While Cellular Therapy and Stem Cell Therapy for Heart Diseases is a rapidly advancing field, many challenges have recently been overcome thanks to the advancement of Cell-based technologies in 2024 and these treatments become widely available just recently. Ongoing research, particularly in clinical trials around the world, continues to refine Cellular Therapy and Stem Cell Therapies and explore their potential to revolutionize the treatment of various cardiovascular conditions.
Unlike mammals, which typically form scar tissue in response to cardiac injury, zebrafish can efficiently replace damaged heart muscle with healthy tissue, restoring normal cardiac function.
Heart and Vessel diseases remain one of the most prevalent and challenging health concerns globally, affecting millions of lives each year. From Coronary Artery Disease (CAD) to Congestive Heart Failure (CHF), the spectrum of Cardiovascular Disorders presents a significant burden on individuals and healthcare systems alike. Despite advancements in Cell-based treatment modalities, the quest for innovative approaches to regenerate damaged cardiac and vascular tissues and restore heart and vessel functions continues to drive research forward.
One area of promising exploration lies in Cellular Therapy and Stem Cells for Heart Disease Regeneration. Stem cells possess remarkable potential for tissue repair and regeneration due to their unique ability to differentiate into various cell types, including cardiomyocytes—the building blocks of the heart muscle. This potential opens doors to revolutionary treatments aimed at addressing the root causes of Heart Disease and promoting functional recovery.
One captivating example of nature’s regenerative prowess is found in the zebrafish—a tiny aquatic creature with a remarkable capacity for cardiac regeneration. Zebrafish have captured the attention of researchers for their ability to regenerate not only fins and other tissues but also their hearts. In a striking demonstration of this phenomenon, studies have revealed the zebrafish’s remarkable ability to regenerate its pericardium-induced heart tissue following injury. This extraordinary regenerative capability is attributed, in part, to the presence of resident cardiac stem cells and the dynamic interplay of various signaling pathways within the zebrafish heart.
The study of zebrafish cardiac regeneration serves as a beacon of hope and inspiration for researchers striving to unlock the secrets of human heart repair. By unraveling the underlying mechanisms governing zebrafish heart regeneration, scientists aim to harness similar regenerative processes in human cardiac tissue through innovative Cellular Therapy and Stem Cell-based interventions.
In this exploration Cellular Therapy and Stem Cells for Heart Diseases, we delve into the fascinating world of Cardiovascular regeneration, drawing insights from nature’s own marvels and translating them into potential treatments for the benefit of patients worldwide. Through interdisciplinary collaboration and relentless pursuit of knowledge, we endeavor to turn the tide against Heart and Vessel Disease and pave the way towards a future where damaged hearts and vessels can heal and thrive once more[1-5].
– ACS affects millions of people worldwide each year, with approximately 1.5 million cases reported in the United States alone annually.
– It is a leading cause of hospital admissions and cardiovascular-related deaths globally.
– Cardiomyopathy is estimated to affect around 1 in every 500 individuals globally.
– It is responsible for a significant proportion of heart failure cases, contributing to increased morbidity and mortality rates.
– CHF is a prevalent condition worldwide, affecting over 26 million people globally.
– It is a major cause of hospitalizations and healthcare costs, posing a significant burden on healthcare systems.
– PVD, PAD, and chronic arterial occlusive disease of lower limbs collectively impact millions of individuals globally.
– They are associated with an increased risk of limb amputations and reduced quality of life for affected individuals.
– Valvular heart disease affects millions of people worldwide, with rheumatic heart disease being a significant contributor in developing countries.
– It is associated with complications such as heart failure, stroke, and increased mortality rates if left untreated.
These statistics highlight the significant burden of heart diseases on global health, emphasizing the urgent need for effective prevention and treatment strategies[6-10].
The heart is a complex organ composed of various types of cells that work together to maintain its function. Here are the primary cell types found in the heart:
1. Cardiomyocytes: These are the muscle cells of the heart responsible for contraction and pumping blood throughout the body.
2. Cardiac Fibroblasts: These cells provide structural support to the heart muscle and play a crucial role in maintaining the extracellular matrix (ECM) of the heart.
3. Endothelial Cells: These cells line the inner surface of blood vessels, including those within the heart (endocardium), and are involved in regulating vascular tone and permeability.
4. Smooth Muscle Cells: Found in the walls of blood vessels, including arteries and veins within the heart, smooth muscle cells help regulate blood flow and pressure.
5. Pericytes: These cells are located around small blood vessels (capillaries) and have roles in blood vessel stability, angiogenesis (formation of new blood vessels), and tissue repair.
6. Valvular Interstitial Cells (VICs): These cells are found in heart valves and contribute to valve structure and function, including the maintenance of valve integrity and flexibility.
7. Macrophages: These immune cells are present in the heart and play roles in inflammation regulation, tissue repair, and immune response to infections or injuries.
8. Progenitor Stem Cells: While not a distinct cell type of the mature heart, stem cells and progenitor cells (such as cardiac progenitor cells) are involved in cardiac development, repair, and regeneration processes.
These cell types work together harmoniously to ensure proper cardiac function, including contraction, relaxation, blood flow regulation, and structural integrity of the heart’s tissues and vessels[11-18].
Despite medical advancements, there are several challenges associated with cardiovascular conditions that continue to impact patients globally.
– Delayed recognition and treatment of ACS/CAD symptoms, leading to missed opportunities for timely intervention and potential complications such as myocardial infarction.
– Variability in healthcare access and disparities in ACS/CAD management, particularly in underserved populations and rural areas.
– Risk of recurrent ACS/CAD events and long-term cardiovascular complications even after initial treatment and recovery.
– Limited options for effective disease-modifying therapies, especially for non-ischemic cardiomyopathy.
– Challenges in early detection and diagnosis of cardiomyopathy, resulting in delayed initiation of appropriate treatment.
– Progressive nature of the disease, leading to irreversible damage to cardiac tissue and increased risk of heart failure and arrhythmias.
– Difficulty in managing fluid overload and maintaining optimal fluid balance in CHF patients, contributing to recurrent hospitalizations.
– Adherence to complex medication regimens and lifestyle modifications, which can be challenging for some patients.
– Coexistence of multiple comorbidities in CHF patients, such as diabetes and chronic kidney disease, complicating treatment and management strategies.
– Underdiagnosis and undertreatment of PVD and PAD, particularly in asymptomatic or mild cases, leading to progression of the disease and increased risk of limb complications.
– Limited awareness and access to non-invasive diagnostic tests for early detection of PVD and PAD in primary care settings.
– High prevalence of risk factors such as smoking, diabetes, and hypertension contributing to the development and progression of arterial occlusive diseases.
– Challenges in timely diagnosis and assessment of valvular heart disease severity, particularly in asymptomatic or minimally symptomatic patients.
– Limited availability of minimally invasive treatment options for valvular heart disease, leading to delays in intervention and management.
– Age-related degenerative changes in heart valves, increasing the risk of valve dysfunction and progressive deterioration.
Addressing these challenges requires a multidisciplinary approach involving healthcare professionals, policymakers, and patient education initiatives to improve outcomes and quality of life for individuals affected by cardiovascular conditions[19-23].
Endothelial and cardiac progenitor stem cells are at the forefront of research and clinical trials as a potential strategy for repairing damaged cardiac tissue and restoring optimal heart function in patients with heart disease. These specialized stem cells, derived from the endothelium and cardiac tissues, respectively, possess remarkable regenerative properties that make them ideal candidates for cardiac repair and regeneration. Here are more details about their potential in treating heart disease:
– Source of Cells: Endothelial progenitor stem cells are derived from the endothelium, which lines blood vessels, while cardiac progenitor stem cells are derived from the heart tissue itself. These cells have the capacity to differentiate into various cell types crucial for cardiac function, such as endothelial cells, cardiomyocytes, and smooth muscle cells.
– Regenerative Potential: Endothelial and cardiac progenitor stem cells exhibit regenerative properties essential for repairing damaged heart tissues, including the myocardium and blood vessels. They can promote angiogenesis (formation of new blood vessels), improve blood flow to the heart, and replace dysfunctional or injured cardiac cells.
– Mechanisms of Action: These stem cells exert their therapeutic effects through multiple mechanisms. They can directly differentiate into mature cardiac cells, secrete growth factors and cytokines that stimulate tissue repair and regeneration, modulate immune responses to reduce inflammation, and promote the recruitment and activation of endogenous cardiac stem cells.
– Potential Therapeutic Applications: Cellular Therapy and Stem Cells using endothelial and cardiac progenitor stem cells holds immense promise for treating various heart conditions, including ischemic heart disease, myocardial infarction, heart failure, and cardiomyopathies. The goal is to enhance cardiac function, prevent further damage, and improve overall heart health.
– Clinical Validation: While still in the experimental stages, early preclinical studies and some initial clinical trials have shown encouraging results regarding the safety, feasibility, and potential efficacy of using endothelial and cardiac progenitor stem cells in heart disease management. Further research and clinical validation are essential to fully realize the therapeutic benefits of these stem cells in cardiac regenerative medicine.
– Future Directions: Ongoing research aims to optimize the delivery, engraftment, and long-term survival of endothelial and cardiac progenitor stem cells in the heart. This includes exploring advanced delivery methods, understanding the ideal dosage and timing of cell therapy, and identifying patient-specific factors that may influence treatment outcomes.
Endothelial and cardiac progenitor stem cells represent a promising avenue for innovative therapies aimed at repairing cardiac tissues, restoring heart function, and improving outcomes for patients with heart disease. Continued research and advancements in stem cell technology are crucial for translating these findings into effective clinical treatments[24-28].
Cellular Therapy and Stem Cells for heart diseases is an area of rapid development with the potential to revolutionize treatment approaches for various cardiac conditions. Although still in its early stages, encouraging findings from preclinical studies and initial clinical trials indicate that Cellular Therapy and Stem Cells could offer innovative strategies for cardiac regeneration and repair.
– Research involving stem cells, particularly mesenchymal stem cells (MSCs), has demonstrated their ability to promote angiogenesis, reduce inflammation, and improve cardiac function in animal models of ACS/CAD during preclinical investigations.
– Initial clinical trials exploring MSC therapy in ACS/CAD patients have shown promising results, such as enhanced myocardial perfusion and improved left ventricular function, suggesting potential benefits in reducing cardiac damage and improving outcomes.
– Studies on stem cell therapy for cardiomyopathy have shown encouraging results in preclinical settings, indicating improved myocardial contractility, reduced fibrosis, and enhanced cardiac function with various stem cell types.
– Early clinical trials in patients with cardiomyopathy have reported potential benefits of stem cell treatments, including improved ejection fraction, reduced heart failure symptoms, and enhanced exercise capacity, although further research is needed for definitive conclusions.
– Preclinical studies utilizing stem cells, such as cardiac progenitor stem cells and MSCs, have demonstrated their ability to promote cardiac repair, reduce fibrosis, and improve ventricular function in CHF animal models.
– Early clinical trials investigating stem cell therapy in CHF patients have reported potential benefits, including improved ejection fraction, reduced hospitalizations for heart failure exacerbations, and enhanced quality of life, highlighting the therapeutic potential of Cellular Therapy and Stem Cells in managing CHF.
– Research on stem cell therapy for peripheral vascular diseases has shown promising outcomes in preclinical studies, indicating enhanced angiogenesis, improved blood flow, and tissue regeneration with various stem cell types.
– Early clinical trials in patients with PVD, PAD, and chronic arterial occlusive disease of lower limbs have reported potential benefits from Cellular Therapy and Stem Cells treatments, such as improved walking distance, reduced pain, and enhanced limb perfusion, suggesting the potential of stem cells in treating vascular disorders.
– Preclinical investigations utilizing stem cells, including cardiac-derived stem cells and MSCs, have shown promising results in improving valve function, reducing valve calcification, and promoting valvular tissue repair.
– Early clinical trials exploring stem cell therapy for valvular heart disease have reported potential benefits, such as improved valve hemodynamics, reduced valve regurgitation, and enhanced functional status, highlighting the potential of stem cells in addressing valvular abnormalities[29-33].
1. Acute Coronary Syndrome (ACS)/ Coronary Artery Disease (CAD): Research and clinical trials aims to develop strategies for myocardial revascularization, angiogenesis (formation of new blood vessels), and myocardial regeneration following acute myocardial infarction (heart attack). Cellular Therapy and Stem Cells target improving myocardial perfusion (blood flow to the heart muscle), reducing infarct size (area of tissue damage), and preventing adverse ventricular remodeling (changes in heart structure and function).
2. Cardiomyopathy: Efforts are directed towards enhancing cardiac contractility, promoting myocardial regeneration, and mitigating myocardial fibrosis (excessive scarring) in patients with cardiomyopathy. Stem cell-based therapies seek to replace damaged myocardium (heart muscle tissue), improve left ventricular ejection fraction (amount of blood pumped out of the heart), and restore cardiac structure and function.
3. Congestive Heart Failure (CHF): The exploration into Cellular Therapy and Stem Cells in CHF focuses on improving ventricular function, reversing adverse remodeling, and enhancing myocardial viability. Cellular Therapy and Stem Cells are utilized to stimulate endogenous repair mechanisms, improve myocardial contractility, and reduce symptoms of heart failure such as dyspnea (shortness of breath) and fatigue.
4. Peripheral Vascular Disease (PVD), Peripheral Arterial Disease (PAD), Chronic Arterial Occlusive Disease of Lower Limbs: The focus includes promoting angiogenesis, neovascularization, and improving tissue perfusion in ischemic peripheral tissues. Cellular Therapy and Stem Cells aim to enhance limb perfusion, stimulate collateral vessel formation (development of new blood vessels), and alleviate symptoms of claudication (painful cramping) and limb ischemia (inadequate blood supply to the limbs).
5. Valvular Heart Disease: Research and clinical trials explores the potential of Cellular Therapy and Stem Cells to regenerate valvular tissues, repair damaged heart valves, and improve valvular function. Stem cell-based approaches aim to enhance valvular structure, reduce stenosis (narrowing) or regurgitation (backflow), and prolong valve durability[34-38].
– Promotion of angiogenesis and vasculogenesis (formation of new blood vessels) to improve tissue perfusion.
– Stimulation of endogenous repair mechanisms and regeneration of damaged cardiac tissues.
– Modulation of inflammatory responses and reduction of myocardial fibrosis.
– Enhancement of cardiac contractility, improvement in ejection fraction, and prevention of adverse remodeling.
– Alleviation of symptoms, improvement in exercise tolerance, and enhancement of quality of life in affected patients.
The mechanisms of action underlying these therapeutic effects involve paracrine signaling (cell-to-cell communication), immunomodulation (regulation of immune responses), anti-inflammatory effects, promotion of angiogenesis and vasculogenesis, stimulation of endogenous cardiac progenitor stem cells, and direct differentiation into cardiomyocytes or endothelial cells.
The clinical implications of these advancements in Cellular Therapy and Stem Cells for heart diseases include the potential for personalized treatment approaches, improved patient outcomes, reduced morbidity and mortality, and enhanced cardiac function and quality of life for individuals with various cardiovascular conditions[39-43].
1. Paracrine Effect: Transplanted heart stem cells from our special treatment protocols exert their effects primarily through paracrine signaling, where they release a variety of bioactive molecules such as growth factors (e.g., vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), transforming Growth Factor (TGF)-β, Stromal Cell-Derived Factor (SDF)-1 ), cytokines, and chemokines. These factors act on neighboring cells and the microenvironment to promote cell survival, proliferation, angiogenesis, and tissue repair while decreasing apoptosis of endogenous cardiomyocytes.[1][2]
2. Differentiation: Endothelial and Cardiac stem cells have the capacity to differentiate into various cardiac contractile cell types of the heart, including cardiomyocytes, endothelial cells, and smooth muscle cells. This differentiation replenishes the pool of functional cells in the damaged myocardium, contributing to tissue regeneration.[3][4]By replacing damaged cardiomyocytes, they contribute directly to restoring cardiac function.
3. Immunomodulation: Cellular Therapy and Stem Cells can modulate the immune response by suppressing inflammation and promoting an anti-inflammatory environment in the injured tissue, which helps prevent excessive tissue damage. This immunomodulatory effect helps to reduce tissue damage and promote a more favorable environment for tissue healing, which can be observed by the presence of certain biomarkers, such as IL-15, IL-5, and SCF, which are correlated with enhanced cardiac function following Cellular Therapy and Cardiac Progenitor Stem Cell treatment at our center.[5]
4. Extracellular Matrix Remodeling: Endothelial and cardiac progenitor stem cells contribute to the remodeling of the extracellular matrix (ECM) by secreting enzymes that degrade scar tissue and promote the synthesis and deposition of new ECM components. Our Biomedical scientists and Stem Cell researchers have shown that this process helps to reduce fibrosis and improve tissue structure and function in all of our patients with heart diseases.
5. Angiogenesis: Our Cellular Therapy and Cardiopoietic Stem cells stimulate the formation of new blood vessels (angiogenesis) by secreting pro-angiogenic factors. Enhanced blood flow to the injured area of the heart improves oxygen and nutrient delivery to the coronary arteries, supporting cardiac tissue repair and local regeneration.
6. Cell Survival and Anti-apoptotic Effects: Our unique Cardiosphere-derived Cells (CDCs) can promote cell survival and inhibit apoptosis (programmed cell death) in the damaged myocardium, thereby preserving existing tissue and preventing further loss of functional cells.
The combined effects of angiogenesis, paracrine signaling, differentiation, immunomodulation, and extracellular matrix remodeling contribute to the beneficial outcomes observed with transplanted endothelial and cardiac progenitor stem cells in cardiac repair and remodeling[44-48].
The most common sources of Endothelial and Cardiac Progenitor Stem Cells used in real clinical settings include:
1. Bone Marrow: Bone marrow is a rich source of stem cells, including endothelial progenitor cells (EPCs) and cardiac progenitor cells (CPCs). These cells can be isolated from the bone marrow aspirate and used for cardiac repair.
2. Peripheral Blood: Peripheral blood also contains circulating endothelial progenitor cells that can be mobilized and collected through apheresis. These cells can then be used for therapeutic purposes in cardiac regeneration.
3. Adipose Tissue: Adipose tissue, commonly known as fat tissue, is another source of stem cells. Adipose-derived stem cells (ADSCs) have shown potential in promoting cardiac repair and angiogenesis.
4. Cord Blood: Umbilical cord blood is a valuable source of stem cells, including endothelial and cardiac progenitor stem cells. These cells can be obtained from umbilical cord blood banks and used for various regenerative therapies.
5. Induced Pluripotent Stem Cells (iPSCs): iPSCs can be generated by reprogramming adult stem cells such as skin cells or blood cells into a pluripotent state. These cells can then be differentiated into endothelial and cardiac progenitor cells for cardiac repair applications.
These sources provide a diverse range of Endothelial and Cardiac Progenitor Stem Cells that can be utilized in clinical settings for cardiac repair and remodeling therapies[49-53].
1. Advanced Research and Development: Our center is at the forefront of stem cell research and development, continuously striving to innovate and optimize treatment protocols for heart disease. We have a dedicated team of researchers and scientists focused on enhancing the efficacy and safety of Cellular Therapy using endothelial and cardiac progenitor stem cells.
2. Tailored Treatment Plans: We believe in personalized medicine and design customized treatment plans for each patient based on their specific medical history, condition severity, and therapeutic goals. This tailored approach ensures that patients receive the most effective and targeted treatment for their heart disease.
3. Cutting-Edge Technology: Our facility is equipped with state-of-the-art technology and infrastructure to support the delivery of Cellular Therapy and Stem Cell treatments. We utilize advanced imaging techniques, cell culture systems, and quality control measures to ensure the highest standards of treatment and patient care.
4. Experienced Medical Team: Our center boasts a highly experienced and multidisciplinary team of medical professionals, including cardiologists, regenerative medicine specialists, and stem cell scientists. This expertise allows us to provide comprehensive and integrated care to patients with heart disease, from diagnosis to treatment and follow-up.
5. Clinical Validation: We have conducted numerous clinical trials and studies to validate the safety, efficacy, and long-term outcomes of Cellular Therapy and Stem Cell treatments for heart disease. Our research findings contribute to the growing body of evidence supporting the use of these innovative therapies in cardiac regeneration and repair.
6. Global Reputation: Our DrStemCellsThailand‘s Anti-Aging and Regenerative Medicine Center of Thailand has earned a global reputation for excellence in regenerative medicine. Patients from around the world seek our expertise and innovative treatments for various age-related conditions, including heart disease.
Our special treatment protocols of Cellular Therapy and Endothelial and Cardiac Progenitor Stem Cells set us apart through advanced research and clinical trials, personalized care, cutting-edge technology, experienced medical professionals, clinical validation, and a global reputation for excellence.
– Enhanced repair and regeneration of damaged cardiac tissue following myocardial infarction.
– Promotion of angiogenesis and blood vessel formation to improve coronary circulation.
– Reduction of inflammation, oxidative stress, and cardiac remodeling post-ACS/CAD events.
– Differentiation of Cellular Therapy and Stem Cells into functional cardiac muscle cells to restore contractility.
– Regulation of myocardial fibrosis, apoptosis, and hypertrophy in cardiomyopathic hearts.
– Improvement in cardiac function, ejection fraction, and reduction in heart failure symptoms.
– Enhancement of cardiac contractility and relaxation through stem cell-mediated repair.
– Modulation of neurohormonal imbalance and improvement in cardiac output.
– Reduction of CHF-related symptoms, such as dyspnea, fatigue, and edema.
– Promotion of angiogenesis and neovascularization in ischemic tissues to restore blood flow.
– Enhancement of endothelial function, vasodilation, and circulation in affected limbs.
– Improvement in claudication, ischemic pain, wound healing, and limb salvage in PAD/PVD patients.
– Stimulation of valve tissue regeneration and repair in patients with valvular disorders.
– Reduction of valve calcification, stenosis, regurgitation, and valve-related symptoms.
– Improvement in cardiac valve function, hemodynamics, and overall cardiovascular health.
These specialized treatment protocols harness the regenerative potential of Cellular Therapy and Endothelial and Cardiac Progenitor Stem Cells to address the underlying pathologies of cardiovascular diseases, improve heart function, enhance vascular health, and ultimately optimize the well-being of patients with these conditions[54-58].
Our team of Cardiologists and Regenerative Specialists utilize clinical assessment and diagnostic tests to assess how much our patients with heart conditions improve.
– Detailed Medical History: Improvement is observed through reduced frequency or severity of symptoms such as chest pain, shortness of breath, fatigue, and palpitations. Better management of risk factors like blood pressure, blood sugar levels, and cholesterol levels indicates improved overall cardiovascular health.
– Physical Examination: Improvement may include normalized heart sounds, absence of murmurs or abnormal heart sounds, and signs of heart failure (edema, jugular venous distention) resolving or diminishing.
– Cardiovascular Risk Factors: Improvement is evident in controlled blood pressure, improved blood glucose and lipid profiles, reduced body weight, and adoption of healthier lifestyle habits.
– Electrocardiogram (ECG): Improvement manifests as normalized or stable heart rhythm, resolution of arrhythmias, and absence of new abnormalities.
– Echocardiogram: Improvement includes increased ejection fraction, better ventricular function, normalized valve function, and reduced chamber sizes.
– Stress Testing: Improved exercise capacity and absence of ischemic changes during stress indicate better cardiovascular fitness and reduced risk of coronary artery disease (CAD) progression.
– Cardiac MRI/CT: Reduction or stabilization of coronary artery calcifications, improvement in cardiac wall motion abnormalities, and decreased cardiac mass indicate positive treatment response.
– Holter Monitoring: Absence of significant arrhythmias or reduction in their frequency suggests improved heart rhythm stability.
– Blood Tests: Decreased levels of cardiac enzymes (troponin, CK-MB) and biomarkers (BNP, NT-proBNP) indicate reduced heart muscle damage, stress, or heart failure severity.
– Coronary Angiography: Improvement includes reduced coronary artery blockages, improved blood flow, and better coronary artery function post-treatment or intervention.
– Electrophysiology Studies: Improved heart rhythm stability, decreased arrhythmia occurrence, and optimized settings for implanted devices (pacemakers, defibrillators) indicate treatment success.
– Follow-Up Appointments: Improvement is assessed through symptom relief, enhanced quality of life, and adherence to treatment plans.
– Diagnostic Tests Follow-Up: Progressive improvement is seen in repeated echocardiograms, stress tests, and other diagnostic imaging showing stable or enhanced cardiac function, reduced disease progression, and better treatment response.
– Advanced Imaging Techniques: Improved accuracy in assessing cardiac function, myocardial strain, and tissue characteristics allows for more precise treatment monitoring and detection of subtle changes indicating improvement or early signs of relapse.
– Collaborative Care: Effective collaboration with other specialists ensures integrated care, optimal treatment adjustments, and improved patient outcomes over time.
By closely monitoring these parameters and observing improvements across clinical assessments and diagnostic tests, our team ensures that patients receive personalized care and achieve tangible benefits in their cardiovascular health and overall well-being[59-63].
Several cardiac biomarkers are used to measure the improvement of patients with heart conditions. These biomarkers provide valuable information about cardiac function, injury, and overall cardiovascular health. Some commonly used cardiac biomarkers include:
1. Troponin: Troponin is a protein released into the bloodstream when there is damage to the heart muscle, such as during a heart attack. Elevated levels of troponin indicate myocardial injury and can help diagnose and monitor acute coronary syndromes and other cardiac conditions.
2. B-type natriuretic peptide (BNP) and N-terminal pro B-type natriuretic peptide (NT-proBNP): BNP and NT-proBNP are hormones released by the heart in response to increased pressure and volume. Elevated levels of these biomarkers are associated with heart failure and can indicate the severity of heart failure and predict prognosis.
3. Creatine kinase-MB (CK-MB): CK-MB is an enzyme released into the bloodstream when there is damage to heart muscle cells. Elevated levels of CK-MB can indicate myocardial infarction (heart attack) or other forms of myocardial injury.
4. Myoglobin: Myoglobin is a protein found in heart and skeletal muscle cells. Elevated levels of myoglobin can indicate muscle damage, including damage to the heart muscle. Myoglobin levels may rise more rapidly than troponin levels in the early stages of a heart attack.
5. C-reactive protein (CRP): CRP is a marker of inflammation in the body, including inflammation of the blood vessels and heart. Elevated levels of CRP may indicate an increased risk of cardiovascular events and can be used to assess the effectiveness of treatment in reducing inflammation.
6. Lipoprotein-associated phospholipase A2 (Lp-PLA2): Lp-PLA2 is an enzyme associated with inflammation of the blood vessels and is considered a marker of increased cardiovascular risk. Elevated levels of Lp-PLA2 may indicate an increased risk of coronary artery disease and other cardiovascular events.
These cardiac biomarkers, when used in combination with other diagnostic tests and clinical assessments, can provide valuable information about the presence, severity, and progression of heart conditions, as well as the effectiveness of treatment interventions[64-68].
Our international patients with chronic heart conditions can complete our special heart regenerative treatment protocols at our DrStemCellsThailand‘s Anti-Aging and Regenerative Medicine Center of Thailand in Bangkok within approximately 10 to 14 days. This timeframe includes alternating infusions of Cellular Therapy with Endothelial, Cardiac Progenitor Stem Cells and Cardiopoetic Growth Factors and intramuscular Regenerative Exosomes with Peptide. Unlike traditional approaches that focus on high doses of Cellular Therapy and Stem Cells in a short period, our protocols prioritize gradual regeneration, allowing the body, especially the heart and blood vessels, sufficient time to heal and regenerate. This approach is tailored to patients with varying degrees of heart disease severity, ensuring optimal outcomes and promoting long-term cardiac health.
Please refer to the table at the end of this page.
Rong Yang, Yonggang Zhang, Xiaoyang Liao, Ru Guo, Yi Yao, Chuanying Huang, Li Qi
2021, Frontiers in Cardiovascular Medicine – Article
The clinical trials investigating Cellular Therapy and Stem Cell therapy for heart diseases registered at ClinicalTrials.gov are mostly interventional studies, and only a few are phase 4 trials. Most trials have a small sample size, and few have a duration of more than 121 months. Most of the completed trials did not publish their results, and some of the registration information was incomplete and illogical. At our Heart Regenerative Center of Thailand, however, our team of researchers and heart specialists always believe in holistic and integrative approach to taking care of all of our heart patients. Incorporating all the Cellular Therapy and Cardiac Stem Cell research all around the world, together with our 20-year experiences on treating patients with cardiac problems all around the globe, we always have a high anticipation of our special treatment protocols’ success in regenerating lost cardiomyocytes in acute cardiac problems such as acute myocardial infarction (AMI) : STEMI, NSTEMI, UA, slowing down progression of chronic heart conditions (chronic heart failure) in patients who may arrive late
1. Enhanced Cardiovascular Function: Cardiac rehabilitation programs are designed to improve cardiovascular health through structured exercise training, education on heart-healthy behaviors, and risk factor management. These interventions help optimize cardiac function, including improvements in cardiac output, stroke volume, and heart rate variability. (Source: American Heart Association)
2. Improved Exercise Capacity: Rehabilitation protocols focus on increasing exercise tolerance and stamina, which is particularly beneficial for individuals with chronic heart conditions. Regular physical activity enhances the heart’s efficiency, improves oxygen delivery to tissues, and promotes overall cardiovascular fitness. (Source: European Society of Cardiology)
3. Risk Factor Modification: Rehabilitation programs emphasize lifestyle modifications such as smoking cessation, dietary changes, weight management, and stress reduction techniques. These interventions target modifiable risk factors like hypertension, hyperlipidemia, and diabetes, thereby reducing the risk of cardiovascular events and disease progression. (Source: National Institutes of Health)
4. Psychological Well-being: Participation in cardiac rehabilitation has psychological benefits, including reduced anxiety, depression, and improved self-confidence. The supportive environment of rehabilitation centers and the focus on holistic health contribute to better mental health outcomes in patients with chronic heart conditions. (Source: American College of Cardiology)
5. Medication Management: Cardiac rehabilitation teams work closely with healthcare providers to optimize medication regimens, ensure medication adherence, and monitor medication side effects. This collaborative approach helps manage symptoms, prevent complications, and improve medication effectiveness in controlling chronic heart conditions. (Source: European Society of Cardiology)
6. Long-term Monitoring and Follow-up: Cardiac rehabilitation programs include regular monitoring of patients’ cardiovascular status, exercise capacity, and adherence to treatment plans. Follow-up assessments help track progress, identify potential complications early, and tailor interventions to individual patient needs for long-term cardiovascular health maintenance. (Source: World Health Organization)
The ongoing endorsement of cardiac rehabilitation by our team is based on its comprehensive approach to improving cardiovascular function, reducing risk factors, enhancing psychological well-being, and promoting long-term heart health in individuals with chronic heart conditions[69-73].
Following Cellular Therapy and Stem Cells for Heart Diseases using Endothelial, Cardiac Progenitor and Cardiopoetic Stem Cell Protocols, individuals with chronic heart diseases frequently benefit from cardiac rehabilitation (cardiac rehab) to enhance their cardiovascular health.
Our team of cardiac physical therapists takes pleasure in customizing rehab programs for each patient, ensuring that the unique needs of every individual are addressed. This approach promotes a comprehensive and effective recovery process, emphasizing personalized care for heart patients during and after regenerative treatments.
1. Enhanced Cardiac Function: Cellular Therapy and Stem Cells for Heart Diseases have the potential to repair damaged cardiac tissues, improve myocardial contractility, and enhance overall heart function. This regenerative approach can complement the benefits of cardiac rehabilitation by promoting tissue healing and restoring normal cardiac physiology. (Source: Journal of Cardiovascular Translational Research)
2. Improved Exercise Capacity: The combination of Cellular Therapy and Stem Cells for Heart Diseases with cardiac rehabilitation can lead to significant improvements in exercise tolerance and functional capacity. Cellular Therapy and Stem Cell therapy may facilitate angiogenesis, improve blood flow to the heart, and enhance oxygen utilization during physical activity, allowing patients to engage in more rigorous exercises and activities. (Source: Journal of the American College of Cardiology)
3. Reduced Symptoms: Patients undergoing Cellular Therapy and Stem Cells for Heart Diseases alongside cardiac rehabilitation often experience a reduction in symptoms such as chest pain (angina), shortness of breath, and fatigue. The regenerative effects of stem cells can mitigate ischemic damage, decrease inflammation, and alleviate myocardial strain, leading to symptom relief and improved quality of life. (Source: Circulation Research)
4. Optimized Medication Response: Cellular Therapy and Stem Cells for Heart Diseases enhance the response to cardiovascular medications by promoting tissue repair and regeneration. This synergistic approach can lead to better medication outcomes, reduced medication doses, and improved control of cardiac risk factors like hypertension, hyperlipidemia, and arrhythmias. (Source: European Heart Journal)
5. Cardiac Remodeling: Cellular Therapy and Stem Cells for Heart Diseases combined with rehabilitation can contribute to beneficial cardiac remodeling, including the regeneration of functional cardiomyocytes, reduction of scar tissue, and improvement in ventricular structure and function. These remodeling effects can lead to long-term improvements in cardiac performance and prevent adverse remodeling associated with chronic heart conditions. (Source: Journal of Molecular and Cellular Cardiology)
6. Psychosocial Support: Cardiac rehabilitation programs offer valuable psychosocial support, education, and counseling to patients and their families. When integrated with Cellular Therapy and Stem Cells for Heart Diseases, this comprehensive approach addresses psychological aspects such as stress, anxiety, and depression commonly experienced by individuals with heart conditions, promoting overall well-being and mental health. (Source: Journal of Cardiopulmonary Rehabilitation and Prevention)
By combining Cellular Therapy and Endothelial and Cardiac Progenitor Stem Cells with cardiac rehabilitation, patients can benefit from synergistic effects that enhance heart function, improve exercise tolerance, alleviate symptoms, optimize medication responses, promote cardiac remodeling, and provide holistic psychosocial support for a comprehensive approach to cardiovascular health management[74-78].
Several innovative strategies have been developed by our team of Cardiologists and Regenerative Specialists to enhance the delivery of Cellular Therapy and Stem Cells for Heart Diseases specifically to the heart, aiming to improve their retention, engraftment, and therapeutic efficacy. Some of these strategies include:
1. Intramyocardial Injection: Direct injection of stem cells into the myocardium during surgical procedures or catheter-based interventions allows for precise delivery to the target site of cardiac injury.
2. Intracoronary Infusion: Stem cells can be delivered through the coronary arteries using catheter-based techniques, enabling widespread distribution throughout the myocardium.
3. Intravenous Delivery with Targeting Moieties: Using targeting moieties such as antibodies, peptides, or nanoparticles can facilitate specific binding of stem cells to receptors expressed on injured cardiac cells, enhancing homing and retention within the heart. This method is widely utilized due to its minimal invasiveness and convenience, particularly in outpatient settings.
4. Biocompatible Scaffolds: Incorporating stem cells into biocompatible scaffolds or matrices provides mechanical support and promotes cell survival and integration upon implantation into the myocardium.
5. Gene Modification: Genetically modifying stem cells to overexpress cardiac-specific markers or homing receptors can enhance their affinity for cardiac tissue and improve retention post-delivery.
6. Magnetic Targeting: Magnetic guidance techniques involve labeling stem cells with magnetic nanoparticles, allowing for external magnetic fields to guide cells to the desired cardiac region, enhancing localization and retention.
7. Ultrasound and Microbubbles: Utilizing ultrasound in combination with microbubbles can transiently disrupt the endothelial barrier, facilitating the extravasation of stem cells into the myocardium.
8. Exosome-Based Delivery: Instead of delivering whole stem cells, utilizing stem cell-derived exosomes, which are nanosized vesicles containing bioactive molecules, can provide paracrine signaling effects without the need for cell engraftment.
9. Hydrogel Encapsulation: Encapsulating stem cells within hydrogels improves their survival, protects them from immune rejection, and allows for controlled release of therapeutic factors within the heart.
10. Optimization of Cell Type and Dosage: Selecting the appropriate type of stem cells (e.g., mesenchymal stem cells, cardiac progenitor cells) and optimizing the cell dosage based on preclinical and clinical studies can maximize the therapeutic benefits and minimize adverse effects.
These strategies, either alone or in combination, aim to overcome the challenges associated with stem cell delivery to the heart and enhance their therapeutic potential for treating various cardiac conditions[79-83].
2.1 Acute Coronary Syndrome (ACS)
2.2 Cardiomyopathy
2.3 Congestive Heart Failure (CHF)
2.4 Peripheral Vascular Disease (PVD), Peripheral Arterial Disease (PAD), Chronic Arterial Occlusive Disease of Lower Limbs
2.5 Valvular Heart Disease
2.6 Cardiac Arrhythmias
2.7 Cardiac Fibrosis
2.8 Cardiac Amyloidosis
2.9 Rheumatic Heart Disease
2.10 Endocarditis
2.11 Congenital Heart Defects
2.12 Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
2.13 Takotsubo Cardiomyopathy
2.14 Cardiac Sarcoidosis
2.15 Hypertension-related Heart Disease
2.16 Pericardial Diseases
2.17 Cardiogenic Shock
2.18 Heart Transplant Rejection (Post-transplant complications)
2.19 Cardiac Arrest Recovery
Abbreviation :
1. BM‐MSCs (Bone Marrow Mesenchymal Stem Cells):
2. hUCB‐MSCs (Human Umbilical Cord Blood Mesenchymal Stem Cells):
3. DPSCs (Dental Pulp Stem Cells):
4. ESCs (Embryonic Stem Cells):
5. iPSCs (Induced Pluripotent Stem Cells):
6. HSCs (Hematopoietic Stem Cells):
7. EPCs (Endothelial Progenitor Cells):
8. Cardiac PCs (Cardiac Progenitor Cells):
9. UCSCs (Umbilical Cord Stem Cells):
10. ADSCs (Adipose-derived Stem Cells):
1. Cardiomyocyte-PSCs: Responsible for heart muscle contraction.
2. Fibroblast-PSCs: Provide structural support to cardiac tissues.
3. Endothelial-PSCs: Line blood vessels and regulate vascular function.
4. Smooth Muscle-PSCs: Control blood flow in arteries and veins.
5. Pericyte-PSCs: Support blood vessel stability and repair.
6. VIC-PSCs: Maintain heart valve integrity and flexibility.
7. Macrophage-PSCs: Regulate inflammation and tissue repair.
8. Stem/Progenitor-PSCs: Contribute to cardiac development and regeneration.
Diseases associated with Heart and Blood Vessels | Sources of Cellular Therapy&Cardiac Stem Cells | Improvement Assessment by |
2.1 Acute Coronary Syndrome/ Coronary Artery Syndrome (ACS/CAD): 2.1.1 Unstable Angina (UA): Mild, Moderate 2.1.2 Severe and Chronic Intractable Angina Pectoris refractory to conventional treatments 2.1.3 Non-ST-elevation MI (NSTEMI) 2.1.4 ST-elevation MI (STEMI) 2.1.5 Myocardial Infarction (MI) or Myocardial Ischemia or Ischemic Heart Disease (IHD) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Autologous/ Allogenic Intracoronary, IV Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in cardiac biomarkers: – Troponin levels: A decrease in troponin levels indicates a reduction in myocardial injury and necrosis. – Creatine kinase-MB (CK-MB) levels: Reduction in CK-MB levels reflects diminished myocardial damage. 2. Improvement in cardiac function parameters: – Left ventricular ejection fraction (LVEF): Increase in LVEF signifies enhanced myocardial contractility and pumping function. – Wall motion abnormalities: Resolution or improvement in regional wall motion abnormalities observed on echocardiography or cardiac MRI scans. 3. Reduction in ischemic events and complications: – Frequency of recurrent myocardial infarction (MI) or angina episodes. – Incidence of major adverse cardiac events (MACE), including revascularization procedures, stroke, or cardiovascular-related death. 4. Improvement in exercise tolerance and functional capacity: – Exercise tolerance tests, such as the six-minute walk test (6MWT), treadmill exercise testing, or cardiopulmonary exercise testing (CPET). – Assessment of symptom-limited exercise duration, peak oxygen consumption (VO2 max), and heart rate response to exercise. 5. Reduction in symptoms and improvement in quality of life: – Assessment using disease-specific quality of life questionnaires, such as the Seattle Angina Questionnaire (SAQ) or the MacNew Heart Disease Health-Related Quality of Life Questionnaire. – Evaluation of symptom severity, including chest pain, dyspnea, and fatigue. 6. Improvement in myocardial perfusion: – Assessment of myocardial perfusion using imaging techniques such as myocardial perfusion scintigraphy (MPS) or single-photon emission computed tomography (SPECT) scans. 7. Evaluation of left ventricular remodeling: – Assessment of left ventricular volumes, dimensions, and shape changes using echocardiography or cardiac MRI scans. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.2 Cardiomyopathy: 2.2.1. Dilated Cardiomyopathy (DCM) 2.2.2. Hypertrophic Cardiomyopathy (HCM) 2.2.3. Restrictive Cardiomyopathy 2.2.4. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) 2.2.5. Takotsubo Cardiomyopathy 2.2.6. Ischemic Cardiomyopathy 2.2.7. Non-ischemic Cardiomyopathy 2.2.8. Peripartum Cardiomyopathy | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in cardiac function parameters: – Left ventricular ejection fraction (LVEF): Increase in LVEF indicates improved myocardial contractility and pumping function. – Reduction in left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD), indicating reverse remodeling of the heart. 2. Reduction in symptoms and improvement in quality of life: – Assessment using disease-specific quality of life questionnaires, such as the Minnesota Living with Heart Failure Questionnaire (MLHFQ) or the Kansas City Cardiomyopathy Questionnaire (KCCQ). – Evaluation of symptom severity, including dyspnea, fatigue, and exercise intolerance. 3. Reduction in hospitalizations and adverse cardiac events: – Frequency of hospital admissions due to heart failure exacerbations or cardiovascular events. – Incidence of major adverse cardiac events (MACE), including heart failure exacerbations, arrhythmias, or sudden cardiac death. 4. Improvement in exercise tolerance and functional capacity: – Exercise tolerance tests, such as the six-minute walk test (6MWT) or cardiopulmonary exercise testing (CPET). – Assessment of symptom-limited exercise duration, peak oxygen consumption (VO2 max), and heart rate response to exercise. 5. Reduction in cardiac biomarkers: – Brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) levels: Decrease in BNP or NT-proBNP levels reflects reduced myocardial stress and improved cardiac function. 6. Improvement in myocardial perfusion: – Assessment of myocardial perfusion using imaging techniques such as myocardial perfusion scintigraphy (MPS) or cardiac MRI scans. 7. Evaluation of left ventricular remodeling: – Assessment of left ventricular volumes, dimensions, and shape changes using echocardiography or cardiac MRI scans. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.3 Congestive Heart Failure (CHF): Cardiac output (CO): 2.3.1 Low-output Cardiac Failure 2.3.2 High-output Cardiac Failure Onset and duration: 2.3.3 Acute CHF 2.3.4 Chronic CHF 2.3.5 Advanced CHF Severity: 2.3.6 Compensated HF 2.3.7 Decompensated HF Type and function: 2.3.8 Left-sided HF 2.3.9 HF with Systolic dysfunction 2.3.10 HF with Diastolic dysfunction 2.3.11 Right-sided HF 2.3.12 Biventricular HF Classification (NYHA): 2.3.13 Stage A: at risk for HF 2.3.14 Stage B: Pre-HF 2.3.15 Stage C: asymptomatic HF 2.3.16 Stage D: Advanced HF | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Autologous/ Allogenic Intracoronary, IV Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in cardiac function parameters: – Left ventricular ejection fraction (LVEF): Increase in LVEF indicates improved myocardial contractility and pumping function. – Reduction in left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD), indicating reverse remodeling of the heart. 2. Reduction in symptoms and improvement in quality of life: – Assessment using disease-specific quality of life questionnaires, such as the Minnesota Living with Heart Failure Questionnaire (MLHFQ) or the Kansas City Cardiomyopathy Questionnaire (KCCQ). – Evaluation of symptom severity, including dyspnea, fatigue, and exercise intolerance. 3. Reduction in hospitalizations and adverse cardiac events: – Frequency of hospital admissions due to heart failure exacerbations or cardiovascular events. – Incidence of major adverse cardiac events (MACE), including heart failure exacerbations, arrhythmias, or sudden cardiac death. 4. Improvement in exercise tolerance and functional capacity: – Exercise tolerance tests, such as the six-minute walk test (6MWT) or cardiopulmonary exercise testing (CPET). – Assessment of symptom-limited exercise duration, peak oxygen consumption (VO2 max), and heart rate response to exercise. 5. Reduction in cardiac biomarkers: – Brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) levels: Decrease in BNP or NT-proBNP levels reflects reduced myocardial stress and improved cardiac function. 6. Improvement in myocardial perfusion: – Assessment of myocardial perfusion using imaging techniques such as myocardial perfusion scintigraphy (MPS) or cardiac MRI scans. 7. Evaluation of left ventricular remodeling: – Assessment of left ventricular volumes, dimensions, and shape changes using echocardiography or cardiac MRI scans. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.4 Peripheral Vascular Disease (PVD), Peripheral Arterial Disease (PAD), Chronic Arterial Occlusive Disease of Lower Limbs: 2.4.1 Chronic Leg and Foot –Wounds/ Ulcers 2.4.2 Arterial Ulcers 2.4.3 Neuropathic 2.4.4 Diabetic Ulcers 2.4.5 Pressure Ulcers 2.4.6 Venous Stadis Ulcers 2.4.7Chronic Limb 2.4.8 Threatening Ischemia (CLTI) from Diabetes Mellitis (DM) patients who are not candidates of standard revascularization 2.4.9 Buerger’s disease (thromboangiitis obliterans) 2.4.10 Peripheral Artery Disease (PAD) 2.4.11 Deep Vein Thrombosis (DVT) 2.4.12 Chronic Venous Insufficiency (CVI) 2.4.13 Varicose Veins 2.4.14 Raynaud’s Disease 2.4.15 Aneurysmal Disease 2.4.16 Peripheral Vascular Trauma | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in claudication symptoms: – Assessment of claudication distance: Measure of the maximum walking distance until the onset of leg pain. – Improvement in pain-free walking distance: Increase in the distance walked without experiencing claudication symptoms. 2. Changes in ankle-brachial index (ABI): – Increase in ABI values: Improvement in arterial blood flow and perfusion to the lower extremities. – Reduction in ABI values suggestive of disease progression or worsening arterial insufficiency. 3. Wound healing and tissue perfusion: – Assessment of wound healing: Evaluation of the rate of wound closure and resolution of ischemic ulcers in the lower extremities. – Improvement in tissue perfusion: Measurement of skin temperature, capillary refill time, and transcutaneous oxygen tension (TcPO2) as indicators of tissue oxygenation. 4. Quality of life and functional outcomes: – Disease-specific quality of life assessments: Use of questionnaires such as the Peripheral Artery Questionnaire (PAQ) to evaluate the impact of PVD on daily activities and overall well-being. – Improvement in functional capacity: Assessment of physical function and activities of daily living, including walking ability and participation in recreational activities. 5. Reduction in critical limb ischemia (CLI) events: – Decrease in the incidence of CLI-related complications: Reduction in the frequency of ischemic rest pain, tissue necrosis, ulceration, or gangrene requiring amputation. 6. Angiographic outcomes: – Improvement in vascular patency: Evaluation of arterial lumen diameter, collateral vessel formation, and reduction in arterial stenosis on angiographic imaging studies. 7. Hemodynamic parameters: – Increase in peak systolic velocity (PSV) and decrease in end-diastolic velocity (EDV) on Doppler ultrasound studies, indicating improved blood flow velocity and reduced resistance in the peripheral arteries. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.5 Valvular Heart Disease: Myxomatous Mitral Valve Disease (MMVD) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in valvular function: – Reduction in valve regurgitation: Assessment of the severity and extent of valvular regurgitation (e.g., mitral regurgitation, aortic regurgitation) using echocardiography. – Decrease in valve stenosis: Evaluation of the degree of valvular stenosis (e.g., aortic stenosis, mitral stenosis) and improvement in valve orifice area. 2. Changes in cardiac function: – Improvement in left ventricular ejection fraction (LVEF): Measurement of the percentage of blood pumped out of the left ventricle with each heartbeat, indicating enhanced cardiac contractility and systolic function. – Reduction in left ventricular volumes: Decrease in left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV), reflecting reverse remodeling and improvement in ventricular chamber dimensions. 3. Symptomatic relief and functional outcomes: – Reduction in heart failure symptoms: Assessment of dyspnea, fatigue, exercise intolerance, and New York Heart Association (NYHA) functional class. – Improvement in exercise capacity: Evaluation of exercise tolerance, peak oxygen consumption (VO2 max), and distance covered during a 6-minute walk test (6MWT). 4. Quality of life (QoL) measures: – Disease-specific QoL assessments: Use of standardized questionnaires (e.g., Minnesota Living with Heart Failure Questionnaire, Kansas City Cardiomyopathy Questionnaire) to evaluate the impact of valvular heart disease on physical, emotional, and social well-being. 5. Reduction in hospitalizations and cardiovascular events: – Decrease in heart failure exacerbations: Reduction in the frequency and duration of hospital admissions for acute decompensated heart failure or valvular-related complications. – Prevention of adverse cardiovascular events: Lower incidence of arrhythmias, thromboembolic events, or sudden cardiac death associated with valvular heart disease progression. 6. Hemodynamic parameters: – Improvement in cardiac output (CO) and stroke volume (SV): Measurement of CO and SV using echocardiography or cardiac catheterization to assess cardiac performance and hemodynamic status. – Reduction in valvular gradients: Decrease in transvalvular pressure gradients across stenotic valves, indicating alleviation of valvular obstruction and improved hemodynamics. |
2.6 Cardiac Arrhythmias 2.6.1. Atrial Fibrillation (AFib) 2.6.2. Atrial Flutter 2.6.3. Ventricular Tachycardia (VT) 2.6.4. Ventricular Fibrillation (VFib) 2.6.5. Supraventricular Tachycardia (SVT) 2.6.6. Bradycardia 2.6.7. Wolff-Parkinson-White Syndrome (WPW) 2.6.8. Long QT Syndrome (LQTS) 2.6.9. Short QT Syndrome (SQTS) 2.6.10. Brugada Syndrome 2.6.11. Sick Sinus Syndrome (SSS) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Arrhythmia Episodes: Assessing the frequency and severity of arrhythmia episodes post-cellular therapy compared to baseline. 2. Improvement in Heart Rate Variability (HRV): Evaluating changes in HRV as an indicator of autonomic nervous system function and arrhythmia risk. 3. Cardiac Function Improvement: Measuring changes in cardiac function parameters such as ejection fraction and cardiac output. 4. Electrocardiogram (ECG) Findings: Analyzing ECG results for any improvements in rhythm regularity and conduction abnormalities. 5. Quality of Life Assessment: Using validated scales to assess improvements in patients’ quality of life related to arrhythmia symptoms and overall well-being. 6. Exercise Tolerance: Evaluating changes in exercise capacity and tolerance following cellular therapy for arrhythmias. 7. Reduction in Cardiovascular Events: Monitoring and comparing the occurrence of adverse cardiovascular events such as stroke, heart failure exacerbations, and sudden cardiac death. 8. Biomarker Levels: Assessing changes in biomarker levels associated with arrhythmia pathophysiology, such as brain natriuretic peptide (BNP) or troponin levels. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.7 Cardiac Fibrosis 2.7.1. Ischemic Cardiac Fibrosis 2.7.2. Non-ischemic (Idiopathic) Cardiac Fibrosis 2.7.3. Hypertensive Cardiac Fibrosis 2.7.4. Valvular Heart Disease-Related Fibrosis 2.7.5. Inflammatory Cardiac Fibrosis 2.7.6. Cardiomyopathy-Associated Fibrosis 2.7.7. Radiation-Induced Cardiac Fibrosis 2.7.8. Age-Related Cardiac Fibrosis 2.7.9. Diabetic Cardiac Fibrosis 2.7.10. Alcoholic Cardiac Fibrosis 2.7.11. Toxic-Medication Induced Cardiac Fibrosis 2.7.12. Autoimmune Cardiac Fibrosis 2.7.13. Genetic Cardiac Fibrosis Syndromes 2.7.14. Infectious Cardiac Fibrosis (e.g., Chagas Disease) 2.7.15. Peripartum Cardiac Fibrosis 2.7.16. Fibrotic Consequences of Cardiac Surgery 2.7.17. Occupational or Environmental Cardiac Fibrosis (e.g., asbestos-related) 2.7.18. Metabolic Syndrome-Associated Cardiac Fibrosis 2.7.19. Connective Tissue Disorder-Associated Cardiac Fibrosis 2.7.20. Neuromuscular Disorder-Associated Cardiac Fibrosis | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Fibrotic Tissue: Assessing the extent and severity of cardiac fibrosis through imaging modalities like cardiac MRI or echocardiography. 2. Improvement in Cardiac Function: Measuring changes in cardiac function parameters such as ejection fraction, stroke volume, and cardiac output. 3. Inflammatory Marker Levels: Monitoring changes in inflammatory markers like C-reactive protein (CRP) and interleukins associated with fibrotic processes. 4. Cardiac Biomarkers: Assessing levels of cardiac biomarkers such as brain natriuretic peptide (BNP) and troponin to evaluate cardiac injury and remodeling. 5. Quality of Life Assessment: Using standardized scales to assess improvements in patients’ quality of life related to heart function and symptoms. 6. Exercise Capacity: Evaluating changes in exercise tolerance and capacity post-cellular therapy for cardiac fibrosis. 7. Electrocardiogram (ECG) Findings: Analyzing ECG results for any improvements in rhythm regularity and conduction abnormalities. 8. Reduction in Adverse Cardiac Events: Monitoring and comparing the occurrence of adverse cardiac events such as heart failure exacerbations or arrhythmias. 9. Fibrosis Regression: Assessing the regression or stabilization of fibrotic tissue over time with cellular therapy interventions. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.8 Cardiac Amyloidosis 2.8.1. Immunoglobulin Light Chain (AL) Amyloidosis 2.8.2. Transthyretin (ATTR) Amyloidosis 2.8.3. Wild-Type ATTR (ATTRwt) Amyloidosis 2.8.4. Hereditary ATTR (ATTRv) Amyloidosis 2.8.5. Dialysis-Related (Beta-2 Microglobulin) Amyloidosis | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Amyloid Deposits: Assessing the extent and severity of amyloid deposits in the heart through imaging modalities like cardiac MRI or PET scans. 2. Improvement in Cardiac Function: Measuring changes in cardiac function parameters such as ejection fraction, diastolic function, and cardiac output. 3. Reduction in Cardiac Biomarkers: Monitoring levels of cardiac biomarkers associated with amyloidosis, such as brain natriuretic peptide (BNP) and troponin. 4. Quality of Life Assessment: Using standardized scales to assess improvements in patients’ quality of life related to cardiac function and symptoms. 5. Exercise Capacity: Evaluating changes in exercise tolerance and capacity post-cellular therapy for cardiac amyloidosis. 6. Electrocardiogram (ECG) Findings: Analyzing ECG results for any improvements in rhythm regularity and conduction abnormalities. 7. Reduction in Cardiac Events: Monitoring and comparing the occurrence of adverse cardiac events such as heart failure exacerbations or arrhythmias. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.9 Rheumatic Heart Disease 2.9.1. Mitral Valve Involvement 2.9.2. Aortic Valve Involvement 2.9.3. Tricuspid Valve Involvement 2.9.4. Pulmonary Valve Involvement 2.9.5. Multivalvular Involvement 2.9.6. Left-Sided Valve Involvement 2.9.7. Right-Sided Valve Involvement 2.9.8. Mitral and Aortic Valve Involvement 2.9.9. Rheumatic Cardiomyopathy | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Inflammatory Markers: Monitoring levels of inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) to assess inflammation reduction. 2. Improvement in Cardiac Function: Measuring changes in cardiac function parameters such as ejection fraction, stroke volume, and cardiac output. 3. Reduction in Valve Dysfunction: Assessing improvements in valve function and reduction in valve regurgitation or stenosis. 4. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to cardiac function and symptoms. 5. Exercise Tolerance: Evaluating changes in exercise capacity and tolerance post-cellular therapy for Rheumatic Heart Disease. 6. Reduction in Disease Progression: Monitoring and comparing disease progression, including the development of heart failure or arrhythmias. 7. Valve Structure Improvement: Assessing changes in valve structure integrity and thickness post-treatment. 8. Cardiac Imaging Findings: Analyzing cardiac imaging results such as echocardiograms or cardiac MRI for improvements in cardiac structure and function. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.10 Endocarditis 2.10.1. Infective Endocarditis – 2.10.1.1. Acute Infective Endocarditis – 2.10.1.2. Subacute Infective Endocarditis – 2.10.1.3. Healthcare-Associated Infective Endocarditis – 2.10.1.4. Community-Acquired Infective Endocarditis – 2.10.1.5. Intravenous Drug Use-Related Infective Endocarditis 2.10.2. Native Valve Endocarditis – 2.10.2.1. Left-Sided Native Valve Endocarditis – 2.10.2.1.1. Mitral Valve Endocarditis – 2.10.2.1.2. Aortic Valve Endocarditis – 2.10.2.1.3. Left Atrial Endocarditis – 2.10.2.2. Right-Sided Native Valve Endocarditis – 2.10.2.2.1. Tricuspid Valve Endocarditis – 2.10.2.2.2. Pulmonary Valve Endocarditis – 2.10.2.2.3. Right Atrial Endocarditis 2.10.3. Prosthetic Valve Endocarditis – 2.10.3.1. Early-Onset Prosthetic Valve Endocarditis – 2.10.3.2. Late-Onset Prosthetic Valve Endocarditis – 2.10.3.3. Intravascular Device-Related Endocarditis – 2.10.3.3.1. Pacemaker Lead-Associated Endocarditis – 2.10.3.3.2. Intravascular Catheter-Associated Endocarditis 2.10.4. Right-Sided Endocarditis – 2.10.4.1. Tricuspid Valve Endocarditis – 2.10.4.2. Pulmonary Valve Endocarditis – 2.10.4.3. Right Atrial Endocarditis 2.10.5. Left-Sided Endocarditis – 2.10.5.1. Mitral Valve Endocarditis – 2.10.5.2. Aortic Valve Endocarditis – 2.10.5.3. Left Atrial Endocarditis 2.10.6. Fungal Endocarditis – 2.10.6.1. Candida Endocarditis – 2.10.6.2. Aspergillus Endocarditis – 2.10.6.3. Histoplasma Endocarditis – 2.10.6.4. Cryptococcus Endocarditis 2.10.7. Culture-Negative Endocarditis – 2.10.7.1. Q Fever Endocarditis – 2.10.7.2. Bartonella Endocarditis – 2.10.7.3. Coxiella burnetii Endocarditis 2.10.8. Nonbacterial Thrombotic Endocarditis (NBTE) – 2.10.8.1. Libman-Sacks Endocarditis (associated with systemic lupus erythematosus) – 2.10.8.2. Marantic Endocarditis (associated with hypercoagulable states) – 2.10.8.3. Verrucous Endocarditis (associated with chronic debilitation) 2.10.9. Infectious Endocarditis Complications – 2.10.9.1. Perivalvular Abscess – 2.10.9.2. Mycotic Aneurysm – 2.10.9.3. Valve Rupture – 2.10.9.4. Septic Emboli | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Infectious Markers: Monitoring levels of infectious markers such as white blood cell count, C-reactive protein (CRP), and procalcitonin to assess infection control. 2. Improvement in Cardiac Function: Measuring changes in cardiac function parameters such as ejection fraction, stroke volume, and cardiac output. 3. Reduction in Vegetations: Assessing the size and resolution of endocardial vegetations through cardiac imaging modalities like echocardiography or MRI. 4. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to cardiac function and infection-related symptoms. 5. Blood Culture Clearance: Monitoring the clearance of blood cultures and resolution of bacteremia or fungemia post-treatment. 6. Reduction in Valvular Damage: Assessing improvements in valve function and reduction in valve regurgitation or stenosis. 7. Cardiac Imaging Findings: Analyzing cardiac imaging results for improvements in cardiac structure and function, including the presence of abscesses or complications. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.11 Congenital Heart Defects 2.11.1. Atrial Septal Defects (ASD) 2.11.2. Ventricular Septal Defects (VSD) 2.11.3. Patent Ductus Arteriosus (PDA) 2.11.4. Tetralogy of Fallot (TOF) 2.11.5. Transposition of the Great Arteries (TGA) 2.11.6. Ebstein’s Anomaly 2.11.7. Coarctation of the Aorta 2.11.8. Hypoplastic Left Heart Syndrome (HLHS) 2.11.9. Atrioventricular Canal Defect (AV Canal) 2.11.10. Truncus Arteriosus 2.11.11. Double Outlet Right Ventricle (DORV) 2.11.12. Total Anomalous Pulmonary Venous Connection (TAPVC) 2.11.13. Pulmonary Atresia 2.11.14. Hypoplastic Right Heart Syndrome 2.11.15. Single Ventricle Defects (e.g., Univentricular Heart) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in Cardiac Function: Measuring changes in cardiac function parameters such as ejection fraction, pulmonary artery pressure, and cardiac output. 2. Reduction in Ventricular Hypertrophy: Assessing changes in ventricular wall thickness and hypertrophy. 3. Improvement in Oxygenation: Monitoring improvements in oxygen saturation levels and reduction in cyanosis. 4. Reduction in Heart Failure Symptoms: Evaluating improvements in heart failure symptoms such as dyspnea, fatigue, and exercise intolerance. 5. Valve Function Improvement: Assessing changes in valve function and reduction in valve regurgitation or stenosis. 6. Reduction in Arrhythmias: Monitoring and comparing the occurrence of arrhythmias such as atrial or ventricular tachycardia. 7. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to cardiac function and symptoms. 8. Exercise Tolerance: Evaluating changes in exercise capacity and tolerance post-cellular therapy for congenital heart defects. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.12 Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Arrhythmias: Monitoring and comparing the occurrence of ventricular arrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF). 2. Improvement in Right Ventricular Function: Measuring changes in right ventricular ejection fraction, dimensions, and contractility. 3. Reduction in Right Ventricular Enlargement: Assessing changes in right ventricular size and volume. 4. Improvement in Exercise Capacity: Evaluating changes in exercise tolerance and capacity post-cellular therapy for ARVC. 5. Reduction in Cardiac Biomarkers: Monitoring levels of cardiac biomarkers associated with ARVC such as troponin and brain natriuretic peptide (BNP). 6. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to ARVC symptoms and cardiac function. 7. Evaluation of Implantable Cardioverter-Defibrillator (ICD) Interventions: Assessing the frequency and effectiveness of ICD therapies for arrhythmia termination. 8. Cardiac Imaging Findings: Analyzing cardiac imaging results such as MRI or echocardiography for improvements in right ventricular structure and function. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.13 Takotsubo Cardiomyopathy | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in Left Ventricular Function: Measuring changes in left ventricular ejection fraction, dimensions, and contractility. 2. Reduction in Myocardial Stunning: Assessing improvements in myocardial function and resolution of wall motion abnormalities. 3. Reduction in Cardiac Biomarkers: Monitoring levels of cardiac biomarkers associated with myocardial injury, such as troponin and brain natriuretic peptide (BNP). 4. Reduction in Heart Failure Symptoms: Evaluating improvements in heart failure symptoms such as dyspnea, fatigue, and edema. 5. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to Takotsubo Cardiomyopathy symptoms and cardiac function. 6. Exercise Tolerance: Evaluating changes in exercise capacity and tolerance post-cellular therapy for Takotsubo Cardiomyopathy. 7. Electrocardiogram (ECG) Findings: Analyzing ECG results for any improvements in rhythm regularity and conduction abnormalities. 8. Cardiac Imaging Findings: Analyzing cardiac imaging results such as echocardiography or cardiac MRI for improvements in ventricular function and structure. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.14 Cardiac Sarcoidosis | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Myocardial Inflammation: Monitoring levels of inflammatory markers such as C-reactive protein (CRP) and interleukins to assess reduction in myocardial inflammation. 2. Improvement in Cardiac Function: Measuring changes in left ventricular ejection fraction, dimensions, and contractility. 3. Reduction in Cardiac Biomarkers: Monitoring levels of cardiac biomarkers associated with myocardial injury and inflammation, such as troponin and brain natriuretic peptide (BNP). 4. Reduction in Arrhythmias: Monitoring and comparing the occurrence of arrhythmias such as ventricular tachycardia or atrioventricular block. 5. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to Cardiac Sarcoidosis symptoms and cardiac function. 6. Exercise Tolerance: Evaluating changes in exercise capacity and tolerance post-cellular therapy for Cardiac Sarcoidosis. 7. Improvement in Cardiac Imaging: Analyzing cardiac imaging results such as cardiac MRI or PET scans for improvements in myocardial function, inflammation, and scar burden. 8. Reduction in Cardiac Complications: Monitoring and comparing the occurrence of cardiac complications such as heart failure exacerbations or thromboembolic events. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.15 Hypertension-related Heart Disease 2.15.1. Hypertensive Heart Disease with Left Ventricular Hypertrophy 2.15.2. Hypertensive Heart Disease with Diastolic Dysfunction 2.15.3. Hypertensive Heart Disease with Systolic Dysfunction 2.15.4. Hypertensive Heart Disease with Heart Failure with Preserved Ejection Fraction (HFpEF) 2.15.5. Hypertensive Heart Disease with Heart Failure with Reduced Ejection Fraction (HFrEF) 2.15.6. Hypertensive Heart Disease with Coronary Artery Disease 2.15.7. Hypertensive Heart Disease with Arrhythmias (e.g., Atrial Fibrillation) 2.15.8. Hypertensive Heart Disease with Valvular Heart Disease (e.g., Aortic Stenosis) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Blood Pressure: Monitoring changes in blood pressure levels, including systolic and diastolic blood pressure measurements. 2. Improvement in Left Ventricular Hypertrophy: Assessing changes in left ventricular mass index and regression of left ventricular hypertrophy. 3. Reduction in Myocardial Fibrosis: Evaluating improvements in myocardial fibrosis using cardiac imaging modalities such as MRI or echocardiography. 4. Improvement in Cardiac Function: Measuring changes in left ventricular ejection fraction, diastolic function, and cardiac output. 5. Reduction in Cardiovascular Events: Monitoring and comparing the occurrence of cardiovascular events such as heart failure exacerbations, myocardial infarction, or stroke. 6. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to hypertension-related heart disease symptoms and overall well-being. 7. Reduction in Arrhythmias: Monitoring and comparing the occurrence of arrhythmias such as atrial fibrillation or ventricular tachycardia. 8. Exercise Capacity: Evaluating changes in exercise tolerance and capacity post-cellular therapy for hypertension-related heart disease. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.16 Pericardial Diseases 2.16.1. Acute Pericarditis 2.16.2. Chronic Pericarditis 2.16.3. Recurrent Pericarditis 2.16.4. Pericardial Effusion without Inflammation (e.g., idiopathic or post-cardiac surgery) 2.16.5. Constrictive Pericarditis 2.16.6. Pericardial Cysts 2.16.7. Pericardial Tumors (e.g., primary or metastatic) 2.16.8. Pericardial Calcification (e.g., due to chronic inflammation or prior infections) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Pericardial Inflammation: Monitoring levels of inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) to assess reduction in pericardial inflammation. 2. Improvement in Pericardial Effusion: Assessing changes in pericardial effusion volume and resolution of pericardial fluid accumulation. 3. Reduction in Pericardial Thickness: Evaluating improvements in pericardial thickness using cardiac imaging modalities such as echocardiography or MRI. 4. Improvement in Cardiac Function: Measuring changes in left ventricular function, including ejection fraction, diastolic function, and cardiac output. 5. Reduction in Pericarditis Symptoms: Monitoring improvements in pericarditis symptoms such as chest pain, dyspnea, and fatigue. 6. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to pericardial disease symptoms and overall well-being. 7. Reduction in Pericardial Complications: Monitoring and comparing the occurrence of complications such as cardiac tamponade or constrictive pericarditis. 8. Cardiac Imaging Findings: Analyzing cardiac imaging results for improvements in pericardial structure, function, and any residual abnormalities post-treatment. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.17 Cardiogenic Shock 2.17.1. Ischemic Cardiogenic Shock (e.g., acute myocardial infarction) 2.17.2. Non-Ischemic Cardiogenic Shock (e.g., acute decompensated heart failure) 2.17.3. Post-Cardiotomy Cardiogenic Shock (e.g., after cardiac surgery) 2.17.4. Acute Valvular Cardiogenic Shock (e.g., severe aortic stenosis, mitral regurgitation) 2.17.5. Cardiogenic Shock due to Arrhythmias (e.g., rapid ventricular tachycardia, atrial fibrillation with rapid ventricular response) 2.17.6. Cardiogenic Shock due to Myocarditis (e.g., viral myocarditis) 2.17.7. Cardiogenic Shock due to Cardiomyopathies (e.g., dilated cardiomyopathy, hypertrophic cardiomyopathy) 2.17.8. Cardiogenic Shock due to Mechanical Complications (e.g., acute mechanical mitral valve dysfunction, acute ventricular septal defect) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Improvement in Hemodynamic Parameters: Monitoring changes in blood pressure, heart rate, cardiac output, and systemic vascular resistance to assess hemodynamic stability. 2. Reduction in Inotropic Support: Evaluating the need for inotropic medications and assessing reductions in their dosage or discontinuation post-treatment. 3. Improvement in Organ Perfusion: Measuring changes in markers of end-organ perfusion such as lactate levels, renal function (e.g., serum creatinine), and hepatic function (e.g., liver enzymes). 4. Reduction in Ventricular Filling Pressures: Assessing improvements in pulmonary capillary wedge pressure (PCWP) or central venous pressure (CVP) as indicators of reduced ventricular filling pressures. 5. Improvement in Cardiac Function: Monitoring changes in left ventricular ejection fraction, stroke volume, and cardiac index to assess improvements in cardiac function. 6. Reduction in Mortality: Comparing mortality rates between pre-treatment and post-treatment periods to evaluate the impact of cellular therapy on survival outcomes. 7. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to cardiogenic shock symptoms and overall well-being. 8. Cardiac Imaging Findings: Analyzing cardiac imaging results such as echocardiography or cardiac MRI for improvements in ventricular function, wall motion abnormalities, and myocardial perfusion. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.18 Heart Transplant Rejection (Post-transplant complications) 2.18.1. Acute Cellular Rejection 2.18.2. Antibody-Mediated Rejection (AMR) 2.18.3. Hyperacute Rejection 2.18.4. Chronic Rejection 2.18.5. Transplant Vasculopathy (e.g., cardiac allograft vasculopathy) 2.18.6. Chronic Allograft Nephropathy (for kidney transplants) 2.18.7. Bronchiolitis Obliterans Syndrome (for lung transplants) 2.18.8. Graft-versus-Host Disease (GVHD) (for hematopoietic stem cell transplants) | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Reduction in Rejection Episodes: Monitoring the frequency and severity of transplant rejection episodes, including acute cellular rejection and antibody-mediated rejection. 2. Improvement in Graft Function: Assessing changes in graft function parameters, such as renal function (e.g., serum creatinine levels for kidney transplant) or cardiac function (e.g., echocardiography parameters for heart transplant). 3. Reduction in Immunosuppressive Medication Doses: Evaluating the need for immunosuppressive medications and assessing reductions in their dosage or discontinuation post-cellular therapy. 4. Improvement in Biopsy Findings: Analyzing transplant biopsy results to assess improvements in histological features of rejection, such as inflammatory infiltrates or tissue damage. 5. Reduction in Donor-Specific Antibodies (DSA): Monitoring changes in DSA levels to assess reductions in alloimmune responses against the transplant. 6. Prevention of Chronic Rejection: Assessing the prevention or delay of chronic rejection manifestations, such as transplant vasculopathy in heart transplants or chronic allograft nephropathy in kidney transplants. 7. Reduction in Infection Rates: Monitoring and comparing the occurrence of infections, including opportunistic infections, post-cellular therapy in transplant recipients. 8. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to transplant-related complications and overall well-being. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
2.19 Cardiac Arrest Recovery 2.19.1. Post-Resuscitation Syndrome 2.19.2. Ischemic Cardiac Arrest Recovery 2.19.3. Non-Ischemic Cardiac Arrest Recovery 2.19.4. Cardiogenic Shock-Associated Cardiac Arrest Recovery 2.19.5. Arrhythmia-Related Cardiac Arrest Recovery 2.19.6. Sudden Cardiac Arrest Recovery due to Structural Heart Disease 2.19.7. Cardiac Arrest Recovery following Myocardial Infarction 2.19.8. Hypoxic-Ischemic Encephalopathy (HIE) following Cardiac Arrest | BM‐MSCs, hUCB‐MSCs, DPSCs, ESCs, and iPSCs, HSCs, iPSCs, EPCs, Cardiac PCs, UCSCs, ADSCs, DPSCs Cardiomyocyte-PSCs Cardiac Fibroblast-PSCs , Endothelial-PSCs , Smooth Muscle-PSCs, Pericyte-PSCs, VIC-PSCs , Macrophage-PSCs | 1. Neurological Function Assessment: Monitoring neurological status using standardized scales such as the Glasgow Coma Scale (GCS) or the Cerebral Performance Category (CPC) score to evaluate cognitive function and consciousness level. 2. Survival Rates: Comparing survival rates between pre-treatment and post-treatment periods to assess the impact of cellular therapy on overall survival following cardiac arrest. 3. Cardiac Function Improvement: Measuring changes in cardiac function parameters such as ejection fraction, cardiac output, and hemodynamic stability. 4. Reduction in Ventricular Arrhythmias: Monitoring and comparing the occurrence of ventricular arrhythmias such as ventricular tachycardia or fibrillation post-cellular therapy. 5. Quality of Life Assessment: Using standardized scales to evaluate improvements in patients’ quality of life related to cardiac arrest recovery, physical function, and overall well-being. 6. Functional Recovery: Assessing improvements in activities of daily living, mobility, and independence post-cellular therapy for cardiac arrest recovery. 7. Cardiac Imaging Findings: Analyzing cardiac imaging results such as echocardiography or cardiac MRI for improvements in ventricular function, wall motion abnormalities, and myocardial perfusion. 8. Prevention of Cardiac Arrest Recurrence: Monitoring and comparing the occurrence of recurrent cardiac arrest events to evaluate the effectiveness of cellular therapy in preventing future episodes. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |