Treatment Trends of Myocarditis with Coxsackievirus B3 infection

2020 ◽  
pp. 19-30
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Mortality Rate ◽  
Viral Myocarditis ◽  
Inflammatory Cells ◽  
Coxsackievirus B3 ◽  
Basic Knowledge ◽  
Cardiac Damage ◽  
Viral Particles ◽  
Treatment Trends

Viral myocarditis occurred after viral invasion of the cardiocytes and followed by the releasing of viral particles and inflammatory cells. Acute viral myocarditis is relatively common phase of the disease cured spontaneously in some cases or leading to sever acute heart failure and cardiac damage ended with chronic heart failure with increased mortality rate. The fully understand mechanism of viral myocarditis is unclear but some hypothesis trying to illustrate the events of the disease. Regardless of etiological cause, myocarditis is treated depending on disease phase and by following the instructions of Heart Failure Society of America guideline. This article provides the basic knowledge available in literatures to review some important informations of viral myocarditis, with a special focusing on viral myocarditis caused by coxsackievirus B3 infection.

Chronic heart failure

2020 ◽  
pp. 217-240
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Mortality Rate ◽  
Adult Population ◽  
Age Groups ◽  
Severe Heart Failure ◽  
Signs And Symptoms ◽  
Developed Countries ◽  
Clinical Syndrome ◽  
The Uk

Heart failure is a complex clinical syndrome of signs and symptoms that suggest the ability of the heart to pump effectively has been impaired. It is distinguished by dyspnoea, effort intolerance, fluid retention, and poor survival. The prevalence of heart failure is around 1–2% in the adult population in developed countries, and 920 000 people in the UK have heart failure. The incidence of heart failure has decreased; however, the number of people newly diagnosed with heart failure has increased. This is thought to be largely due to an ageing population, improvement in the management and survival of people with ischaemic heart disease, and effective treatment of heart failure. The condition can occur in all age groups; however, the incidence and prevalence steeply increase with age. The average age at first diagnosis is typically 77yrs. Chronic heart failure (CHF) has a poor prognosis, the mortality rate for CHF being worse than for many cancers. It is estimated that 70% of those hospitalized for the first time with severe heart failure will die within 5yrs. However, this has been improving, with 6mth mortality rate ↓ from 26% in 1995, 15% in 2009, to 8.9% in 2016. This chapter will outline the aetiology, pathophysiology, and management of CHF, including considerations for palliative care.

scholarly journals Ventricular septal rupture presented with chronic heart failure symptoms: a case report

2019 ◽  
Vol 3 (2) ◽  
Author(s):  
Ioannis Michelis ◽  
Ioannis Kontonasakis ◽  
Christina Tsakliadou ◽  
Nikolaos Kouvelas
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Mortality Rate ◽  
High Mortality ◽  
Medical Attention ◽  
Mechanical Complication ◽  
Ventricular Septal Rupture ◽  
Elective Repair ◽  
Very High

Abstract Background Ventricular septal rupture (VSR) is a rare mechanical complication following acute myocardial infarction, with very high mortality rate. Haemodynamic deterioration and cardiogenic shock is common in such cases. Rarely, however, patients may show only signs of chronic heart failure or be completely asymptomatic. Case summary We report a case of a 72-year-old male patient with VSR following a transmural myocardial infarction. He sought medical attention only after gradually experiencing symptoms of chronic heart failure, weeks after the onset of the myocardial infarction. The patient successfully underwent elective repair surgery, after optimizing the medical therapy and completing the necessary workup. Discussion Ventricular septal rupture repair is necessary in all cases due to the high mortality rate if left untreated. The timing of the operation, however, should be decided individually for every patient. Haemodynamically unstable patients may require early surgery, but in stable patients responding to medical treatment, delayed repair may be the best option.

scholarly journals Severe T-System Remodeling in Pediatric Viral Myocarditis

2021 ◽  
Vol 7 ◽  
Author(s):  
Dominik J. Fiegle ◽  
Martin Schöber ◽  
Sven Dittrich ◽  
Robert Cesnjevar ◽  
Karin Klingel ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Acute Myocarditis ◽  
Viral Myocarditis ◽  
Left Ventricular ◽  
Length Ratio ◽  
Transverse Tubular System ◽  
Ec Coupling ◽  
T Tubules ◽  
T System

Chronic heart failure (HF) in adults causes remodeling of the cardiomyocyte transverse tubular system (t-system), which contributes to disease progression by impairing excitation-contraction (EC) coupling. However, it is unknown if t-system remodeling occurs in pediatric heart failure. This study investigated the t-system in pediatric viral myocarditis. The t-system and integrity of EC coupling junctions (co-localization of L-type Ca2+ channels with ryanodine receptors and junctophilin-2) were analyzed by 3D confocal microscopy in left-ventricular (LV) samples from 5 children with myocarditis (age 14 ± 3 months), undergoing ventricular assist device (VAD) implantation, and 5 children with atrioventricular septum defect (AVSD, age 17 ± 3 months), undergoing corrective surgery. LV ejection fraction (EF) was 58.4 ± 2.3% in AVSD and 12.2 ± 2.4% in acute myocarditis. Cardiomyocytes from myocarditis samples showed increased t-tubule distance (1.27 ± 0.05 μm, n = 34 cells) and dilation of t-tubules (volume-length ratio: 0.64 ± 0.02 μm2) when compared with AVSD (0.90 ± 0.02 μm, p < 0.001; 0.52 ± 0.02 μm2, n = 61, p < 0.01). Intriguingly, 4 out of 5 myocarditis samples exhibited sheet-like t-tubules (t-sheets), a characteristic feature of adult chronic heart failure. The fraction of extracellular matrix was slightly higher in myocarditis (26.6 ± 1.4%) than in AVSD samples (24.4 ± 0.8%, p < 0.05). In one case of myocarditis, a second biopsy was taken and analyzed at VAD explantation after extensive cardiac recovery (EF from 7 to 56%) and clinical remission. When compared with pre-VAD, t-tubule distance and density were unchanged, as well as volume-length ratio (0.67 ± 0.04 μm2 vs. 0.72 ± 0.05 μm2, p = 0.5), reflecting extant t-sheets. However, junctophilin-2 cluster density was considerably higher (0.12 ± 0.02 μm−3 vs. 0.05 ± 0.01 μm−3, n = 9/10, p < 0.001), approaching values of AVSD (0.13 ± 0.05 μm−3, n = 56), and the measure of intact EC coupling junctions showed a distinct increase (20.2 ± 5.0% vs. 6.8 ± 2.2%, p < 0.001). Severe t-system loss and remodeling to t-sheets can occur in acute HF in young children, resembling the structural changes of chronically failing adult hearts. T-system remodeling might contribute to cardiac dysfunction in viral myocarditis. Although t-system recovery remains elusive, recovery of EC coupling junctions may be possible and deserves further investigation.

scholarly journals EPIDEMIOLOGICAL CHARACTERISTICS OF CHRONIC HEART FAILURE PATIENTS IN ROSTOV REGION

2011 ◽  
Vol 2 (1) ◽  
pp. 74-78
Author(s):  
N P Dorofeeva ◽  
S A Pleskachev ◽  
S V Shlyk ◽  
E V Tchigaeva ◽  
E A TherAnanyanz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Mortality Rate ◽  
Arterial Hypertension ◽  
Differential Treatment ◽  
Prospective Evaluation ◽  
Heart Failure Patients ◽  
Rostov Region ◽  
Epidemiological Characteristics

Objective. Assesment of chronic heart failure (CHF) prevalence and differential treatment in Rostov Region based on retrospective and prospective evaluation. Materials and methods. Retrospective analysis of 3059 casehistories of CHF patients hospitalized in cardiology departments of Rostov Region in 2008. 745 patients prospective followup. Results. Inpatients demonstrate a 52% CHF prevalence with a mortality rate of 3%. Major CHF development factors (in 82% cases) were determined to be ischaemic heart disease and arterial hypertension. Optimal medical treatment with basic pharmacological groups of drugs was conducted in 82% of inpatients the number decreasing to 53% during a year after discharge.

THE RELATIONSHIP PREDICE SCORE AND MORTALITY 30 DAYS IN CHRONIC HEART FAILURE PATIENTS

2021 ◽  
pp. 207-209
Author(s):  
Dwi Handayani Nasution ◽  
Zainal safri ◽  
Refli Hasan
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Mortality Rate ◽  
Good Treatment ◽  
Heart Failure Patients ◽  
Background Mortality ◽  
The Mean ◽  
Prospective Research ◽  
The Relationship

The Background : Mortality rate of heart failure patients are increasing even they have a good treatment. Therefore, it should be possible to make a prognostic for chronic heart failure patients with use an easy parameter namely predice score. The aim of the study : To assess the ability of the predice score to predict mortality within 30 days in patients with chronic heart failure. The Method : We did this prospective research started from 1st July 2016 until 31st December 2016 with concerned chronic heart failure patients as many as 44 patients. We counted the association grade with use Man whitney U. The Result : The results showed that there was a signicant relationship between predice score and mortality (p = 0.004). The mean predice score in the living subjects was 11.77 (SD: 4.07) Meanwhile, the mean predice score of the subjects who died was 17.18 ( SD:2,85). The Conclusion: Predice Score can be used to predict 30-day mortality in chronic heart failure patients who experience worsening because it is statistically signicant (p<0,05).

scholarly journals A Family History of Dilated Cardiomyopathy Induced by Viral Myocarditis

2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Thomas Cognet ◽  
Olivier Lairez ◽  
Pauline Marchal ◽  
Jérôme Roncalli ◽  
Michel Galinier
Keyword(s):  
Heart Failure ◽  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Chronic Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Viral Myocarditis ◽  
Fulminant Myocarditis ◽  
Electrical Storm ◽  
The Family ◽  
History Of

Myocarditis can lead to acute heart failure, cardiogenic shock, or sudden death and later, dilated cardiomyopathy (DCM) with chronic heart failure. We report the cases of two DCM induced by acute and past myocarditis in the same family and expressed by its two main complications within few weeks: an hemodynamic presentation as a fulminant myocarditis rapidly leading to cardiac tranplantation and a rythmologic presentation as an electrical storm leading to catheter ablation of ventricular tachycardia. These cases ask the question of the family predisposition to viral myocarditis leading to DCM.

scholarly journals CD11b is involved in coxsackievirus B3-induced viral myocarditis in mice by inducing Th17 cells

2020 ◽  
Vol 15 (1) ◽  
pp. 1024-1032
Author(s):  
Heng Wei ◽  
Chong-Kai Lin ◽  
Sheng-Jian Lu ◽  
Yu-Xin Wen ◽  
Shuai Yuan ◽  
...  
Keyword(s):  
Immune Responses ◽  
Th17 Cells ◽  
Cytotoxic Effect ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Rt Pcr ◽  
Cardiac Damage ◽  
Cvb3 Infection ◽  
Life Threatening

AbstractViral myocarditis (VMC) caused by coxsackievirus B3 (CVB3) infection is a life-threatening disease. The cardiac damage during VMC is not mainly due to the direct cytotoxic effect of the virus on cardiomyocytes but mostly involves the induction of immune responses. Integrin CD11b plays an important role in immune response, for instance, in the induction of Th17 cells. However, the role of CD11b in the pathogenesis of VMC remains largely unknown. In the present study, a mouse model of VMC was established by CVB3 infection and CD11b was knocked down in the VMC mice by transfection with siRNA-CD11b. The expression of CD11b and IL-17 in heart tissues, frequency of Th17 cells in spleen tissues and serum IL-17 levels were measured using quantitative RT-PCR, Western blot, immunohistochemistry, flow cytometry and ELISA. Results showed that CVB3 infection caused the pathological changes in heart tissues with the increases in the following indexes: expression of CD11b and IL-17 in heart tissues, frequency of Th17 cells in spleen tissues and serum IL-17 levels. The expression of CD11b was positively correlated with IL-17 expression in heart tissues. Depletion of CD11b attenuated the damage caused by CVB3 and decreased the frequency of Th17 cells in spleen tissues as well as in IL-17, IL-23 and STAT3 expression in heart tissues. In summary, our findings reveal that disruption of CD11b function reduced CVB3-induced myocarditis, suggesting that CD11b may be a novel therapeutic target for VMC.

Abstract 569: Both Young and Old ACE2-transgenic Mice are More Resistant to Cardiac Dysfunction Induced by Myocardial Infarction

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Juan Zhang ◽  
Yanfei Qi ◽  
Colleen Jeffery ◽  
Andrew Espejo ◽  
Mohan Raizada ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Function ◽  
Renin Angiotensin System ◽  
Inflammatory Cells ◽  
Protective Role ◽  
Cardiac Damage ◽  
Monocytes And Macrophages ◽  
Old Mice ◽  
Young Mice

Background: Increased activity of the classic renin-angiotensin system (RAS) is associated with cardiovascular diseases (CVD) such as heart failure and hypertension. Angiotensin-converting enzyme 2 (ACE2) is reported to provide a protective role in CVD. In addition, there is a shift in the balance of the ACE2/Angiotensin-(1-7) axis towards the ACE/Angiotensin II axis during aging, making the cardiovascular system more vulnerable to damages. We hypothesized that global ACE2-overexpression could correct the imbalance between the two axes by providing a cardiovascular protective role against heart failure both in young and aged mice. Methods: Both young (10 weeks old) and old (12 months old) ACE2-transgenic and wild type (WT) mice underwent myocardial infarction surgery. Cardiac function was measured using echocardiography four weeks after MI. The number of circulating inflammatory cells (CD11b) in the blood for these animals was also measured using flow cytometry. Results: In the MI animals, the WT-old mice had a significant reduction in ejection fraction (47.67±4.23%: from 72.63±8.52% to 24.96±4.29%). However, the reduction in EF for ACE2-old mice was 37% lower (26.26±1.90%: from 60.06±7.56% to 29.18±5.66%) than that of WT-old mice. Meanwhile, the MI-induced decrease in EF of 14.60±1.56% for ACE2-young mice (from 59.09±8.38% to 44.49±6.82%) also was significantly less than the 26.97±1.21% reduction observed in WT-young mice (from 53.23±7.67% to 26.26±6.46%). Thus, ACE2 overexpression provides some protection of cardiac function from ischemia-induced injury in both young and old animals. Moreover, the circulating monocytes and macrophages in the blood of ACE2-young MI mice (22.65±6.86%) was also less than which observed in the WT control (31.37±4.90%), suggesting that there is less cardiac damage in these animals. Conclusions: Collectively, our observation suggests that global ACE2 overexpression has a consistent cardiac protection both in the young and old and as a result, the heart may be more resistant to heart failure damage during aging. This protective effect may be partly due to its systematic anti-inflammatory effect.

scholarly journals Renal denervation improves cardiac function in rats with chronic heart failure: Effects on expression of β-adrenoceptors

2016 ◽  
Vol 311 (2) ◽  
pp. H337-H346 ◽  
Author(s):  
Hong Zheng ◽  
Xuefei Liu ◽  
Neeru M. Sharma ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricle ◽  
Cardiac Function ◽  
Renal Denervation ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Cardiac Damage ◽  
Sprague Dawley Rats

Chronic activation of the sympathetic drive contributes to cardiac remodeling and dysfunction during chronic heart failure (HF). The present study was undertaken to assess whether renal denervation (RDN) would abrogate the sympathoexcitation in HF and ameliorate the adrenergic dysfunction and cardiac damage. Ligation of the left coronary artery was used to induce HF in Sprague-Dawley rats. Four weeks after surgery, RDN was performed, 1 wk before the final measurements. At the end of the protocol, cardiac function was assessed by measuring ventricular hemodynamics. Rats with HF had an average infarct area >30% of the left ventricle and left ventricular end-diastolic pressure (LVEDP) >20 mmHg. β1- and β2-adrenoceptor proteins in the left ventricle were reduced by 37 and 49%, respectively, in the rats with HF. RDN lowered elevated levels of urinary excretion of norepinephrine and brain natriuretic peptide levels in the hearts of rats with HF. RDN also decreased LVEDP to 10 mmHg and improved basal dP/d t to within the normal range in rats with HF. RDN blunted loss of β1-adrenoceptor (by 47%) and β2-adrenoceptor (by 100%) protein expression and improved isoproterenol (0.5 μg/kg)-induced increase in +dP/d t (by 71%) and −dP/d t (by 62%) in rats with HF. RDN also attenuated the increase in collagen 1 expression in the left ventricles of rats with HF. These findings demonstrate that RDN initiated in chronic HF condition improves cardiac function mediated by adrenergic agonist and blunts β-adrenoceptor expression loss, providing mechanistic insights for RDN-induced improvements in cardiac function in the HF condition.

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