Cardiac Dysfunction In Patients Research Articles

Effectiveness of exercise-based interventions in preventing cancer therapy-related cardiac dysfunction in patients with breast cancer: A systematic review and network meta-analysis

Effectiveness of exercise-based interventions in preventing cancer therapy-related cardiac dysfunction in patients with breast cancer: A systematic review and network meta-analysis

The SARAH trial: more evidence on the role of neurohormonal blockers in prevention of anthracycline-induced cardiotoxicity.

This mini-review highlights the results of the SARAH trial, which evaluated the efficacy of sacubitril/valsartan in preventing subclinical cardiac dysfunction in patients undergoing anthracycline-based chemotherapy. The trial demonstrated a significant reduction in GLS decline in the treatment group compared to placebo. The findings are discussed in context with other trials investigating neurohormonal blockade for the prevention of cancer therapy-related cardiac dysfunction.

Association Between Advanced TNM Stages and Increased Risk of Cardiac Dysfunction in Patients with LVEF < 50.

Background and Objectives: Cardio-oncology addresses the growing concern of cardiovascular complications arising from cancer therapies. Although cancer treatments have greatly enhanced survival outcomes, they frequently carry substantial risks to cardiovascular health. This research examines the cardiovascular toxicity associated with HER2-targeted therapies, focusing on the interconnection between tumor characteristics, including histopathological profiles and TNM classification, and the development of cardiovascular complications. The objective is to identify key correlations that inform better prevention and management strategies for cardiotoxicity in oncology patients. Materials and Methods: This retrospective study analyzed cancer patients undergoing cytostatic treatments, particularly anthracyclines, radiotherapy, and HER2-targeted therapies. Cardiac function was monitored using echocardiographic assessments, including global longitudinal strain and left ventricular ejection fraction (LVEF). Patients were stratified based on TNM cancer staging and histopathological findings to evaluate correlations between treatment regimens and cardiovascular outcomes. Results: The analysis revealed a significant association between advanced TNM stages and reduced LVEF, with patients in stage T4 showing the highest prevalence of cardiac dysfunction. Cytostatic treatments, such as anthracyclines and HER2-targeted therapies, were identified as key contributors to cardiotoxicity, particularly in advanced-stage cancer patients. These findings emphasize the importance of regular cardiac monitoring to detect early signs of cardiotoxicity, as patients with pre-existing cardiovascular risk factors demonstrated a higher prevalence of complications. Conclusions: This study highlights the need for personalized treatment approaches and tailored cardioprotective strategies to improve outcomes and enhance the quality of life for oncology patients. Future studies should prioritize developing improved strategies to reduce the cardiovascular complications linked to contemporary cancer treatments.

Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne Muscular Dystrophy.

Absence of dystrophin protein causes cardiac dysfunction in patients with Duchenne muscular dystrophy (DMD). Unlike boys with DMD, the common mouse model of DMD (B10-mdx) does not manifest cardiac deficits until late adulthood. This has limited our understanding of the mechanism and therapeutic approaches to target the pediatric onset of cardiac pathology in DMD. Here we show that the mdx mouse model on the DBA/2J genetic background (D2-mdx) displays juvenile-onset cardiac degeneration. Molecular and histological analysis revealed that cardiac damage in this model is linked to increased leukocyte chemotactic signaling and an inability to resolve inflammation. These deficiencies result in chronic inflammation and fibrotic conversion of the extracellular matrix (ECM) in the juvenile D2-mdx heart. To address these pathologies, we tested the utility of pro-resolution therapy to clear chronic cardiac inflammation. Use of an N-formyl peptide receptor (FPR) agonist helped physiologically resolve inflammation and mitigate the downstream events that lead to fibrotic degeneration of cardiomyocytes, preventing juvenile onset cardiac muscle loss. These results establish the utility of D2-mdx model to study events associated with pediatric-onset cardiac damage and demonstrates pro-resolution therapy as an alternate to anti-inflammatory therapy for treating cardiac degenerative pathology responsible for cardiomyopathy in DMD patients.

Metabolic flux analysis in hiPSC-CMs reveals insights into cardiac dysfunction in propionic acidemia Eva Richard.

Propionic acidemia is an inborn error of metabolism caused by mutations in either the PCCA or PCCB genes. Patients with propionic acidemia experience a range of complications, including life-threatening cardiac dysfunctions. However, the pathological mechanisms underlying propionic acidemia-associated cardiac diseases remain largely unknown. To gain insights into the metabolic alterations in propionic acidemia, we studied human induced pluripotent stem cell-derived cardiomyocytes generated from a patient with propionic acidemia with two pathogenic PCCA mutations (p.Cys616_Val633del and p.Gly477Glufs9*) and from a healthy individual. Using stable isotope-based metabolic flux analysis, we confirmed that the PCCA mutations lead to impaired propionyl-CoA carboxylase activity in human induced pluripotent stem cell-derived cardiomyocytes. In addition to being converted to propionylcarnitine, the accumulated propionyl-CoA can also be hydrolyzed to propionate and exported out of the cell, serving as a secondary "pressure valve" to regulate cellular propionyl-CoA levels. Interestingly, the deficiency of propionyl-CoA carboxylase was found to shift fuel metabolism from fatty acid oxidation to increased glucose metabolism human in induced pluripotent stem cell-derived cardiomyocytes from patients with propionic acidemia. This metabolic switch is less energy-efficient and may contribute to the development of chronic cardiac dysfunction in patients with propionic acidemia.

Association between Alpha- Klotho Protein, Calcium, and Phosphate concentrations in Adult Iraqi Patients with Beta-Thalassemia Major

Background: Beta-thalassemia major is a prevalent global condition characterized by a rapid breakdown of red blood cells. Regular blood transfusions can give rise to problems such as cardiovascular disease, diabetes, osteoporosis, and renal disorders. Alpha-Klotho protein is a protein that has anti-aging properties and is involved in several functions, including reducing oxidative stress, regulating energy metabolism through several routes, and managing calcium and phosphate metabolism. Objective: This study aimed to assess changes in calcium and phosphate levels, Alpha-Klotho protein concentration, and their associations with cardiac dysfunction in patients with Beta-thalassemia major. Methods: The study was conducted at Al-Sadr General Hospital and Ibn Albaladi Center of Blood Diseases, Baghdad, and involved 90 participants who were grouped into three groups: Group A: 30 patients with Beta-thalassemia major and heart dysfunction; Group B:30 patients with Beta-thalassemia major without any signs of heart dysfunction; and Group C:30 healthy individuals as a control group. The indicators examined were serum levels of Alpha-klotho protein, calcium, phosphate, and Ferritin. ELISA method was used to assess serum Alpha-klotho protein, whereas serum Ca, serum phosphate, and serum Ferritin were analyzed using the Beckman Coulter AU clinical chemistry analyzers. Results: The mean values of Serum Alpha-Klotho protein, phosphate, and Ferritin in the patients with beta-thalassemia were greater than those in the control group with P value&lt;0.05. Patients with thalassemia had decreased levels of serum calcium compared to the control group. Additionally, a strong negative association was observed between serum calcium and phosphate levels. Conclusion: Patients with beta-thalassemia major have significant alterations in calcium and phosphate levels under the control of Klotho protein levels.

Left ventricular global longitudinal strain in patients treated with immune checkpoint inhibitors.

Immune checkpoint inhibitors (ICI) are generally associated with rare cardiac side effects, yet instances like myocarditis can be fatal. Therefore, detecting and managing left ventricular dysfunction early in ICI therapy is vital. This study aims to evaluate whether left ventricular global longitudinal strain (LV GLS) is a predictor for early detection of cardiac dysfunction in patients receving ICI. This retrospective cohort study included 44 cancer patients who received ICI therapy and underwent pre- and post- treatment assessments of left ventricular ejection fraction (LVEF) and LV GLS between May 2022 and November 2023. Retrospective comparisons and evaluations were conducted on pre-treatment and 3-month interval LVEF and LV GLS measurements during the first year of treatment. The median follow-up duration was 5.3 months (0.5-18.9). No statistically significant difference between baseline and subsequent time points was observed in LVEF and LV GLS values (p>0.05). At the 3-month evaluation, a notable decrease in LVEF and LV GLS was observed in two patients. One patient with reduced LVEF and LV GLS succumbed to myocarditis, and another experienced sudden death of unknown etiology. The other two patients had decreased LV GLS with normal LVEF. Subsequent follow-ups of the patients exhibiting decreased LV GLS alone revealed no further decline in LVEF or LV GLS. In our study, a reduction in LV GLS did not demonstrate a significant role in the early prediction of ICI-related myocarditis or cardiac dysfunction. Further validation through multicenter, large-scale, prospective studies with extended follow-up periods is needed to confirm these findings.

Muscle Pathology Associated With Cardiac Function in Duchenne Muscular Dystrophy.

To compare the progression of muscle fibrosis of various site and its relation between cardiac deterioration in Duchenne muscular dystrophy (DMD). In this study aimed to examine the associations between echocardiogram-based cardiac function indices and fibrosis of the abdominal and lower extremity muscles in patients with DMD to facilitate early detection of cardiac dysfunction and identify its predictors. Twenty-one patients with DMD patients were enrolled in the study. The association between cardiac dysfunction and fibrosis of the abdominal and lower extremity muscles was determined by analyzing the echocardiography and elastography. Non-parametric Spearman rank correlation coefficients were used to examine the pairwise relationships between cardiac function and muscle elasticity. All patients were male and non-ambulant. Their mean age was 18.45±4.28 years. The strain ratios of the abdominal muscle and quadriceps muscles were significantly higher than those of the medial gastrocnemius. The strain ratio of the rectus abdominis muscle has a significant negative correlation with left ventricular ejection fraction. Cardiac function and valvular insufficiency were not significantly correlated with muscle strain ratio. According to the result of our study, the only skeletal muscle which showed significant correlation with cardiac dysfunction was degree abdominal muscle fibrosis. The degree of fibrosis of respiratory muscles was also significantly associated with cardiac dysfunction; therefore, it can be used as a predictor of cardiac dysfunction in patients with DMD in clinical practice.

Evaluation of Subclinical Cancer Therapy-Related Cardiac Dysfunction in Patients Undergoing Hematopoietic Stem Cell Transplantation: An Echocardiography Study.

Background: Hematopoietic stem cell transplantation (HSCT) is a potentially curative procedure that is used in various hematological malignancies. However, among an increasing number of HSCT, the amount of cancer therapy-related cardiac dysfunction (CTRCD) is increasing as well. This study aimed to determine the prevalence of subclinical CTRCD in HSCT patients 12 months after HSCT and to assess the impact of clinical factors on the development of CTRCD. Material and Methods: We included 55 patients who underwent autologous or allogeneic HSCT. The patients were assessed using an echocardiography method before and 12 months after a HSCT procedure. Results: Our study revealed that during the 12-month follow-up period, asymptomatic CTRCD was observed in 15 patients (27.3%), 6 experienced moderate CTRCD, and 9 experienced mild CTRCD. Patients with previous use of anthracyclines tended to have CTRCD more often: nine patients (60%) in the CTRCD group and nine patients (22.5%) in non-CTRCD group. Patients who received the BEAM regimen for conditioning also experienced CTRCD more often: five patients (33.3%) in CTRCD group vs. two patients (5%) in the non-CTRCD group. Conclusions: Our study showed that asymptomatic CTRCD was found in 27.3% of the patients 12 months after HSCT. The BEAM chemotherapy conditioning protocol following prior anthracycline use were identified as factors contributing to the development of CTRCD.

Iron chelation therapy failed to improve cardiac dysfunction caused by mitochondrial injury in rats with iron overload cardiomyopathy a 7T Cardiac MR research in vivo

Abstract Purpose To assess the efficacy of iron chelation therapy in improving cardiac function in iron overload cardiomyopathy (IOC) rats by using Cardiac magnetic resonance feature-tracking (CMR-FT). Methods The IOC rat model was induced by intraperitoneal injection of iron dextran over 2 months. Subsequently, 7 rats with IOC were assigned as IOC group to receive continued intraperitoneal injections of saline for an additional 2 months, while another group of 5 rats received intraperitoneal injections of deferoxamine (DFO) for the same duration, forming the IOC+DFO group. Meanwhile, a control group consisting of 7 healthy rats received intraperitoneal injections of saline for the entire duration of 4 months. All rats underwent a 7T CMR scan to assess cardiac function, myocardial iron overload, and myocardial fibrosis via cine, T2 mapping, and late gadolinium enhancement (LGE) scanning, respectively. The cardiac function analysis included left ventricular ejection fraction (LVEF) and left ventricular global longitudinal strain (GLS) using cine images. Following CMR scans, all rats underwent open-chest blood collection to detect serum iron levels, and cardiac gross specimens were then subjected to pathological staining, including hematoxylin and eosin (HE) for cardiomyocytes injury, Prussian blue for iron deposition , and Masson staining for myocardial fibrosis. Furthermore, the ultrastructure of cardiomyocyte was examined using transmission electron microscopy (TEM). Results The T2 value, measured in the septum wall at the mid-layer of the LV, and LVEF, and GLS exhibited a significant decrease in the IOC or IOC+DFO group, compared to the control group, while there were no significant difference observed between the IOC and IOC+DFO group (Fig. 1A, B, C). Myocardial fibrosis was not detected in the LGE images in both IOC and IOC+DFO group. Compared to the control group (37.5±12.5μmol/L) , serum iron levels were significantly elevated in the IOC group (368.6±181.0μmol/L) and in chelation treatment group (106.1±32.2μmol/L). Histological examination with HE staining revealed a normal arrangement of myocardial cells in all rats, without cellular degeneration or necrosis. Prussian blue staining highlighted the presence of iron particles within the myocardial interstitium in the IOC and IOC+DFO groups. Masson staining demonstrated intact myocardial muscle bundles without any evidence of myocardial fibrosis. Transmission electron microscopy (TEM) revealed myocardial mitochondria injury, characterized by ruptured outer membranes, reduced cristae, and vacuolization. Conclusions Following iron chelation therapy, the excessive iron burden in the bloodstream was alleviated. However, myocardial iron overload persisted in IOC rats, with no significant improvement in cardiac function observed. This persistence may be attributed to mitochondrial injury. The findings underscore the importance of monitoring cardiac dysfunction in patients with iron overload.CMR parameters analysis in IOC rats

Metabolic dysfunction-associated steatotic liver disease-associated fibrosis and cardiac dysfunction in patients with type 2 diabetes.

Metabolic dysfunction-associated steatotic liver disease (MASLD), particularly in the presence of liver fibrosis, increases the risk of cardiovascular morbidity and mortality, but the nature of the cardio-hepatic interaction in the context type 2 diabetes mellitus (T2DM) is not fully understood. To evaluate the changes in cardiac morphology and function in patients with T2DM and MASLD-associated liver fibrosis. T2DM patients with MASLD underwent a medical evaluation that included an assessment of lifestyle, anthropometric measurements, vital signs, an extensive laboratory panel, and a standard echocardiography. Liver fibrosis was evaluated using two scores [Fibrosis-4 (FIB4) and Non-alcoholic fatty liver disease-Fibrosis Score (NFS)], and subjects were classified as having advanced fibrosis, no fibrosis, or an indeterminate risk. The correlations between structural and functional cardiac parameters and markers of liver fibrosis were evaluated through bivariate and multiple regression analyses. Statistical significance was set at P < 0.05. Data from 267 T2DM-MASLD subjects with complete assessment was analyzed. Patients with scores indicating advanced fibrosis exhibited higher interventricular septum and left ventricular (LV) posterior wall thickness, atrial diameters, LV end-systolic volume, LV mass index (LVMi), and epicardial adipose tissue thickness (EATT). Their mean ejection fraction (EF) was significantly lower (49.19% ± 5.62% vs 50.87% ± 5.14% vs 52.00% ± 3.25%; P = 0.003), and a smaller proportion had an EF ≥ 50% (49.40% vs 68.90% vs 84.21%; P = 0.0017). Their total and mid LV wall motion score indexes were higher (P < 0.05). Additionally, they had markers of diastolic dysfunction, with a higher E/e' ratio [9.64 ± 4.10 vs 8.44 (2.43-26.33) vs 7.35 ± 2.62; P = 0.026], and over 70% had lateral e' values < 10 cm/second, though without significant differences between groups. In multiple regression analyses, FIB4 correlated with left atrium diameter (LAD; β = 0.044; P < 0.05), and NFS with both LAD (β = 0.039; P < 0.05) and right atrium diameter (β = 0.041; P < 0.01), Moreover, LVMi correlated positively with age and EATT (β = 1.997; P = 0.0008), and negatively with serum sex-hormone binding protein (SHBP) concentrations (β = -0.280; P = 0.004). SHBP also correlated negatively with LAD (β = -0.036; P < 0.05). T2DM patients with markers of MASLD-related liver fibrosis exhibit lower EF and present indicators of diastolic dysfunction and cardiac hypertrophy. Additionally, LVMi and LAD correlated negatively with serum SHBP concentrations.

Myocardial strain analysis by feature tracking cardiac magnetic resonance to identify subclinical cardiac dysfunction in patients with MINOCA

BackgroundTo investigate whether feature tracking cardiac magnetic resonance (FT-CMR) can identify subclinical myocardial dysfunction in patients with myocardial infarction with non-obstructed coronary arteries (MINOCA).MethodsClinical data and CMR images of MINOCA patients (N = 46) and control individuals (N = 12) were compared. The infarct and edema volume to total myocardium, peak global longitudinal strain (GLS), global longitudinal strain rate (GLSR), peak global circumferential strain (GCS), global circumferential strain rate, peak global radial strain, and global radial strain rate were measured. Diagnostic performances of strain parameters for MINOCA were evaluated by logistic regression and receiver operating characteristics analysis.ResultsExcept smoking history, the two groups showed no significant differences in cardiovascular risk factors and traditional heart function. GLS (-14.67 ± 1.96% vs. -19.19 ± 2.05%), GLSR (-0.94 ± 0.16 S− 1 vs. -1.23 ± 0.14 S− 1) and GCS (-17.59 ± 1.81% vs. -19.22 ± 1.76%) were impaired in MINOCA patients compared with the control group. MINOCA patients with normal routine CMR showed abnormalities in GLS (-16.23 ± 1.16%) and GLSR (-1.04 ± 0.16 S− 1). GLS and GLSR were predictive for MINOCA diagnosis (P = 0.002 vs. P = 0.033). GLS correlated strongly with myocardial infarction and edema. The optimal diagnostic threshold for GLS was <-16.9% for MINOCA diagnosis (sensitivity 87.1%, specificity 92.9%); the area under the receiver operating characteristic curve was 0.968.ConclusionsMyocardial strain by FT-CMR may effectively detect early myocardial impairment with MINOCA, especially in patients with normal routine MRI.

Proteomics-Based Machine-Learning Approach for Predicting Cardiac Dysfunction in Patients on Hemodialysis

Proteomics-Based Machine-Learning Approach for Predicting Cardiac Dysfunction in Patients on Hemodialysis

Correlation between mitral annular plane systolic excursion (MAPSE) at different degrees of ejection fraction in patients with diabetes mellitus

Background and aim. Diabetic cardiomyopathy is characterized by myocardial structure and function abnormality in the absence of other cardiovascular risk factors. Early detection of cardiac dysfunction is crucial for timely intervention and improved patient outcomes. The purpose of this study is to determine how mitral annular plane systolic excursion (MAPSE) is a sensitive marker of early cardiac dysfunction in patients with diabetes mellitus by examining the relationship between MAPSE values and different levels of ejection fraction. Methods and material. An analytical cross-sectional study was carried out at Dr. Wahidin Sudirohusodo Hospital in Indonesia's Integrated Heart Center. The sample included 79 patients with ages from 18 to 65 years old and a type 2 diabetes diagnosis. Data collected included age, gender, ejection fraction, and MAPSE. Statistical methods included descriptive analysis and Spearman correlation tests. Results. The study population was predominantly male (71%), with a mean age of 55.5 years for those without EF impairment and 59.5 years for those with impairment. The average impaired EF was 37.69%. MAPSE examination in septal, lateral, and average segments showed significant differences. There is a strong positive association between MAPSE and EF in all study samples. In patients with preserved EF (average EF 58%), MAPSE was 14.4 mm, and in those with reduced EF (average EF 29%), MAPSE was 6.31mm, with significant positive correlations. No significant results were observed in subjects with mid-range EF. Conclusions. This research revealed that mitral annular plane systolic excursion (MAPSE) is significantly associated with ejection fraction (EF) in individuals with diabetes mellitus (DM), mainly when EF is either well-maintained or diminished.

Cardiac Function and Functional Capacity in Patients With Long COVID: A Comparison to Propensity-Matched Community Controls

Cardiac Function and Functional Capacity in Patients With Long COVID: A Comparison to Propensity-Matched Community Controls

SGLT2i and Primary Prevention of CancerTherapy-Related Cardiac Dysfunction in Patients With Diabetes.

SGLT2i and Primary Prevention of CancerTherapy-Related Cardiac Dysfunction in Patients With Diabetes.

The clinical relevance of the new criteria for cirrhotic cardiomyopathy and future directions.

Cardiac dysfunction in patients with liver disease has been recognized since the 1950s. Initially attributed to shared risk factors, it is now evident that cardiac dysfunction in patients with cirrhosis can occur in the absence of known cardiac, i.e., coronary artery and valvular heart disease, and across all etiologies for cirrhosis. In 1996 this myocardial dysfunction was termed cirrhotic cardiomyopathy (CCM). The pathophysiologic mechanisms underlying CCM include impaired beta-adrenergic membrane function and circulating proinflammatory and cardiotoxic substances. In 2005, the first diagnostic criteria for CCM were introduced enabling greater sensitivity and accuracy of diagnosis. Since 2005, advancements in echocardiographic methods and better understanding of the pathophysiology of cardiac dysfunction in patients with cirrhosis necessitated revision of CCM criteria. Changes in CCM criteria included removal of blunted contractile or heart rate response on stress testing and addition of global longitudinal systolic strain. Refinement of criteria for diastolic dysfunction were also incorporated into the new diagnostic approach. Since 2020, the prevalence of the disorder and clinical considerations for pre-transplant, peritransplant, and post-transplant patients with cirrhosis have been further evaluated and CCM was found to adversely impact clinical outcomes during all three phases of care. Future research considerations should address the timing of universal echocardiographic screening for patients with cirrhosis, utility of biomarkers in aiding CCM diagnosis, impact of CCM on right heart function, and role of anti-remodeling agents post-liver transplant (post-LT).

Comparison of predictive value of cardiac troponins and creatine phosphokinase MB fraction for in-hospital mortality and cardiac dysfunction in patients with AMI after thrombolysis

Comparison of predictive value of cardiac troponins and creatine phosphokinase MB fraction for in-hospital mortality and cardiac dysfunction in patients with AMI after thrombolysis

Detection of Subclinical Cardiac Dysfunction in Patients With Sickle Cell Disease Using Speckle-Tracking Echocardiography

Detection of Subclinical Cardiac Dysfunction in Patients With Sickle Cell Disease Using Speckle-Tracking Echocardiography

Imatinib Mesylate Causes Potential Cardiac Dysfunction in Patients With Chronic Myeloid Leukemia: the Results of a Case-control Study.

Unlike second-generation tyrosine kinase inhibitors, effects of imatinib on the cardiovascular (CV) system are debatable. The current case-control study aimed to evaluate the CV effects of imatinib in patients with chronic myeloid leukemia (CML) using non-invasive 2D-echocardiography testing. Patients with CML ≥ 13 years attending the adult haematology clinic of a tertiary care hospital in north India were prospectively enrolled over 1.5 years. The study population (n = 110) consisted of 35 newly diagnosed patients (treatment-naïve group) and 75 patients under imatinib therapy ≥ 1 year (treated group). All the eligible patients were subjected to 2D-echocardiography to calculate pulmonary artery systolic pressure (PASP), left ventricular ejection fraction (LVEF) and deceleration time (DT). These parameters were compared between the two groups. P-value < 0.05 was considered statistically significant. The median age of study population was 40 years (range, 13-73) and M:F ratio was 1.14:1. Both the groups had similar demographics at the diagnosis including CV risk factors. The median PASP of the treated group was 2 mm Hg higher than the treatment-naïve group (25 vs 23 mm Hg, p-value = 0.919). The median LVEF of the treated group was 3.2% lower than the treatment-naïve group (58.5% vs 61.72%, p-value = 0.577). The median DT of the treated group was 7 ms shorter than treatment-naïve group (211 vs 204 ms, p-value = 0.411). Imatinib causes potential cardiac dysfunction in patients with CML. Large scale prospective follow-up trials in the same cohort of patients are needed to validate the findings of our study.