further studies with larger populations are necessary to establish its predictive value for SCD, similar to GLS. As strain measurements are generally robust and reproducible, papillary muscle strain has the potential to replace traditional parameters like left atrial dimension, wall thickness, and ejection fraction. Moreover, this paper highlights the importance of considering papillary muscle involvement in HCM, drawing attention to abnormalities such as bifid papillary muscles and anterior displacement during strain measurement. Ultimately, by integrating papillary muscle free strain with GLS, RV, and LA strain, we can enhance our ability to predict sudden cardiac death and ensure more appropriate ICD implantation. For clinicians focused on managing HCM, these are exciting times, and this paper provides valuable insights into the field.Maurizi N, Olivotto I, Maron M, et al. Lifetime clinical course of hypertrophic cardiomyopathy: Outcome of the historical Florence cohort over five decades. JACC Adv. 2023;2(4). doi:10.1016/j.jacadv.2023.100337Maron MS, Rowin EJ, Maron BJ. The paradigm of sudden death prevention in hypertrophic cardiomyopathy. Am J Cardiol. 2024;212S:S64-S76. doi:10.1016/j.amjcard.2023.10.076Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;26:ehac262. doi:10.1093/eurheartj/ehac262Monda E, Limongelli G. Integrated sudden cardiac death risk prediction model for patients with hypertrophic cardiomyopathy. Circulation. 2023;147(4):281-283. doi:10.1161/CIRCULATIONAHA.122.063019Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2020;142:e558–e631. doi:10.1161/CIR.0000000000000937Shirani J, Pick R, Roberts WC, Maron BJ. Morphology and significance of the left ventricular collagen network in young patients with hypertrophic cardiomyopathy and sudden cardiac death. J Am Coll Cardiol. 2000;35(1):36-44. doi:10.1016/s0735-1097(99)00492-1Nikoo MH, Zarrabi M, Moaref A, Razeghian-Jahromi I. Global longitudinal strain may be the one that appropriately identifies candidates for ICD implantation. Cardiol Res Pract. 2024;2024:2214072. doi:10.1155/2024/2214072Hiemstra YL, Debonnaire P, Bootsma M, et al. Global longitudinal strain and left atrial volume index provide incremental prognostic value in patients with hypertrophic cardiomyopathy. Circ Cardiovasc Imaging. 2017;10(7): e005706. doi:10.1161/CIRCIMAGING.116.005706Hussain K, Nso N, Tsourdinis G, et al. A systematic review and meta-analysis of left atrial strain in hypertrophic cardiomyopathy and its prognostic utility. Curr Probl Cardiol. 2024;49(1 Pt C):102146. doi:10.1016/j.cpcardiol.2023.102146Zhu X, Shi Y, Lian J, et al. Left atrial and left ventricular strain in feature-tracking cardiac magnetic resonance for predicting patients at high risk of sudden cardiac death in hypertrophic cardiomyopathy. Quant Imaging Med Surg. 2024;14(5):3544-3556. doi:10.21037/qims-23-1615Sherrid MV, Adams DH. The mitral valve in hypertrophic cardiomyopathy: Other side of the outflow tract. J Am Coll Cardiol. 2020;76(19):2248-2251. doi:10.1016/j.jacc.2020.09.580Kwon DH, Setser RM, Thamilarasan M, et al. Abnormal papillary muscle morphology is independently associated with increased left ventricular outflow tract obstruction in hypertrophic cardiomyopathy. Heart. 2008;94(10):1295-1301. doi:10.1136/hrt.2007.118018Klues HG, Maron BJ, Dollar AL, Roberts WC. Diversity of structural mitral valve alterations in hypertrophic cardiomyopathy. Circulation. 1992;85(5):1651-1660. doi:10.1161/01.cir.85.5.1651Gruner C, Chan RH, Crean A, et al. Significance of left ventricular apical-basal muscle bundle identified by cardiovascular magnetic resonance imaging in patients with hypertrophic cardiomyopathy. Eur Heart J. 2014;Rajiah P, Fulton NL, Bolen M. Magnetic resonance imaging of the papillary muscles of the left ventricle: Normal anatomy, variants, and abnormalities. Insights Imaging. 2019;10(1):83. doi:10.1186/s13244-019-0761-3Kılıcgedik A, Kahveci G, Gurbuz AS, et al. Papillary muscle free strain in patients with severe degenerative and functional mitral regurgitation. Arq Bras Cardiol. 2017;108(4):339-346. doi:10.5935/abc.20170035

Fusion imaging (FI) technology using Echo-Navigator that integrates live transesophageal echocardiogram (TEE) and overlays on real-time fluoroscopy. We present our experience placing a right ventricular (RV) support device, a ProtekDuo, in our patient with post-operative RV failure using FI to guide the implantation.

Concomitant inferior sinus venosus atrial septal defect and hypoplasia of the posterior mitral valve leaflet in a 65-year-old female with a history of surgical ostium secundum atrial septal defect repair decades ago. Transesophageal echocardiography with bubble study using agitated saline contrast and cardiac magnetic resonance confirmed the previously undetected diagnosis

Mitral valve prolapse is a common valve disorder that usually has a benign prognosis unless there is significant regurgitation or left ventricular impairment. However, a subset of patients are at an increased risk of ventricular arrhythmias and sudden cardiac death, which has led to the recognition of ‘arrhythmic mitral valve prolapse’ as a clinical entity. Emerging risk factors include mitral annular disjunction and myocardial fibrosis. While echocardiography remains the primary method of evaluation, cardiac magnetic resonance has become crucial in managing this condition. Cine-MR sequences provide accurate characterization of prolapse and annular disjunction, assessment of ventricular volumes and function, identification of early dysfunction and remodeling, and quantitative assessment of mitral regurgitation when integrated with flow imaging. However, the unique strength of magnetic resonance lies in its ability to identify tissue changes. T1 mapping sequences identify diffuse fibrosis, in turn related to early ventricular dysfunction and remodeling. Late gadolinium enhancement sequences detect replacement fibrosis, an independent risk factor for ventricular arrhythmias and sudden cardiac death. There are consensus documents and reviews on the use of cardiac magnetic resonance specifically in arrhythmic mitral valve prolapse. However, in this article, we propose an algorithm for the broader use of cardiac magnetic resonance in managing this condition in various scenarios. Future advancements may involve implementing techniques for tissue characterization and flow analysis, such as 4D flow imaging, to identify patients with ventricular dysfunction and remodeling, increased arrhythmic risk, and more accurate grading of mitral regurgitation, ultimately benefiting patient selection for surgical therapy.

Type Ⅲ redundancy of the foramen ovale flap (RFOF) mimics hemodynamic changes of mitral stenosis(MS), which has not been particularly highlighted in previous literature. This type of MS carries a favorable prognosis.

Congenitally correct transposition of the great arteries (cc-TGA) is an extremely rare congenital cardiac malposition. They are usually detected by echocardiography in the fetal period. This case report describes a 58-year-old female patient who presented with tachycardia. The combination of cc-TGA and isolated levocardia is incidentally diagnosed by transthoracic echocardiography and cardiac magnetic resonance imaging.

Purpose: Point-of-care cardiovascular left ventricle ejection fraction (LVEF) quantification is established, but automatic tablet-based stroke volume (SV) quantification with handheld ultrasound devices is unexplored. We evaluated a tablet-based monoplane LVEF and LV volume quantification tool (AutoEF) against a computer-based tool (Tomtec) for LVEF and SV quantification. Methods: Patients underwent handheld ultrasound scans, and LVEF and SV were quantified using AutoEF and computer-based software that utilized either apical four-chamber views (AS-mono) or both apical four-chamber and apical two-chamber views (AS-bi). Correlation and Bland-Altman analysis were used to compare AutoEF with AS-mono and AS-bi. Results: Out of 43 participants, 8 were excluded. AutoEF showed a correlation of 0.83 [0.69:0.91] with AS-mono for LVEF and 0.68 [0.44:0.82] for SV. The correlation with AS-bi was 0.79 [0.62:0.89] for LVEF and 0.66 [0.42:0.81] for SV. The bias between AutoEF and AS-mono was 4.88% [3.15:6.61] for LVEF and 17.46 ml [12.99:21.92] for SV. The limits of agreement (LOA) were [-5.50:15.26]% for LVEF and [-8.02:42.94] ml for SV. The bias between AutoEF and AS-bi was 6.63% [5.31:7.94] for LVEF and 20.62 ml [16.18:25.05] for SV, with LOA of [-1.20:14.47]% for LVEF and [-4.71:45.94] ml for SV. Conclusion: LVEF quantification with AutoEF software was accurate and reliable, but SV quantification showed limitations, indicating non-interchangeability with neither AS-mono nor AS-bi. Further refinement of AutoEF is needed for reliable SV quantification at the point of care.