Impaired Myocardial Function Research Articles

M6A-mediated upregulation of miRNA-193a aggravates cardiomyocyte apoptosis and inflammatory response in sepsis-induced cardiomyopathy via the METTL3/ miRNA-193a/BCL2L2 pathway

The impact of N6-methyladenosine (m6A) modification on pri-miRNA in sepsis-induced cardiomyopathy (SICM), and its underlying regulatory mechanism, have not been fully elucidated. We successfully constructed a SICM mice model through cecal ligation and puncture (CLP). In vitro, a lipopolysaccharide (LPS)-induced HL-1 cells model was also established. The results showed that sepsis frequently resulted in excessive inflammatory response concomitant with impaired myocardial function in mice exposed to CLP, as indicated by decreases in ejection fraction (EF), fraction shortening (FS), and left ventricular end diastolic diameters (LVDd). miR-193a was enriched in CLP mice heart and in LPS-treated HL-1 cells, while overexpression of miR-193a significantly increased the expression levels of cytokines. Sepsis-induced enrichment of miR-193a significantly inhibited cardiomyocytes proliferation and enhanced apoptosis, while this was reversed by miR-193a knockdown. Furthermore, under our experimental conditions, enrichment of miR-193a in SICM could be considered excessively maturated on pri-miR-193a by enhanced m6A modification. This modification was catalyzed by sepsis-induced overexpression of methyltransferase-like 3 (METTL3). Moreover, mature miRNA-193a bound to a predictive sequence within 3′UTRs of a downstream target, BCL2L2, which was further validated by the observation that the BCL2L2-3′UTR mutant failed to decrease luciferase activity when co-transfected with miRNA-193a. The interaction between miRNA-193a and BCL2L2 resulted in BCL2L2 downregulation, subsequently activating the caspase-3 apoptotic pathway. In conclusion, sepsis-induced miR-193a enrichment via m6A modification plays an essential regulatory role in cardiomyocyte apoptosis and inflammatory response in SICM. The detrimental axis of METTL3/m6A/miR-193a/BCL2L2 is implicated in the development of SICM.

Cardiac involvement in polymyositis and dermatomyositis: diagnostic approaches.

Polymyositis (PM) and dermatomyositis (DM) are rare idiopathic inflammatory myopathies (IIM). Myocardial involvement in patients with IIM is an unfavorable prognostic factor and one of the most common cause of mortality in this group of patients. The purpose of this review is to present current knowledge on cardiovascular manifestations observed in IIM. Data published in English until December 2021 were selected. Clinical symptoms suggesting cardiac involvement are non-specific and require a differential diagnosis in accordance with cardiological guidelines. Troponin I is specific to cardiac injury and should be preferred to other markers to evaluate the myocardium in IIM. Abnormalities in electrocardiography are common in IIM, especially non-specific changes of the ST-T segment. In standard echocardiography left ventricular diastolic dysfunction is reported frequently. New diagnostic technologies can reveal clinically silent myocardial abnormalities. However, the prognostic value of subclinical impairment of myocardial function require further studies.

Effect of Sacubitril/Valsartan and enalapril on left ventricular function in patients with hematologic malignancies after bone marrow transplantation

Abstract Funding Acknowledgements Type of funding sources: None. Background and Aims Chemotherapy is known for its potential adverse effects on myocardium. Optimal medical treatment for heart failure may reverse myocardial dysfunction in the early stages of toxicity development. We hypothesized that early initiation of treatment with sacubitril/valsartan (s/v) or enalapril (ena) might prevent cardiotoxicity. Patients and methods 90 patients (mean age 45.7 ± 14,1 years old, 52 male) with preserved ejection fraction, who suffered from hematologic malignancies (lymphoma, leukemia) and underwent bone marrow transplantation, were randomized to receive sacubitril/valsartan 24/26 mg bid daily or enalapril 5 mg bid daily or placebo. We measured at baseline, before transplantation and after six months: i) Global Longitudinal Strain (GLS) of left ventricle (LV) by speckle tracking imaging, ii) myocardial global work index (GWI), global constructive work (GCW), global wasted work (GWW) and myocardial global work efficiency (GWE), by longitudinal strain-peripheral blood pressure loops, and iii) Left Ventricular Ejection Fraction (LVEF Simpson’s Method). Results The two treatment groups had similar age, sex atherosclerotic risk factors and cardiotoxic medication before and after bone marrow transplantation. Compared to baseline, patients treated with sacubitril/valsartan or enalapril for six months did not show a deterioration of LV GLS (−19.8±2.8 vs −19.3±4.1%, p = 0.403 for s/v, −20.3±2.8 vs −20.0±3.6%, p = 0.634 for ena). Conversely, patients treated with placebo for six months, presented a significant impairment of LV GLS (−20.9±2.1% vs −18.5±2.2, p = 0,001). No significant changes were found in LVEF after treatment with sacubitril/valsartan or enalapril for six months (57.5±4.9 vs 57.9±6.8%, p = 0.826 for s/v, 58.8±5.4 vs 60.7±7.1%, p = 0.419, for ena), while a borderline deterioration was noticed after treatment with placebo for six months (60.6±5.4 vs 57.7±6.7%, p = 0,045). We did not notice any alteration in GWi, GCW, GWW, GWE in patients treated with enalapril. On the other hand, in patients treated with sacubitril/valsartan GWE was improved (94.2±3.1 vs 95.8±1.8 %, p = 0.030) and GWW was diminished (111.5±75.7 vs 86.4±43.1 mmHg%, p = 0.045), while GWI and GCW did not show any significant alteration. Conversely, in the placebo group, GWI was reduced (1909.9±336.4 vs 1727.9±340.9 mmHg%, p = 0.027), GWW was increased (80.7±60.6 vs 110.6±65.1 mmHg%, p = 0.045), GWE was diminished (95.9±2.1 vs 94.1±3.9 %, p = 0.039) and GCW did not change. Conclusions Treatment with sacubitril/valsartan or enalapril prevented deterioration of myocardial function six months after bone marrow transplantation in patients with hematologic malignancies and preserved ejection fraction. Moreover, sacubitril/valsartan showed a more favorable effect on myocardial work.

Relationship between NT-proBNP and myocardial deformation in obese patients with acute myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): This research was funded by “Iuliu Haţieganu” University of Medicine and Pharmacy, Dept. of Cardiology, Cluj-Napoca, Romania, grant number 1529/66/18.01.2019. Introduction In addition to promoting coronary artery disease, obesity increases the risk of cardiovascular complications. The obesity paradox, however, refers to the observation that a high body mass index (BMI) may be protective of outcomes following an acute myocardial infarction (AMI). In patients with AMI, both NT-proBNP and novel echocardiographic markers (global longitudinal strain - GLS) provide additional information; nevertheless, there is limited research on the association between these parameters and obesity in this clinical setting. Material and methods This was a prospective study that included 55 patients admitted with AMI and preserved or mildly reduced LVEF (>40%), which all underwent successful percutaneous revascularization. At 48 hours after PCI, echocardiography was performed using a Vivid E95 scanner and the automated function-imaging (AFI) tool was used to determine GLS. NT-proBNP was measured using ELISA. All patients were divided into two groups according to their BMI (group 1 included 18 patients with normal BMI<25 kg/m2, and group 2 included 37 obese patients, with a BMI>30 kg/m2). Results The mean age of the patients was of 66±14 years, 58% were male and 65.5% had STEMI. Other than obesity, there was no difference between groups in the other cardiovascular risk factors (smoking, dyslipidemia, arterial hypertension, diabetes, age, gender). In both groups, the anterior descending coronary artery was the most frequent culprit vessel (44% vs. 40%, p=0.9). The majority of the patients had single- or two- vessel coronary artery disease (72% vs. 73%), but there were no differences between groups (p=0.74). The values of NT-proBNP were significantly lower in the obese group (300 [117-713] vs. 756 [450-1800] pg/mL, p=0.02). However, regarding the echocardiographic evaluation of myocardial function, there was no difference between the values of GLS (-10.5% vs. -10.8%, p=0.77) or LVEF (56.7% vs. 49.2%, p=0.27) among groups. GLS showed a stronger correlation to NT-proBNP values in the normal weight group (r=0.63) than in the obese group (r=0.27). Conclusion Despite the fact that increased BMI is linked to lower values of NT-proBNP following AMI, non-obese patients do not demonstrate more impaired myocardial longitudinal function. These findings might offer more insights on the perspectives of obese AMI patients.

Regional contributions to impaired myocardial mechanical function in heart failure with preserved ejection fraction.

Hypertensive heart disease (HHD) is recognized as a key clinical precursor to heart failure with preserved ejection fraction (HFPEF). However, pathophysiological transition from HHD to HFPEF is not well understood. We sought determine whether regional differences in impaired myocardial function may underlie the greater mechanical dysfunction seen in HFPEF compared to HHD. We used standardized echocardiography to assess regional myocardial deformation in a cohort of n = 327 adults with preserved left ventricular (LV) ejection fraction (≥45%), including: n = 129 with HFPEF, n = 158 with HHD and no heart failure, and n = 40 normotensive controls. From detailed measurements of LV systolic strain performed in multiple views, we derived and then compared regional measures of basal, mid-ventricular, and apical longitudinal strains. In models adjusting for clinical covariates, basal and mid-ventricular LV myocardial deformation was more impaired in HHD than in controls (P ≤ 0.003), whereas apical deformation was more impaired in HFPEF than in HHD (P = 0.005). In multivariable-adjusted analyses, only apical strain remained independently associated with HFPEF vs. HHD status [odds ratio 1.18 (1.02-1.37), P = 0.030 per 1% decrease in apical strain]. Compared to other regional strains, apical longitudinal strain optimally differentiated HFPEF from HHD (area under the receiver operating curve: apical longitudinal strain = 0.67; mid-ventricular longitudinal strain = 0.59; basal longitudinal strain = 0.60). We found that while apical mechanical function is preserved in HHD, it was impaired in HFPEF and may contribute to the transition from an asymptomatic heart disease to a symptomatic heart disease.

TREKING: TaRgEting NK cells in post-Ischemic cardiac remodeliNG

Acute myocardial infarction is a common condition responsible for heart failure and sudden death. We precedently showed that CD8+ T lymphocytes are recruited and activated in the ischemic heart tissue and release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling and deterioration of myocardial function. NK cells, belonging to innate immunity cells are playing an important role in anti-viral and anti-tumor immunity. These cells release also Granzyme B and secrete IFNg, TNFa and GM-CSF. The goal of this study was to unravel the distinct role of NK cells in post-ischemic injury. Acute MI was induced in mice by permanent ligation of the left anterior descending coronary artery. Cardiac function and remodeling were assessed by using echocardiography and histology. To determine the specific role of NK cells, the study used mice with and without NK cell depletion but also with and without hyperactivation of these NK cells. We assessed cardiac NK cells and innate populations using flow cytometry and RNA sequencing. We found that NK cells levels were increased in the heart after experimental MI. Depletion of NK cells restored cardiac function whereas hyperactivation of these cells via anti-NKG2A antibody showed worst cardiac function and left ventricle remodeling. Co cultured NK cells with cardiomycoytes showed apoptosis via Granzyme B. NK cells depletion by anti-NK1.1 antibody decreased monocyte recruitment after MI leading to anti-inflammatory environment permitting a less adverse post-ischemic cardiac remodeling. NK cells altered cardiac healing and aggravate the recovery of heart function after MI in mice. Depletion of NK cells could be a novel therapeutic strategy to promote a reparative response after MI.

Transmembrane BAX inhibitor motif containing 6 suppresses presenilin-2 to preserve mitochondrial integrity after myocardial ischemia-reperfusion injury.

Myocardial ischemia-reperfusion (I/R) damage is characterized by mitochondrial damage in cardiomyocytes. Transmembrane BAX inhibitor motif containing 6 (TMBIM6) and presenilin-2 (PS2) participate in multiple mitochondrial pathways; thus, we investigated the impact of these proteins on mitochondrial homeostasis during an acute reperfusion injury. Myocardial post-ischemic reperfusion stress impaired myocardial function, induced structural abnormalities and promoted cardiomyocyte death by disrupting the mitochondrial integrity in wild-type mice, but not in TMBIM6 transgenic mice. We found that TMBIM6 bound directly to PS2 and promoted its post-transcriptional degradation. Knocking out PS2 in mice reduced I/R injury-induced cardiac dysfunction, inflammatory responses, myocardial swelling and cardiomyocyte death by improving the mitochondrial integrity. These findings demonstrate that sufficient TMBIM6 expression can prevent PS2 accumulation during cardiac I/R injury, thus suppressing reperfusion-induced mitochondrial damage. Therefore, TMBIM6 and PS2 are promising therapeutic targets for the treatment of cardiac reperfusion damage.

Predictive value of cardiac magnetic resonance mechanical parameters for myocardial fibrosis in hypertrophic cardiomyopathy with preserved left ventricular ejection fraction.

Myocardial fibrosis leads to systolic dysfunction in hypertrophic cardiomyopathy (HCM) patients. This study aims to investigate the relationship between cardiac magnetic resonance mechanical parameters for evaluating the left ventricular function in HCM with preserved left ventricular ejection fraction (LVEF ≥50%) and the association between myocardial fibrosis defined by late gadolinium enhancement (LGE). This study was a retrospective analysis of CMR images of 93 patients with HCM with preserved ejection fraction (HCMpEF) and 96 controls diagnosed by cardiac magnetic resonance (CMR) at our hospital from July 2019 to January 2022. The myocardial contraction fraction (MCF) was calculated, and myocardial mechanical parameters, including global myocardial longitudinal strain (GLS), circumferential strain (GLS), and myocardial strain (GLS), were obtained by tissue tracking and LGE quantitative modules of dedicated software, respectively. The correlation between myocardial strain and LGE was analyzed, and a multivariate logistic regression model was developed to discuss the risk predictors of LGE. Compared to the control group, the left ventricular mechanical parameters GLS (-13.90 ± 3.80% versus -18.20 ± 2.10%, p < 0.001), GCS (-16.62 ± 3.50% versus -18.4 ± 2.69%, p < 0.001), GRS (28.99 ± 10.38% versus 33.02 ± 6.25%, p < 0.01), and MCF (64 ± 16% versus 99 ± 18%, p < 0.001) were found significantly lower in HCM group. Moreover, even in LGE-negative HCM patients, GLS (-16.3 ± 3.9%) and MCF (78 ± 19%) were significantly lower compared to the control group. Left ventricular GLS [OR = 1.61, (1.29, 2.02), p = 0.001] and MCF [OR = 0.90, (0.86, 0.94), p = 0.001] independently predicted myocardial late gadolinium enhancement (LGE). In participants of HCM with preserved ejection fraction, the early onset of reduced left ventricular GLS and MCF in patients with HCMpEF may provide new evidence for evaluating impaired myocardial systolic function. The reduction of myocardial mechanical indexes may reflect the presence and extent of myocardial fibrosis, and the more significant the reduction, the more severe the myocardial fibrosis; GLS and MCF may be ideal predictors for LGE.

Speckle tracking echocardiography in patients with systemic sclerosis: a meta-analysis

Abstract Background Myocardial dysfunction is well established in systemic sclerosis (SSc). The utility of standard echocardiography is limited to detect the onset of myocardial dysfunction. Speckle tracking echocardiography (STE) and strain imaging has emerged as a useful technique to quantify left ventricle hemodynamics and myocardial function in early stages of myocardial dysfunction. We aimed to systematically analyze the existing literature on the application of STE and strain analysis in identifying SSc associated myocardial dysfunction Methods PubMed, Cochrane, and Google Scholar were queried for studies from the inception of the databases to 2022. Case control studies that used 2D STE for assessment of strain in SSc patients and controls, were included for the analysis. PRISMA guidelines were followed for selections of studies. Two independent reviewers extracted data. Analysis was done using Cochrane Review Manager 5.0. Results Total of 19 studies were included in the analysis that compared strain analysis in SSc patient's vs healthy controls. Of the 16 studies that reported left ventricular (LV) global longitudinal strain, we found significantly lower LV global longitudinal strain in SSc patients (mean difference 1.92; 95% CI 0.98–2.87). Six studies reported LV circumferential strain which was noted to be lower in SSc patients compared to healthy controls (mean difference 3.55; 95% CI 1.60–5.51). Five studies reported LV global radial strain with a similar decrease in radial strain among SSc patients compared to controls (mean difference 4.39; 95% CI −6.95 to −1.83). 10 studies reported right ventricular longitudinal strain with a decrease in longitudinal strain in SSc patient's vs controls (mean difference 2.57; 95% CI 2.03–3.12). Conclusions SSc patients have lower strain values compared to controls, which is suggestive of an impaired myocardial function in left and right ventricle. Strain analysis by STE could help with early detection of myocardial dysfunction. Funding Acknowledgement Type of funding sources: None.

Dynamics of structural and functional characteristics of the heart in patients after myocardial infarction with ST segment elevation as a marker of progression of chronic heart failure

Objective. To identify the association of a number of clinical features and structural and functional characteristics of the heart with the progression of chronic heart failure (CHF) in patients one year after ST-segment elevation myocardial infarction (MI) (STEMI) with preserved and reduced left ventricular ejection fraction (EF) (LVEF).Design and methods. 120 patients with STEMI were included in a prospective study. During the study, all patients underwent an echocardiographic study using a Sonos 2500 device (Hewlett Packard, USA) on the 1st day (point I), on the 12th day (point II) of hospitalization, and also after 1 year (point III). Depending on the parameters of EF on the 1st day of the disease, the total sample of patients was divided into two: the 1st group — with preserved LVEF was represented by 86 (71,7 %), the 2nd group — with a reduced LVEF was represented by 34 (28,3 %) patients.Results. A total of 19 (15,8 %) adverse events were registered. In two cases, a fatal outcome (1,7 %) was recorded, the cause of which was repeated MI, in five (4,2 %) patients decompensation of СHF was noted, in eight (6,7 %) patients a clinic of progressive angina was traced, in four (3, 3 %) of patients were diagnosed recurrent MI. Deterioration of systolic and diastolic function was established one year after STEMI with preserved (≥ 50 %) LVEF: 17,6 % of patients began to correspond to the intermediate range of EF (40-49 %), the number of patients with diastolic dysfunction increased by 10 % compared to with acute study.Conclusions. Within a year after a STEMI with initially preserved LVEF, there is a deterioration in myocardial function in the form of a decrease in myocardial contractility and an increase in the number of patients with diastolic dysfunction.

Non-invasive myocardial work index contributes to early identification of impaired left ventricular myocardial function in uremic patients with preserved left ventricular ejection fraction

BackgroundCardiac damage is the leading cause of death in uremic patients. This study aimed to evaluate the application of non-invasive myocardial work index (NIMWI) by echocardiography in assessing the left ventricular (LV) systolic function in uremic patients.MethodsTwenty-six uremic patients and 27 age- and sex-matched healthy volunteers were enrolled in the study. Except for the conventional echocardiographic parameters, the LV myocardial work (MW) parameters including GWI (myocardial global work index), GCW (global constructive work), GWW (global wasted work), and GWE (global work efficiency) were calculated in study participants. Differences in MW parameters between the uremic and normal groups were compared by independent-sample t-test. Receiver operating characteristic (ROC) curves were constructed for MW parameters to detect abnormal LV systolic function in uremic patients.ResultsCompared with the normal group, GWW was significantly increased and GWE decreased in the uremic group (P < 0.05). Area under the curve (AUC) for GWE by the ROC analysis was 0.966. The best threshold, sensitivity and specificity values of GWE to detect abnormality of LV systolic function in uremic patients were 92.5%, 0.89 and 0.96, respectively.ConclusionsNIMWI may be applied to assess the global MW of uremic patients. The presence of reduced GWE can help identify impaired left ventricular myocardial function in uremic patients with preserved LV ejection fraction with a high sensitivity and specificity.

THE SOLUBLE ST2 BLOOD LEVEL IN PATIENTS WITH DEPRESSIVE DISORDERS AND ISCHEMIC HEART FAILURE SYNDROME

&#x0D; Mental disorders are among the leading causes of the global health-related burden. This burden was high across the entire lifespan, for both sexes, and across many locations. Heart failure (HF) persists as an increasing global epidemic; indeed, its estimated prevalence is currently more than 37.7 million people worldwide. ST2 (growth stimulation expressed gene 2) is a member of the interleukin (IL)-1 receptor family. Recent studies revealed that elevated levels of sST2 were associated with adverse outcomes in patients with acute dyspnoea, acute coronary syndromes, and HF. The purpose of this study: to evaluate the relationship between ST2 levels in the blood of patients with heart failure and depression. Material and methods: there were examined 129 patients with depression of varying severity together with the syndrome of HF of ischemic genesis, FC II-IV (NYHA). Depressive disorders were screened using the Hospital Anxiety and Depression Scale, which showed 8 or more points to indicate depressive episodes. The severity of depressive disorders was determined using the Hamilton scale. Transthoracic echocardiography was performed; the plasma content of soluble ST2 (sST2) and the titers of the N-terminal fragment of the brain natriuretic peptide (NT-proBNP) in the blood were determined by ELISA. Statistical analysis was performed using the standard software package "Statistica for Windows 12.0" (StatSoft, Tulsa, OK, USA).Results: The average age of the examined patients was (67.21 ± 11.73) years; among them - 41 women (31.8%). It was noted that the levels of soluble ST2 and NT-pro-BNP in the blood of patients with depressive disorders and HF of ischemic origin increased with decreasing LV EF. According to the Hamilton questionnaire, the majority of patients with HF suffered from depressive disorders of moderate intensity - 96 (74.4%) people. Univariate correlation analysis showed a direct relationship between soluble ST2 levels in the blood of the examined patients and the severity of depressive symptoms (rs = 0.33; p = 0.041); blood content of NT-pro-BNP (rs = 0.51; p = 0.015); resting heart rate (rs = 0.31; p = 0.011) and feedback from LV EF (rs = -0.39; p = 0.043).Conclusion. Patients with depressive disorders and concomitant heart failure of ischemic origin more often showed elevated levels of soluble ST2 molecule in the blood, which depend on the intensity of depression and impaired myocardial contractile function.

Assessment of Myocardial Work of the Left Ventricle before and after PCI in Patients with Non-ST-Segment Elevation Acute Coronary Syndrome by Pressure-Strain Loop Technology.

Objectives Noninvasive left ventricular pressure-strain loop (PSL) is a new method for quantitative evaluation of myocardial work, which is developed on the basis of speckle tracking echocardiography. It is necessary to fit the noninvasive left ventricular pressure and the strain by speckle tracking echocardiography to construct a pressure-strain loop. Compared with traditional left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS), it has potential application value and is a useful supplement for clinical evaluation of left ventricular systolic function. We perform this study to evaluate the changes of myocardial function in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) before and after percutaneous coronary intervention (PCI) with noninvasive left ventricular pressure-strain loop (PSL). Methods 33 NSTE-ACS patients admitted to the Department of Cardiovascular Medicine of the Affiliated Lianyungang Hospital of Xuzhou Medical University who successfully underwent early PCI were included as the PCI group. At the same time, 30 healthy patients matched in age and sex were selected as the control group. All patients received routine echocardiography. The parameters such as GWI, GCW, GWW, and GWE were obtained by EchoPAC 203 software. The differences in the general clinical data and echocardiographic parameters between the two groups, including controls and patients 1 day before surgery and 1 month after surgery, were compared. Results Compared with the control group, GWI, GCW, and GWI in the PCI group were decreased 1 day before surgery and 1 month after surgery, while GWW was increased, with statistical significance (P < 0.05). In the PCI group, compared with 1 day before surgery, GWI and GCW were all increased 1 month after surgery (P < 0.05), and GWW and GWE were not significantly different between the two groups (P > 0.05). Conclusion The noninvasive left ventricular PSL technology can early and accurately evaluate the myocardial function impairment in NSTE-ACS patients and the recovery of myocardial function after PCI, providing a new noninvasive method for clinical postoperative myocardial function evaluation.

TakoTsubo Syndrome: First an Acute Coronary Vasculitis and Then Prolonged Myocarditis?

Since its initial description by Japanese investigators 30 years ago, TakoTsubo Syndrome (TTS) has variously been regarded as a form of acute coronary syndrome and also as a form of cardiomyopathy (or more accurately, a myocarditis). There is actually good evidence that TTS embodies both of these concepts, and the main purpose of this review is to present data that they occur sequentially. The initial phase of the disorder (over perhaps the first 48 hours post onset of symptoms) represents a form of vasculitis, with associated damage to the endothelial glycocalyx and associated permeabilization of blood vessels. This is followed by a more prolonged phase of myocardial inflammation and oedema, associated with inflammatory activation and energetic impairment within the entire myocardium. Although this phase subsides after several months, it may be followed by longstanding impairment of myocardial function, reflecting residual fibrosis. Understanding of this gradual transition in TTS pathogenesis from vasculature towards myocardium remains an important limitation of patient management, especially as many patients are still told that their hearts have "recovered" within 1-2 weeks. A number of important uncertainties remain. These include development of specific early and ongoing therapeutic strategies to be used to match the sequential pathogenesis of TTS. "And so these men of Indostan Disputed loud and long, Each in his own opinion Exceeding stiff and strong, Though each was partly in the right, And all were in the wrong!" From: Six wise men of Hindustan.

Association between diabetic nephropathy and left ventricular longitudinal myocardial function in type 1 diabetes mellitus patients with preserved ejection fraction.

Left ventricular (LV) longitudinal myocardial dysfunction can be observed even in type 2 diabetes mellitus (DM) (T2DM) patients with preserved LV ejection fraction (LVEF), and is considered the earliest marker of DM-related cardiac dysfunction. Furthermore, diabetic nephropathy (DN), a common complication in DM, is strongly associated with LV longitudinal myocardial function in T2DM patients, but its association with type 1 DM (T1DM) has not been fully investigated. We studied 125 asymptomatic T1DM patients with preserved LVEF, and 75 age-, gender-, LVEF-matched non-diabetic healthy controls. Two-dimensional speckle-tracking strain LV was used to assess longitudinal myocardial function as global longitudinal strain (GLS). GLS of T1DM patients was significantly lower than that of normal controls (19.7 ± 3.6% vs. 20.6 ± 1.8%, P = 0.049). GLS of T1DM patients with DN was significantly lower that of T1DM patients without DN (17.3 ± 3.7% vs. 20.2 ± 3.5%, P < 0.001), but that of T1DM patients without DN was similar compared to normal controls (20.6 ± 1.8% vs. 20.2 ± 3.5%, P = 0.37). Moreover, multiple regression analysis identified DN the independent determinant parameters for GLS of T1DM patients also correlated significantly with duration of T1DM. Impaired LV longitudinal myocardial function was observed in asymptomatic T1DM patients with preserved LVEF, and DN was associated with LV longitudinal myocardial dysfunction. These findings are clinically useful for better management of T1DM patients to prevent impending development of cardiovascular disease.

Arrhythmia and impaired myocardial function in heritable thoracic aortic disease: An international retrospective cohort study

BackgroundHeritable thoracic aortic diseases (HTAD), typically entailing aortic complications, can be caused by pathogenic variants or likely pathogenic variants (PV/LPVs) in several genes, including fibrillin1 (FBN1), Actin Alpha2 (ACTA2) and genes encoding components of the transforming growth factor (TGF)-β signaling pathway. In addition to aortic complications, non-aortic cardiac disease such as impaired myocardial function and/or arrhythmia have been increasingly reported, mainly in Marfan syndrome with underlying FBN1 PV/LPVs and are acknowledged as additional causes of morbidity and mortality. The prevalence of these manifestations in the various HTAD entities is largely unknown. MethodsThis international multicentre retrospective study collected data on patients with HTAD presenting non-aortic cardiac disease. A total of 9 centers from 7 different countries participated. Patients 12 years or older carrying a PV/LPV in one of the following genes: FBN1, TGFBR1, TGFBR2, TGFB2, TGFB3, SMAD3 and ACTA2 were screened. Non-aortic cardiac disease included impaired myocardial function and/or arrhythmia. Impaired myocardial function was defined as (a)symptomatic reduced ejection fraction (EF<50%). Arrhythmias included atrial fibrillation (AF), atrial flutter (AFL), ventricular tachycardia (VT), ventricular fibrillation (VF) and (aborted) sudden cardiac death (presumed arrhythmogenic) (SCD). ResultsMedical records of 3219 patients with HTAD were screened (2761, 385 and 73 carrying a PV/LPV in FBN1, in a TGF-β signaling gene and in ACTA2 respectively). Non-aortic cardiac disease was reported 142 times in 101 patients (3.1%) (age 37 [range 12–77] years, 39% female): 88 patients carrying an FBN1 PV/LPV and 13 carrying a PV/LPV in one of the TGF-β signaling genes. Neither impaired myocardial function nor arrhythmia was reported in screened patients carrying a PV/LPV in ACTA2. Among the 142 reported non-aortic cardiac diseases, 68 (48%) were impaired myocardial function, 47 (33%) were AF/AFL and 27 (19%) were VT/VF/SCD. Among the patients with non-aortic cardiac disease, prior cardiac surgery was noted in 80% and severe valvular disease (valvular surgery or severe valvular regurgitation) in 58%, while 18% of the patients developed non-aortic cardiac disease in the absence of any of the latter. ConclusionsIn patients with HTAD, arrhythmia and impaired myocardial function was reported in patients with PV/LPVs in FBN1 and in the TGF-β signaling genes and not in patients harboring PV/LPVs in ACTA2. Though infrequent, non-aortic cardiac disease should be acknowledged as potentially severe, also occurring in young patients with no underlying significant valvular or aortic disease.

Assessment of nurses' knowledge toward myocardial infraction at coronary unit in Al-Imam Al-Sadiq Teaching Hospital, Babylon Province, Iraq

Background: Acute myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. The world health organization has defined Ischemic heart disease as myocardial function impairment due to imbalance between coronary blood flow and myocardial requirement the most common cause being atherosclerosis. The aim of the Study: The aims of this study was to assess nurses' knowledge toward myocardial function, and to assess their socio-demographic characteristics in relation to knowledge. Methodology:: A descriptive design study was conducted to accomplish the objectives. Which study was conducted at coronary unit in Al- Imam Al-Sadiq Teaching Hospital, Babylon province, Iraq. Purposive - non-probability sample were selected . In order to collect the data, the researcher prepared specific questionnaire to assess the nurses' knowledge toward myocardial function, and to assess their socio-demographic characteristics in relation to knowledge after reviewing of relevant literature and studies.Results: the majority of the study participants were male who accounted for (60%) of the total participants. Regarding age (58%) were from the age group (40- 49 years); (40%) of the nurses were experience in nursing at period ranging (1- 5 years). Conclusion: The study has confirmed that (28%) the sample have good level of knowledge about myocardial infarction.

Amino Acid and Phospholipid Metabolism as an Indicator of Inflammation and Subtle Cardiomyopathy in Patients with Marfan Syndrome.

Patients with Marfan syndrome (MFS) have an increased risk of aortic aneurysm formation, dissection and development of a subtle cardiomyopathy. We analyzed amino acid and lipid metabolic pathways in MFS patients, seeking biomarker patterns as potential monitoring tools of cardiovascular risk with deterioration of myocardial function. We assessed myocardial function in 24 adult MFS patients and compared traditional laboratory values and mass spectrometry-based amino acid, phospholipid and acylcarnitine metabolomes in patients with those in healthy controls. Analytes for which values differed between patients and controls were subjected to regression analysis. A high proportion of patients had signs of impaired diastolic function and elevated serum levels of NT-proBNP. Patients had lower serum levels of taurine, histidine and PCaeC42:3 than controls. The evidence of diastolic dysfunction, aortic root dimensions and history of aortic root surgery correlated with NT-proBNP and taurine levels. Alterations in serum levels of metabolism derived analytes link MFS pathophysiology with inflammation, oxidative stress and incipient cardiomyopathy.

Dengue and the heart.

Dengue is a neglected viral arthropod-borne tropical disease transmitted by the bite of infected Aedes spp. mosquitoes. It is responsible for a significant global burden of disease and corresponding socio-economic implications. There are four different virus serotypes, all of which are found predominantly in countries with tropical climates. Patients with dengue may present with cardiovascular (CV) manifestations, contributing to associated death and disability. A systematic review was conducted to identify CV manifestations of dengue, wherein 30 relevant studies were identified in the MEDLINE and PubMed databases. CV complications of dengue include rhythm abnormalities, hypotension, myocarditis, pericarditis and deterioration in myocardial function. Prompt recognition and treatment of CV complications of dengue are essential to reduce morbidity and mortality in these patients, who are at risk of progressing to cardiogenic shock and heart failure.

Incomplete functional reverse remodelling of the left ventricle one year after bariatric surgery. Insights from the prospective FatWest study

Abstract Background Patients with severe obesity are predisposed to development of left ventricular (LV) hypertrophy with subsequent increased myocardial oxygen demand and impaired myocardial function. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. Purpose To assess whether LV systolic function, wall mechanics, and cardiac power improve 1 year after bariatric surgery. Methods 91 severely obese patients (43±10 years, 70% women, body mass index [BMI] 41.7±4.9 kg/m2, 55% with hypertension, 17% with diabetes mellitus) underwent echocardiography before, 6 and 14 months after Roux-en-Y gastric bypass surgery in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV systolic function by biplane ejection fraction (EF), LV wall mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), and cardiac power normalized for LV mass by 0.222 x cardiac output x mean blood pressure (BP)/LV mass. Results Surgery induced a significant reduction in BMI, heart rate, systolic BP, and LV mass (Figure 1). Prevalence of LV hypertrophy fell from 34 to 20% 14 months after surgery (p&amp;lt;0.001), while that of concentric geometry remained stable: 8 vs 10% (p=0.36). GLS improved by 28%, however LV EF and MWS did not change (Figure 2). LV power at rest decreased postoperatively, reflecting the lower BP and heart rate, but was unaltered when normalized for LV mass (Figure 2). In backward stepwise multivariate regression analyses, 1 year improvement in GLS was predicted by the systolic BP reduction (p&amp;lt;0.05) (R2 0.73, p&amp;lt;0.001), while low 1-year MWS was independently associated with female gender, concentric geometry and higher myocardial oxygen demand (all p&amp;lt;0.01) (Nagelkerke R2 0.44, p&amp;lt;0.001), and lower 1-year LV power-mass with female gender and LV hypertrophy (p&amp;lt;0.01) (R2 0.24, p&amp;lt;0.001). Conclusion In severely obese patients, LV longitudinal function normalizes 1 year after bariatric surgery, mainly due to the BP reduction. LV midwall mechanics and power do not improve, especially in women and patients with persistent LV geometric abnormalities. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2