[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"conditionNormalized\":\"sepsis-induced-cardiomyopathy\",\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:sepsis-induced-cardiomyopathy":86},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,4,0,[8,40,73,97],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":14,"acronym":4,"eligibilityCriteria":15,"healthyVolunteers":11,"sex":16,"minAge":17,"maxAge":18,"enrollmentInfo":19,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":23,"conditions":24,"keywords":4,"overallStatus":27,"whyStopped":4,"lastUpdateSubmitDate":28,"lastUpdatePostDateStruct":29,"startDateStruct":32,"completionDateStruct":34,"leadSponsor":36,"locationsCount":39},"100631166","sepsis-induced-myocardial-injury-in-critically-ill-children-100631166",false,"NCT07497139","Sepsis Induced Myocardial Injury in Critically Ill Children","Predictors and Outcome Of Sepsis Induced Myocardial Injury In Critically Ill Children; A Prospective Observational Study","Inclusion Criteria:\n\n1. Pediatric population aged 1month to 18 years.\n2. Critically ill children (who has an illness or injury impairing one or more vital organ systems such that there is high probability of imminent or life-threatening deterioration in the patient's condition)\n3. Has clinically and laboratory manifestations of sepsis\n\nExclusion Criteria:\n\n1. Neonates and adults ( \\\u003C1 month or \\>18 years)\n2. Children with congenital heart disease\n3. Children with Acquired heart disease ( Rheumatic, Myocarditis or Cardiomyopathy)\n4. Cardiac surgery","ALL","1 Month","18 Years",{"count":20,"type":21},84,"ESTIMATED","OBSERVATIONAL","Sepsis is a dysregulated immune response due to infection, leading to life-threatening organ dysfunction affecting respiratory, renal, immunological, digestive, neurological, and cardiovascular organs. The prevalence of cardiovascular dysfunction caused by sepsis may reach up to 50%, and the symptoms may comprise vasodilatory shock, myocardial injury, arrhythmia, and sepsis-induced cardiomyopathy. (1) Sepsis-induced cardiomyopathy occurs frequently in critically ill patients, but the clinical features and prognostic impact of sepsis-induced cardiomyopathy on sepsis outcome remain controversial.\n\nCardiac troponins I and T are regulatory proteins that control the calcium-mediated interaction of actin and myosin, producing myocardial contraction. Since troponins do not occur in extracellular space, their appearance in serum is sensitive and specific marker of myocardium damage. They have been established as the gold standard biochemical markers for myocardial necrosis .\n\nElevated cardiac troponins levels have been detected in critically ill children with congenital heart disease before and after cardiac surgery.(2) Echocardiography is the cornerstone for the diagnosis of septic cardiomyopathy. There is consensus and expert opinion that every hemodynamically unstable patient should receive critical care echocardiography.(3) Improved understanding of sepsis induced myocardial injury is important for multiple reasons. First, cardiac function is crucial for maintaining hemodynamic stability in patients with septic shock. Second, by understanding the clinical features and predictors of sepsis induced myocardial injury, the investigators can discriminate sepsis-induced cardiomyopathy from other cardiac diseases and avoid unnecessary invasive procedures, such as coronary angiography, a risky procedure in critically ill patients. Thus, the investigators aimed to define clinical predictors of sepsis-induced cardiomyopathy and assess the clinical course and outcome of sepsis-induced cardiomyopathy in patients with sepsis.",[25,26],"Sepsis Induced Cardiomyopathy","Sepsis Induced Myocardial Dysfunction","NOT_YET_RECRUITING","2026-03-23",{"date":30,"type":31},"2026-03-27","ACTUAL",{"date":33,"type":21},"2026-04-01",{"date":35,"type":21},"2028-04-01",{"name":37,"class":38},"Assiut University","OTHER",1,{"id":41,"slug":42,"hasResults":11,"nctId":43,"briefTitle":44,"officialTitle":44,"acronym":45,"eligibilityCriteria":46,"healthyVolunteers":11,"sex":16,"minAge":18,"maxAge":4,"enrollmentInfo":47,"targetDuration":4,"studyType":49,"phases":50,"briefSummary":52,"conditions":53,"keywords":54,"overallStatus":27,"whyStopped":4,"lastUpdateSubmitDate":64,"lastUpdatePostDateStruct":65,"startDateStruct":67,"completionDateStruct":69,"leadSponsor":71,"locationsCount":4},"100589263","hemodynamic-effects-of-ketone-esters-in-patients-with-sepsis-induced-cardiomyopathy-100589263","NCT06952140","Hemodynamic Effects of Ketone Esters in Patients With Sepsis Induced Cardiomyopathy","KetoSIC","Inclusion Criteria:\n\n* Patients ≥ 18 years of age admitted to the the intensive care unit (ICU)\n* LVEF \\\u003C 50% determined by a screening echocardiography and analysed according to the Simpson biplane method\n* Ability for study personnel to perform transthoracic echocardiography\n* Suspected or documented infection (suspected infection is defined as ongoing antibiotic treatment and\u002For body fluid culture sampling performed within 72 hours before screening)\n\nExclusion Criteria:\n\n* Diagnosis of heart failure with reduced ejection fraction prior to ICU admission according to health records\n* Surgical cause of ICU admission\n* For patients in shock: Other primary causes of shock than sepsis (i.e. hypovolemia, haemorrhage, cardiogenic etiology, pulmonary embolism, anaphylaxis)\n* Blood pH \\\u003C 7.20\n* Severe gastroparesis\n* Inability to position a nasogastric tube",{"count":48,"type":21},12,"INTERVENTIONAL",[51],"NA","Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection and is associated with a high mortality rate in the ICU. Sepsis induced cardiomyopathy (SICM) is a multi-factorial process that appears in approximately 50% of patients with sepsis\u002Fseptic shock and is associated with increased mortality. It is suggested that ketone bodies are more efficient substrates of energy metabolism than glucose, with a lower oxygen consumption per ATP-molecule produced and that the failing human heart increases the capacity to metabolize ketones. Previous studies have found acute beneficial hemodynamic effects of ketone esters in patients with chronic heart failure and cardiogenic shock, respectively. Improved hemodynamics and reduced systemic oxygen consumption as an effect of ketone esters might be of great benefit in patients admitted to the ICU. Thus, the investigators aim to investigate the hemodynamic effects of ketone esters in patients with sepsis induced cardiomyopathy in this randomized, placebo-controlled, double-blinded, cross-over, acute intervention study. .",[25],[55,56,57,58,59,60,61,62,63],"Sepsis induced cardiomyopathy","Sepsis","Hemodynamics","Ketone ester","Ketones","Echocardiography","Randomized controlled trial","Cross-over trial","Cardiovascular","2026-03-03",{"date":66,"type":31},"2026-03-04",{"date":68,"type":21},"2026-03-10",{"date":70,"type":21},"2027-12-31",{"name":72,"class":38},"Tor Biering-Sørensen",{"id":74,"slug":75,"hasResults":11,"nctId":76,"briefTitle":77,"officialTitle":78,"acronym":79,"eligibilityCriteria":80,"healthyVolunteers":11,"sex":16,"minAge":18,"maxAge":4,"enrollmentInfo":81,"targetDuration":4,"studyType":49,"phases":83,"briefSummary":84,"conditions":85,"keywords":4,"overallStatus":27,"whyStopped":4,"lastUpdateSubmitDate":88,"lastUpdatePostDateStruct":89,"startDateStruct":91,"completionDateStruct":93,"leadSponsor":95,"locationsCount":4},"100573355","recombinant-human-brain-natriuretic-peptide-for-the-recovery-stage-of-septic-shock-100573355","NCT06745206","Recombinant Human Brain Natriuretic Peptide for the Recovery Stage of Septic Shock","Recombinant Human Brain Natriuretic Peptide for the Recovery Stage of Septic Shock: An Interventional Pilot Study","rh-BNP-RSS","Inclusion criteria:\n\n1. Age \\>18 years.\n2. Septic shock in recovery phase with decreasing vasopressor requirements, which is defined as:\n\n   1. Fulfilling the Sepsis-3 definition of septic shock at initial stage.\n   2. Hemodynamic stability achieved after adequate initial resuscitation and individualized hemodynamic optimization.\n   3. Controlled infection source with 48-hour trend of improving temperature, white blood cell count, and procalcitonin.\n   4. 48-hour trend of decreasing vasopressor requirements and transition to negative fluid balance.\n   5. Adequate perfusion with warm extremities, and capillary refill time \\\u003C3 seconds.\n3. Ongoing pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and sinus rhythm.\n4. Volume indicators above the lower limit of normal range, with global end-diastolic volume index (GEDI) \\>680 mL\u002Fm2 and central venous pressure (CVP) \\>8 mmHg.\n5. Signs of cardiac dysfunction: BNP\\>200\\[10\\] or NT-proBNP \\>900 pg\u002Fml\\[6\\] or reduced ejection fraction (LVEF) \\\u003C 50%.\n6. No bolus dose of diuretics had been administered in the previous 6 hours.\n7. Informed consent obtained from patient\u002Flegal representative.\n\nExclusion Criteria:\n\n1. Pregnancy or lactation.\n2. Arrhythmia.\n3. Advanced renal dysfunction (Acute Kidney Injury \\[AKI\\] stage 3 or Chronic Kidney Disease \\[CKD\\] stage 3b or higher) based on Kidney Disease: Improving Global Outcomes (KDIGO) criteria.\n4. Inadequate ultrasound window preventing acquisition of diagnostic-quality images.\n5. Trauma or neurological diseases (including intracerebral hemorrhage and cerebral infarction).\n6. Pre-existing severe heart failure (New York Heart Association \\[NYHA\\] class III-IV) or acute myocardial infarction within the past 30 days.\n7. Concurrent enrollment in interventional trials that could confound study outcomes.\n\nCriteria for withdrawing from the study:\n\n1. Withdrawal of the informed consent.\n2. Severe hemodynamic deterioration necessitating the discontinuation of all vasodilatory medications.\n3. Treating clinician's decision.",{"count":82,"type":21},30,[51],"As infection control improves and circulation stabilizes, treatment de-escalation of septic shock begins, accompanied by fluid redistribution from interstitial spaces to the vasculature, increasing cardiac volume load. Synthetic recombinant human BNP (rh-BNP) plays a role in inducing vasodilation, particularly in the venous system, alleviating cardiac congestion, and enhancing natriuresis and diuresis. Thus the investigators designed a single-center, prospective physiological study to evaluate the efficacy of standard rh-BNP infusion in reducing venous return and enhancing fluid removal, with a secondary objective of assessing the maintenance of perfusion pressure and tissue perfusion.",[86,87],"Sepsis-induced Cardiomyopathy","the Recovery Phase of Septic Shock","2025-07-23",{"date":90,"type":31},"2025-07-29",{"date":92,"type":21},"2025-12",{"date":94,"type":21},"2026-09",{"name":96,"class":38},"Sichuan Provincial People's Hospital",{"id":98,"slug":99,"hasResults":11,"nctId":100,"briefTitle":101,"officialTitle":102,"acronym":103,"eligibilityCriteria":104,"healthyVolunteers":11,"sex":16,"minAge":18,"maxAge":4,"enrollmentInfo":105,"targetDuration":4,"studyType":49,"phases":107,"briefSummary":108,"conditions":109,"keywords":111,"overallStatus":118,"whyStopped":4,"lastUpdateSubmitDate":119,"lastUpdatePostDateStruct":120,"startDateStruct":122,"completionDateStruct":124,"leadSponsor":126,"locationsCount":39},"100500188","characterization-of-primary-and-secondary-stress-related-takotsubo-100500188","NCT05793008","Characterization of priMary And sEcondary STress Related takOtsubo","Characterization of priMary And sEcondary STress Related takOtsubo: the MAESTRO Pilot Study","MAESTRO","Inclusion Criteria:\n\nFor patients with TTS:\n\n* Informed consent signed by the patient or parent\u002Fguardian\u002Flegal representative.\n* TTS diagnosed based on modified Mayo Clinic Diagnostic Criteria as: (i) transient wall motion abnormality in the left ventricle beyond a single epicardial coronary artery distribution; (ii) absence of obstructive coronary artery disease or angiographic evidence of acute plaque rupture, which can explain the wall motion abnormality; (iii) new electrocardiographic abnormalities or elevation in cardiac troponin values; (iv) absence of pheochromocytoma or myocarditis. N.B. - All TTS diagnosis made according to Mayo Clinic Diagnostic Criteria will be a posterior compared to fulfil the new InterTAK Diagnostic Criteria (19). Myocarditis will be suspected based on clinical presentation (e.g. previous flu-like symptoms, increased inflammatory biomarkers) and confirmed by cardiac magnetic resonance.N.B. - Of note, primary TTS mainly concerns post-menopausal women with symptoms resulting from myocardial damage, emotional trigger, and evidence of normal coronary arteries at coronary angiography, whilst secondary TTS equally affects men and women, with physical triggers and in the presence of possible coronary artery disease at coronary angiography.\n\nFor patients with sepsis:\n\n* Informed consent signed by the patient or parent\u002Fguardian\u002Flegal representative.\n* Diagnosis of sepsis, defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, which can be represented by an increase in the Sequential \\[Sepsis-related\\] Organ Failure Assessment (SOFA) score of 2 points or more.\n* Septic a shock, defined as vasopressor requirement to maintain a mean arterial pressure of 65 mmHg or greater and serum lactate level greater than 2 mmol\u002FL (\\>18 mg\u002FdL) in the absence of hypovolemia.\n* Sepsis-induced cardiomyopathy, defined as left ventricular systolic dysfunction (LVSD) and\u002For LV diastolic dysfunction (LVDD) following sepsis in patients without known structural or functional cardiac disease.\n\nExclusion Criteria:\n\n* Alternate diagnosis for the clinical presentation.\n* Contraindication to PET for patients with TTS (pregnancy, breast-feeding or patients considering becoming pregnant during the study period);\n* Patients with comorbidities having an expected survival \\\u003C1-year.",{"count":106,"type":21},60,[51],"Takotsubo syndrome (TTS) is an acute and reversible form of myocardial injury often preceded by a physical or emotional trigger. Although TTS was generally considered a benign disease for its reversible nature, it is now clear that hemodynamic and electrical instability during the acute phase exposes patients to frequent serious adverse in-hospital complications. However, the pathophysiology of TTS is far from being completely understood. Consistent evidence demonstrated that the environmental events experienced by most of these patients and perceived as stressful (both physical or emotional) induce a brain activation and a stress-related response, with increasing bioavailability of local and circulating stress mediators, such as catecholamine and cortisol, which showed to play a major role in the etiology of to the \"neurogenic stunning myocardium\" responsible for this clinical condition.\n\nPrimary and secondary TTS showed an important clinical heterogeneity identifying two different subtypes of patients with different outcomes and risk profiles. the invastigators hypothesize that a different activation of the brain structures involved in acute stress response, as well as a different exposure to chronic stress, may subtend the different clinical and risk profiles observed in primary vs. secondary TTS patients. Moreover, the invastigators hypothesize that distinct signatures of circulating biomarkers may be associated with these two categories of TTS patients. Therefore, identifying these specific signatures may help in the diagnosis of these patients and pave the way for the identification of specific pathophysiologic pathways and the development of future therapies.",[110,86],"Takotsubo Cardiomyopathy",[112,113,114,115,116,117],"Takotsubo Syndrome","Fisical trigger","Emotional trigger","Biomarker","Precision Medicine","Neuroimaging approach","RECRUITING","2024-02-23",{"date":121,"type":31},"2024-02-26",{"date":123,"type":31},"2023-03-30",{"date":125,"type":21},"2026-09-02",{"name":127,"class":38},"Fondazione Policlinico Universitario Agostino Gemelli IRCCS"]