ABSTRACT
BACKGROUND: Gunshot wounds (GSW) to the heart are lethal, and most patients die before they arrive to the hospital. Survival decreases with number of cardiac chambers involved. We report a case of a 17-year-old male who survived a GSW injury involving two cardiac chambers with acute severe tricuspid regurgitation (TR) who subsequently developed cardiogenic shock requiring extracorporeal membrane oxygenation (ECMO) support. CASE PRESENTATION: A 17-year-old male sustained a single gunshot wound to the left chest, resulting in pericardial tamponade and right hemothorax. Emergency sternotomy revealed injury to the right ventricle and inferior cavoatrial junction with the adjacent pericardium contributing to a right hemothorax. The cardiac injuries were repaired primarily. Tricuspid regurgitation was confirmed immediately postoperatively. Five days after presentation, the patient developed cardiogenic shock secondary to TR requiring emergent stabilization with ECMO. He subsequently underwent successful tricuspid valve replacement. CONCLUSIONS: This is the first report to our knowledge of successful ECMO support of severe TR due to gunshot injury to the heart.
Subject(s)
Extracorporeal Membrane Oxygenation , Heart Injuries , Tricuspid Valve Insufficiency , Wounds, Gunshot , Wounds, Penetrating , Male , Humans , Adolescent , Shock, Cardiogenic/etiology , Tricuspid Valve Insufficiency/complications , Wounds, Gunshot/complications , Extracorporeal Membrane Oxygenation/methods , Hemothorax/complications , Heart Injuries/complicationsABSTRACT
INTRODUCTION: The management of even large pericardial effusions in asymptomatic patients is still a matter of debate. Aim of the present study is to explore, in a multicenter setting, the rate of post-cardiac injury syndromes (PCIS) and pericardial effusion recurrence after pericardial effusion drainage procedure. MATERIAL AND METHODS: This is a multicenter international retrospective study including a consecutive cohort of patients diagnosed with large, chronic and idiopathic pericardial effusions, prospectively evaluated from January 2003 to December 2021 who underwent a clinically indicated pericardial drainage procedure. Two separate end-points were recorded: 1) recurrence of pericardial effusion after drainage without any sign of pericardial inflammation 2) occurrence of PCIS, defined as the new onset of pericarditis 1 to 6 weeks after pericardial intervention. RESULTS: 124 patients were enrolled (50 % female, mean age 64 years old). A mean follow-up of 29.6 ± 25.6 months was obtained in 110 patients (88 %). 110 patients were treated with pericardiocentesis (89 %), 25 with pleuro-pericardial windows (20 %), and 1 with pericardiectomy (1 %). PCIS occurred in 21 out of 124 patients followed for at least 6 weeks (16.9%). Recurrence of pericardial effusion after drainage without any sign of pericardial inflammation occurred in 68 out of 110 patients at a longer follow-up (61.8 %). At multivariate analysis only inflammatory cells in pericardial fluid was associated with PCIS and pericardiocentesis with pericardial effusion recurrency. CONCLUSION: Our data support the need of caution with the use of pericardiocentesis in asymptomatic patients with large pericardial effusion as it is often associated with pericardial effusion recurrence. Of interest the presence of inflammatory cells in the pericardial fluid is associated with PCIS after pericardial drainage procedures.
Subject(s)
Drainage , Pericardial Effusion , Pericardiocentesis , Recurrence , Humans , Pericardial Effusion/etiology , Female , Male , Middle Aged , Retrospective Studies , Aged , Pericarditis/etiology , Pericardial Window Techniques , Pericardiectomy , Heart Injuries/complicationsABSTRACT
Myocardial contusion should be suspected in a selected patient group with blunt thoracic trauma, who have elevated troponin, ECG changes and/or haemodynamical instability. Echocardiography is useful for direct visualisation of possible complications. In stable conditions, MRI allows for good visualisation of the heart and can confirm a suspected myocardial contusion as well as demonstrate the extent of myocardial damage. Based on the present literature, the authors developed a diagram for the diagnostic approach of a patient with suspected myocardial contusion.
Subject(s)
Contusions , Heart Injuries , Myocardial Contusions , Thoracic Injuries , Wounds, Nonpenetrating , Humans , Heart Injuries/etiology , Heart Injuries/complications , Myocardial Contusions/diagnostic imaging , Myocardial Contusions/complications , Troponin , Echocardiography , Wounds, Nonpenetrating/complications , Wounds, Nonpenetrating/diagnostic imaging , Thoracic Injuries/complications , Thoracic Injuries/diagnostic imaging , Contusions/diagnostic imaging , Contusions/etiology , ElectrocardiographyABSTRACT
BACKGROUND: Although chest trauma happens very often, accompanying tricuspid valve injuries occur rarely and may be manifested by scarce symptoms and signs. Pericardial rupture with cardiac herniation is even a bigger rarity. Transthoracic echocardiography plays a key role in the diagnosis of valve injuries but is of limited value in cardiac herniation. CASE PRESENTATION: We present the case of 58-year-old man who experienced severe chest trauma in a car accident. Symptoms of right heart failure occurred 10 years after the injury, due to the loss of tricuspid leaflet support caused by the rupture of tendinous chords with significant tricuspid regurgitation. Intraoperatively, old posttraumatic pericardial rupture into left pleura was also found, with partial cardiac herniation and pressure of the edge of pericardium on all left-sided coronary arteries simultaneously. The patient was successfully operated and is free of symptoms 4 years later. CONCLUSIONS: This case emphasizes the importance of timely diagnosis and underlines a mechanism that leads to delayed rupture of the tricuspid valve apparatus. Repeated echocardiography in all patients who experienced chest trauma could be of great importance. Also, given the limited value of echocardiography in posttraumatic pericardial rupture and cardiac herniation, cardiac computed tomography should be performed.
Subject(s)
Heart Injuries , Thoracic Injuries , Tricuspid Valve Insufficiency , Wounds, Nonpenetrating , Male , Humans , Middle Aged , Tricuspid Valve/diagnostic imaging , Tricuspid Valve/surgery , Wounds, Nonpenetrating/complications , Wounds, Nonpenetrating/diagnostic imaging , Wounds, Nonpenetrating/surgery , Tricuspid Valve Insufficiency/diagnostic imaging , Tricuspid Valve Insufficiency/etiology , Tricuspid Valve Insufficiency/surgery , Echocardiography/adverse effects , Thoracic Injuries/diagnosis , Pericardium/diagnostic imaging , Pericardium/surgery , Rupture/complications , Heart Injuries/complications , Heart Injuries/diagnostic imagingABSTRACT
INTRODUCTION: Myocardial injury is a serious complication in sepsis with high mortality. Zero-valent iron nanoparticles (nanoFe) displayed novel roles in cecal ligation and puncture (CLP)-induced septic mouse model. Nonetheless, its high reactivity makes it difficult for long-term storage. OBJECTIVES: To overcome the obstacle and improve therapeutic efficiency, a surface passivation of nanoFe was designed using sodium sulfide. METHODS: We prepared iron sulfide nanoclusters and constructed CLP mouse models. Then the effect of sulfide-modified nanoscale zero-valent iron (S-nanoFe) on the survival rate, blood routine parameters, blood biochemical parameters, cardiac function, and pathological indicators of myocardium was observed. RNA-seq was used to further explore the comprehensive protective mechanisms of S-nanoFe. Finally, the stability of S-nanoFe-1d and S-nanoFe-30 d, together with the therapeutic efficacy of sepsis between S-nanoFe and nanoFe was compared. RESULTS: The results revealed that S-nanoFe significantly inhibited the growth of bacteria and exerted a protective role against septic myocardial injury. S-nanoFe treatment activated AMPK signaling and ameliorated several CLP-induced pathological processes including myocardial inflammation, oxidative stress, mitochondrial dysfunction. RNA-seq analysis further clarified the comprehensive myocardial protective mechanisms of S-nanoFe against septic injury. Importantly, S-nanoFe had a good stability and a comparable protective efficacy to nanoFe. CONCLUSIONS: The surface vulcanization strategy for nanoFe has a significant protective role against sepsis and septic myocardial injury. This study provides an alternative strategy for overcoming sepsis and septic myocardial injury and opens up possibilities for the development of nanoparticle in infectious diseases.
Subject(s)
Heart Injuries , Sepsis , Mice , Animals , Iron , Myocardium/pathology , Heart Injuries/drug therapy , Heart Injuries/complications , Heart Injuries/pathology , Sepsis/drug therapy , Sepsis/complications , Sulfides/therapeutic useABSTRACT
Diabetes increases the production of free radicals and inflammatory agents in the heart tissue and alters the expression of genes associated with the induction of apoptosis. Considering the importance of common cardiovascular disorders in diabetes, this study investigated the effect of eight weeks of aerobic exercise and crocin use, as well as tissue damage and oxidative stress caused by diabetes in the hearts of adult rats. Streptozotocin 50 mg/kg was injected as a single dose intraperitoneally to cause the diabetes. After 72 hours, a glucometer monitored blood glucose levels, and blood glucose above 250 mg/dl was considered diabetes. Continuous treadmill exercise was performed for eight weeks by placing the animal on the treadmill. Next, the animals were anesthetized, and samples were taken from the hearts and frozen in liquid nitrogen. Then, superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA) were measured in the cardiac tissue. Finally, the hearts of half of the animals were immediately immersed in a formalin solution for histological changes. According to our findings, diabetes increased lipid peroxidation, characterized by increased MDA levels in the control diabetes group and decreased SOD and GPx levels (P <0.05). It also changes the balance of expression of genes associated with apoptosis control, increased Bcl-2-associated X (Bax) expression, and decreased Bcl-2 expression (P <0.05). Also, we observed the induction of apoptosis in cardiac tissue. Using eight weeks of continuous exercise and administration of crocin significantly reduced blood sugar levels and lipid peroxidation and increased the activity of antioxidant enzymes and Bcl-2 gene expression compared to the diabetes control group. In addition, continuous exercise and crocin improved the oxidative stress parameters in the control group. This study showed that diabetes could cause oxidative stress and heart dysfunction. Moreover, simultaneously and separately, aerobic exercise with a treadmill and crocin administration can reduce these disorders and prevent apoptosis in the heart tissue.
Subject(s)
Diabetes Mellitus, Experimental , Heart Injuries , Rats , Animals , Diabetes Mellitus, Experimental/metabolism , Blood Glucose/metabolism , Rats, Wistar , Antioxidants/metabolism , Oxidative Stress , Superoxide Dismutase/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , Heart Injuries/complicationsABSTRACT
As sepsis is associated with a 50% increase in mortality, sepsis-induced cardiomyopathy has become a critical topic. A multidisciplinary approach is required for the diagnosis and treatment of septic cardiomyopathy. This study looked at Sulforaphane, a natural product that aims to evaluate cardiac function after sepsis, and its likely mechanism of action. Twenty-four adult male Swiss albino mice were randomly divided into 4 equal groups (n=6): sham, CLP, vehicle Sulforaphane (the same amount of DMSO injected IP one hour before the CLP), and Sulforaphane group (one hour before the CLP, a 5mg/kg dose of Sulforaphane was injected). Cardiac tissue levels of toll-like receptor 4 (TLR-4), pro-inflammatory mediators, anti-inflammatory markers, oxidative stress markers, apoptosis markers, and serum cardiac damage biomarkers were assessed using ELISA. Statistical analyses, including t-tests and ANOVA tests, were performed with a significance level of 0.05 for normally distributed data. Compared to the sham group, the sepsis group had significantly elevated levels of TLR-4, IL-6, TNF-α, MIF, F2-isoprostane, caspase-3, cTn-I, and CK-MB (p<0.05). In contrast, the Sulforaphane pre-treated group demonstrated significantly lower levels of these markers (p<0.05). Additionally, Bcl-2 levels were significantly reduced (p<0.05) in the Sulforaphane group. Sulforaphane administration also significantly attenuated cardiac tissue injury (p<0.05). The findings suggest that Sulforaphane can decrease heart damage in male mice during CLP-induced polymicrobial sepsis by suppressing TLR-4/NF-kB downstream signal transduction pathways.
Subject(s)
Cardiomyopathies , Heart Injuries , Sepsis , Mice , Male , Animals , Toll-Like Receptor 4/metabolism , Toll-Like Receptor 4/therapeutic use , Cardiomyopathies/etiology , Cardiomyopathies/complications , Heart Injuries/complications , Sepsis/complications , Sepsis/drug therapyABSTRACT
AIMS: The heart rejuvenating effects of circulating growth differentiation factor 11 (GDF11), a transforming growth factor-ß superfamily member that shares 90% homology with myostatin (MSTN), remains controversial. Here, we aimed to probe the role of GDF11 in acute myocardial infarction (MI), a frequent cause of heart failure and premature death during ageing. METHODS AND RESULTS: In contrast to endogenous Mstn, myocardial Gdf11 declined during the course of ageing and was particularly reduced following ischaemia/reperfusion (I/R) injury, suggesting a therapeutic potential of GDF11 signalling in MI. Unexpectedly, boosting systemic Gdf11 by recombinant GDF11 delivery (0.1â mg/kg body weight over 30 days) prior to myocardial I/R augmented myocardial infarct size in C57BL/6 mice irrespective of their age, predominantly by accelerating pro-apoptotic signalling. While intrinsic cardioprotective signalling pathways remained unaffected by high circulating GDF11, targeted transcriptomics and immunomapping studies focusing on GDF11-associated downstream targets revealed attenuated Nkx2-5 expression confined to CD105-expressing cells, with pro-apoptotic activity, as assessed by caspase-3 levels, being particularly pronounced in adjacent cells, suggesting an indirect effect. By harnessing a highly specific and validated liquid chromatography-tandem mass spectrometry-based assay, we show that in prospectively recruited patients with MI circulating GDF11 but not MSTN levels incline with age. Moreover, GDF11 levels were particularly elevated in those at high risk for adverse outcomes following the acute event, with circulating GDF11 emerging as an independent predictor of myocardial infarct size, as estimated by standardized peak creatine kinase-MB levels. CONCLUSION: Our data challenge the initially reported heart rejuvenating effects of circulating GDF11 and suggest that high levels of systemic GDF11 exacerbate myocardial injury in mice and humans alike. Persistently high GDF11 levels during ageing may contribute to the age-dependent loss of cardioprotective mechanisms and thus poor outcomes of elderly patients following acute MI.
Subject(s)
Growth Differentiation Factors , Heart Injuries , Myocardial Infarction , Aged , Animals , Humans , Mice , Aging/metabolism , Bone Morphogenetic Proteins , Growth Differentiation Factors/genetics , Growth Differentiation Factors/metabolism , Heart , Heart Injuries/complications , Heart Injuries/metabolism , Mice, Inbred C57BL , Myocardial Infarction/complications , Myocardial Infarction/metabolismABSTRACT
BACKGROUND Cardiac perforation is a rare complication of cardiac implantable electronic devices, with a reported incidence ranging from 0.1% to 5.2%. Delayed perforation, defined as perforation occurring more than 1 month after implantation, is more uncommon. In this report, we present a case of cardiac perforation involving the right ventricle wall that occurred 9 years after pacemaker implantation. CASE REPORT A 79-year-old woman presented with symptoms of dyspnea and was subsequently admitted to a hospital. She had undergone pacemaker implantation for a complete atrioventricular block 9 years prior to the presentation. The patient had right ventricular failure to capture and a resultant complete atrioventricular block. Computed tomography imaging revealed that the right ventricular lead had clearly protruded outside the heart; however, no pericardial effusion was observed. When the patient underwent open surgical repair, the ventricular tined lead was noted to be traversing the right ventricular apex. Device interrogation revealed a sudden increase followed by a gradual decrease in the right ventricular pacing threshold over the course of 2 months, indicating that the lead had slowly traversed the right ventricular muscle before ultimately rupturing through it. CONCLUSIONS This study described the case of a delayed right ventricular pacemaker lead perforation that occurred 9 years after implantation, which was managed via open surgical repair.
Subject(s)
Atrioventricular Block , Heart Injuries , Pacemaker, Artificial , Pericardial Effusion , Female , Humans , Aged , Heart Ventricles/surgery , Atrioventricular Block/therapy , Atrioventricular Block/complications , Pacemaker, Artificial/adverse effects , Pericardial Effusion/etiology , Heart Injuries/surgery , Heart Injuries/complicationsABSTRACT
INTRODUCTION: The diagnosis of cardiac contusion, caused by blunt chest trauma, remains a challenge due to the non-specific symptoms it causes and the lack of ideal tests to diagnose myocardial damage. A cardiac contusion can be life-threatening if not diagnosed and treated promptly. Several diagnostic tests have been used to evaluate the risk of cardiac complications, but the challenge of identifying patients with contusions nevertheless remains. AIM OF THE STUDY: To evaluate the accuracy of diagnostic tests for detecting blunt cardiac injury (BCI) and its complications, in patients with severe chest injuries, who are assessed in an emergency department or by any front-line emergency physician. METHODS: A targeted search strategy was performed using Ovid MEDLINE and Embase databases from 1993 up to October 2022. Data on at least one of the following diagnostic tests: electrocardiogram (ECG), serum creatinine phosphokinase-MB level (CPK-MB), echocardiography (Echo), Cardiac troponin I (cTnI) or Cardiac troponin T (cTnT). Diagnostic tests for cardiac contusion were evaluated for their accuracy in meta-analysis. Heterogeneity was assessed using the I2 and the QUADAS-2 tool was used to assess bias of the studies. RESULTS: This systematic review yielded 51 studies (n = 5,359). The weighted mean incidence of myocardial injuries after sustaining a blunt force trauma stood at 18.3% of cases. Overall weighted mean mortality among patients with blunt cardiac injury was 7.6% (1.4-36.4%). Initial ECG, cTnI, cTnT and transthoracic echocardiography TTE all showed high specificity (> 80%), but lower sensitivity (< 70%). TEE had a specificity of 72.1% (range 35.8-98.2%) and sensitivity of 86.7% (range 40-99.2%) in diagnosing cardiac contusion. CK-MB had the lowest diagnostic odds ratio of 3.598 (95% CI: 1.832-7.068). Normal ECG accompanied by normal cTnI showed a high sensitivity of 85% in ruling out cardiac injuries. CONCLUSION: Emergency physicians face great challenges in diagnosing cardiac injuries in patients following blunt trauma. In the majority of cases, joint use of ECG and cTnI was a pragmatic and cost-effective approach to rule out cardiac injuries. In addition, TEE may be highly accurate in identifying cardiac injuries in suspected cases.
Subject(s)
Heart Injuries , Myocardial Contusions , Thoracic Injuries , Wounds, Nonpenetrating , Humans , Thoracic Injuries/complications , Thoracic Injuries/diagnosis , Wounds, Nonpenetrating/complications , Wounds, Nonpenetrating/diagnosis , Heart Injuries/diagnosis , Heart Injuries/complications , Myocardial Contusions/diagnosis , Myocardial Contusions/complications , Troponin I , Troponin T , Diagnostic Tests, RoutineABSTRACT
Macrophage activation syndrome (MAS), a secondary hemophagocytic lymphohistiocytosis characterized by an excessive systemic inflammatory response, is a life-threatening and rare disease. Cardiovascular damage is a common and severe complication of the disease, however, it is easily ignored and not well studied. Herein, we report two cases of patients with MAS-associated heart damage and review the clinical characteristics, mechanism, and treatment. Case 1 along with systemic lupus erythematosus and Kikuchi necrotizing lymphadenitis occurred in fatal acute heart failure, and case 2 complicated adult-onset Still's Disease began with atrial fibrillation and had some improvement with the treatment of high dose corticosteroids. MAS-associated heart damage is a critical issue in clinical settings, and the etiology and mechanisms of MAS-associated cardiovascular diseases are likely multifactorial. The manifestations were various and high levels of the cytokines and cardiac damage may contribute to poor prognosis. Therefore, early intensive immunosuppressive therapy probably improves the treatment outcome.
Subject(s)
Heart Diseases , Heart Injuries , Lymphohistiocytosis, Hemophagocytic , Macrophage Activation Syndrome , Adult , Humans , Macrophage Activation Syndrome/complications , Macrophage Activation Syndrome/diagnosis , Immunosuppressive Agents/therapeutic use , Lymphohistiocytosis, Hemophagocytic/complications , Lymphohistiocytosis, Hemophagocytic/diagnosis , Lymphohistiocytosis, Hemophagocytic/drug therapy , Heart Diseases/complications , Heart Diseases/drug therapy , Heart Injuries/complications , Heart Injuries/drug therapyABSTRACT
BACKGROUND: Long-term symptoms are frequent after coronavirus disease 2019 (COVID-19). We studied the prevalence of post-acute myocardial scar on cardiac magnetic resonance imaging (CMR) in patients hospitalized due to COVID-19 and its association with long-term symptoms. MATERIALS AND METHODS: In this prospective observational single-center study, 95 formerly hospitalized COVID-19 patients underwent CMR imaging at the median of 9 months after acute COVID-19. In addition, 43 control subjects were imaged. Myocardial scar characteristic of myocardial infarction or myocarditis were noted from late gadolinium enhancement images (LGE). Patient symptoms were screened using a questionnaire. Data are presented as mean ± standard deviation or median (interquartile range). RESULTS: The presence of any LGE was higher in COVID-19 patients (66% vs. 37%, p<0.01) as was the presence of LGE suggestive of previous myocarditis (29% vs. 9%, p = 0.01). The prevalence of ischemic scar was comparable (8% vs. 2%, p = 0.13). Only two COVID-19 patients (7%) had myocarditis scar combined with left ventricular dysfunction (EF <50%). Myocardial edema was not detected in any participant. The need for intensive care unit (ICU) treatment during initial hospitalization was comparable in patients with and without myocarditis scar (47% vs. 67%, p = 0.44). Dyspnea, chest pain, and arrhythmias were prevalent in COVID-19 patients at follow-up (64%, 31%, and 41%, respectively) but not associated with myocarditis scar on CMR. CONCLUSIONS: Myocardial scar suggestive of possible previous myocarditis was detected in almost one-third of hospital-treated COVID-19 patients. It was not associated with the need for ICU treatment, greater symptomatic burden, or ventricular dysfunction at 9 months follow-up. Thus, post-acute myocarditis scar on COVID-19 patients seems to be a subclinical imaging finding and does not commonly require further clinical evaluation.
Subject(s)
COVID-19 , Heart Injuries , Myocarditis , Humans , Myocarditis/complications , Contrast Media , Cicatrix/complications , Ventricular Function, Left , COVID-19/complications , Gadolinium , Magnetic Resonance Imaging , Magnetic Resonance Spectroscopy , Heart Injuries/complications , Magnetic Resonance Imaging, Cine/methods , Predictive Value of TestsABSTRACT
INTRODUCTION: Cardiac perforation is a rare life-threatening complication of cardiac catheterization. There is very little published literature detailing risk factors for cardiac perforation and outcomes from this complication in children. MATERIALS AND METHODS: This was a retrospective study analyzing the cardiac catheterization case registry of the Congenital Cardiovascular Interventional Study Consortium. Children aged < 18 years were included during the study period of 9 years (January 2009-December 2017). The primary outcome measures were incidence of cardiac perforation, risk factors for and outcomes of patients who experience cardiac perforation during cardiac catheterization. RESULTS: Cardiac perforation occurred in 50 patients from a total of 36,986 (0.14%). Cardiac perforation was more likely to occur in younger, smaller patients undergoing urgent/emergent and interventional procedures (p < 0.01). Cardiac peroration risk was significantly different across diagnostic and procedure categories (p < 0.01). Higher CRISP score (Area Under Curve [AUC] = 0.87), lower age, and procedure category (radiofrequency perforation of pulmonary valve, AUC = 0.84) were independent predictors of cardiac perforation. Cardiac perforation was associated with a significantly higher rate of mortality (14%), further emergency procedure (42%), ECMO (14%), and cardiac arrest (6%), p < 0.01. CONCLUSIONS: Cardiac perforation during cardiac catheterization is a life-threatening complication with a range of associated secondary complications. Higher CRISP score, lower age, and radiofrequency perforation of pulmonary valve are independent predictors.
Subject(s)
Heart Defects, Congenital , Heart Injuries , Child , Humans , Retrospective Studies , Incidence , Heart Defects, Congenital/epidemiology , Heart Defects, Congenital/surgery , Heart Defects, Congenital/complications , Treatment Outcome , Cardiac Catheterization/adverse effects , Cardiac Catheterization/methods , Heart Injuries/etiology , Heart Injuries/complicationsABSTRACT
Structural cardiac injury after blunt trauma is uncommon but usually life-threatening. While tricuspid injury is very rare and potentially lethal, the right heart can accommodate larger volumes and higher pressures in acute tricuspid insufficiency and facilitate initial stabilization prior to definitive valvular repair. ECMO may be used to ameliorate resulting right heart failure. The traumatic force required to cause cardiac structural injury is also associated with pulmonary complications related to pneumothorax, hemothorax, effusion, acute pain secondary to rib fractures, and pulmonary contusions causing hypoxia. We present an unusual case of hypoxia in a trauma patient caused by acute tricuspid regurgitation with pre-existing patent foramen ovale.
Subject(s)
Foramen Ovale, Patent , Heart Injuries , Tricuspid Valve Insufficiency , Wounds, Nonpenetrating , Humans , Tricuspid Valve/diagnostic imaging , Tricuspid Valve/injuries , Foramen Ovale, Patent/complications , Foramen Ovale, Patent/diagnostic imaging , Tricuspid Valve Insufficiency/diagnostic imaging , Tricuspid Valve Insufficiency/etiology , Heart Injuries/complications , Heart Injuries/diagnostic imaging , Hypoxia/complications , Wounds, Nonpenetrating/complicationsABSTRACT
BACKGROUND: Chronic pre-procedural and acute post-procedural myocardial injury are frequently observed in patients with aortic stenosis undergoing transcatheter aortic valve implantation (TAVI). The aim of our study was to investigate the prognostic role of high sensitivity cardiac troponins (hs-cTns) elevation before and after TAVI. METHODS: 106 patients with severe aortic stenosis who underwent TAVI were enrolled. High sensitivity cardiac troponin T (hs-cTnT) was measured before and after TAVI (6, 24, 48, 72 hours). Post-procedural myocardial damage was defined as a 15-fold rise in hs-cTnT upper reference limit (URL) after TAVI. The clinical endpoints were all cause death, cardiovascular death and re-hospitalization at 24 months follow-up. RESULTS: Before TAVI, hs-cTnT median value was 0.03 µg/L (2.3±2.1 fold over URL). After TAVI procedure, myocardial damage (MD), as defined by VARC-2 criteria, was observed in 40 patients (38%) (MD group). In our population, logarithmically transformed hs-cTnTs were independently associated with all-cause mortality at 24 months F/U (pre-TAVI hs-cTnT: Hazard ratio [HR] 2.2, 95% confidence interval [CI]: 1.1 to 4.4, P=0.027). No significant differences were observed between the MD and non-MD groups for the three endpoints of all cause death (p log rank: 0.15), cardiovascular death (p log rank: 0.86) and re-hospitalization (p log rank: 0.87). CONCLUSIONS: Only baseline hs-cTnT levels correlated with outcomes at 24 months of follow-up. Chronic pre-procedural myocardial injury significantly affects prognosis after TAVI.
Subject(s)
Aortic Valve Stenosis , Heart Injuries , Transcatheter Aortic Valve Replacement , Humans , Prognosis , Transcatheter Aortic Valve Replacement/adverse effects , Transcatheter Aortic Valve Replacement/methods , Biomarkers , Risk Factors , Aortic Valve Stenosis/surgery , Aortic Valve Stenosis/complications , Troponin T , Heart Injuries/etiology , Heart Injuries/complicationsABSTRACT
BACKGROUND: This study reviews our experience with combined cardiac and abdominal stab wounds over 12 years and reviews how changes in technology and clinical approaches have impacted our management of these patients. MATERIALS AND METHODS: A retrospective cohort study was conducted from January 2008 to January 2020 at a major trauma centre in South Africa. All patients with concurrent SWs to the chest and the abdomen and required both a thoracotomy for cardiac injury and a laparotomy for an intra-abdominal injury at the same setting were included. RESULTS: Twenty-two cases were identified (100% male, mean age: 27 years). Mean values of admission physiology: systolic blood pressure (SBP): 85 mmHg, pH: 7.2, base excess: -10.2 mmol/L and serum lactate 6.7 mmol/L. Thirty-two percent (7/22) of cases underwent a Focused Assessment with Sonography in Trauma (FAST) scan (5 positive and 2 negative). All 7 cases had intraoperatively confirmed cardiac injuries. The thoracotomy first approach was used in 18 cases (82%), and the laparotomy first approach was used in the remaining 4 cases (18%). Nineteen (86%) of the 22 laparotomies were positive. A total of 6 patients (27%) experienced one or more complications. The mean length of hospital stay was 9 days. The overall mortality was 18% (4/22) and all mortality occurred prior to 2013. DISCUSSION: Double jeopardy is still associated with an increased risk of mortality. The use of FAST and Subxiphoid Pericardial Windows (SPWs) have reduced clinical uncertainty, decreasing the need for concomitant thoracotomy and laparotomy to be performed.
Subject(s)
Abdominal Injuries , Heart Injuries , Wounds, Penetrating , Wounds, Stab , Humans , Male , Adult , Female , Retrospective Studies , Clinical Decision-Making , Uncertainty , Wounds, Stab/diagnostic imaging , Wounds, Stab/surgery , Wounds, Stab/complications , Heart Injuries/diagnostic imaging , Heart Injuries/surgery , Heart Injuries/complications , Abdominal Injuries/diagnostic imaging , Abdominal Injuries/surgery , Abdominal Injuries/complications , Abdomen/surgery , Laparotomy/methods , Wounds, Penetrating/surgeryABSTRACT
Penetrating heart injuries are associated with higher mortality rates. Coronary lesions caused by penetrating trauma are considered even rarer and universally fatal. We present a case of a fortunate survivor who had complete transection of left anterior descending (LAD) artery with right ventricular (RV) tear after being stabbed by knife, arriving in emergency unit with massively bleeding chest wound. Complex cardiac trauma involving coronaries and cardiac chambers is a challenge to surgeons if patients miraculously reach the hospital alive. This patient had complete transection of LAD artery with penetration into RV cavity, he was successfully managed by timely and prompt surgical intervention by on call team. This case highlights the importance of team dynamics working in harmony during emergency situations, we stress upon conducting routine drills to train surgical residents, perfusionists and operation theatre staff.
Subject(s)
Heart Injuries , Thoracic Injuries , Wounds, Penetrating , Wounds, Stab , Male , Humans , Wounds, Stab/surgery , Wounds, Stab/complications , Wounds, Penetrating/complications , Thoracic Injuries/complications , Heart Injuries/complications , Heart Injuries/surgery , Coronary Vessels/injuries , Coronary Vessels/surgeryABSTRACT
BACKGROUND: Cardiac injury in trauma patients can be secondary to either blunt or penetrating trauma and is a significant cause of death. The commonest etiological factors for blunt cardiac injury include motor vehicle collisions, falls, and crush or blast injuries. The incidence of blunt cardiac injury following falls is reported to be between 5 and 50%.CASE REPORT: A combat pilot lost his life in an aircraft accident. Although he had ejected successfully just before the aircraft caught fire and his parachute had deployed fully, it was engulfed in the ball of fire rising up from the burning aircraft wreckage, causing the parachute to burn up. As a result, the pilot had a free fall from an estimated height of 70-80 ft (21-24 m). Autopsy revealed a ruptured right atrium and endocardial tears at the right atrioventricular junction. The left side of the heart and the coronary arteries were unscathed. The histopathological finding showed evidence that the cardiac injuries sustained were antemortem. The cause of death was ascertained to be due to cardiac rupture, leading to hemorrhagic shock.DISCUSSION: Cardiac rupture in this case appears to be a case of the 'water hammer' effect, the right atrium being the commonest site of blunt cardiac rupture. It is possible that the individual landed on his feet after his parachute got burnt in the ball of fire and the violent compression of the lower limb and abdominal veins, caused by the sudden hyperflexion of the lower limbs over the abdomen, caused the cardiac rupture in this case.CONCLUSION: The possibility of blunt cardiac trauma should always be kept in mind while dealing with survivors of ejection at low levels.Sharma MD, Gupta N, Rajkumar T, Sharma A. Cardiac rupture due to a fall from height: the 'water hammer' effect. Aerosp Med Hum Perform. 2022; 93(10):755-757.
Subject(s)
Heart Injuries , Heart Rupture , Myocardial Contusions , Wounds, Nonpenetrating , Heart Injuries/complications , Heart Injuries/pathology , Heart Rupture/complications , Humans , Male , Myocardial Contusions/complications , Water , Wounds, Nonpenetrating/complications , Wounds, Nonpenetrating/pathologyABSTRACT
INTRODUCTION: Albeit described since 1763, cardiac contusions is still an under-recognised clinical condition in the acute care setting. This evidence-based review aims to provide an overview of the topic by focusing on etiopathogenesis, classification and clinical presentation of patients with cardiac contusions, as well as on the diagnostic work-up and therapy options available for this subset population in the acute care setting. METHODS: A targeted research strategy was performed using PubMed, MEDLINE, Embase and Cochrane Central databases up to June 2022. The literature search was conducted using the following keywords (in Title and/or Abstract): ("cardiac" OR "heart" OR "myocardial") AND ("contusion"). All available high-quality resources written in English and containing information on epidemiology, etiopathogenesis, clinical findings, diagnosis and management of cardiac contusions were included in our research. RESULTS: Biochemical samples of cardiac troponins together with a 12lead ECG appear to be sufficient screening tools in hemodynamically stable subjects, while cardiac ultrasound provides a further diagnostic clue for patients with hemodynamic instability or those more likely to have a significant cardiac contusion. CONCLUSIONS: The management of patients with suspected cardiac contusion remains a challenge in clinical practice. For this kind of patients a comprehensive diagnostic approach and a prompt emergency response are required, taking into consideration the degree of severity and clinical impairment of associated traumatic injuries.
Subject(s)
Contusions , Heart Injuries , Myocardial Contusions , Wounds, Nonpenetrating , Humans , Wounds, Nonpenetrating/complications , Myocardial Contusions/complications , Contusions/diagnosis , Contusions/therapy , Contusions/etiology , Heart Injuries/diagnosis , Heart Injuries/therapy , Heart Injuries/complications , TroponinABSTRACT
Neuroinflammation in the cardiovascular center plays a critical role in the progression of hypertensive heart disease. And microglial autophagy is involved in the regulation of neuroinflammation. Cyclic GMP-AMP synthase (cGAS), a cytosolic DNA sensor, senses mitochondrial DNA (mtDNA) and regulates autophagy. The detailed mechanisms of central cGAS affects neuroinflammatory response in hypertensive heart disease via regulating autophagy remain unknown. Angiotensin II (Ang II, 1.5 mg·kg-1·12 h-1, 2 weeks) was intraperitoneally injected to induce hypertension in mice. The cGAS-STING pathway was activated in the paraventricular nucleus (PVN) of Ang II-induced hypertensive mice. The contractile dysfunction of heart was alleviated in Ang II-induced hypertensive cGAS-/- mice. To observe the central effects of cGAS on regulating hypertensive heart disease, the RU.521 (a cGAS inhibitor) was intracisternally infused in hypertensive mice. Intracisternal infusion of the RU.521-alleviated myocardial interstitial fibrosis, cardiomyocyte hypertrophy, and the contractile dysfunction in Ang II-induced hypertensive mice. Intracisternal infusion of RU.521 attenuated the microglial activation, neuroinflammation, sympathetic/parasympathetic activity ratio, and lowered blood pressure. The autophagic flux in the PVN cells was blocked, while intracisternal infusion of RU.521 alleviated this effect in the Ang II-induced hypertensive mice. In vitro, it was found that cGAS-STING activation-induced autophagic flux blockage, while when the impaired autophagic flux was facilitated by rapamycin, an autophagy inducer, the microglial M1 polarization was decreased correspondingly. In conclusion, cGAS induces the inflammatory phenotype of microglia via impairing autophagic flux, thereby participating in neuroinflammation, which leads to sympathetic overactivation in hypertension and further caused hypertensive myocardial injury.