Myocardial Abnormalities Research Articles

Myocardial Disorders in BDNF-Deficient Rats: Limited Recovery Post-Moderate Endurance Training.

The study aimed to determine whether heterozygous BDNF-deficient (BDNF-knockout, SD-BDNF) rats exhibit pathological changes in the myocardium and to assess whether a 5-week moderate-intensity endurance training program can reverse adverse changes in the heart muscle. Experiments were conducted on four groups of rats: control wild-type, control BDNF knockout, trained wild-type and trained BDNF knockout. Knockout rats were selected due to the presence of symptoms resembling metabolic syndrome in serum and liver while 5-week moderate endurance training was used as an intervention targeted at restoring heart function. Measurements of BDNF/Trk-B concentrations and molecules levels and activities, such as cardiac specific enzymes like creatine kinase and creatine kinase myocardial band, lipids as total cholesterol, low-density lipoprotein and triglycerides, metabolic enzymes including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase and lactate dehydrogenase and interleukin-1 were carried out in myocardium homogenates. In BDNF-deficient rats, the myocardium showed significantly reduced lipid concentrations, decreased metabolic and cardiac enzyme activity, and elevated Trk-B levels, all of which are indicative of myocardial ischemia or hypoxia. These changes in critical biomarkers were consistent with those earlier observed in the livers of BDNF-deficient rats, suggesting a link between the liver and cardiac function. Moderate endurance training led to an increase in creatine kinase activity in the myocardium of trained rats, suggesting increased production and utilization of energy required for myocardial contraction in trained wild-type and knockout populations of rats. BDNF-deficient rats exhibited numerous myocardial abnormalities, most of which were not reversible after moderate-intensity endurance training. These findings provide a basis for a deeper understanding of the mechanisms underlying myocardial disorders in BDNF-deficient rats, which appear to be a suitable model for studying various aspects of metabolic disorders.

Clinical guideline for non-invasive imaging techniques in diagnosing adult cardiomyopathies (2024 edition)

Cardiomyopathies encompass a spectrum of disorders characterized by alterations in cardiac structure, function, histology, and the conduction system due to myocardial cell injury, with significant variability in clinical presentation and prognosis. Despite overlapping morphological features among different types of cardiomyopathies, phenotypic similarities limit the precision of diagnosis and consequently affect the development of therapeutic strategies and prognosis assessment. Diagnosis begins with the screening of myocardial morphology and function abnormalities, primarily relying on multimodal non-invasive imaging techniques such as echocardiography, CT scans, and cardiac magnetic resonance imaging. These techniques comprehensively summarize the structural, functional, and tissue characteristics of various cardiomyopathies, highlighting differences among them. In view of the unique needs and current situation in this field in China, an expert group has jointly developed the"Clinical guideline for non-invasive imaging techniques in diagnosing adult cardiomyopathies (2024 edition)."These guidelines integrate the latest evidence, and systematically introduce the diagnosis and monitoring of cardiomyopathy, the application of non-invasive imaging techniques, and the analysis of features of cardiomyopathies, thereby to enhance the precise diagnosis of cardiomyopathy and aid in offering information for therapeutic decision-making, aiming to provide reasonable recommendations for clinicians in China.

A Highly Sensitive Surface Electrode for Electrophysiological Monitoring

AbstractSurface electrodes monitoring various electrophysiological activities with high sensitivity are crucial for studying electrical phenomena in living organisms. However, the sensitivity of current surface electrodes is limited due to electron transmission losses and signal attenuation at the electrode‐skin interface. Here, a bicontinuous liquid metal/polymer film electrode is developed, in which up to 92 wt.% of liquid metal is stably immobilized within a 3D continuous polymer network via electrostatic interactions. This electrode facilitates fast electron transport, enhances skin adhesion through hydrogen bonding, and ensures conformal contact due to its flexibility. As a result, the electrode achieves a sensitivity of 20 µV N−1, representing an improvement of 400% over the highest performance reported to date. This leap in sensitivity enables the high‐resolution monitoring of electrophysiological signals, allowing for earlier and more accurate identification of myocardial infarction abnormalities. Moreover, this high‐sensitivity electrode has the potential to develop an intelligent sensory system for material recognition and provide real‐time warnings in hazardous situations for individuals with tactile impairments.

Abstract 4124677: Left ventricular function and myocardial longitudinal strain analysis in patients with Chagas disease: case series and systematic literature review.

Introduction: Chagas disease is a significant cause of tropical disease-related mortality. It presents in acute, indeterminate, and chronic phases, with chronic cardiomyopathy being the most severe form, leading to heart failure, arrhythmias, and sudden cardiac death. Conventional echocardiography often fails to detect early subclinical dysfunction, whereas Global longitudinal strain (GLS) may provide earlier detection of myocardial strain abnormalities. Left ventricular dysfunction is an independent predictor of mortality and GLS is an emerging modality that may aid early detection of cardiac involvement. Objective: This study aims to compare left ventricular function using multiple echocardiographic parameters between patients with indeterminate and chronic forms of Chagas disease and to perform a systematic literature review. Methods: The observational study involved 11 patients (mean age 76.36 years) from a tertiary hospital in Brazil, classified as indeterminate (45%) or chronic (55%). Serological confirmation and detailed echocardiographic evaluations, including GLS, were performed. A systematic literature review was also conducted on GLS in Chagas cardiomyopathy. Results: Patients with chronic Chagas disease showed significantly lower LVEF and GLS compared to those with the indeterminate form. Segmental strain analysis revealed consistent contractility reductions across specific ventricular segments in both groups. Discussion: Chagas cardiomyopathy often leads to dilated cardiomyopathy with significant arrhythmias and heart failure. GLS can detect early myocardial changes even before a significant drop in LVEF, indicating its potential for early diagnosis and better management of Chagas cardiomyopathy. Literature review supports the use of GLS for detecting early cardiac involvement and predicting adverse outcomes. Conclusion: Incorporating GLS with conventional echocardiography offers enhanced early detection of myocardial changes in Chagas disease. While promising, further research is needed to establish the clinical significance and impact of these techniques in routine practice.

Abstract 4119187: Association of CMR derived Global Longitudinal Strain with adverse Outcomes in Arrhythmogenic Cardiomyopathy.

Background: Arrhythmogenic cardiomyopathy (ACM) is associated with high risk of ventricular arrhythmias (VA) and heart failure (HF). Different predictive models and diagnostic criteria include parameters related to myocardial structural abnormalities and right ventricular (RV) ejection fraction (EF). Nevertheless, the value of global longitudinal strain (GLS) ascertained from cardiac magnetic resonance (CMR) for risk-stratification in the context of ACM is unknown. Aim: We aim to study the association of low CMR-derived GLS with adverse outcomes in ACM patients. Methods: This was a retrospective cohort study of ACM patients seen at a single quaternary center. ACM diagnosis followed the modified 2010 ARVC modified task force criteria. Primary outcome was a composite of life-threatening VAs, heart transplant or HF hospitalization during follow up. We excluded patients who suffered events prior to diagnosis, and those with missing or inadequate CMR protocol. Imaging parameters were acquired by CMR including EF, GLS, and late gadolinium enhancement (LGE). Results: A total of 82 patients with suspected ACM were included, with a median age of 40 years, and 43 (52.4%) were females. Most common reason of initial visit was family history of genetic cardiomyopathy in 46 (56%), while 16 (20%) patients visited our clinic due to history of syncope. Out of 60 patients who had genetic testing, 21 (35%) had mutations of DSP gene. Left ventricular involvement (non-ischemic LV-LGE by CMR) was present in 42 (56.8%) out of 74 patients who had CMR with gadolinium. Median LVEF was 62% (56, 66), and RVEF of 53% (48, 59), both by CMR. Median LVGLS was -17.01% (-14.71, -18.43), while median RVGLS was -20.5% (-18.3, -24.4). A total of 15 (18%) patients suffered the composite endpoint during an average follow up period of 8 years. Patients who suffered the composite endpoint had significantly lower mean LVGLS (-15.04% vs -16.70%, p= 0.048), and lower average RVGLS (-18.45% vs -21.33%, p=0.035) compared to patients free from the adverse outcome. Meanwhile there was no significant difference in LVEF (60.13% vs 61.18%, p=0.67), nor in RVEF (49.13% vs 54.01%, p=0.065) between the two groups. Conclusion: Lower GLS was significantly associated with VAs and HF hospitalizations in our patient population. CMR derived GLS can be used as an important prognostic parameter of adverse outcomes in patients with suspected ACM. Especially in those with LV involvement and high genetic predisposition as our cohort.

Exploring cardiovascular involvement in IgG4-related disease: a case series approach with cardiovascular magnetic resonance

BackgroundIgG4-related disease (IgG4-RD) is a relapsing–remitting, fibroinflammatory, multisystem disorder. Cardiovascular involvement from IgG4-RD has not been systematically characterised. In this study, we sought to evaluate consecutive patients with IgG4-RD using...

Concealed cardiomyopathy as an emerging cause of sudden cardiac arrest and sudden cardiac death.

The inherited cardiomyopathies exhibit a broad spectrum of disease, with some patients remaining asymptomatic throughout life, while, for others, the first symptom of disease is sudden cardiac death at a young age. The risk of malignant ventricular arrhythmia in these conditions has traditionally been linked to the degree of structural myocardial abnormalities and functional impairment. However, recent advances in genetic testing and knowledge of the genetic basis of the diseases have led to the identification of concealed cardiomyopathy, in which sudden cardiac arrest or sudden cardiac death occurs in the absence of observable clinical features of cardiomyopathy, with a diagnosis being made only after the identification of a causative genetic variant. Increased awareness of concealed cardiomyopathy, a better understanding of mechanisms of arrhythmia and identification of risk modulators will be vital to improve care for families with concealed cardiomyopathy.

Coordinate-Independent 3-D Ultrasound Principal Stretch and Direction Imaging.

In clinical ultrasound, current 2-D strain imaging faces challenges in quantifying three orthogonal normal strain components. This requires separate image acquisitions based on the pixel-dependent cardiac coordinate system, leading to additional computations and estimation discrepancies due to probe orientation. Most systems lack shear strain information, as displaying all components is challenging to interpret. This paper presents a 3-D high-spatial-resolution, coordinate-independent strain imaging approach based on principal stretch and axis estimation. All strain components are transformed into three principal stretches along three normal principal axes, enabling direct visualization of the primary deformation. We devised an efficient 3-D speckle tracking method with tilt filtering, incorporating randomized searching in a two-pass tracking framework and rotating the phase of the 3-D correlation function for robust filtering. The proposed speckle tracking approach significantly improves estimates of displacement gradients related to the axial displacement component. Non-axial displacement gradient estimates are enhanced using a correlation-weighted least-squares method constrained by tissue incompressibility. Simulated and in vivo canine cardiac datasets were evaluated to estimate Lagrangian strains from end-diastole to end-systole. The proposed speckle tracking method improves displacement estimation by a factor of 4.3 to 10.5 over conventional 1-pass processing. Maximum principal axis/direction imaging enables better detection of local disease regions than conventional strain imaging. Coordinate-independent tracking can identify myocardial abnormalities with high accuracy. This study offers enhanced accuracy and robustness in strain imaging compared to current methods.

Targeting DUSP26 to drive cardiac mitochondrial dynamics via FAK-ERK signaling in diabetic cardiomyopathy

Diabetic cardiomyopathy (DCM) is a severe cardiac complication of diabetes mellitus, characterized by structural and functional myocardial abnormalities. The molecular mechanisms underlying DCM, particularly the role of dual-specificity phosphatase 26 (DUSP26), remain insufficiently understood. Our study reveals that DUSP26 expression is markedly downregulated in the cardiomyocytes of diabetic db/db mice and under glucolipotoxic stress. Overexpression of DUSP26 in db/db mice significantly improved cardiac function, as demonstrated by enhanced left ventricular ejection fraction and fractional shortening, alongside reduced myocardial fibrosis and hypertrophy. Mitochondrial analysis indicated that DUSP26 overexpression led to increased ATP production, enhanced mitochondrial fusion, and improved structural integrity. In addition, lipid accumulation was reduced, reflecting enhanced metabolic function. We also discovered that DUSP26 is necessary for regulating the focal adhesion kinase (FAK)-extracellular signal-regulated kinase (ERK) pathway, with pharmacological activation of FAK partially offsetting the benefits of DUSP26 overexpression in rescue experiments. These findings underscore the pivotal role of DUSP26 as a potential therapeutic target, highlighting the importance of developing targeted molecular interventions to address diabetic cardiac complications.

Activation of protein kinase B rescues against thapsigargin-elicited cardiac dysfunction through regulation of NADPH oxidase and ferroptosis

Endoplasmic reticulum (ER) stress is a known contributor to cardiac remodeling and contractile dysfunction. Although NADPH oxidase has been implicated in ER stress-induced organ damage, its specific role in myocardial complications resulting from ER stress remains unclear. This study aimed to investigate the possible involvement of NADPH oxidase in ER stress-induced myocardial abnormalities and to evaluate the impact of Akt constitutive activation on these myocardial defects. Mice with cardiac-specific overexpression of active mutant of Akt (Myr-Akt) and their wild-type (WT) littermates were treated with ER stress instigator thapsigargin (1 mg/kg, i. p. 72 hrs) before evaluating myocardial morphology and function. Our results noted that thapsigargin significantly impaired echocardiographic parameters and cell shortening indices, including elevated LVESD, decreased ejection fraction, fractional shortening, peak shortening, electrically-stimulated intracellular Ca2+ release, and cardiomyocyte survival. These functional deteriorations were accompanied by upregulation of NADPH oxidase, O2− production, mitochondrial damage, carbonyl formation, lipid peroxidation, apoptosis, and interstitial fibrosis, with unchanged myocardial size. Constitutive Akt hyperactivation did not generate any response on myocardial morphology and function, although it greatly suppressed or nullified thapsigargin-induced myocardial remodeling and dysfunction. Thapsigargin also triggered dephosphorylation of Akt and its downstream signal GSK3β, along with development of ferroptosis, all of which were nullified by Akt hyperactivation. In vitro studies further revealed that thapsigargin provoked cardiomyocyte mechanical anomalies and lipid peroxidation, similar to in vivo results. These effects were reverted by inhibitors of NADPH oxidase and ferroptosis (apocynin and LIP1). Collectively, our data denote an important protective role for Akt hyperactivation in thapsigargin-evoked myocardial anomalies, likely through NADPH oxidase-mediated regulation of ferroptosis.

Implications of a new clinical classification of acute myocardial infarction

Abstract Background The Universal Definition of Myocardial Infarction has provided standardisation of the diagnostic criteria for myocardial infarction. However, there remain significant challenges in adopting some of the current recommendations in practice. The diagnostic criteria for type 2 myocardial infarction identify a heterogenous group of patients with variable clinical outcomes and no clear treatment implications to date. Purpose To determine the implications of a new clinical classification for myocardial infarction with more objective diagnostic criteria using cardiac imaging.(1) Methods In a prospective cohort study,(2) patients with type 2 myocardial infarction underwent coronary angiography and cardiac magnetic resonance imaging or echocardiography. The new classification was applied to identify (a) spontaneous myocardial infarction due to acute coronary pathology, (b) secondary myocardial infarction precipitated by acute illness in the presence of obstructive coronary artery disease, a new regional wall motion abnormality or infarct pattern scarring, and (c) no myocardial infarction in the absence of obstructive disease or new myocardial abnormality. The diagnostic outcome was the proportion of patients with type 2 myocardial infarction reclassified as having spontaneous, secondary or no myocardial infarction by the new clinical classification. The prognostic outcome was a composite of all-cause death, any recurrent myocardial infarction, or heart failure hospitalisation during follow up. Results In 100 patients (65 years, 43% women) with type 2 myocardial infarction, the new classification identified 25 and 31 patients with spontaneous and secondary myocardial infarction, respectively, and 44 without myocardial infarction (Figure 1). Compared to patients without myocardial infarction, those with secondary myocardial infarction were older, had more risk factors, and higher troponin concentrations (P<0.05 for all). In patients who underwent cardiac magnetic resonance imaging, there was evidence of infarct-pattern late gadolinium enhancement in 95% (19/20) and 60% (15/25) of patients with spontaneous and secondary myocardial infarction, respectively, which was more likely to be transmural in the former. In patients reclassified as secondary myocardial infarction, just 45% and 58% were established on aspirin or a lipid lowering therapy. During a median follow up of 4.4 years, death, myocardial infarction or heart failure hospitalization was more common in secondary myocardial infarction compared to those without myocardial infarction (55% [17/31] versus 16% [7/44], P<0.001; Figure 2). Conclusions A new clinical classification of myocardial infarction informed by cardiac imaging would reduce the diagnosis of myocardial infarction in acute illness and identify those patients at highest risk who are most likely to benefit from treatment.Figure 1:Alluvial plotFigure 2:Kaplan Meier curve

Prevalence of cardiomyopathies and myocardial scar in patients with non-complicated premature ventricular beats: a CMR study

Abstract Introduction Frequent or symptomatic premature ventricular beats (PVBs) in subjects with no personal or family history of cardiac disease or sudden death is a recurrent motive for cardiac magnetic resonance (CMR) prescriptions. This represents a significant burden on healthcare services, given the low availability of CMR technique. If CMR is a recommended imaging modality in patients with history of cardiac arrest due to ventricular arrhythmia, sustained ventricular arrhythmias or when first-line tests are abnormal, its diagnostic value in this specific setting has not been evaluated. Purpose To determine the prevalence of significant CMR abnormalities (myocardial fibrosis, arrhythmogenic cardiomyopathies) in patients with no personal nor family history of cardiac disease and non-complicated PVBs. Methods Between September 2010 and July 2021, 416 healthy adults with no personal nor family cardiac disease history underwent CMR at our institution to explore non complicated PVBs, and were retrospectively included (Figure 1). Right and left ventricular (RV/LV) function and dimensions were systematically evaluated on CMR, as the presence of myocardial late gadolinium enhancement (LGE). Criteria for cardiomyopathies (hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), ARVD), the presence and location of myocardial fibrosis were looked after. Results A total of 605 patients were referred for CMR to explore frequent PVBs, representing 14% of all tests performed during this period. Among them, 12 patients (3%) presented significant myocardial abnormalities possibly related to PVBs: 2 patients had sequelae of myocardial infarction and 3 of myocarditis, 1 patient had criteria of HCM and 1 of ARVD, finally 5 presented non-specific myocardial fibrosis (septal mid-wall LGE). In addition, after a mean follow-up of 5 years, there was no death in patients with abnormal CMR, and only 2 patients underwent transcatheter ablation for focal non complicated but symptomatic PVBs. There was no hospitalization for heart failure. Conclusion In patients with non-complicated PVBs and no history of cardiac disease, the rate of cardiomyopathy pattern or myocardial scar on CMR is very low (3%). In this specific population, events were very rare: frequent isolated PVBs, even when associated with myocardial abnormalities, were a benign condition in our study. Given the high volume of patients referred for this indication in daily practice (14% of total CMRs in our center), the limited availability and high costs of CMR, and the difficulties of CMR sequences acquisition in the context of frequent PVBs (possibly leading to misdiagnosis), these data suggest that we should refine the selection of patients undergoing CMR for PVBs exploration.

Cardiac biomarkers can detect and track subclinical HIV-associated myocardial disease in newly diagnosed people living with HIV

Abstract Background Cardiovascular disease (CVD) in people living with HIV (PLWH) remains poorly understood, and the profile of disease differs between high-income and low- and middle-income settings[1]. Subclinical cardiovascular abnormalities may be present at the time of HIV diagnosis and serve as potential substrate for future CVD[2]. Biochemical markers are fundamental in cardiac evaluation, and various novel assays have recently been discovered. Purpose To assess the presence and evolution of subclinical myocardial disease, we prospectively assessed the hearts of newly diagnosed PLWH and matched, HIV-uninfected controls using cardiac biomarkers and correlated our findings with cardiovascular magnetic resonance imaging (CMR). Methods Newly diagnosed, antiretroviral treatment (ART) naïve PLWH were recruited along with HIV uninfected, age- and sex-matched controls in the Western Cape Province of South Africa. All participants underwent measurement of high-sensitivity cardiac troponin T (hs-cTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), soluble ST2 (sST2), Galectin-3, and a CMR study with multiparametric mapping. The HIV group started ART and was re-evaluated 9 months later. The cardiac biomarkers and their correlation with CMR parameters were evaluated in, and between groups. Results Compared with controls (n=22), hs-cTnT (4.0 ng/l vs 5.1 ng/l; p=0.004) , NT-proBNP (23.2 ng/l vs 40.8 ng/l; p=0.02), and Galectin-3 (6.8 ng/ml vs 9.0 ng/ml; p=0.002) were all significantly higher in the ART naïve group (n=73). After 9 months of ART, hs-cTnT (5.1 ng/l vs 4.3 ng/l; p=0.02) and NT-proBNP (40.8 ng/l vs 28.5 ng/l; p=0.03) both decreased significantly, and a trend of decrease was seen in sST2 (16.5 ng/ml vs 14.8 ng/l; p=0.08). Galectin-3 did not demonstrate decrease over time (9.0 ng/ml vs 8.8 ng/ml; p=0.6). The cardiac biomarkers that showed the best correlation with CMR measurements native T1, T2, and ECV, were NT-proBNP (rs≥0.4, p<0.001) and Galectin-3 (rs≥0.3, p<0.01). Conclusion Our cardiac biomarker data supports the presence of subclinical myocardial injury, remodelling, and fibrosis at HIV diagnosis and ART had a positive influence on these blood markers. It remains unclear if the underlying pathological processes were fully addressed by ART. The elevation of Galectin-3 despite ART may be indicative of ongoing cardiac remodelling that may incur future risk of CVD, and necessitates further study. The ability of cardiac biomarkers to detect and track tissue abnormalities diagnosed with CMR, showed promise. With additional research, this could lead to improvements in screening and monitoring myocardial abnormalities, even in CMR-limited settings.

Cardiomyopathies: The Role of Non-Coding RNAs

Cardiomyopathies are the structural and functional disorders of the myocardium. Etiopathogenesis is complex and involves an interplay of genetic, environmental, and lifestyle factors eventually leading to myocardial abnormalities. It is known that non-coding (Nc) RNAs, including micro (mi)-RNAs and long non-coding (lnc) RNAs, play a crucial role in regulating gene expression. Several studies have explored the role of miRNAs in the development of various pathologies, including heart diseases. In this review, we analyzed various patterns of ncRNAs expressed in the most common cardiomyopathies: dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic cardiomyopathy. Understanding the role of different ncRNAs implicated in cardiomyopathic processes may contribute to the identification of potential therapeutic targets and novel risk stratification models based on gene expression. The analysis of ncRNAs may also be helpful to unveil the molecular mechanisms subtended to these diseases.

Distinguishing hypertensive cardiomyopathy from cardiac amyloidosis in hypertensive patients with heart failure: a CMR study with histological confirmation

PurposeDifferentiation of the cause of left ventricular hypertrophy (LVH) is challenging in cases with co-existing hypertension. CMR offers assessment of diffuse myocardial abnormalities via T1 mapping with extracellular volume fraction (ECV) and macroscopic fibrosis via late gadolinium enhancement imaging (LGE). The goal of the study was to understand if CMR parameters can differentiate hypertensive cardiomyopathy (HC) from cardiac amyloidosis (CA) in patients with hypertension and heart failure, using endomyocardial biopsy (EMB) as the gold standard.MethodsWe retrospectively analyzed patients with hypertension, LVH, and heart failure undergoing EMB due to uncertain diagnosis. CMR parameters including cine, LGE characteristics, T1 mapping, and ECV were analyzed.ResultsA total of 34 patients were included (mean age 66.5 ± 10.7 years, 79.4% male). The final EMB-based diagnosis was HC (10, 29%), light chain (AL) CA (7, 21%), and transthyretin (ATTR) CA (17, 50%). There was a significant difference in subendocardial LGE (p = 0.03) and number of AHA segments with subendocardial LGE (p = 0.005). The subendocardial LGE pattern was most common in AL-CA (85.7%) and African American with HC (80%). ECV elevation (≥ 29%) was present in all patients with CA (AL-CA: 57.6 ± 5.2%, ATTR-CA: 59.1 ± 15.3%) and HC (37.3 ± 4.5%).ConclusionsExtensive subendocardial LGE pattern is not pathognomonic for CA but might also be present in African American patients with longstanding or poorly controlled HTN. The ECV elevation in HC with HF might be more significant than previously reported with an overlap of ECV values in HC and CA, particularly in younger African American patients.Graphical Abbreviations: CMR, cardiovascular magnetic resonance imaging; LVH, left ventricular hypertrophy; HTN, hypertension; HF, heart failure; ECV, extracellular volume fraction; HC, hypertensive heart disease; CA, cardiac amyloidosis; AA, African American; LGE, late gadolinium enhancement

Cardiovascular toxicity of anaplastic lymphoma kinase inhibitors for patients with non-small cell lung cancer: a network meta-analysis.

Aim: We conducted network meta-analysis to assess cardiovascular toxicity of anaplastic lymphoma kinase-tyrosine kinase inhibitors (ALK-TKIs).Materials & methods: Eleven articles involving 2855 patients and six interventions including crizotinib, alectinib, ceritinib, lorlatinib, brigatinib and chemotherapy were analyzed.Results: No significant difference was observed in overall cardiovascular risk among ALK-TKIs. Subgroup analysis showed that for cardiac toxicity, crizotinib and alectinib were more likely to cause myocardial rhythm abnormalities. Crizotinib and ceritinib had a higher risk of Q-T prolongation than chemotherapy. For vascular toxicity, crizotinib and ceritinib had a higher risk of thrombotic events than brigatinib. Crizotinib and lorlatinib were more likely to cause blood pressure abnormalities.Conclusion: Clinicians should carefully monitoring cardiovascular events when ALK-TKIs used in NSCLCs patients with baseline cardiovascular diseases.

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.

Sickle Cell Disease Revealed by Simultaneous Occurrence of Acute Coronary Syndrome and Pulmonary Embolism: A Case Report

The simultaneous occurrence of acute coronary syndrome (ACS) and pulmonary embolism (PE) in patients with sickle cell disease (SCD) presents notable diagnostic and management challenges. This case report describes a 25-year-old woman with SCD who, after an uncomplicated laparoscopic cholecystectomy, developed acute retrosternal chest pain, severe dyspnea, and tachycardia. Diagnostic workup included several key methods: thoracic CT angiography was performed, revealing massive bilateral pulmonary embolism and a pulmonary infarct. Echocardiography demonstrated myocardial abnormalities, such as wall motion defects and a mildly reduced ejection fraction. Electrocardiography showed ST-segment depression and T-wave inversions in the anteroseptal leads. To confirm the presence of coronary artery disease, coronary angiography identified significant thrombotic stenosis in the proximal left anterior descending artery. Sickle cell disease was confirmed through a positive sickle cell test, which identified the characteristic hemoglobin S. Despite aggressive treatment, the patient’s condition rapidly deteriorated, leading to death within 24 hours. This case underscores the critical role of a comprehensive diagnostic approach, including specific tests for SCD, in managing severe cardiovascular complications and highlights the need for tailored treatment strategies to improve patient outcomes.

Potential cardioprotective effect of Vitamin D and sodium-glucose transport protein 2 inhibitor in improving cardiac hypertrophy and fibrosis in Type 2 diabetic rats

Background: Diabetes mellitus (DM) is a major risk factor for cardiovascular diseases. The progression of myocardial abnormalities due to DM occurs slowly but is progressive and asymptomatic. Sodium-glucose transport protein 2 inhibitors (SGLT-2i) and Vitamin D have potential cardioprotective properties that inhibit cardiomyocyte fibrosis and hypertrophy, which are early structural changes that occur in the heart of DM patients. Aim: The study aimed to determine the potential protective effects of SGLT-2i and Vitamin D administration on cardiac hypertrophy and fibrosis in Type 2 diabetic rats.Methods: This is an experimental study with a post-test-only control group design. Thirty-two male Wistar rats were given a high-fat/high-glucose (HF/HG) diet. After 3 weeks, rats were given an injection of streptozotocin (STZ 35 mg/kg) to induce pancreatic damage. The diabetic rats were then divided into four groups (n = 8 per group): untreated diabetic group (HF/HG/STZ), the diabetic group treated with empagliflozin (EMPA) 10 mg/kg body weight (BW) (HF/HG/ STZ+EMPA), the diabetic group treated with Vitamin D 225 IU/day (HF/HG/STZ+VitD), and the diabetic group treated with a combination of EMPA 10 mg/kg BW and Vitamin D 225 IU/day (HF/ HG/STZ+EMPA+VitD). Treatments were given by oral gavage for 8 weeks. Left ventricular biopsy was performed at week 13 to examine collagen deposition, the cardiomyocyte cross-sectional area (CSA), and the mRNA expression of β-myosin heavy chain (β-MHC) and transforming growth factor-β (TGF-β). All the obtained data were analyzed statistically. Results: The administration of EMPA, Vitamin D, and combination therapy of EMPA and Vitamin D reduced the mRNA expression of β-MHC and TGF-β in diabetic rats compared to the untreated diabetic group. The administration of EMPA, Vitamin D, and combination therapy also resulted in a decrease in both the cardiomyocyte CSA and collagen deposition. Compared to monotherapy, combination therapy led to significantly better parameter reduction. Conclusion: Administration of EMPA, Vitamin D, and combination therapy improved cardiac hypertrophy and fibrosis in type 2 diabetic rats.Relevance for Patients: The combination of Vitamin D and SGLT-2i may be proposed as a cardioprotective strategy and preventive measure to reduce the incidence of cardiovascular disease in patients with Type 2 DM.

Clinical Applications of Cardiac Magnetic Resonance Parametric Mapping.

Cardiovascular magnetic resonance (CMR) imaging is widely regarded as the gold-standard technique for myocardial tissue characterization, allowing for the detection of structural abnormalities such as myocardial fatty replacement, myocardial edema, myocardial necrosis, and/or fibrosis. Historically, the identification of abnormal myocardial regions relied on variations in tissue signal intensity, often necessitating the use of exogenous contrast agents. However, over the past two decades, innovative parametric mapping techniques have emerged, enabling the direct quantitative assessment of tissue magnetic resonance (MR) properties on a voxel-by-voxel basis. These mapping techniques offer significant advantages by providing comprehensive and precise information that can be translated into color-coded maps, facilitating the identification of subtle or diffuse myocardial abnormalities. As unlikely conventional methods, these techniques do not require a substantial amount of structurally altered tissue to be visually identifiable as an area of abnormal signal intensity, eliminating the reliance on contrast agents. Moreover, these parametric mapping techniques, such as T1, T2, and T2* mapping, have transitioned from being primarily research tools to becoming valuable assets in the clinical diagnosis and risk stratification of various cardiac disorders. In this review, we aim to elucidate the underlying physical principles of CMR parametric mapping, explore its current clinical applications, address potential pitfalls, and outline future directions for research and development in this field.