Shahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Editorial1253110.18502/cbj.v6i1.22783ENSeyed JalilMirhosseiniYazd Cardiovascular Research Center, Non- communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran0000-0003-3281-4714Journal Article20260724Cardiovascular medicine is increasingly moving beyond the question of whether a patient has disease toward a more important question: how much biological damage is already present when conventional measures still appear reassuring?The five contributions in this issue illustrate this transition from different perspectives. Together, they highlight a common theme: clinically meaningful myocardial dysfunction may precede symptoms, reduction in left ventricular ejection fraction, or other conventional markers of disease progression.The focused meta-analysis of global longitudinal strain (GLS) during exercise in asymptomatic severe aortic stenosis is particularly illustrative. Resting GLS was consistently worse in patients with abnormal exercise responses, while the difference became substantially greater during exercise. These findings support GLS as a sensitive marker of early myocardial involvement. At the same time, the considerable heterogeneity of exercise-derived measurements reminds us that physiological promise must be followed by methodological standardisation and prospective validation before a new parameter becomes a routine treatment trigger.The articles addressing myocardial deformation, stress physiology, and cardiovascular risk similarly reinforce the importance of contractile reserve rather than resting function alone. A preserved ejection fraction should increasingly be regarded as one component of ventricular assessment, not as proof of myocardial integrity.A complementary message emerges from the article on artificial intelligence in cardiac amyloidosis. AI can identify subtle echocardiographic phenotypes and potentially increase diagnostic suspicion, but its value will depend on how intelligently it is integrated into clinical practice. An algorithm can identify a pattern; it cannot replace clinical context, expert interpretation, or responsibility for the final diagnosis. These observations lead to a broader principle.The future of cardiovascular imaging will be defined less by individual measurements and more by the integration of structure, function, physiology, and computation.GLS, exercise response, valve haemodynamics, myocardial fibrosis, biomarkers, and AI-derived phenotypes may ultimately become components of a multidimensional assessment of myocardial reserve. The challenge is not simply to detect more abnormalities, but to determine which abnormalities represent clinically actionable disease.This distinction is especially important in asymptomatic severe aortic stenosis and other conditions in which irreversible myocardial injury may begin before symptoms become apparent. Earlier recognition may create an opportunity for earlier intervention—but only if the diagnostic signal has been adequately validated and shown to improve decision-making and outcomes.As technology becomes increasingly capable of detecting what the human eye cannot easily see, the role of the clinician will not diminish. It will change. The future expert will be the clinician who can critically interpret increasingly sophisticated measurements and artificial intelligence without becoming dependent upon them.Ultimately, the goal of innovation in cardiovascular imaging should remain simple:To recognize myocardial disease earlier, understand its biological significance more precisely, and intervene at the moment when treatment can make the greatest difference. This is the direction in which cardiovascular medicine is movinand the articles in this issue offer valuable steps along that path.https://cbj.ssu.ac.ir/article_531_0fcbc61acd0479dc77e3cccc0f5ffca7.pdfShahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Global longitudinal strain in stress test of asymptomatic severe aortic stenosis: a focused meta-analysis31452510.18502/cbj.v6i1.22784ENOliverMcConnelMacclesfield District General Hospital, East Cheshire NHS Trust, Macclesfield, England, UK0009-0008-9715-3965VenusShahabi RaboriDepartment of Cardiology, King’s College Hospital, London, England, UK0000-0002-2589-5360Journal Article20260607Objectives: In asymptomatic severe aortic stenosis (AS) with preserved ejection fraction, subclinical myocardial dysfunction often precedes symptoms by years. Left ventricular ejection fraction (LVEF) is not a determining factor of this early impairment. Global longitudinal strain (GLS) can detect subtle impairment earlier, but its behaviour during exercise stress testing in this context has not been thoroughly assessed. We examined whether GLS at rest and during exercise can distinguish patients with abnormal stress test responses from those with normal responses, and whether exercise‑derived strain adds information beyond resting measurements.Methods: The researchers conducted a comprehensive review of studies published up to August 21, 2025, using databases including PubMed, Scopus, and Web of Science. They included studies reporting Global Longitudinal Strain (GLS) in asymptomatic patients with severe aortic stenosis (AS) who had a left ventricular ejection fraction (LVEF) of 55% or greater. The studies compared responses to normal versus abnormal exercise stress tests. Two reviewers independently extracted the data. The researchers used the Newcastle-Ottawa Scale to assess study quality. A meta-analysis was performed using random-effects models with Hedges’ g to calculate standardized mean differences, conducted in STATA-MP version 17.Results: Four studies involving 887 patients were included in the analysis. Resting GLS was worse in patients with abnormal stress responses (SMD -0.37; 95% CI -0.51 to -0.22; p<0.001), with no heterogeneity across studies (I²=0%). During exercise, the difference more than doubled (SMD -0.86; 95% CI -1.40 to -0.32; p=0.002), though substantial heterogeneity was present (I²=82%). Delta GLS showed a non-significant trend (SMD -0.34; p=0.22), also with high heterogeneity (I²=84%), likely related to differences in imaging timing across studies. All studies scored 6–8 on the Newcastle-Ottawa Scale.Conclusions: GLS identifies subclinical myocardial dysfunction in this population. The exercise signal is stronger than the resting signal but requires standardisation before clinical application. Prospective studies with pre-specified GLS thresholds are needed.https://cbj.ssu.ac.ir/article_525_69421f032498c97020180038fddb8e24.pdfShahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Cardiovascular adaptation and dysfunction in fighter pilots exposed to G-Forces and hypobaric environments: a comprehensive review152952610.18502/cbj.v6i1.22785ENMohammadMoradiDepartment of Biomedical Engineering, Faculty of Khajeh Nasir al Din Tusi Faculty, Tabriz University of Technology (Sahand), Sahand, Tabriz, Iran0009-0002-1506-865XHaniehHabibi JirdehiDepartment of Biomedical Engineering, Faculty of Khajeh Nasir al Din Tusi Faculty, Tabriz University of Technology (Sahand), Sahand, Tabriz, Iran0009-0004-9372-4485Journal Article20260622Objectives: Military fighter pilots routinely experience extreme physiological stressors, including high acceleration forces (+Gz), hypobaric hypoxia, rapid atmospheric pressure changes, and intense operational workloads. These environmental challenges impose substantial demands on the cardiovascular system and may affect cardiac function, autonomic regulation, vascular adaptation, and long-term cardiovascular health. Understanding the cardiovascular consequences of these stressors is essential for optimizing pilot performance, improving flight safety, and guiding aerospace medicine practice. This review study aimed to critically evaluate the effects of acceleration forces and atmospheric pressure changes on cardiovascular physiology in fighter pilots, with particular emphasis on hemodynamic regulation, autonomic nervous system responses, hypoxia-related cardiac effects, decompression sickness, and long-term cardiovascular adaptation.Methods: This literature review utilized peer-reviewed publications indexed in major scientific databases, including PubMed, Scopus, Web of Science, and Google Scholar. The samples included all studies published from 1986 to early 2025, including experimental and clinical studies, physiological research, aerospace medicine reports, and review articles examining cardiovascular responses to acceleration stress and hypobaric exposure.Results: Exposure to positive acceleration (+Gz) produces significant cardiovascular alterations through blood redistribution toward the lower extremities, reduced venous return, decreased stroke volume, and diminished cerebral perfusion. Recent evidence suggests that improved G tolerance is mediated primarily by peripheral vascular adaptation rather than solely by enhanced baroreflex sensitivity. High-altitude exposure causes hypobaric hypoxia, increasing heart rate, elevating cardiac output, and enhancing sympathetic activation to preserve tissue oxygenation. Decompression sickness remains a potentially serious complication, with cardiovascular manifestations ranging from pulmonary vascular obstruction to coronary gas embolism. Heart rate variability studies consistently demonstrate increased sympathetic nervous system activity during military flight, with autonomic disturbances persisting for several hours after mission completion. Despite these acute physiological stresses, current evidence indicates that most healthy fighter pilots maintain preserved long-term cardiovascular function, although continued surveillance remains necessary.Conclusions: The cardiovascular system exhibits remarkable adaptive capacity in response to the combined effects of acceleration forces and hypobaric environments encountered in military aviation. However, these stressors generate substantial acute hemodynamic and autonomic challenges that may affect operational performance and, in rare cases, contribute to serious cardiovascular events. Continued research into vascular adaptation, autonomic regulation, hypoxia tolerance, and long-term cardiovascular outcomes is required to improve pilot health, optimize training strategies, and enhance flight safety.https://cbj.ssu.ac.ir/article_526_85422afb467e9456013a2a51d4dff702.pdfShahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Assessment of Endothelial Function Changes Following Repeated Hyperbaric Exposure in Divers: A Comprehensive Review303853010.18502/cbj.v6i1.22786ENMohammadMoradiDepartment of Biomedical Engineering, Faculty of Khajeh Nasir al Din Tusi Faculty, Tabriz University of Technology (Sahand), Sahand, Tabriz, Iran0009-0002-1506-865XHaniehHabibi JirdehiDepartment of Biomedical Engineering, Faculty of Khajeh Nasir al Din Tusi Faculty, Tabriz University of Technology (Sahand), Sahand, Tabriz, Iran0009-0004-9372-4485Journal Article20260622Objectives: Repeated exposure to hyperbaric pressure and decompression during diving induces unique physiological challenges for the cardiovascular system. The vascular endothelium plays a critical role in maintaining vascular homeostasis through regulating vascular tone, nitric oxide (NO) bioavailability, inflammatory responses, and oxidative balance. Previous investigations have shown that acute hyperbaric exposure may impair endothelial function through oxidative stress, inflammatory activation, and intravascular bubble formation; however, the long-term effects of repeated diving exposure on endothelial health remain unclear. Therefore, this review was conducted to summarize current evidence regarding alterations in endothelial function following repeated hyperbaric exposure in divers and to describe the underlying molecular mechanisms involved in endothelial injury and vascular adaptation. This review aimed to evaluate the effects of repeated hyperbaric exposure on endothelial function in divers and to summarize the potential mechanisms associated with endothelial dysfunction and vascular adaptation.Methods: A comprehensive literature search was performed in PubMed, ScienceDirect, and Scopus databases using combinations of relevant keywords, including "endothelial function," "diving," "hyperbaric exposure," "decompression," "oxidative stress," "endothelial microparticles (EMPs)," "nitric oxide (NO)," and "heat shock proteins (HSPs)." The review focused on human and animal studies that assessed objective markers of endothelial function following hyperbaric exposure or diving activities.Results: Current evidence indicates that acute hyperbaric exposure and decompression are associated with increased circulating gas bubbles, oxidative stress, inflammatory activation, and transient endothelial dysfunction. Reduced flow-mediated dilation (FMD) and increased endothelial microparticles (EMPs) have been reported following deep and repetitive diving exposures. Experimental studies have demonstrated enhanced oxidative responses after simulated deep dives, including alterations in lipid peroxidation and antioxidant activity. However, repeated diving training may induce adaptive responses, including decreased bubble formation and improved tolerance to hyperbaric stress, without necessarily causing persistent endothelial impairment. These responses appear to involve regulation of NO bioavailability, heat shock protein (HSP) expression, oxidative pathways, and vascular protective mechanisms.Conclusions: Repeated hyperbaric exposure induces a complex interaction between endothelial stress and physiological adaptation. Although acute diving-related stress may cause temporary endothelial dysfunction, long-term repetitive exposure may promote protective vascular adaptations. Further longitudinal investigations are required to determine the long-term cardiovascular consequences of these adaptations in professional divers.https://cbj.ssu.ac.ir/article_530_d64a340bcb633f536d56e51874281454.pdfShahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Congenital absence of the right coronary artery, with the LCX supplying the entire RCA territory394352910.18502/cbj.v6i1.22787ENHosseinNoughYazd Cardiovascular Research Center, Non-communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran0000-0001-7255-5310MohammadtaghiSarebanhassanabadiYazd Cardiovascular Research Center, Non-communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran0000-0002-8867-4717MahmoudEmamiYazd Cardiovascular Research Center, Non-communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran0000-0002-5121-0054ParisaPeiganYazd Cardiovascular Research Center, Non-communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran0000-0001-5035-5692FatemehRahmanidehnaviDepartment of Cardiology, Clinical Research Center, Paster Educational Hospital, Bam University of Medical Sciences, Bam, Iran0009-0003-6644-4763Journal Article20260628Objectives: Congenital absence of the right coronary artery (RCA) is an exceedingly rare coronary anomaly in which the left coronary system supplies the entire myocardium. We report a case of congenital absence of the RCA with a superdominant left circumflex artery (LCX) supplying the entire RCA territory in a patient presenting with stable angina, highlighting the diagnostic and clinical importance of recognizing this unusual coronary anatomy.Methods: A 57-year-old man with hypertension and type 2 diabetes mellitus presented with a one-month history of typical anginal chest pain. Clinical evaluation included electrocardiography, transthoracic echocardiography, single-photon emission computed tomography myocardial perfusion imaging (SPECT MPI), and coronary angiography to assess myocardial ischemia and coronary anatomy.Results: SPECT MPI demonstrated a small-to-moderate reversible perfusion defect in the apical region. Coronary angiography revealed no identifiable RCA ostium in the right coronary sinus, confirming congenital absence of the RCA. Selective left coronary angiography demonstrated a markedly enlarged, superdominant LCX that coursed through the left atrioventricular groove, crossed the crux, and extended into the right atrioventricular groove, supplying the territories normally perfused by the RCA. A myocardial bridge was also observed in the mid-left anterior descending artery without significant compression at rest, and no significant obstructive coronary artery disease was identified. Medical treatment with bisoprolol was initiated, and the patient remained asymptomatic during follow-up.Conclusions: Congenital absence of the RCA with compensatory perfusion by a superdominant LCX is a rare coronary anomaly that may present with angina and evidence of myocardial ischemia. Accurate delineation of coronary anatomy is essential to establish the diagnosis, avoid unnecessary attempts to cannulate a nonexistent RCA ostium, and guide future interventional or surgical management.https://cbj.ssu.ac.ir/article_529_37f0e884fbad9667e38940169d0a3c95.pdfShahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Scrimmage with 'Coronary Sinus Muscle Bridge': case series and clinical implications444852810.18502/cbj.v6i1.22788ENMahdiMoeiniDepartment of Cardiology, Seyyed-al-Shohada Educational Heart Hospital, Urmia University of Medical Sciences, Urmia, Iran0000-0002-0899-0518MohammadrezaDehghaniDepartment of Cardiology, Seyyed-al-Shohada Educational Heart Hospital, Urmia University of Medical Sciences, Urmia, Iran0009-0005-7083-0135Journal Article20260816Objectives: The coronary sinus (CS) plays a key role in cardiac electrophysiology, including cardiac resynchronization therapy (CRT) and ablation of arrhythmias such as left-sided accessory pathways, premature ventricular complexes (PVCs), and atrial fibrillation (AF). Some procedures cannot be performed without CS access, requiring alternative approaches when cannulation fails. CS cannulation can be difficult and, rarely, unsuccessful. Known causes include anatomical abnormalities such as atresia, diverticulum, anomalous ostial location, and fixed stenosis at the ostium or along the vessel course. Here, we present three cases of difficult CS cannulation due to dynamic obstruction — a novel anatomical variant.Methods: We describe three consecutive patients referred for CRT-D implantation in whom CS cannulation or lead advancement was unexpectedly difficult. In each case, standard CS sheath and catheter techniques were used via subclavian venous access. When resistance to catheter or lead advancement was encountered, contrast venography (with balloon occlusion in select cases) was performed to delineate CS anatomy across the cardiac cycle, and catheter/lead manipulation timed to the non-systolic phase was used to overcome the obstruction.Results: In all three patients, venography revealed dynamic narrowing of the CS main trunk or a branch during ventricular systole, with resolution of the compression during diastole — a pattern consistent with an underlying muscle bridge rather than a fixed structural lesion. Case 1 showed severe systolic compression of the CS main trunk at the posterolateral branch takeoff; Case 2 showed a similar constriction in the mid-CS body; Case 3 showed compression confined to the distal lateral branch. Despite these dynamic obstructions, successful CS lead placement was achieved in all three patients using gentle catheter manipulation and advancement timed to diastole, without need for alternative pacing approaches.Conclusions: Dynamic, systole-phase compression of the coronary sinus or its branches — attributable to an epicardial-to-intramyocardial muscle bridge — represents a previously underrecognized and reversible cause of CS cannulation difficulty, distinct from fixed anatomical anomalies. Recognition of this pattern on cine-venography, combined with balloon-occlusion imaging and diastole-timed catheter advancement, allows most cases to be managed successfully without abandoning the CS approach.https://cbj.ssu.ac.ir/article_528_f4be00279ee2e0a53eafdaa94a151e2c.pdfShahid Sadoughi University of Medical SciencesCardiovascular Biomedicine2783-297X6120260901Artificial intelligence in diagnosing cardiac amyloidosis by standard echocardiography: opportunity or threat for sonographers?495052410.18502/cbj.v6i1.22789ENRaziehParizadCardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran0000-0002-4492-637XMohammadrezaTaban SadeghiCardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran0000-0001-9577-0099Journal Article20260528Dear Editor,Cardiac amyloidosis (CA) remains an underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) (1). Standard transthoracic echocardiography (TTE) continues to serve as the first-line screening tool; however, classic red flags, including increased left ventricular (LV) wall thickness with normal or low voltage, reduced global longitudinal strain (GLS), and the relative apical sparing pattern, are frequently overlooked (2). The rapid integration of artificial intelligence (AI) into echocardiography laboratories raises a critical question: does AI represent an opportunity or a threat for sonographers? AI as an OpportunityAI algorithms can detect subtle CA patterns that may escape human visual assessment. A deep learning (DL) model using a single apical four-chamber video clip achieved an area under the receiver operating characteristic (ROC) curve (AUROC) of 0.93, 85% sensitivity, and 93% specificity during external validation across 18 global sites (3). Another model discriminated CA from hypertensive heart disease (area under the curve [AUC] 0.92), hypertrophic cardiomyopathy (AUC 0.91), and aortic stenosis (AUC 0.93) (4). A systematic review confirmed that AI models perform comparably to or better than professional cardiologists (5). For sonographers, AI functions as a real-time "second pair of expert eyes," transforming them from passive data collectors into active clinical screeners. AI as a ThreatThere are three principal threats. First, overreliance on AI may lead to false-positive findings. For instance, the apical sparing pattern has only 72% sensitivity and 66% specificity for CA, and 32% of non-CA controls exhibit the same pattern (6). Second, overreliance on automated measurements might weaken pattern recognition skills and potentially lead to a gradual loss of diagnostic proficiency. Third, professional autonomy is likely to weaken if AI-driven automated reports bypass sonographer input entirely, thereby reducing their role primarily to image acquisition. Furthermore, implementation barriers, including cost, interoperability with electronic health records (EHRs), regulatory challenges, and liability concerns, remain unresolved (7). ConclusionAI will not replace sonographers who understand CA pathology; however, it may replace those who refuse to adopt AI-assisted diagnosis. Therefore, AI literacy should be a fundamental part of sonography training. Sonography training should include basic principles of machine learning, recognition of AI-generated false positives, and integration of AI alerts into the clinical workflow. Table 1 presents the key opportunities and threats with supporting references.https://cbj.ssu.ac.ir/article_524_ba2fd310dcaa8781a9a652a31baf3c68.pdf