Introduction: Systemic lupus is a disseminated inflammation of the conjunctive tissue. Cardiovascular lesions are the first cause of morbidity and mortality in the course of that disease. These lesions are prevalent in 30 to 62% of cases, depending on whether the diagnostic tool is clinical, echocardiographic, or autopsic. Any part of the heart can be affected, yielding manifestations of pericarditis, endocarditis, coronary heart disease, conduction disorders, and rarely myocarditis.
Objective: Describe cardiac manifestations during the follow up of patients diagnosed with systemic lupus.
Patients and Methods: We conducted a transversal descriptive study over a period of 27 months, in the departments of Internal Medicine, Dermatology, and Cardiology of Yalgado Ouedraogo University Hospital of Ouagadougou. All patients diagnosed with systemic lupus according to the American College of Rheumatology criteria, and having done an EKG, a Holter EKG, or a transthoracic echocardiography, were included in the study. Data were collected from inpatient medical records, outpatient follow up registry and booklets.
Results: Cardiovascular lesions were prevalent in 7 cases (43.75%) out of 16 patients diagnosed with systemic lupus. Mean age of patients was 36 years, with extremes of 23 and 51 years. Only female patients were affected in our study. Cardiac manifestations were mainly benign pericarditis, heart failure, and conduction disorders.
Conclusions: Cardiovascular manifestations are frequent during the course of systemic lupus, and occur after few years of disease progression. Transthoracic echocardiography and EKG remain useful non-invasive explorations for the assessment of cardiovascular lesions, despite minor shortcomings.
Background: Patients with myocardial infarction (MI) often experience anxiety, depression and poor quality of life (QoL) compared with a normative population. Mood disturbances and QoL have been extensively investigated, but only a few studies have examined the long-term effects of MI on these complex phenomena.
Aims: To examine the levels and associated predictors of anxiety, depression, and QoL in patients 2 years after MI.
Methods: This was a single center, observational study of patients with MI (n=377, 22% women, median age 66 years). Two years after MI (2012-2014), the patients were asked to answer the Hospital Anxiety and Depression Scale (HADS) and EuroQol 5-dimension (EQ-5D-3L) questionnaires.
Results: Most patients experienced neither anxiety (87%, 95% confidence interval [CI]: 83-90%) nor depression (94%, 95% CI: 92-97%) 2 years post-MI. Elderly patients experienced more depression than younger patients (p=0.003) and women had higher anxiety levels than men (p=0.009).
Most patients had “no problems” with any of the EQ-5D-3L dimensions (72-98%), but 48% (95% CI: 43%-53%) self-reported at least “some problems” with pain/discomfort. In a multiple logistic regression model (EQ-5D-3L) higher age (p<0.001) and female sex (p<0.001) were associated with more pain/discomfort. Female sex (p=0.047) and prior MI (p=0.038) were associated with anxiety/depression. History of heart failure was associated with worse mobility (p=0.005) and problems with usual activities (p=0.006). The median total health status of the patients (EQ-VAS) was 78 (95% CI: 75-80)
The results of the 20 years studies of the presence in blood serum and other body fluids of endogenous modulators of adrenergic and M-cholinergic impact as a component of humoral link of autonomic nervous system. The article is devoted to the endogenous sensitizer of beta-adrenergic receptor (ESBAR) - water-soluble low molecular weight substances, analogs of which are histidine, tryptophan, tyrosine, mildronat and preductal. It is shown, that separate dilutions of human serum and animal (as a source of ESBAR) and analogs of ESBAR ways to enhance the effectiveness of activation of beta-adrenoceptors (AR) of smooth muscle (uterus, coronary and renal arteries, trachea, stomach), myocardium, erythrocytes and platelets (respectively influenced of histidine and tryptophan). It is reported that content of ESBAR in human serum (according to the titers of its dilution) depends on the sex and the presence of somatic diseases, and at women are also on the stage of reproduction and obstetric complications It is discussed possible mechanisms of ESBAR action, its physiological role, including as a component of beta-adrenoceptor inhibitory mechanism for myometrium, as well as the prospect of the use of analogs of ESBAR, including for the prevention of preterm labor, and for the treatment of bronchial asthma, coronary heart disease, hypertension and heart failure.
Cardiomyopathy is a heart muscle disease with structural and functional myocardial abnormalities in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease. However, it has become clear that diverse etiologies and clinical manifestations (e.g. arrhythmogenic right-ventricular cardiomyopathy/dysplasia (ARVC/D), ARVD/C, left-ventricular non-compaction cardiomyopathy (LVNC)) are responsible for the clinical picture of dilated cardiomyopathy (DCM).
The American Heart Association (AHA) classification grouped cardiomyopathies into genetic, mixed and acquired forms, while the European Society of Cardiology (ESC) classification proposed the subgrouping of each major type of cardiomyopathy into familial or genetic, and nonfamilial or nongenetic, forms [1-4].
Cardiomyopathies are clinically heterogeneous diseases, and there are differences in sex, age of onset, rate of progression, risk of development of overt heart failure and likelihood of sudden death within each cardiomyopathy subtype .
Because of the complex etiology and clinical presentation, the diagnostic spectrum in cardiomyopathies spans the entire range of non-invasive and invasive cardiological examination techniques including genetic analysis. The exact verification of certain cardiomyopathies necessitates additional investigations. So, histological, immunohistological and molecular biological/virological investigations of endomyocardial biopsies are the gold standard to confirm the diagnosis of an inflammatory cardiomyopathy (DCMi) [6-10].
This review focuses on myocarditis and inflammatory cardiomyopathies underlying an immune-mediated process or persistent viral infection.
Background: The prognostic significance of impaired left ventricular (LV) relaxation and increased LV stiffness as precursor of heart failure with preserved ejection fraction and death is still largely unknown in apparently healthy subjects.
Methods: We constituted a cohort of 353 patients with normal ejection fraction (>45%) and no significant heart disease, based on a total of 3,575 consecutive left-sided heart catheterizations performed. We measured peak negative first derivative of LV pressure (-dP/dt) and operating chamber stiffness (Κ) using a validated equation. Patients were categorized as having: 1) normal diastolic function, 2) isolated relaxation abnormalities (-dP/dt > 1860mm Hg/sec and K <0.025mm Hg/ml), or 3) predominant stiff heart (K ≥0.025mm Hg/ml).
Results: During a follow-up of at least 5 years, the incidence of the primary composite endpoint (death, major arterial event, heart failure, and arrhythmia) was 23.2% (82 patients). Compared to isolated relaxation abnormalities, predominant stiff heart showed stronger prognostic significance for all events (p=0.002), namely heart failure (HR, 2.9; p=0.0499), cardiac death (HR, 5.8; p=0.03), and heart failure and cardiac death combined (HR, 3.7; p=0.003).
Conclusion: In this apparently healthy population referred to our center for cardiac catheterization, the prevalence of diastolic dysfunction was very high. Moreover, predominant stiff heart was a better predictor of cardiovascular outcomes than isolated relaxation abnormalities.
Blunt chest trauma leads to a wide range of lesions, relatively minor parietal injuries to potentially fatal cardiac lesions, making diagnosis and management difficult. The diagnosis is currently facilitated by imaging, however, these lesions may go unnoticed and be discovered late through complications.
We report the case of a neglected heart wound revealed by a heart failure. This case is notable due to a favourable outcome despite a delay in diagnosis due to a lack of pericardial effusion and the absence of cardiac symptoms, and a long delay from injury to appropriate treatment in the presence of a penetrating cardiac wound deep enough to cause a muscular ventricular septal defect and lacerate the anterior mitral leaflet.
Background: Current guidelines for diagnosis and management of heart failure (HF) rely on clinical findings and natriuretic peptide values, but evidence suggests that recently identified cardiac biomarkers may aid in early detection of HF and improve risk stratification. The aim of this study was to assess the diagnostic and prognostic utility of multiple biomarkers in patients with HF and left ventricular systolic dysfunction (LVSD).
Methods: High-sensitivity cardiac troponin I (cTnI), N-terminal pro b-type natriuretic peptide (NT-proBNP), interleukin-6 (IL-6), endothelin-1 (ET-1), pro-matrix metalloproteinase-9 (pMMP-9), and tumor necrosis factor-alpha (TNF-α) were measured using single-molecule counting technology in 200 patients with varying stages of HF. Plasma detection with cross-sectional associations of biomarkers across all HF stages, and advanced-therapy and transplant-free survival were assessed using multivariate analysis and Cox regression analyses, respectively.
Results: NTproBNP, pMMP-9, IL-6 were elevated in early, asymptomatic stages of HF, and increased with HF severity. Higher circulating levels of combined IL-6, NTproBNP, and cTnI predicted significantly worse survival at 1500-day follow-up. Cox regression analysis adjusted for ACC/AHA HF stages demonstrated that a higher concentration of IL-6 and cTnI conferred greater risks in terms of time to death, implantation of left ventricular assist device (LVAD), or heart transplantation.
Conclusion: Biomarkers of inflammation, LV remodeling, and myocardial injury were elevated in HF and increased with HF severity. Patients had a significantly higher risk of serious cardiac events if multiple biomarkers were elevated. These findings support measuring NTproBNP, cTnI and IL-6 among patients with HF and LVSD for diagnostic and prognostic purposes.
Background: Anemia is an accelerating problem among patients with heart failure (HF) and its presence is associated with more symptoms. In this study, we investigated whether anemia in heart failure was related to hepcidin concentration.
Methods: 50 patients with heart failure and 20 healthy subjects with no history of a chronic illness including heart failure as control group, were included in the study. Heart failure was verified by echocardiography in each subject and patients were defined as ones with reduced ejection fraction (HFrEF) if EF ≤ 40% and with preserved ejection fraction (HFpEF) if EF 40% - 50%. Blood samples were taken from all patients after 10-12 hours fasting. Anemia assessment was performed according to World Health Organization (WHO) criterias.
Results: There was a positive correlation between hepcidin concentration and urea, ferritin, hemoglobin, hematocrite, C-reactive protein (p < 0,05). Hepcidin concentrations of anemic heart failure patients were significantly lower than the non-anemic heart failure patients (p < 0,05).
Conclusion: We found that serum hepcidin concentration in anemic patients with heart failure was lower than in heart failure patients without anemia. We believe that iron defiency occurs as a result of inflammatory process in heart failure and therefore hepcidin concentrations decrease as a response. However, long-term follow up studies are needed.
Chronic heart failure has been extensively characterized as a disorder arising from a complex interaction between impaired ventricular performance and neurohormonal activation. Since beta adrenoceptor blocking agents are currently considered an integral component of therapy for the management of patients with severe chronic heart failure; several well designed clinical trials have been conducted to determine the morbidity and mortality benefits of these agents these studies, however did not yield the same results in terms of morbidity and mortality benefits. Currently only Bisoprolol, Carvedilol and sustained release metoprolol succinate have clinically proven and convincing morbidity and mortality benefits the current list of approved medicines of the National Health Insurance Scheme (NHIS) of the republic of Ghana does not provide coverage for these lifesaving therapeutic agents. The objective of this review was to collate the relevant scientific evidence that will convince the authorities at the National Health Insurance Authority (NHIA) of the Republic of Ghana to include at least one of the evidence based beta adrenoceptor blocking agents in the list of approved medicines.
A thorough search on the internet was conducted using Google scholar to obtain only the clinically relevant studies associated with the benefits of beta adrenoceptor blocking agents in patients with chronic heart failure published in the English language. The phrases beta adrenoceptor blocking agents and chronic heart failure were used as search engines.
The search engine yielded several studies that met the predefined inclusion criteria. However, only the Cardiac Insufficiency BIsoprolol Studies (CIBIS-I and CIBIS-II), Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) and Metoprolol CR/XL Randomized Intervention Trial (MERIF-HF) because of the clinical relevance of their findings Beta adrenoceptor blocking agents such as atenolol and propranolol have been used in the management of patients with chronic heart failure. However, their efficacy and optimal dose in reducing mortality have not been scientifically established not all beta adrenoceptor blocking agents scientifically studied provide the same degree of clinically meaningful and convincing morbidity and mortality benefits in patients with chronic heart failure.
Background: Contrast-induced acute kidney injury (CI-AKI) is an important cause of increasing the hospital stay and in-hospital mortality. By increasing intra-renal vasoconstriction, left ventricular ejection fraction (LVEF) can increase the risk of CI-AKI. We sought to investigate whether LVEF can impact the incidence of CI-AKI after cardiac catheterization and whether it can be used to predict CI-AKI.
Methods: Patients underwent cardiac catheterization from December 2017 to February 2018 at Jersey Shore University Medical Center were enrolled in the study. Contrast-induced acute kidney injury (CI-AKI) was defined as an increase in serum creatinine of ≥ 0.5 mg/dL or an increase of ≥ 25% from the pre-procedure value within 72 hours post-procedure. The maximum allowable contrast dose was calculated using the following formula: (5* (weight (kg)/creatinine level (mg/dL)). A multivariable logistic regression analyses, controlling for potential confounders, were used to test associations between LVEF and CI-AKI.
Results: 9.6% had post catheterization CI-AKI. A total of 18 out of 44 (44%) of patients who had CI-AKI also had ongoing congestive heart failure. No statistically significant association found neither with maximum allowable contrast (p = 0.009) nor ejection fraction (p = 0.099) with the development of CI-AKI.
Conclusion: In spite of the fact that no statistically significant relationship found between the percentage maximum contrast dose and the ejection fraction with the post-procedure CI-AKI, we heighten the essential of employing Maximum Allowable Contrast Dose (MACD) and ejection fraction in patients undergoing PCI to be used as a clinical guide to predict CI-AKI.
Biventricular (BiV) pacing revolutionized the heart failure management in patients with sinus rhythm and left bundle branch block; however, left ventricular-lead placement is not always technically possible. Also, BiV pacing does not fully normalize ventricular activation and, therefore, the ventricular resynchronization is imperfect. On the other hand, right ventricular pacing for bradycardia may cause or worsen heart failure in some patients by causing dyssynchronous ventricular activation. His bundle pacing comes as an alternative to current approaches as it activates the ventricles via the native His-Purkinje system, resulting in true physiological pacing, and, therefore, is a promising site for pacing in bradycardia and traditional CRT indications in cases where it can overcome left bundle branch block. Furthermore, it has the potential to open up new indications for pacing therapy in heart failure, such as targeting patients with PR prolongation, but a narrow QRS duration. In this article we explore the history, clinical evidence, proposed mechanisms, procedural characteristics, and the role in current therapy of His bundle pacing in the prevention and treatment of heart failure.
Background: Infants of diabetic mothers (IDMs) are at increased risk of developing congenital anomalies including cardiac defects. Pathological left ventricular hypertrophy, asymmetrical septal hypertrophy and outflow tract obstruction is a rare but known cardiac comorbidity in infants of diabetic mothers. The severity of this condition in IDMs can vary from an incidental finding on echocardiography to an infant with severe symptoms of congestive heart failure and specific management of the condition varies.
Aim: The aim of this article is to report this clinical entity in a Nigerian infant born to a mother with poor glycaemic control in pregnancy and highlight management.
Case report: We report a term neonate who was diagnosed as a case of pathological left ventricular hypertrophy, asymmetrical septal hypertrophy and outflow tract obstruction delivered to a mother with gestational diabetics with poor glycaemic control in pregnancy. Child was treated successfully with β-adrenergic blocker and showed resolution of hypertrophy in follow-up echocardiography.
Conclusion: Infants of diabetic mothers are very high risk infants. Pathological left ventricular hypertrophy in IDM have good prognosis. Early recognition and prompt intervention is advocated.
Implantable cardioverter defibrillators (ICDs) are electronic devices that can prevent sudden cardiac death (SCD) caused by arrhythmic events in patients.
The latest ESC/EAS and ACC/AHA Guidelines deem the placement of an ICDs appropriate in patients with heart failure class NYHA II and III in the presence of an ejection fraction less than or equal to 35% [1,2]. ICDs are usually not indicated in either class I or IV patients. The Guidelines recommendations for primary prevention of SCD with ICD implantation do not take into account the age of the patients but only their life expectancy which must be at least 1 year.
Our patients usually are over eighty years old with heart failure and severely reduced ejection fraction. We must consequently decide if it is right to implant these patients with an ICD. Is the use of ICD in the patients over 80, in particular over 90 years old, really make sense becomes particularly important considering demographic changes that await us in the coming decades.
Background: Sudden cardiac death is a major healthcare issue in reduced ejection fraction heart failure (HFrEF) patients. Recently, the new association of sacubitril/valsartan showed a reduction of both ventricular arrhythmias (VA) and mortality even at low dose compared to enalapril in HF patients. The purpose of our study was to assess whether the highest dose of sacubitril/valsartan compared to lower doses may improve the rate of death and VA in a population of patients with HFrEF and with an implantable cardiac defibrillator (ICD).
Methods: 104 HF patients with reduced EF under sacubitril/valsartan with an ICD were divided in 2 groups: the first one with the lower doses of sacubitril/valsartan (24/26 mg or 49 mg/51 mg twice daily) and the second with the maximal dose (97mg/103mg twice daily). The primary outcome was a composite of death or appropriate ICD therapy for VA.
Results: After a median follow-up of 14 months, 39 patients were treated with lower doses and 65 patients with the highest dose. Patients from the lower doses group were older (70 [60-80] vs. 66 [60-70]; p = 0,03), more symptomatic at initiation (NYHA 3: 44% vs. 19%; p < 0,01) and more often in atrial fibrillation (31% vs. 12%; p = 0,04). The primary composite endpoint occurred in 14 patients (36%) in the low doses group versus 7 patients (11%) in high dose group (p < 0,01). This difference was particularly observed in the subgroup of patients with ischemic cardiomyopathy. In a multivariable analysis, the higher dose was independently associated with the primary outcome with an HR = 2,934 [IC 95% 1,147 – 7,504]; p = 0,03. Kaplan-Meier curve showed an early effect of the highest dose of sacubitril/valsartan association.
Conclusion: Patients with HFrEF under the highest dose of sacubitril/valsartan showed better clinical outcomes with a decrease of both mortality or appropriated ICD therapies related to ventricular arrhythmias.
Taryètba André Arthur Seghda*, Théodore Boro, Jean Eudes Bambara, Kadari Cisse, Andrés Miguel Lopez, André K Samadoulougou, Taryètba André Arthur Seghda*, Théodore Boro, Jean Eudes Bambara, Kadari Cisse, Andrés Miguel Lopez and Patrice Zabsonre
Peripartum cardiomyopathy is one of the curable cardiomyopathy. It’s a severe and frequent disease arising among women of childbearing age. Its evolution in the long-term among some patients leads to chronic heart failure. Our study aims to determine from a prospective cohort, the factors associated with the non-recovery of myocardial function upon 12 months of diagnosis. Sociodemographic, clinical and echocardiographic data were collected at the time of diagnosis and then in months 3, 6 and 12. The outcome was the non-recovery of myocardial function at one year, defined by a left ventricular ejection fraction (LVEF) below 50%. 60 patients were analyzed after 12 months of follow-up. Mortality was about 13.3% and recovery rate of myocardial function reached 42.3%. After logistic regression, delay diagnosis and observance were the factors related to non- recovery of myocardial function.
The normal adult heart is a well maintained machine that has a mechanism for growth replacement of the sarcomere that is lost by natural degeneration. This process ensures the heart has the strength of contraction to function correctly giving blood supply to the whole body. Some of the force of contraction of the sarcomere is transmitted to its major protein titin where its strength results in unfolding of a flexible section and release of a growth stimulant. The origin of all the cardiomyopathies can be traced to errors in this system resulting from mutations in a wide variety of the sarcomeric proteins. Too much or chronic tension transfer to titin giving increased growth resulting in hypertrophic cardiomyopathy (HCM) and too little leading to muscle wastage, dilated cardiomyopathy (DCM). HCM can ultimately lead to sudden cardiac death and DCM to heart failure. In this paper I show (1) a collection of the tension/ATPase calcium dependencies of cardiac myofibrils that define the mechanism of Ca2+ cooperativity. (2) I then reintroduce the stress/strain relationship to cardiomyopathies. (3) I then review the cardiomyopathy literature that contains similar Ca2+ dependency data to throw light on the mechanisms involved in generation of the types of myopathies from the mutations involved. In the review of cardiomyopathy there are two sections on mutations, the first dealing with those disrupting the Ca2+ cooperativity, i.e. the Hill coefficient of activation, leading to incomplete relaxation in diastole, chronic tension, and increased growth. Secondly dealing with those where the Ca2+ cooperativity is not affected giving either increased or decreased tension transfer to titin and changes in sarcomere growth.
Ventricular assist device is a portable machine which is also called an artificial heart for the patients who have terminal heart failure. The device maintains the heart’s vital functions until the suitable donor is found for the heart transplantation. It can be applied to either ventricles or both (biventricular). Although the device provides independence for the patient, it also has life-threatening complications. Such as infection, stroke secondary to thromboembolism, hemorrhage depending on anticoagulant use, right heart failure… and most of the time it is really hard to manage those complications. We will present a case, who had ischemic stroke as a complication of VAD even though he has been using aspirin, warfarin and had effective INR value.
The shapes and sizes of human cardiomyocytes are accessible to systematic observation under most circumstances only at autopsy. This constraint has seriously curbed the study of these topics, thereby leaving a crippling gap in our understanding of heart failure. In recent years the only published ongoing findings have come from this laboratory. This article is a condensation of these reports, using those sources to develop fresh analyses designed to construct a set of organizing principles. The data are entirely retrospective thereby forbidding hypothesis testing and permitting only hypothesis formation. The hypotheses generated in this way are novel and surprising. In spite of the severe limitations in this methodology is seems possible that some useful new directions of inquiry might evolve from pursuing these original observations.
Introduction: Congestive heart failure is one of the main causes of morbidity and mortality in the XXI century given the promising to date of ABMDSCs and HFDSCs we investigate the safety and efficacy for the implantation of those stem cells for the treatment of idiopathic cardiomyopathy. This is the first pilot clinical study to assess the safety and feasibility of HFDSC in humans. We totally implanted 13 patients: 3 patients were implanted with ABMDSC by Mini-invasive surgical technique in March 2004 in Montevideo, Uruguay, and 10 patients were implanted with HFDSCs by using 2 different surgical techniques: minimally invasive technique (1 patient) and full sternotomy technique (9 patients) between January and February of 2005 in Guayaquil Ecuador.
The HFDSCs were obtained from fetuses of 5 to 12 weeks´ gestation from legally consent, no compensated donors who have undergone terminated ectopic pregnancies, elective abortions, or spontaneous miscarriages. At that gestation´s period, totipotent stem cells´ fetus haven´t develop yet the HLA histocompatibility complex, so there´s no possible antigenicity between donor and recipient.
Results: Patients with HFDSCs improved in association with increased contractility in these regions. Compared with baseline assessments, we noted other improvements: The mean (±SD) NYHA class decreased from 3.4±0.5 to 1.33±0.5 (P=.001); the mean EF increased 31%, from 26.6% ± 4.0% to 34.8%±7.2% (P=.005); performance in the ETT increased 291.3%, from 4.25 minutes to 16.63 minutes (128.9% in metabolic equivalents, 2.45 to 5.63) (P<.0001); the mean LVEDD decreased 15%, from 6.85±0.6cm to 5.80±0.58cm (P<.001); mean performance in the 6-minute walk test increased 43.2%, from 251±113.1 seconds to 360±0 seconds (P=.01); the mean distance increased 64.4%, from 284.4±144.9m to 468.2±89.8m (P=.004); and the mean result in the Minnesota congestive HF test decreased from 71±27.3 to 6±5.9 (P<.001) The Kaplan-Maier probability of survival at 48 months was 66%.
It is not observed rejection, these patients have not developed malignance nodules or cancer at all in the follow-up. In the AMBCSs. The preoperative average NYHA functional class was 3.4; at. 6 months of follow up the average functional class value was 1.3 (p<0,005);. After 6 months all of them remained in functional class I/II. Baseline values of LVEF were 25,28 and 30%.; at 6 months increased to 38, 40 and 46%. (p<0,05). LVESV went from 50mm to 42mm (p<0.05). After 24 months, 2 of the patients still maintained this improvement, while the 3er patient returned to the earlier values after suffering from pneumonia. At 12 years and 5 months 2 patients are alive both received a Resynchronization Therapy; at 8 years and 3 months and 9 years and 1,6 month the actual average EF are 28 and 30 %. The 3er patient died of sudden death at 10 years after the implantation. We can´t demonstrate the cause of this sudden death.
Conclusion: Irrespective of the improvement seen in this study, it is still premature to determine accurately the mechanism of action, indications, doses and type of stem cells. Therefore, is imperative and extremely important that more research is needed.
Stem cell treatments depend not only on the type of cell to be used but also on the different implantation techniques. Intravascular cell injections are known to rapidly separate from the vessels. On the other hand, it is also well known that direct injection into the myocardium provides better coupling within the heart muscle. That were the cases of Embriofetal stem cell (HFDSC) or Autologous stem cells (ABMSC) in our experience focused on direct approaches.
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