Infective Endocarditis

2014 ◽  
pp. 18-26
Author(s):  
Anju Nohria
Keyword(s):  
Heart Failure ◽  
Infective Endocarditis ◽  
Heart Valves ◽  
Interventricular Septum ◽  
Inflammatory Cells ◽  
Chordae Tendineae ◽  
Systemic Complications ◽  
Fungal Endocarditis ◽  
Mycotic Aneurysms ◽  
Endocardial Surface

Infective endocarditis (IE) is an infection of the endocardial surface of the heart. It is characterized by one or more vegetations, which comprise a mass of platelets, fibrin, microorganisms, and inflammatory cells. IE primarily involves the heart valves (native or prosthetic). Other structures may also be involved, including the interventricular septum, the chordae tendineae, the mural endocardium, or intracardiac devices such as a pacemaker. The most common infective causes are bacterial; however, fungal endocarditis can be seen in patients who are immunocompromised. There is controversy about the existence of viral endocarditis. Valvular involvement in IE may lead to congestive heart failure, conduction abnormalities, and myocardial abscesses. Systemic complications in IE include embolization of both sterile and infected emboli, abscess formation, and mycotic aneurysms.

scholarly journals Infektif Endokarditis Pada Penyakit Jantung Tiroid

2020 ◽  
Vol 9 (1) ◽  
pp. 113
Author(s):  
Pradita Diah Permatasari
Keyword(s):  
Heart Failure ◽  
Infective Endocarditis ◽  
Blood Culture ◽  
Mitral Regurgitation ◽  
Heart Valves ◽  
Clinical Symptoms ◽  
Predisposing Factor ◽  
Duke Criteria ◽  
Cardiac Lesions ◽  
Endocardial Surface

Infective endocarditis is an endocardial surface infection of the heart including heart valves that can be fatal. Occurs because there is damage to the surface of the endocardium and the entry of bacteria into the circulation. The presence of cardiac lesions such as mitral regurgitation can be a predisposing factor for infective endocarditis. Patients were diagnosed with infective endocarditis based on a scoring system consisting of clinical symptoms, imaging, and blood culture findings, namely: modified Duke criteria. Treatment of infective endocarditis consists of giving antibiotics and evacuating vegetation by surgery. Surgical action is indicated if there is symptoms of heart failure, uncontrolled infections and vegetation size are too large, causing the risk of embolism.

Prevention and Management of Infective Endocarditis

1991 ◽  
Vol 4 (5) ◽  
pp. 295-313
Author(s):  
Julie McMorrow ◽  
Milap C. Nahata
Keyword(s):  
Infective Endocarditis ◽  
Heart Valves ◽  
Hospital Admissions ◽  
Pediatric Hospital ◽  
Invasive Procedures ◽  
Congenital Cardiac Defects ◽  
Septal Defects ◽  
Endocardial Surface ◽  
Diagnosis Therapy ◽  
Heart Wall

Infective endocarditis is an infection of the endocardial surface of the heart and usually involves one or more heart valves but may occur on septal defects or the heart wall. Its incidence is approximately 1 per 1,000 adults and 0.5 per 1,000 pediatric hospital admissions. Factors predisposing to infective endocarditis include degenerative heart disease, survivable congenital cardiac defects, use of invasive procedures, chronic immunosuppression, and intravenous drug abuse. This article discusses the pathophysiology, diagnosis, therapy, and prevention of infective endocarditis.

scholarly journals Neurologic Manifestations of Infective Endocarditis

2019 ◽  
Vol 16 (3) ◽  
pp. 63-68
Author(s):  
Cristina Dumitrescu ◽  
Alin Badea ◽  
Ioana Păltineanu ◽  
Dan Mitrea ◽  
Radu Mihăilescu ◽  
...  
Keyword(s):  
Nervous System ◽  
Infective Endocarditis ◽  
Heart Valves ◽  
Transoesophageal Echocardiography ◽  
Mitral Valves ◽  
The Past ◽  
Streptococcus Gallolyticus ◽  
Potential Source ◽  
Gradual Onset ◽  
Endocardial Surface

AbstractInfective endocarditis is an infection of the endocardial surface of the heart. Usually, it affects one or more heart valves or an intracardiac device. Neurologic events (silent or symptomatic) account for 20 to 40% of all patients with infective endocarditis.We are presenting the case of a 57 -year-old man with cardiovascular risk factors admitted to our clinic for aphasia. His medical history included a recent stroke and small fiber neuropathy with a gradual onset for the past six months. Despite extensive investigations, no cause for strokes and neuropathy could be found. To identify a potential source of embolism, a transoesophageal echocardiography was performed. It revealed vegetation attached to both aortic and mitral valves. Blood cultures were positive for Streptococcus gallolyticus. The patient underwent emergency aortic and mitral valve replacement and a 6-week course of antibiotic treatment with ceftriaxone and gentamicin with the improvement of both aphasia and peripheral neuropathy.Central nervous system complications such as encephalopathy, seizures, stroke or severe cerebral hemorrhage are commonly described in infective endocarditis, but peripheral nervous system involvement is rarely reported in the literature. Although no cause for neuropathy has been found, it is difficult to asses whether it was a complication of the infective endocarditis.

Infective and inflammatory cardiac conditions

2010 ◽  
pp. 191-224
Author(s):  
Juan Carlos Kaski
Keyword(s):  
Clinical Practice ◽  
Infective Endocarditis ◽  
Heart Valves ◽  
Antimicrobial Prophylaxis ◽  
Current Clinical Practice ◽  
Cardiac Tissues ◽  
Prosthetic Valves ◽  
Fungal Endocarditis ◽  
Culture Negative

Infective endocarditis 192 Treatment of endocarditis 194 Enterococcal endocarditis 204 Endocarditis caused by HACEK organisms 210 Fungal endocarditis 212 Culture-negative endocarditis 214 Antimicrobial prophylaxis 218 Pericarditis 220 Myocarditis 223 Infective endocarditis is an infection of the endocardium which usually involves the heart valves. In current clinical practice, endocarditis encompasses a heterogeneous collection of infections that may involve native cardiac tissues, prosthetic valves, pacing systems, and a variety of intracardiac implants. Endocarditis is mainly caused by bacteria, but fungi are occasionally implicated....

scholarly journals Infective endocarditis or myxoma? Description of a patient with new diagnosis of congestive heart failure

2015 ◽  
Vol 78 (2) ◽  
Author(s):  
Marzia Testa ◽  
Enrico Lombardo ◽  
Enrico Avogadri ◽  
Marco Agostini ◽  
Giuseppe Forte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Infective Endocarditis ◽  
Inflammatory Disease ◽  
Diagnostic Tool ◽  
Heart Valves ◽  
New Diagnosis

ABSTRACT: Infective endocarditis (IE) is an inflammatory disease which interests heart endothelium and mostly heart valves. IE is not a uniform disease, but presents in a variety of different forms that makes the diagnosis difficult. Echocardiography is a crucial diagnostic tool for the diagnosis, especially in those patients who have no typical symptoms as in the case here presented, in which the possibility of a myxoma was also considered.

Early Surgical Intervention for Infective Endocarditis

2002 ◽  
Vol 10 (4) ◽  
pp. 298-301 ◽  
Author(s):  
Hong Sheng Zhu ◽  
Pei Yan Yao ◽  
Jia Hao Zheng ◽  
A Thomas Pezzella
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Heart Disease ◽  
Infective Endocarditis ◽  
Complex Disease ◽  
Surgical Intervention ◽  
Elective Surgery ◽  
Postoperative Bleeding ◽  
Arterial Embolization ◽  
Early Surgical Intervention

Infective endocarditis remains a serious and complex disease with significant morbidity and mortality. Sixty cases of infective endocarditis were retrospectively reviewed, consisting of 41 males and 19 females aged 7 to 50 years (mean, 30 years). Congenital heart disease was diagnosed in 19 of the patients and rheumatic heart disease in 41. Congestive heart failure occurred in 36 and systemic embolism in 8 cases. Blood cultures were positive in only 21.7% of the cases, while vegetations were detected by 2-dimensional echocardiography in 70%. Elective surgery was performed in 57 patients and emergent operation for systemic arterial embolization and/or intractable congestive heart failure in 3 patients. Two patients required reoperation for postoperative bleeding. All but 2 patients had been followed up for 6 to 160 months with no evidence of reinfection. Three patients with mechanical valve implantation later died of intracranial bleeding due to over-anticoagulation. The remaining 55 resumed normal activity. The encouraging outcomes were the result of an aggressive diagnostic approach and early surgical intervention.

Abstract WP335: Intracranial Mycotic Aneurysms in Infective Endocarditis: Incidence, Predictors and Outcome

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Mehmet A Topcuoglu ◽  
Oguzhan Kursun ◽  
Ferdinando S Buonanno ◽  
Aneesh B Singhal
Keyword(s):  
Infective Endocarditis ◽  
Mitral Regurgitation ◽  
Multivariable Analysis ◽  
Native Valve ◽  
Duke Criteria ◽  
Mycotic Aneurysms ◽  
Mean Size ◽  
Pre Treatment ◽  
Cardiac Valve Disease

Introduction: Intracranial mycotic aneurysms (IMA) are rare but serious complications of infective endocarditis (IE). Methods and Results: In this retrospective study (1980-2011) we used original Duke criteria to diagnose IE in 1149 episodes (1081 patients; 81% definite, 80% native valve). Neuro complications occurred in 28%, stroke in 22% (202 infarcts, 53 hemorrhages) and 1% had TIA/TMB. N=33 IMA were detected in 23 (2%) patients. IMA were detected in 8% with focal neuro deficits, 13% with seizures, and 3% with encephalopathy. IMA-related symptoms were present in 22 of 23 cases: headache 48%, seizure 13%, altered sensorium 35% and focal deficits 61%. IMA were detected in 0/885 without stroke, 5.4% with infarcts and 22.6% with hemorrhages (p<0.001); the latter included 9/36 (25%) with ICH, 3/13 (23%) with SAH, and 0/4 with SDH. Of the 23 IMA patients 61% had hemorrhage, 30% had SAH and 57% had infarcts. IMAs were detected by DSA in 21/166 (12.7%). The mean size was 3.6±2.4 mm; 30% multiple; 61% located in distal segments; and 67% in MCA branches. On MRI, 31 had any SAH and 45 had any ICH; IMA detected in 6/9 with diffuse SAH, 2/22 with convexal SAH, 11/45 with ICH, and 11/202 with infarcts. Patients with IMA had higher rates of women, hypertension, known cardiac valve disease, mitral regurgitation, mitral vegetation and S.viridians infection (all p<0.05). On multivariable analysis, mitral regurgitation with vegetation (OR 5.9, 95% CI 2.5-14.0, p<0.001) was the only independent predictor of IMA. Clipping was performed in 8 (all pre-2000); endovascular treatment in 7 (all post-1997); 2 died pre- treatment; 1 detected on autopsy; 1 no follow-up available, and 4 regressed/disappeared with antibiotics. Patients with and without IMA showed no difference in rates of in-hospital mortality (22% v. 19%, p=0.93), and length of stay (32d v. 24d, p=0.28). IMA rates did not decrease during the study period (2.2% in 784 episodes 1980-2000 vs. 1.6% of 365 episodes 2001-2011, p=0.653). Conclusion: IMA are invariably heralded by neurological symptoms and stroke (especially hemorrhages) on brain imaging. Mitral IE has the highest risk for IMA. IMAs can resolve with antibiotics however studies are needed to determine the efficacy of different treatment approaches.

Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca 2+ -ATPase Expression in Cardiomyocytes

Circulation ◽  
2021 ◽  
Author(s):  
Mortimer Korf-Klingebiel ◽  
Marc R. Reboll ◽  
Felix Polten ◽  
Natalie Weber ◽  
Felix Jäckle ◽  
...  
Keyword(s):  
Heart Failure ◽  
Bone Marrow ◽  
Endoplasmic Reticulum ◽  
Growth Factor ◽  
Plasma Concentrations ◽  
Pressure Overload ◽  
Inflammatory Cells ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Wild Type

Background: Inflammation contributes to the pathogenesis of heart failure, but there is limited understanding of inflammation's potential benefits. Inflammatory cells secrete myeloid-derived growth factor (MYDGF) to promote tissue repair after acute myocardial infarction. We hypothesized that MYDGF has a role in cardiac adaptation to persistent pressure overload. Methods: We defined the cellular sources and function of MYDGF in wild-type, Mydgf -deficient ( Mydgf -/- ), and Mydgf bone marrow-chimeric or bone marrow-conditional transgenic mice with pressure overload-induced heart failure after transverse aortic constriction surgery. We measured MYDGF plasma concentrations by targeted liquid chromatography-mass spectrometry. We identified MYDGF signaling targets by phosphoproteomics and substrate-based kinase activity inference. We recorded Ca 2+ transients and sarcomere contractions in isolated cardiomyocytes. Additionally, we explored the therapeutic potential of recombinant MYDGF. Results: MYDGF protein abundance increased in the left ventricular (LV) myocardium and in blood plasma of pressure-overloaded mice. Patients with severe aortic stenosis also had elevated MYDGF plasma concentrations, which declined after transcatheter aortic valve implantation. Monocytes and macrophages emerged as the main MYDGF sources in the pressure-overloaded murine heart. While Mydgf -/- mice had no apparent phenotype at baseline, they developed more severe LV hypertrophy and contractile dysfunction during pressure overload than wild-type mice. Conversely, conditional transgenic overexpression of MYDGF in bone marrow-derived inflammatory cells attenuated pressure overload-induced hypertrophy and dysfunction. Mechanistically, MYDGF inhibited G protein coupled receptor agonist-induced hypertrophy and augmented sarco/endoplasmic reticulum Ca 2+ ATPase 2a (SERCA2a) expression in cultured neonatal rat cardiomyocytes by enhancing PIM1 serine/threonine kinase expression and activity. Along this line, cardiomyocytes from pressure-overloaded Mydgf -/- mice displayed reduced PIM1 and SERCA2a expression, greater hypertrophy, and impaired Ca 2+ cycling and sarcomere function compared to cardiomyocytes from pressure-overloaded wild-type mice. Transplanting Mydgf -/- mice with wild-type bone marrow cells augmented cardiac PIM1 and SERCA2a levels and ameliorated pressure overload-induced hypertrophy and dysfunction. Pressure-overloaded Mydgf -/- mice were similarly rescued by adenoviral Serca2a gene transfer. Treating pressure-overloaded wild-type mice subcutaneously with recombinant MYDGF enhanced SERCA2a expression, attenuated LV hypertrophy and dysfunction, and improved survival. Conclusions: These findings establish a MYDGF-based adaptive crosstalk between inflammatory cells and cardiomyocytes that protects against pressure overload-induced heart failure.

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