Development Of Left Ventricular Dysfunction Research Articles

USE OF SGLT2–INHIBITORS IN THE TREATMENT OF ANTHRACICLINE CARDIOTOXICITY

Abstract The survival rate of cancer patients has significantly increased in the last 25 years thanks to the extraordinary advances in anti-tumor therapies. However, many chemotherapeutic agents are potentially cardiotoxic. In particular, anthracycline-induced cardiotoxicity is a clinical condition caused by chemotherapy drugs that lead to morpho-functional alterations and cell death of cardiomyocytes; the most typical clinical manifestation of this cardiotoxicity is the development of left ventricular dysfunction, which over time can evolve towards full-blown heart failure. It is therefore characterized by a reversible asymptomatic stage that progresses to an irreversible stage, often difficult to treat. For an early individualization of this toxicity, a dedicated clinic has been established in our center for the monitoring of patients undergoing treatment with cardiotoxic chemotherapy. We describe the case of a 53-year-old patient with preserved biventricular systolic function undergoing neoadjuvant treatment for breast cancer, who at the end of the second infusion of anthracyclines presented with mild exertional dyspnoea associated with radiological signs of pulmonary congestion and an increase in the indices of myocardionecrosis and BNP. The echocardiogram revealed a sudden worsening of the left ventricular systolic function which was 48%. It was therefore decided to hospitalize the patient and initiate infusional diuretic therapy with a rapid clinical and instrumental response. An SGLT2 inhibitor with indication for the treatment of heart failure with moderately reduced ejection fraction was also added to the therapy. At the one-month check-up, there was an almost complete recovery of left ventricular function and a clear symptomatic benefit with associated normalization of laboratory markers of myocardial damage and heart failure, with the possibility for the patient to undergo surgery to remove the left ventricle. tumor mass. This clinical case could represent a starting point to start considering therapy with SGLT2 inhibitors for the prevention and early treatment of cardiac toxicities from some chemotherapeutics, in order to avoid the process of irreversibility of myocardial damage with subsequent poor response to anti-inflammatory therapies. – conventional compensation.

ASSESSMENT OF RIGHT VENTRICULAR FUNCTION FOLLOWING PERMANENT PACEMAKER IMPLANTATION BY ECHOCARDIOGRAPHY (INCLUDING 3D ECHOCARDIOGRAPHY)

Objective: Several studies have shown that unfavorable ventricular remodelling & mechanical dyssynchrony caused by Right ventricular (RV) pacing leading to development of Left Ventricular dysfunction. Nevertheless, impact of RV pacing on Right Ventricle function has not been thoroughly assessed. Hence, prospective study was done to assess RV dimensions & function by 2D and three-dimensional (3D) echocardiography at 3 months & 6 months after pacemaker implantation Design and method: This study was a prospective single-centre study. All patients who underwent pacemaker implantation were assessed for RV function by 2D and 3D Echocardiography at baseline (pre-procedure), 3 months & 6 months after pacemaker implantation. The change in follow-up period was evaluated by using single factor analysis of variance ANOVA with repeated measures in normally distributed data & Bonferroni post-hoc test. A p value of <0.05 is considered to be statistically significant Results: From January 2022 to December 2022, a total of 66 patients with permanent pacemaker were enrolled in the study. There was statistically non-significant changes in mean LVEF (%) during follow up (62.13±3.92(Baseline) vs. 62.21±4.15(3-month) vs 62.03+3.83 (6-months), p value>0.05).However, there was statistically significant changes in mean PASP (mm Hg) during follow up (18.45±3.45 (Baseline) vs. 22.18±3.76 (3-month) vs 26.45+3.97, p value <0.05). Also, there was statistically significant changes in mean RIMP during follow up (0.48±0.04(Baseline) vs. 0.50±0.04(3-month) vs 0.50+0.03(6-month),p value<0.05).Likewise, there was statistically significant changes in mean RV E/E’ during follow up (4.47±0.57(Baseline) vs. 4.70±0.74(3-month) vs 4.95+0.82(6-month),p value <0.05).In addition, there was statistically significant changes in mean TR Jet Area (cm2) during follow up (1.68±0.26(Baseline) vs. 2.22±0.43(3-month) vs 2.56+0.53(6-month), p value <0.05). But, there was statistically non-significant changes in mean RVEF % (3D Echo) during follow up (53.51± 2.75(Baseline) vs. 53.02±2.64 (3-month) vs 53.48+2.34 (6-month), p value >0.05).Other echocardiographic parameters of RV function did not show any change in 3-months & 6-months follow-up. Conclusions: There is change in Right Ventricular function after Pacemaker implantation which can be documented as early as 6 months post implantation. Permanent pacemaker was associated with changes in RIMP, RV E/E’, PASP, TR JET AREA during 6 months after Right ventricular pacing

Changes in hemodynamic parameters and atrial fibrillation risk in patients after permanent pacemaker implantation

Data on the development of left ventricular dysfunction after permanent pacemaker implantation are available. According to data from the DAVID (The Dual Chamber and VVI Implantable Defibrillator) study, it was shown that DDDR-paced patients had significantly more fatal events and HF deterioration cases requiring hospitalization. Similar were the results of the MOde Selection Trial (MOST), which poses serious questions to the cardiology community. For that reason it is important to understand how PPM implantation changes the hemodynamic parameters of the heart and what consequences this may have. On the one hand, asynchronous contraction of the paced heart and increase in AF risk with advancing age require active screening of asymptomatic paroxysms of tachyarrhythmias to promptly adjust therapy. On the other hand, minimizing the rate of ventricular pacing through proper programming of the devices should not be overlooked. Recently, various biomarkers have been validated to select high-risk patients in which the therapeutic strategy can be modulated on time.

Permanent Pacemaker Implantation: Early Post-Implantation Data

Abstract Introduction: Data on the development of left ventricular dysfunction after permanent pacemaker implantation are available. Myocardial collagen deposition is a well-known mechanism that occurs in left ventricular remodelling. This gave us reason to dynamically monitor the levels of the main molecules involved in collagen synthesis, PIPC (carboxy-terminal propeptide of type I procollagen) and PIIINP (amino-terminal propeptide of type III procollagen). Materials and Methods: PIPC and PIIINP levels were studied using enzyme-linked immunoassays in plasma from 45 patients (25 men, 20 women, 72.1 ± 9 years) and 46 controls (24 men, 22 women, 71.9 ± 8.7 years) without known cardiovascular diseases (except arterial hypertension, conduction disorder, indication for the procedure) at baseline (immediately before PPM implantation for patients), at 12 and 24 weeks. Results: There was no difference in baseline levels of PICP and PIIINP between patients and controls (p > 0.05, Table abstract). At week 12, PICP levels increased significantly in patients compared to baseline in controls (p < 0.05, Table abstract). At week 24, values continued to increase and were again significantly higher than baseline in the controls (p < 0.001, Table abstract). At the 12-week follow-up visit, PIIINP values in patients were significantly higher than those at baseline in controls (p < 0.001, Table abstract). At week 24, the values of the patients were still higher than those of the controls, but the difference was not significant (p > 0.05, Table abstract). Conclusion: This study showed early activation of collagen synthesis < 6 months after PPM (permanent pacemaker) implantation. Due to the selection of patients without concomitant cardiovascular pathology, we have reason to assume that it is a result of the procedure itself and a serious prerequisite for increased collagen deposition in the myocardium.

Once in a blue moon: coronavirus disease complicates pregnancy in a patient with unknown pulmonary hypertension and subsequent left ventricular dysfunction

During COVID-19 pandemic, several clinical manifestations have been described beyond respiratory compromise that characterizes the viral disease. Cardiovascular manifestations are one of the main complications. In this case, we report an unusual association between the novo diagnosis of pulmonary arterial hypertension in a pregnant patient with SARS Cov-2, with subsquent development of left ventricular dysfunction.

Therapeutic S100A8/A9 blockade inhibits myocardial and systemic inflammation and mitigates sepsis-induced myocardial dysfunction

Background and AimsThe triggering factors of sepsis-induced myocardial dysfunction (SIMD) are poorly understood and are not addressed by current treatments. S100A8/A9 is a pro-inflammatory alarmin abundantly secreted by activated neutrophils during infection and inflammation. We investigated the efficacy of S100A8/A9 blockade as a potential new treatment in SIMD.MethodsThe relationship between plasma S100A8/A9 and cardiac dysfunction was assessed in a cohort of 62 patients with severe sepsis admitted to the intensive care unit of Linköping University Hospital, Sweden. We used S100A8/A9 blockade with the small-molecule inhibitor ABR-238901 and S100A9−/− mice for therapeutic and mechanistic studies on endotoxemia-induced cardiac dysfunction in mice.ResultsIn sepsis patients, elevated plasma S100A8/A9 was associated with left-ventricular (LV) systolic dysfunction and increased SOFA score. In wild-type mice, 5 mg/kg of bacterial lipopolysaccharide (LPS) induced rapid plasma S100A8/A9 increase and acute LV dysfunction. Two ABR-238901 doses (30 mg/kg) administered intraperitoneally with a 6 h interval, starting directly after LPS or at a later time-point when LV dysfunction is fully established, efficiently prevented and reversed the phenotype, respectively. In contrast, dexamethasone did not improve cardiac function compared to PBS-treated endotoxemic controls. S100A8/A9 inhibition potently reduced systemic levels of inflammatory mediators, prevented upregulation of inflammatory genes and restored mitochondrial function in the myocardium. The S100A9−/− mice were protected against LPS-induced LV dysfunction to an extent comparable with pharmacologic S100A8/A9 blockade. The ABR-238901 treatment did not induce an additional improvement of LV function in the S100A9−/− mice, confirming target specificity.ConclusionElevated S100A8/A9 is associated with the development of LV dysfunction in severe sepsis patients and in a mouse model of endotoxemia. Pharmacological blockade of S100A8/A9 with ABR-238901 has potent anti-inflammatory effects, mitigates myocardial dysfunction and might represent a novel therapeutic strategy for patients with severe sepsis.Graphical

PO-03-146 PREMATURE VENTRICULAR CONTRACTIONS IN CHILDREN AND YOUNG ADULTS: RISK FACTORS FOR LEFT VENTRICULAR DYSFUNCTION

Premature ventricular contractions (PVCs) are common in children and are often perceived as benign. However, frequent PVCs can lead to left ventricular (LV) dysfunction. Risk factors for PVC-mediated LV dysfunction are not well defined in children. Characterize the frequency of and risk factors for LV dysfunction in children with frequent PVCs. Retrospective cohort study from 2003-18 including patients aged 1-21 years with frequent PVCs (>0.5% on Holter monitoring), a 12-lead ECG with 1+ PVC, and an echocardiogram. Risk factors for LV dysfunction (LVEF <50%) at time of presentation and during follow up in the subset of patients with echocardiographic follow up were evaluated using logistic regression and Cox proportional hazards analysis, respectively. Exclusion criteria included significant congenital heart disease and known personal or family history of primary arrhythmic or cardiomyopathic disease. We identified 202 patients and four were excluded due to diagnoses made after presentation with PVCs: Andersen-Tawil syndrome (2 siblings), and cardiomyopathy (2), leaving 198 for analysis with a median age 12.3 years. LV dysfunction was present at time of presentation in 4%, developed in an additional 6% during follow up, and was mild in most (LVEF <40% in only 1). Risk factors for LV dysfunction included older age; higher PVC burden; longer PVC duration; couplets, triplets, NSVT, and polymorphic ventricular ectopy (table 1). A PVC burden threshold of ≥15% was 100% sensitive and 76% specific for LV dysfunction at time of presentation (fig. 1) while a PVC duration threshold of ≥151ms was 100% sensitive and 74% specific. No risk factors were identified for developing LV dysfunction during follow up. In children who never received PVC-directed therapy or had serial Holter monitors before therapy was started, PVC burden decreased from a median of 10.2 to 1.8% (p < 0.001) over a median follow up period of 3.2 years. PVC-mediated LV dysfunction is rare in children and is mild in nearly all cases. Younger patients with <15% PVCs, PVC duration <151ms, and without complex ventricular ectopy are at extremely low risk for LV dysfunction. The natural history shows a reduction in PVC burden over time in most, but not all, patients. A minority of children who come to attention due to frequent PVCs have a serious underlying cardiovascular diagnosis.Tabled 1Table 1No LV Dysfunction (n = 191)LV Dysfunction (n = 7)OR [95% CI]p-valueDemographicsMale sex108 (57)6 (86)4.6 [0.5-39.0]0.161Age (years)12.1 (7.8-15.6)17.6 (16.2-17.6)4.5 [1.3-16.1] per 5 year increase0.021CHD8 (4)1 (14)3.8 [0.4-35.5]0.240PresentationPVCs incidentally noted140 (73)6 (86)2.2 [0.3-18.6]0.474Initial Holter Results%PVCs8.6 [3.9-14.9]33.6 [18.5-36.8]1.6 [1.3-2.2] per 5% increase<0.001Sustained VT3 (2)1 (14)10.4 [0.9-115.7]0.056NSVT11 (6)4 (57)21.8 [4.3-109.8]<0.001*Couplets73 (38)7 (100)*0.001Triplets26 (14)4 (57)8.5 [1.8-40.0]0.007Polymorphic ectopy9 (5)2 (29)8.1 [1.4-47.5]0.021ECG PVC CharacteristicsInferior QRS axis156 (82)6 (86)1.3 [0.2-11.5]0.786LBBB morphology141 (74)5 (71)0.9 [0.2-4.7]0.888Outflow tract morphology118 (62)5 (71)1.5 [0.3-8.2]0.608PVC coupling interval (ms)477 (420-531)467 (399-497)0.9 [0.7-1.1] per 25 ms increase0.420PVC duration (ms)135 (119-151)160 (157-168)4.0 [1.5-10.9] per 25 ms increase0.007ETT results (n = 99)PVC suppression during test78 (85)4 (57)0.2 [0.1-1.2]0.080VT during test3 (3)1 (14)4.9 [0.4-55.0]0.194∗Odds ratio cannot be estimated as all patients with dsyfunction are in one group; p-value estimated from Fisher's exact test. CHD = congenital heart disease, VT = ventricular tachycardia, NSVT = non-sustained ventricular tachycardia, LBBB = left bundle branch block, ETT = exercise tolerance test Open table in a new tab

Strain echocardiography in predicting LV dysfunction in RV apical pacing

Right ventricular (RV) pacing is associated with a reduction in left ventricular (LV) systolic function, thought to be mediated by pacing-induced ventricular dyssynchrony. The prevalence of heart failure after RV pacing is reported to range from 31±3%. We studied 60 subjects with high-grade atrioventricular block and Complete Heart Block (CHB) scheduled to undergo right ventricular apical pacing. 2D echocardiography was done at baseline, 1 month and 12 months. Pacing-induced cardiomyopathy was defined as a reduction in LVEF to <45%. Strain was evaluated off-line from digitally stored images using all advanced software package (cardiac wall motion quantification (CMQ); Toshiba Medical Systems). Longitudinal strain for individual myocardial segments was measured from the apical four-chamber, two-chamber and long axis views (16 segment AHA/ASE model). None had LV dysfunction at baseline based on 2D and strain echo imaging. Subsequently 18 patients were detected to develop low GLS score (less than -14.5) at 1 month. On subsequent follow up at 1 year, all 18 patients developed LV dysfunction on 2D Echocardiography. Thus Strain imaging with GLS score helped in early detection of LV dysfunction in RV apical pacing subjects. Pacing-induced cardiomyopathy had significant association with high grade AV block with pacemaker dependency. It had no significant associations with other comorbidities like diabetes, hypertension, ischemic heart disease or with the type of medication intake. However there was a statistically significant association with heart failure.

High-sensitivity troponin I as a predictor of left ventricular dysfunction in the use of cardiotoxic anticancer agents for breast cancer in patients with predominantly low and moderate risk of cardiotoxicity

Aim. To study the significance of monitoring high-sensitivity troponin I (hs-cTnI) for predicting anthracycline-induced left ventricular (LV) dysfunction in the treatment of breast cancer in patients with moderate and low risk of cardiotoxicity (CT).Material and methods. The study involved 49 patients with breast cancer aged 50±10 years who underwent neoadjuvant or adjuvant chemotherapy, which included doxorubicin at a course dose of 60 mg/m2 and an average cumulative dose of 251±60 mg/m2. The level of hs-cTnI was determined by an ultrasensitive method before the start of chemotherapy, after each course of anthracyclines and in 18 patients before the administration of anthracyclines. The level of hscTnI &gt;0,017 ng/ml was considered elevated. Echocardiography was performed before the start of chemotherapy, after the end of anthracycline therapy, and every 3 months for 12 months thereafter. CT was defined as a decrease in LV ejection fraction (EF) by ≥10% to &lt;53%.Results. CT risk before chemotherapy was considered low and moderate in 96% of patients. An increase in hs-сTnI was detected ≥1 times in 56,8% of patients: before chemotherapy — in 13,5%, after 1 and 2 courses of anthracycline therapy — in 13,9%, after 3, 4, 5 and 6 courses — in 44%, 62%, 71% and 66% of patients, respectively. The levels of hs-cTnI before and after administration of anthracyclines did not differ significantly. The development of LV dysfunction was observed in 16,3% of patients. There were following prognostic significance of an increase in hs-cTnI at any time of chemotherapy for a decrease in LV EF: sensitivity — 87,5%, specificity — 50%, the positive predictive value — 28%, the negative predictive value — 94,7%. The closest relationship was noted between CT and hs-cTnI value before the start of chemotherapy (β=0,45, p=0,005) and after the 3rd course of anthracycline therapy (β=0,56, p=0,002).Conclusion. An increase in hs-cTnI level before and during anthracycline thera py in patients with a low risk of cardiotoxicity has a prognostic value in relation to the development of left ventricular dysfunction. Hs-cTnI assessment should be performed before the start of therapy, and then starting from the 3rd course of anthracycline therapy in all patients, regardless of the risk of cardiotoxicity.

Detection of early cardiac disease manifestation in propionic acidemia - Results of a monocentric cross-sectional study.

In propionic acidemia (PA) myocardial involvement is common and includes development of cardiomyopathy, life-threatening acute heart failure, and acquired long-QT syndrome. We sought to investigate which echocardiographic parameters of left ventricular systolic and diastolic function indicate early cardiac disease manifestation in PA. This is a prospective observational study (cross-sectional design) in a Tertiary Medical Care Center. Individuals with confirmed PA were enrolled and the following cardiac investigations were performed in all study individuals: echocardiographic measurements of systolic and diastolic left ventricular (LV) function (LV fractional shortening (LV-FS), LV ejection fraction by biplane modified Simpson's (LV-EF), mitral annular plane systolic excursion (MAPSE), LV global longitudinal strain (LV-GLS) by speckle tracking echocardiography (STE), pulsed Doppler analyses of mitral valve (MV) inflow velocities (MV E/A) and MV deceleration time (DT-E), tissue doppler imaging (TDI) of the mitral annulus (MV E/e'), and LV myocardial performance index (LV-MPI). LV and left atrial (LA) diameters were assessed. 12‑lead electrocardiograms (ECG) were recorded and corrected QT intervals (QTc) calculated. Clinical phenotype and laboratory parameters at the time of cardiac investigation were assessed. Besides descriptive analyses we analyzed frequency, onset, and combinations of echocardiographic and ECG data as well as their correlations with clinical and biochemical findings. The effects of 'age at visit' and LV functional parameters on QTc were analyzed with multiple regression. A total of 18 patients with confirmed PA were enrolled. Median age at PA onset was 6 days (range 1-357 days). Median age at visit for cardiac evaluation was 13.1 years (range 0.6-28.1 years). LV-GLS was abnormal in 72.2%, LV-EF in 61.1%, MAPSE in 50%, MV E/e' in 44.4%, LV-MPI in 33.3%, LV-FS in 33.3%, and MV E/A in 27.8%. In cases with normal or near normal LV-FS, LV-GLS was pathological in 5/10, LV-EF in 4/10, and MAPSE in 3/10. The probability of developing LV dysfunction - systolic and diastolic - increases with age. LV-MPI is a reliable parameter to indicate systolic LV-dysfunction in combination with a dilated LV, i. e. dilated cardiomyopathy (DCM) in PA. Multiple regression reveals a significant positive association between LV diameters and QTc. Abnormal LV-GLS significantly correlates with reduced muscle strength, muscle tone and/or abnormal gross motor function. Our data suggests a high prevalence of cardiac disease manifestation in PA, considerably higher than in previous studies, where only LV-FS was used to assess LV function. Usage of advanced echocardiographic techniques, such as LV-GLS assessment, may allow for early detection of subtle LV dysfunction in PA, and may lead to timely cardiac treatment but also consideration of liver transplantation to prevent development of manifest cardiac complications.

Rationale and Design of the Cardiac CARE Trial: A Randomized Trial of Troponin-Guided Neurohormonal Blockade for the Prevention of Anthracycline Cardiotoxicity.

Anthracyclines are effective cytotoxic drugs used in the treatment of breast cancer and lymphoma but are associated with myocardial injury, left ventricular dysfunction, and heart failure. Anthracycline-induced cardiotoxicity is highly variable in severity and without a proven therapeutic intervention. β-Adrenergic receptor blockers and renin-angiotensin-system inhibitor therapies have been associated with modest cardioprotective effects in unselected patients. The Cardiac CARE trial is a multicentre prospective randomized open-label blinded end point trial of combination β-adrenergic receptor blocker and renin-angiotensin-system inhibitor therapy in patients with breast cancer and non-Hodgkin lymphoma receiving anthracycline chemotherapy that is associated with myocardial injury. Patients at higher risk of cardiotoxicity with plasma high-sensitivity cTnI (cardiac troponin I) concentrations in the upper tertile at the end of chemotherapy are randomized to standard of care plus combination candesartan and carvedilol therapy or standard of care alone. All patients undergo cardiac magnetic resonance imaging before and 6 months after anthracycline treatment. The primary end point is the change in left ventricular ejection fraction at 6 months after chemotherapy. In low-risk nonrandomized patients, left ventricular ejection fraction before and 6 months after anthracycline will be compared with define the specificity of the high-sensitivity cTnI assay for identifying low-risk participants who do not develop left ventricular systolic dysfunction. Cardiac CARE will examine whether cardiac biomarker monitoring identifies patients at risk of left ventricular dysfunction following anthracycline chemotherapy and whether troponin-guided treatment with combination candesartan and carvedilol therapy prevents the development of left ventricular dysfunction in these high-risk patients.

Study of cardiotoxicity in patients with oncological pathology during chemotherapy

Background. Cardiological complications occur in 20% of all patients receiving chemotherapy for oncological diseases (the most severe are cardiac rhythm and conduction disturbances, myocardial ischemia and the development of heart failure), which complicates further high-quality antitumor therapy. In addition, 44% of all cancer patients have concomitant cardiovascular pathology, more often coronary artery disease and essential hypertension are detected. Carrying out cardiotoxic chemotherapy in this group of patients worsens the prognosis of concomitant disease.Aim. Conduct a retrospective analysis of 237 patients undergoing antitumor therapy at different stages of treatment. The analysis included those patients who received drugs with a mechanism of myocardial damage according to type 1 cardiotoxicity — doxorubicin, cyclophosphamide, Herceptin.Methods. Review of case histories of 237 patients treated in 2021 with doxorubicin (146 patients), cyclophosphamide (86 patients), Herceptin (5 patients).Results. The use of chemotherapy with the drugs listed above causes irreversible myocardial dysfunction due to the death of cardiomyocytes with the development of left ventricular dysfunction and heart failure, and also worsens the course of concomitant cardiovascular pathology in patients. For more detailed data, further research is needed, which is continuously ongoing.Conclusion. To date, the fact of the negative impact of chemotherapy on the cardiovascular system is indisputable, however, detailed studies are required. At Meshalkin National Medical Research Center, it is planned to conduct an electrocardiography, an echocardiography with an assessment of the ejection fraction, a general longitudinal strain of the left ventricle myocardium and left ventricle diastolic dysfunction, laboratory tests (troponin T and I, B-type Natriuretic Peptide (BNP), NT-proBNP) and also a comparison of these data with perfusion tomoscintigraphy of the myocardium of each patient undergoing chemotherapy treatment to identify early criteria for the development of cardiotoxicity after each cycle and at the end of chemotherapy, taking into account the total doses of drugs to obtain more accurate and up-to-date data.

Artificial intelligence-based ECG analysis: current status and future perspectives-Part2 : Recent studies and future

Während grundlegende Aspekte der Anwendung von künstlicher Intelligenz (KI) zur Elektrokardiogramm(EKG)-Analyse in Teil 1 dieser Übersicht behandelt wurden, beschäftigt sich die vorliegende Arbeit (Teil 2) mit einer Besprechung von aktuellen Studien zum praktischen Einsatz dieser neuen Technologien und Aspekte ihrer aktuellen und möglichen zukünftigen Anwendung. Die Anzahl der zum Thema KI-basierte EKG-Analyse publizierten Studien steigt seit 2017 rasant an. Dies gilt vor allem für Untersuchungen, die Deep Learning (DL) mit künstlichen neuronalen Netzen (KNN) einsetzen. Inhaltlich geht es nicht nur darum, die Schwächen der klassischen EKG-Diagnostik mit Hilfe von KI zu überwinden und die diagnostische Güte des Verfahrens zu verbessern, sondern auch die Funktionalität des EKGs zu erweitern. Angestrebt wird die Erkennung spezieller kardiologischer und nichtkardiologischer Krankheitsbilder sowie die Vorhersage zukünftiger Krankheitszustände, z. B. die zukünftige Entwicklung einer linksventrikulären Dysfunktion oder das zukünftige Auftreten von Vorhofflimmern. Möglich wird dies, indem KI mittels DL in riesigen EKG-Datensätzen subklinische Muster findet und für die Algorithmen-Entwicklung nutzt. Die KI-unterstützte EKG-Analyse wird somit zu einem Screening-Instrument und geht weit darüber hinaus, nur besser als ein Kardiologe zu sein. Die erzielten Fortschritte sind bemerkenswert und sorgen in Fachwelt und Öffentlichkeit für Aufmerksamkeit und Euphorie. Bei den meisten Studien handelt es sich allerdings um Proof-of-Concept-Studien. Häufig werden private (institutionseigene) Daten verwendet, deren Qualität unklar ist. Bislang ist nur selten eine klinische Validierung der entwickelten Algorithmen in anderen Kollektiven und Szenarien erfolgt. Besonders problematisch ist, dass der Weg, wie KI eine Lösung findet, bislang meistens verborgen bleibt (Blackbox-Charakter). Damit steckt die KI-basierte Elektrokardiographie noch in den Kinderschuhen. Unbestritten ist aber schon absehbar, dass das EKG als einfach anzuwendendes und beliebig oft wiederholbares diagnostisches Verfahren auch in Zukunft nicht nur weiterhin unverzichtbar sein wird, sondern durch KI an klinischer Bedeutung gewinnen wird.

Basal interventricular septum thinning and long-term left ventricular function in patients with sarcoidosis.

Basal interventricular septum (IVS) thinning on transthoracic echocardiography (TTE) is highly specific to cardiac sarcoidosis. Although basal IVS thinning is listed as one of the five major diagnostic criteria for cardiac sarcoidosis, its association with long-term cardiac function has not been investigated. This study aimed to evaluate the epidemiology and clinical relevance of basal IVS thinning in a clinic-based cohort of patients with sarcoidosis. This retrospective observational study was conducted at a general sarcoidosis clinic. The incidence of basal IVS thinning and associations with variables at baseline and a delayed onset of left ventricular (LV) dysfunction (LV ejection fraction [LVEF]<50%) were analyzed. Of the 1009 patients, 23 (2.3%) had basal IVS thinning. Basal IVS thinning was associated with cardiac pacemaker (PM) implantation at baseline (adjusted odds ratio=20.5; 95% confidence interval [CI]=7.9-53.2; P<0.01). Of the 768 patients with an LVEF of ≥50% at baseline who underwent one or more longitudinal TTEs after baseline, 36 (4.7%) developed LV dysfunction over a median observation period of 88.9 months. Basal IVS thinning and PM implantation at baseline were the independent predictors of a delayed onset of LV dysfunction (basal IVS thinning, adjusted hazard ratio [HR]=3.7; 95% CI=1.5-9.6; PM implantation, adjusted HR=15.7; 95% CI=7.4-33.3). Basal IVS thinning in patients with sarcoidosis can predict a delayed onset of LV dysfunction even when the LV function is preserved at the time of detection.

Mechanism of Pacemaker-Induced Left Ventricular Dysfunction: Study Protocol

A permanent pacemaker (PPM) is currently the definitive treatment for patients with a total atrioventricular block (TAVB). The number of pacemaker implantation has been increasing every year. However, PPM implantation increases the risk of developing left ventricular (LV) dysfunction and becoming pacemaker-induced cardiomyopathy (PICM). There has never been a published study on the cellular mechanism of LV dysfunction caused by PPM implantation. The mechanism of pacemaker-induced left ventricular dysfunction (PILVD) study is a multi-center, quasi-experimental, etiognostic study with a time-series design. This etiognostic study aims to investigate the mechanism of cellular level changes in TAVB patients who had PPM implanted. In particular, the difference in serum miR-155 levels and plasma levels of IL-6, sTNFR-2, MMP-9, N-Cad, and ZO-1 in TAVB patients had LV dysfunction caused by right ventricular dysfunction septal PPM implantation measured by global longitudinal strain (GLS) obtained from echocardiography. Blood samples and echocardiographic examinations will be performed on patients who satisfied the inclusion criteria prior to pacemaker implantation, one month after, and three months following pacemaker implantation. The ELISA method will be used to assess IL-6, sTNFR-2, MMP-9, ZO-1, and N-Cad from plasma samples. MiR-155 levels in serum will be determined using the reverse-transcriptase polymerase chain reaction (RT-PCR) technique. The main findings are a decrease in serum miR-155 levels and increased plasma IL-6, sTNFR-2, MMP-9, N-Cad, and ZO-1 levels in TAVB patients who developed LV dysfunction due to right ventricular septal pacemaker implantation measured by GLS at 1 and 3 months.

Mid-term results of mitral valve replacement and repair: current clinical experience, technical aspects, and risk factor analysis

Aim: We evaluated the short- and mid-term results of mitral valve replacement (MVR) and mitral valve repair (MV-repair). Methods: In total, 168 patients (mean age 67 ± 11 years) underwent MVR (n = 104) and MV-repair (n = 64). To treat posterior leaflet disease, MV-repair techniques included triangular or quadrangular resection (n = 38), P1-P2 plication (n = 4), side-to side P1-P2 (n = 1), posterior-medial commissure-plasty (n = 1), and annuloplasty (n = 20). A prosthetic ring was implanted in all patients. In the presence of degenerative disease involving the anterior leaflet, extensive myxomatous and/or prolapsing pathology of the entire valve, and/or rheumatic and endocarditis degeneration, surgical orientation was to perform MVR directly. When possible, the sub-valvular apparatus with its papillary muscle was partially preserved. The mean follow-up was 38 ± 22 months. Results: Operative mortality (0.96% vs. 1.56%) and six-year survival (94% vs. 100%) were similar in MVR and MV-repair. The only independent predictor of late survival was advanced age at the operation (79.2 years vs. 66.4 years; P = 0.012). Freedom from redo-operation was 100%. Partial preservation of the sub-valvular apparatus with its papillary muscle during MVR allowed postoperatively a better left ventricular function with similar values achieved with MV-repair (P = 0.05), and it was a protective factor against the development of left ventricular dysfunction during follow-up (P = 0.01). Conclusion: MVR and MV-repair are associated with satisfactory results in the short and medium term. MV-repair to treat posterior leaflet disease is associated with a stable and long-lasting result; MVR allows equally satisfactory results in the presence of more extensive and more complex mitral valve disease. Partial preservation of the sub-valvular apparatus favors a better left ventricular systolic function.

IVIG Compared to IVIG Plus Infliximab in Multisystem Inflammatory Syndrome in Children.

OBJECTIVES To compare initial treatment with intravenous immunoglobulin (IVIG) versus IVIG plus infliximab in multisystem inflammatory syndrome in children (MIS-C). METHODS Single-center retrospective cohort study of patients with MIS-C who met Centers for Disease Control and Prevention criteria and received treatment from April 2020 to February 2021. Patients were included and compared on the basis of initial therapy of either IVIG alone or IVIG plus infliximab. The primary outcome was need for additional therapy 24 hours or more after treatment initiation. RESULTS Seventy-two children with MIS-C met inclusion criteria. Additional therapy was needed in 13 of 20 (65%) who received IVIG alone and 16 of 52 (31%) who received IVIG plus infliximab (P = .01). The median (interquartile range) ICU lengths of stay were 3.3 (2.2 to 3.8) and 1.8 (1.1 to 2.1) days, respectively (P = .001). New or worsened left ventricular dysfunction developed in 4 of 20 (20%) and 2 of 52 (4%) (P = .05), and new vasoactive medication requirement developed in 3 of 20 (15%) and 2 of 52 (4%), respectively (P = .13). The median percentage changes in the C-reactive protein level at 24 hours posttreatment compared with pretreatment were 0% (−29% to 66%) and −46% (−62% to −15%) (P &amp;lt; .001); and at 48 hours posttreatment, −5% (−41% to 57%) and −70% (−79% to −49%) respectively (P &amp;lt; .001). There was no significant difference in hospital length of stay, time to fever resolution, vasoactive medication duration, or need for diuretics. CONCLUSIONS Patients with MIS-C initially treated with IVIG plus infliximab compared with those treated with IVIG alone were less likely to require additional therapy and had decreased ICU length of stay, decreased development of left ventricular dysfunction, and more rapid decline in C-reactive protein levels.

Bone Morphogenetic Protein 7 Gene Delivery Improves Cardiac Structure and Function in a Murine Model of Diabetic Cardiomyopathy.

Diabetes is a major contributor to the increasing burden of heart failure prevalence globally, at least in part due to a disease process termed diabetic cardiomyopathy. Diabetic cardiomyopathy is characterised by cardiac structural changes that are caused by chronic exposure to the diabetic milieu. These structural changes are a major cause of left ventricular (LV) wall stiffness and the development of LV dysfunction. In the current study, we investigated the therapeutic potential of a cardiac-targeted bone morphogenetic protein 7 (BMP7) gene therapy, administered once diastolic dysfunction was present, mimicking the timeframe in which clinical management of the cardiomyopathy would likely be desired. Following 18 weeks of untreated diabetes, mice were administered with a single tail-vein injection of recombinant adeno-associated viral vector (AAV), containing the BMP7 gene, or null vector. Our data demonstrated, after 8 weeks of treatment, that rAAV6-BMP7 treatment exerted beneficial effects on LV functional and structural changes. Importantly, diabetes-induced LV dysfunction was significantly attenuated by a single administration of rAAV6-BMP7. This was associated with a reduction in cardiac fibrosis, cardiomyocyte hypertrophy and cardiomyocyte apoptosis. In conclusion, BMP7 gene therapy limited pathological remodelling in the diabetic heart, conferring an improvement in cardiac function. These findings provide insight for the potential development of treatment strategies urgently needed to delay or reverse LV pathological remodelling in the diabetic heart.

Predictors of Right ventricular Pacing induced Left Ventricular dysfunction in Pacemaker Recipients with Preserved Ejection Fraction

Abstract Background Pacemaker (PM) has been an effective treatment in the management of patients with brady-arrhythmias. Chronic RV pacing may cause electrical and mechanical dyssynchrony which lead finally to reduced left ventricular ejection fraction (LVEF). This deterioration of LVEF has been defined as pacemaker induced cardiomyopathy (PICM). The incidence of PICM was described by many studies and ranged between 10% to 26%. The predictors for PICM have not been well studied. These studies were limited by variation in follow-up period and definition of PICM. Objective to study the incidence and predictors of PICM in patients who underwent pacemaker implantation in Ain shams University hospital. Patients and Methods This retrospective study included 160 patients who underwent single or dual chamber pacemaker implantation in Ain shams university hospital between 2010 and 2017 with the mean period 4.7±2.0 years. Implantable cardioverter defibrillator (ICD) and cardiac resynchronization therapy (CRT) patients were excluded. Individuals who had baseline transthoracic echocardiography (TTE) with normal LVEF ≥ 50% before implantation were included. Results This study included 160 patients who had single or dual chamber pacemaker implantation between 2010 and 2017. 45% were males and 55% were females, mean age was 55.5 years. It showed that the incidence of PICM is 7.5%. Wider native QRS durations, particularly &amp;gt;140 ms (p &amp;lt; 0.001), wider pQRS duration &amp;gt;150 ms (p &amp;lt; 0.001), Low normal ejection fraction &amp;lt;56 % preimplantation (p = 0.023) and increased LVEDD&amp;gt;53 mm and LVESD&amp;gt;38 mm (p &amp;lt; 0.001) are predictors for the development of PICM. Female gender was independent predictor for PICM (p = 0.058). There was no association between burden of right ventricular pacing (p = 0.782) or pacing site (p = 0.876) with the risk of development of left ventricular dysfunction. Conclusion The incidence of right ventricular pacing-induced left ventricular dysfunction is not uncommon, with an observed incidence of 7.5% in the current study. Wider native and paced QRS durations, Low normal ejection fraction (&amp;lt; 56 %) pre-implantation and increased LVEDD /LVESD post implantation are the most important predictors for the development of PICM. List of abbreviations PM= pacemaker, RV= Right ventricle, PICM = pacemaker induced cardiomyopathy, TTE= transthoracic echocardiography, DM= Diabetes Mellitus, HTN= Hypertension, BMI= Body Mass index, pQRSd= Paced QRS duration, SWMA= segmental wall motion abnormality, AF= Atrial fibrillation, SSS= Sick sinus syndrome, CHB= Complete heart block, AVB= Atrioventricular block, LVEF = left ventricular ejection fraction, LVEDD= Left ventricular end diastolic diameter, LVESD= Left ventricular end systolic diameter, ms= milli second.

Cardiac Toxicity: Using Angiotensin-Converting Enzyme Inhibitors to Prevent Anthracycline-Induced Left Ventricular Dysfunction and Cardiomyopathy

Anthracycline chemotherapies are effective in many different types of cancer. However, cumulative doses are associated with irreversible cardiac toxicity, most frequently manifested in the development of left ventricular dysfunction, cardiomyopathy, and congestive heart failure. The onset of cardiomyopathy and subsequent heart failure can result in the interruption or discontinuation of therapy. Cardioprotective agents, particularly angiotensin- converting enzyme inhibitors, have been shown to slow the progression of left ventricular dysfunction and prevent heart failure. This review assesses the efficacy of angiotensin-converting enzyme inhibitors in the prevention of anthracycline-induced left ventricular dysfunction. A literature search was performed using four electronic databases. Evidence from this review suggests that angiotensin-converting enzyme inhibitors may be effective in preventing or reducing anthracycline- induced left ventricular dysfunction and subsequent cardiomyopathy and heart failure.