This narrative review analyses the development of microfluidic technologies specifically applied to the IVF treatment, and their translation into clinical solution. Starting with an analysis of the latest scientific publications, the patent scenario and the current clinical trials were analysed aiming to identify the most developed applications, the challenges, and barriers for regulatory approval and clinical validation in different countries. Searches were completed in English, by using a combination of these keywords (exceptions are included in the text in the different sections): Microfluidic, IVF, Assisted, clinical, fertility, human fertility, women fertility, reproduction, pregnancy, Assisted Reproductive Technology. These were used for previously published reviews and scientific journal papers using PubMed (National Center for Biotechnology Information at the U.S. National Library of Medicine), and Google Scholar, limited to the last decade (2013-2025); for completed or ongoing clinical trials using Clinicaltrials.gov; for existing patents and intellectual properties commercialization using lens.org, and crosschecked on espacenet.com from 2000 to 2025. It is approximately 20 years since the design of the first microfluidic systems for IVF. In the last 5 years, there have been over 130 publications proposing new microfluidic solutions, with pre-clinical validation data in animal models and humans. Our analysis highlighted three main areas of development that are discussed in terms of trends and advancements in oocyte and sperm processing and handling; proposed solutions to support in vitro embryo development; and microfluidic-based approaches and techniques for cryopreservation and female fertility preservation. In the last 20 years, progression of the microfluidic technology and improvement of manufacturing processes have led to an exponential rise of patents (1405) where microfluidics is applied to different steps of the assisted conception cycle. However, of these innovative techniques, only a limited number have progressed to clinical validation (19 trials commenced since 2009) and these have focused primarily on microfluidic sperm sorting and selection with multiple trials investigating its effectiveness in enhancing sperm quality and fertilization rates, and microfluidic embryo culture systems, where additional research is still needed to establish benefits over traditional culture environments. The key barriers to adoption include the need for long-term clinical outcome data, standardization of results across various patient populations, and regulatory challenges. We summarize the pathways needed to ensure compliance with quality standards and regulations in different countries. This analysis evaluates the different clinical trial requirements and challenges for participant recruitment, as well as study design complexity, and the definition of achievable endpoints and establishment of appropriate control groups or comparators. Finally, this review highlights complementary technologies recently combined with microfluidics (e.g. automatic and artificial intelligence-powered imaging, in situ non-invasive metabolic sensing) which can guarantee a more precise and safe handling of biological samples, favour automation of sample processing (e.g. gametes), and provide new information and higher level of control of the laboratory techniques used by clinics to treat patients in the next 5-10 years. N/A.
Social disconnection, both in the form of social isolation and loneliness, is increasingly recognized as a clinically significant but underappreciated risk factor for cardiovascular disease (CVD), affecting 16-25% of individuals. Population studies have consistently linked social disconnection to a higher risk of all-cause mortality, myocardial infarction, stroke, and cardiovascular death, yet routine screening for social disconnection is uncommon in everyday clinical practice. Even when identified, due to both lack of strong evidence-based interventions and awareness about them, meaningful clinical changes are seldom observed. In light of growing recognition by major health authorities, including the World Health Organization and the U.S. Surgeon General, and of the Harvard Study of Adult Development, showing that social integration and strong relationships are the most powerful predictors of healthy aging, we conducted a narrative literature review synthesizing current evidence on the relationship between social disconnection and CVD. The mechanism mediating social disconnection and cardiovascular events is still a matter of debate. We focus on cortisol-oxytocin imbalance and highlight that it is central in causing CVD through autonomic dysregulation, nutritional imbalance and gut microbiome alterations. Alongside psychosocial comorbidities, these factors may converge on endothelial dysfunction as an initiating mechanism of CVD. Our review also aims to foster discussion on how to recognize and address social disconnection in clinical practice, emphasizing the need for structured, multidisciplinary pathways as well as trials assessing their effect on improving both social disconnection and the associated CVD risk.
Pacemaker implantation rates are increasing worldwide, raising concerns about pacing-induced cardiomyopathy a complication of chronic right ventricular pacing (RVP). Pacing-induced cardiomyopathy results in adverse remodeling leading to left ventricular dysfunction and heart failure. pacing-induced cardiomyopathy treatment includes cardiac resynchronization therapy (CRT) and cardiac physiologic pacing upgrades, while preventative strategies include de novo implantation of CRT or cardiac physiologic pacing. Identification of patients who may be suitable for de novo CRT/cardiac physiologic pacing due to high risk for developing pacing-induced cardiomyopathy remains challenging, in part due to limited assessment of patient characteristics. A narrative review of pertinent literature was conducted to examine the definitions, pathophysiology, prevalence, risk factors, novel screening tools, and treatment options for pacing-induced cardiomyopathy in adult populations. Accurate assessment of pacing-induced cardiomyopathy prevalence is limited by center-to-center variability, as well as a variety of lead implantation sites and pacing options. Effective risk stratification, facilitated by a thorough collection and analysis of notable risk factors for pacing-induced cardiomyopathy, can help identify patients that may benefit from early use of cardiac physiologic pacing or CRT to prevent pathologic remodeling.
Parkinson's disease (PD) is a synucleinopathy best known for its motor symptoms, but emerging research shows it also impacts the cardiovascular system. In this paper, we explore the association between PD and cardiovascular disease (CVD), reviewing six key categories: cardiac dysautonomia, coronary artery disease, arrhythmias, cardiomyopathy, heart valve disease, and heart failure. We also discuss risk factors, epidemiology, and overlapping pathophysiology. Cardiac dysautonomia is the most frequently reported cardiovascular issue in PD and includes orthostatic hypotension, postprandial hypotension, supine hypertension, and nocturnal non-dipping blood pressure. PD also appears to be positively associated with coronary artery disease. Early-stage PD is linked to atrial fibrillation, but overall, there is no consistent increase in arrhythmias outside of certain PD medications. Structural and functional cardiac changes such as left ventricular hypertrophy and diastolic dysfunction have also been reported in PD, which may predispose to heart failure and cardiomyopathy. Dopamine agonists pergolide and cabergoline are associated with valve regurgitation, but this seems to be drug-related rather than caused by PD. Shared risk factors like aging, male sex, diabetes, and inflammation help explain the PD-CVD connection. However, some CVD risk factors like high LDL and smoking are associated with lower PD risk. Autonomic dysfunction, impaired lipid and glucose metabolism, and chronic inflammation may all contribute to disease overlap. Our review consolidates existing research to highlight the importance of recognizing cardiovascular manifestations in PD, which may present before motor symptoms. This has important implications for earlier diagnosis, better screening, and more effective management of PD.
Postoperative atrial fibrillation (POAF) is a common complication that can affect up to 20-44% of patients undergoing cardiac surgery. Evidence suggests that atrial fibrosis is a key factor in the development of POAF due to the disruption of the myocardial electric properties. This systematic review examines the correlation between pre-existing atrial fibrosis and the development of POAF after cardiac surgery. A systematic literature search was conducted in MEDLINE, Embase, and Google Scholar (2000 to March 2025) to identify studies that conducted comparative analysis of atrial fibrosis levels between those who did and did not develop POAF, using histological assessment methods. Extracted data, included study characteristics, histopathological staining methods and analysis findings, fibrosis quantification methods, and overall POAF incidence. Thirteen studies met the inclusion criteria, resulting in a total of 1222 patients, primarily undergoing coronary artery bypass surgery. The incidence of POAF ranged from 14%-42.4% (median 31.6%). In more than half of the studies (7/13), patients who developed POAF demonstrated statistically significant higher degrees of atrial fibrosis compared to those that remained in sinus rhythm postoperatively (four exhibited p < 0.001). Of the eight studies that conducted multivariate analyses, three identified atrial fibrosis as an independent POAF predictor. High heterogeneity precluded pooling of results into a meta-analysis. The current evidence examining the link between pre-existing atrial fibrosis and the development of POAF is restricted by methodological heterogeneity and inconsistent findings. Further efforts to standardize fibrosis quantification methods and POAF definitions are warranted before histopathological assessments can reliably inform POAF risk before cardiac surgery.
As cannabis use accelerates globally with expanding legalization and availability of high-potency formulations, concerns regarding its cardiovascular safety have grown. However, the evidence remains unclear and often inconsistent. This narrative review aimed to summarize the current evidence on the cardiovascular effects of cannabis. We performed a narrative review of peer-reviewed studies on cannabis and cardiovascular outcomes, searching PubMed and Google Scholar for relevant human research published 2014-August 2025. Included evidence encompassed observational cohorts, randomized trials, meta-analyses, Mendelian randomization studies, and mechanistic investigations, supplemented by reference screening. Observational studies reveal mixed associations between THC use and myocardial infarction, stroke, and MACE, with many findings attenuated after adjustment for confounders. A stronger and more consistent association exists for atrial arrhythmias. Evidence for venous thromboembolism remains inconsistent. Interpretation of the available evidence is also hindered by exposure misclassification (e.g., dose, route, frequency), reliance on administrative coding, insufficient differentiation between medical and recreational use, residual confounding (e.g., tobacco, other substances), and limited translational data. Cannabis use is rising, and while mechanistic data suggest THC-related autonomic, endothelial, and platelet effects, overall cardiovascular evidence remains mixed with the most consistent signal seen for atrial arrhythmias. Risk appears influenced by dose, route, and co-use of substances, and current studies are limited by heterogeneity and exposure misclassification. Until higher-quality data emerge, clinicians should adopt a precautionary, harm-reduction approach, especially in patients with cardiovascular comorbidities.
Artificial intelligence (AI) offers new opportunities in cardio-oncology for early detection, risk stratification, and personalized management of cardiovascular complications in cancer patients. By leveraging data from electronic health records, blood biomarkers, imaging tests such as echocardiography, electrocardiograms, and wearables, AI models can facilitate prediction, detection and response to treatment of cardiovascular disease entities, pre-existing and developing as a consequence of cancer therapy. Specific to the latter, referred to as cardiotoxicity, widespread adoption has been hindered by the limited availability of large datasets for model training, insufficient external validation, and challenges in integrating AI tools into routine clinical workflows. Future progress will depend on advancements in AI technologies, rigorous multi-center validation, development of explainable models, and seamless integration into clinical practice. Barriers, not only from a systems perspective, but also from a provider and most importantly from a patient perspective will need to be addressed for successful implementation. With a broad multidisciplinary perspective and patient focus, AI can advance cardio-oncology care and improve outcomes for patients with cancer.
Stretch-Induced Syncope is an uncommon form of situational syncope triggered by stretching upper-back, neck, and shoulder muscles. A review of 133 publications in PubMed, Embase, Scopus, Web of Science, Scielo, and Google Scholar, using search terms such as "stretch syncope," "syncope with stretch," and "stretch-induced syncope," identified 12 studies describing 30 patient cases (ages 5-26). Stretch-induced syncope episodes were triggered by neck hyperextension and upper-back stretching, producing brief loss of consciousness. Early reports attributed these events to vertebral artery compression or carotid baroreceptor stimulation. However, recent data from simulated stretch testing demonstrate a pronounced vasodepressor response with diminished compensatory tachycardia compared to the heart rate increment during an active standing maneuver in the same patient; these findings are best accounted for by a neural reflex-mediated mechanism rather than mechanical vascular obstruction. Diagnosis is best achieved through careful history taking in the clinic and symptom reproduction with simultaneous video-EEG and beat-by-beat blood pressure monitoring during autonomic testing. No pharmacologic therapy has proven effective; patient education and avoidance of provoking maneuvers remain the mainstays of management. Greater awareness of stretch-induced syncope may prevent misdiagnosis, reduce unnecessary testing, and guide future investigation into the autonomic mechanisms of this reflex.
Arrhythmogenic cardiomyopathy (ACM) is a genetically determined myocardial disease characterized by myocyte loss, fibro-fatty replacement, and electrical instability. In a subset of patients, episodes of chest pain with troponin release and electrocardiographic abnormalities occur in the absence of ischemic causes. These events, commonly referred to as "hot phases" (HP), often mimic acute myocarditis and raise important diagnostic and prognostic considerations. Among ACM-related genes, desmoplakin (DSP) variants are most frequently associated with HP, although episodes have also been observed in carriers of genes not classically associated with this presentation. Evidence suggests that HP presentation may vary across genotypes and ACM phenotypes, with DSP carriers more often exhibiting left sided or biventricular involvement. Growing data indicate that inflammation, autoimmunity, and innate immune activation play a central role in HP expression and ACM pathobiology, supported by findings of myocardial inflammatory infiltrates, circulating anti-desmosomal and anti-intercalated disc autoantibodies, and activation of NLRP3-inflammasome pathways. These mechanisms may contribute to disease progression and arrhythmic vulnerability. Therapeutic strategies remain empirical, but recent observations suggest that immunosuppressive therapy may modulate arrhythmic and heart-failure outcomes in DSP carriers. This review summarizes current knowledge on the clinical, genetic and immunologic features of HP in ACM, and discusses how these findings may refine the diagnostic approach and clinical interpretation of myocarditis-like presentations.
Modern cancer therapies, particularly immune checkpoint inhibitors (ICIs) and tyrosine kinase inhibitors (TKIs), have markedly improved cancer outcomes through more selective tumor targeting. However, as survivorship increases, there is growing recognition of long-term treatment-related complications, including a range of cardiometabolic disturbances. These include hyperglycemia, dyslipidemia and accelerated atherosclerosis, thyroid dysfunction and adrenal insufficiency, which significantly elevate long-term cardiovascular and metabolic risk in cancer survivors. The cardiometabolic sequelae of ICIs and TKIs are often under-recognised and under-monitored, despite their potential to contribute to serious morbidity. The mechanisms underpinning these toxicities are diverse and agent-specific, involving immune-mediated endocrine disruption, insulin resistance, and altered lipid metabolism. Current guideline recommendations remain limited across different therapeutic classes and clinical scenarios. In this review, we synthesise available evidence regarding the prevalence, mechanisms, and clinical management of cardiometabolic complications associated with ICIs and TKIs. We highlight key gaps in monitoring and therapeutic guidance and advocate for a multidisciplinary approach to early detection and management. Greater awareness and standardised care pathways will be essential to prevent avoidable complications and optimise long-term health in cancer survivors.
Pharmacological and electrical cardioversion of atrial fibrillation (AF) is associated with markedly increased (>10-fold) risk of thromboembolic events clustering within 7 days following sinus rhythm restoration. Current evidence indicates that post-cardioversion thrombus formation from atrial stunning, rather than preexisting thrombus, causes most thromboembolic complications. Risk factors include traditional CHA2DS2-VASc components (particularly heart failure), AF duration ≥12 h, mitral valve stenosis, cardiac amyloidosis and hypertrophic cardiomyopathy. While placebo-controlled randomized trials are lacking, there is overwhelming observational evidence that oral anticoagulation (OAC) reduces post-cardioversion thromboembolism by 60-80 % to a residual risk of approximately 0.5 %. This benefit seems independent of CHA2DS2-VASc and AF duration (including <48 h). Current guidelines recommend OAC for ≥3 weeks before and ≥4 weeks after cardioversion, or to rule out intracardiac thrombus by imaging, with OAC immediately before cardioversion and for ≥4 weeks. The safety of this strategy was validated in large prospective trials. However, alternative durations of pre-/post-cardioversion OAC have never been tested in randomized trials. The optimal duration of pre-cardioversion OAC remains unclear. Shorter pre-cardioversion delay is associated with increased success of cardioversion, reduced AF recurrence, reduced severity and duration of atrial stunning, and possibly reduced thromboembolic complications. Likewise, antiarrhythmic drug (AAD) pre-treatment improves cardioversion outcomes but is sometimes withheld by fear of early sinus rhythm restoration and associated thromboembolic risk. Randomized data from the ACUTE trial have shown that early AAD introduction was safe. Given the short-lived but dramatic increase in thromboembolic risk post-cardioversion, intensifying OAC immediately before cardioversion might further reduce risk, as suggested by observational studies.
Plastics serve multiple functions in an industrialized society, including major applications in all aspects of healthcare such as single use syringes, coatings and implantable devices. Plastics break down into smaller particles called microplastics (MP; diameter smaller than five millimeters) and nanoplastics (NP; diameter smaller than one micrometer), which are resistant to degradation. Recent evidence suggest that the smallest of these particles may accumulate in the human body throughout multiple organ systems. There has been particular interest on the effects of MP and NP accumulation in the cardiovascular system. In this review, we will discuss MP/NP formation, describe the clinical evidence supporting cardiovascular effects of these particles, with also a discussion on the possible molecular mechanisms behind these interactions. Finally, we will discuss the major knowledge gaps and current controversies involving MP and NP research as they relate to cardiovascular disease. Current evidence linking MP/NPs to cardiovascular disease remains largely correlative, with limited mechanistic validation.
Atrial fibrillation (AF) increases the risk of stroke and cognitive decline. While anticoagulation with vitamin K antagonists (VKAs) and direct oral anticoagulants (DOACs) prevents stroke, their role in reducing dementia risk in patients with AF remains unclear. To evaluate the effect of anticoagulation therapy on dementia incidence in patients with AF, comparing DOACs versus VKAs. We systematically reviewed PubMed, Scopus, Web of Science, Embase, and Cochrane. Systematic reviews and meta-analyses evaluating the effects of anticoagulation therapies on dementia were included. A total of 11 systematic reviews and meta-analyses were included in this umbrella review. Findings from 6 systematic reviews showed that OAC use was associated with a reduced risk of incident dementia in patients with AF, with effect estimates (RR/HR) ranging from 0.46 [0.28-0.78] to 0.79 [0.67-0.93]. For DOACs versus VKAs, most studies found a lower risk of dementia with DOACs, with effect sizes ranging from HR: 0.51 [0.37-0.71] to RR: 0.88 [0.82-0.94]. However, two studies found no significant difference between DOACs and warfarin in dementia risk (OR: 0.65 [0.34-1.25] and RR: 0.91 [0.75-1.12], respectively). Anticoagulation therapy, particularly with DOACs, may help reduce the risk of dementia in AF patients. The evidence remains of moderate to low certainty, and further high-quality, long-term randomized controlled trials are needed to confirm these findings and explore the neuroprotective mechanisms of OACs.
The 2025 European Society of Cardiology (ESC) guidelines and the 2024-2025 American College of Cardiology (ACC) consensus documents redefine the management of myocarditis and pericarditis, with notable convergence, yet key differences. Both emphasize early, accurate diagnosis, particularly through cardiac magnetic resonance (CMR), which now often supersedes immediate biopsy in stable, uncomplicated cases of acute myocarditis. The ESC introduces a unified "inflammatory myopericardial syndrome" (IMPS) framework encompassing myocarditis, pericarditis, and overlap syndromes, while the ACC provides separate pathways, including a novel four-stage clinical classification of myocarditis. Therapeutically, both endorse non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine for pericarditis and myopericarditis, and heart failure-directed therapy for myocarditis, while reserving immunosuppression for select cases. Importantly, interleukin-1 (IL-1) blockade has emerged as a pivotal therapy in recurrent pericarditis, receiving a Class I recommendation in ESC guidelines and strong endorsement in ACC guidance. Prognostic assessment focuses on identifying high-risk features and structured follow-up with imaging and biomarkers. Divergences in terminology, staging, and diagnostic thresholds underscore opportunities for further harmonization. The ESC and ACC documents align in a patient-tailored, evidence-informed approach to management.
Out-of-hospital cardiac arrest (OHCA) remains a leading global mortality challenge, with survival rates below 10% despite significant advancements. This review addresses persistent challenges across the spectrum of OHCA care, highlighting key areas for improvement in alignment with contemporary guidelines, including the recently updated European Resuscitation Council 2025 recommendations. Epidemiologically, progress is hindered by the lack of standardized, multi-territorial registries that prevent effective geospatial analysis and limit the reduction of health inequities. Improving the "Chain of Survival" requires easier, faster public access to defibrillation through the mandatory and widespread installation of Public Access Defibrillators (PADs) and integration with digital tools. Management of refractory ventricular fibrillation is evolving to include alternative defibrillation techniques (Vector-Change and Double Sequential External Defibrillation), as well as novel therapies such as stellate ganglion block. Post-resuscitation care requires defining optimal strategies for complete coronary revascularization and P2Y12 inhibition. Crucially, the long-term phase is inconsistent: the high prevalence of unassessed cognitive and psychological impairments among survivors necessitates enhanced interdisciplinary collaboration and routine long-term follow-up, as emphasized by current guidelines. Overcoming these challenges, from data collection to recovery support, is vital not only for enhancing post-OHCA survival but also for enabling functional recovery and quality of life.
The background for this review includes negative emotions-including anger, sadness, and chronic stress-that are biologically active contributors to atherothrombosis but remain under-integrated in prevention. The objective is to synthesize epidemiologic, mechanistic, and interventional evidence linking emotional dysregulation to the pathogenesis and acute expression of ASCVD, and to contextualize effect sizes alongside traditional risk factors. The methods include a narrative review of large cohorts and case-crossover studies, neural and immunologic mechanisms (amygdala-bone marrow-arterial axis), and trials of β-blockers, SSRIs, cognitive behavioral therapy (CBT), mindfulness, and endothelial function responses to provoked emotions. We found that depressive symptoms and trait anger confer ∼30-50 % higher incident MI risk; intense anger outbursts transiently raise MI risk up to ∼8-9 ×, and bereavement up to ∼20 × within 24 h. Stress-evoked amygdalar activity predicts myelopoiesis, arterial inflammation, and events. Mechanisms include HPA axis activation, IL-6/NLRP3 signaling, eNOS uncoupling, and catecholamine-driven platelet activation. Interventions such as β-blockers, SSRIs, CBT, and mindfulness improve vascular/inflammatory markers and may reduce event susceptibility. We conclude that emotions are causal drivers of atherothrombosis and acute coronary events. Incorporating emotion metrics, inflammatory biomarkers, and targeted behavioral/pharmacologic strategies into preventive cardiology can close residual risk gaps.
Sudden cardiac death (SCD) causes 4 to 5 million deaths each year globally. Electrical vortices (tornadoes or rotors) are the origin of ventricular fibrillation (VF), which often causes SCD. Cardiac electrical vortices have complex dynamics and have been shown in many mammalian species. During VF, the heart fails to contract suitably and is unable to pump blood. Once VF is initiated, drug treatments are ineffective and even make things worse. The only effective treatment is electrical shock to the ventricles. Our current understanding of VF mechanisms is fragmentary, hindering the development of personalized therapies. Yet recent insights into the roles of the most critical sarcolemmal ion channels in VF in controlling the excitation-recovery process provide hope. Substantial evidence indicates that the molecular interplay between the main cardiac sodium channel (NaV1.5) and the strong inward-rectifier potassium current (Kir2.1) controls cardiac excitability, wave propagation velocity, and rotor formation, as well as rotor stability and frequency during VF. Studies at the cellular, molecular, and ion channel levels are helping us understand how rotors generate the turbulence that characterizes VF, providing insights into how to prevent their initiation and identifying new therapeutic targets to avert premature death.
Cardiogenic shock (CS) remains a major clinical challenge, with persistently high short-term mortality despite advances in reperfusion therapy, pharmacological support, and mechanical circulatory support. This review reassesses the conceptual evolution of CS and examines why hemodynamic-centric diagnostic and therapeutic strategies have failed to yield meaningful improvements in outcomes. Historically, CS has been defined by cardiac-oriented macrocirculatory compromise, and contemporary definitions and staging systems have improved risk stratification but remain largely hemodynamics-focused and primarily validated in intensive care settings. Increasing evidence indicates that inflammatory activation, microcirculatory dysfunction, endothelial injury, and metabolic derangements are central determinants of shock progression and organ failure. Integrating multimodal diagnostic approaches-including bedside assessment of microcirculation and inflammation, omics-based phenotyping, advanced echocardiographic techniques, and artificial intelligence-assisted risk stratification-may enable earlier recognition, more precise classification, and improved risk stratification across the continuum of care. Reframing cardiogenic shock as a dynamic, multisystem disorder supports a shift from hemodynamic-centric paradigms toward multimodal precision care, with important implications for clinical management and future trial design.
Cardiogenic shock (CS) is a life-threatening condition characterized by severe systemic hypoperfusion that may progress into multi-organ failure. Immediate optimization of organ perfusion is therefore considered a critical priority. However, first-line therapy with inotropes and vasopressors carries significant risks, adding stress to an already severely failing heart, and may eventually contribute to further clinical deterioration. Subsequent temporary mechanical circulatory support (tMCS) has been traditionally viewed upon as a means to restore systemic circulation. Recent approaches have, however, suggested that the hemodynamic buffer provided by tMCS may create a therapeutic window for the initiation of evidence-based heart failure therapies. Nevertheless, interfering in a jeopardized hemodynamic and failing homeostasis is extremely challenging and the devices carry a significant risk of serious adverse events. In this review, we discuss the potential use of heart failure therapies in patients with CS who are supported with tMCS. We highlight the feasibility and potential efficacy of this combined therapeutic approach from the perspective of a novel, aviation-inspired safety framework referred to as the 'hemodynamic envelope'. This concept may inspire future study designs and support clinicians in initiating established heart failure therapies during tMCS.
Inherited cardiac conditions (ICCs) such as hypertrophic cardiomyopathy and Marfan syndrome pose significant global health challenges, often rooted in complex genetic mutations. Recent advances in gene editing, particularly the CRISPR/Cas9 system, have opened new avenues for precise, personalized interventions. This review examines the current landscape of gene editing in cardiology, with emphasis on its scientific promise, integration with epigenetics, gene therapy, and artificial intelligence, and its potential to transform clinical outcomes. Key gene editing strategies are analyzed for their efficacy and translational potential. The review also explores ongoing clinical trials and emerging research, offering practical insights for future studies. Ethical implications are critically evaluated, with proposed frameworks to address concerns around safety, equity, and long-term consequences. By synthesizing these developments, this review underscores the urgent need for continued interdisciplinary research in the quest to mitigate inherited cardiac diseases.