scholarly journals Acute Heart Failure in a Healthy Young Patient after Severe Carbon Monoxide Poisoning

2019 ◽  
Author(s):  
Christos E Lampropoulos ◽  
Evagelia Sklavou ◽  
Charalampos Anastogiannis ◽  
Vasiliki Papanikolaou ◽  
Dimitris Tsilivarakis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Carbon Monoxide ◽  
Troponin I ◽  
Carbon Monoxide Poisoning ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Co Poisoning ◽  
Jugular Veins ◽  
X Ray ◽  
Cellular Hypoxia

Introduction: Carbon monoxide (CO) poisoning may cause severe cellular hypoxia. Materials and methods: A 28-year-old male presented reduced levels of consciousness and dyspnoea after CO exposure. Clinical examination revealed tachypnoea, bilateral rales, dilated jugular veins and confusion. Troponin I, lactate and carboxyhaemoglobin levels were increased. Thoracic X-ray depicted pulmonary oedema and an echocardiogram, severe heart failure (HF; EF<25%). He was intubated due to clinical deterioration. Results: He remained intubated for 5 days with excellent improvement of left ventricular function (EF>55%). He was discharged 1 week later with full recovery. Discussion: Acute HF is a rare serious complication of CO poisoning, even in healthy young individuals.

scholarly journals High-Sensitivity Troponin I and Creatinine Kinase-Myocardial Band in Screening for Myocardial Injury in Patients with Carbon Monoxide Poisoning

Diagnostics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 242 ◽  
Author(s):  
June-Sung Kim ◽  
Byuk Sung Ko ◽  
Chang Hwan Sohn ◽  
Youn-Jung Kim ◽  
Won Young Kim
Keyword(s):  
Carbon Monoxide ◽  
Troponin I ◽  
Myocardial Dysfunction ◽  
Carbon Monoxide Poisoning ◽  
Right Ventricular Dysfunction ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Co Poisoning ◽  
High Sensitivity Troponin ◽  
Poor Outcomes

Myocardial dysfunction due to acute carbon monoxide (CO) poisoning is common and associated with poor outcomes. The role of cardiac markers, including creatine kinase-myocardial band (CK-MB), high-sensitivity troponin I (hsTnI), and brain natriuretic peptide (BNP), in identifying patients with CO-induced cardiomyopathy were evaluated. This single-center, retrospective cohort study included 905 consecutive adult patients in the CO poisoning registry from February 2009 to December 2019. Cardiomyopathy was defined as any abnormality on transthoracic echocardiography (TTE), including left ventricular systolic and diastolic dysfunction, right ventricular dysfunction, and wall motion abnormalities. The areas under receiver operating curves (AUCs) for biomarkers were compared. Of the 850 included patients, 101 (11.9%) had CO-induced cardiomyopathy. Initial and peak hsTnI and CK-MB concentrations, and initial BNP concentrations were significantly higher in patients with than without cardiomyopathy (all P-values < 0.01), but the AUCs were higher for hsTnI (0.894) and CK-MB (0.864) than for BNP (0.796). Initial TnI > 0.01 ng/mL and CK-MB > 1.5 ng/mL each had 95% sensitivity and 97% negative predictive value for CO-induced cardiomyopathy. Higher hsTnI or CK-MB levels on admission can identify patients at high-risk of CO-induced cardiomyopathy and can be a screening tool for CO poisoning.

Incidence and severity of cardiotoxicity in metastatic renal cell carcinoma (RCC) patients treated with targeted therapies.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 4610-4610 ◽  
Author(s):  
Philip S Hall ◽  
Ronald Witteles ◽  
Sandy Srinivas ◽  
Lauren Christine Harshman
Keyword(s):  
Heart Failure ◽  
Targeted Therapies ◽  
Troponin I ◽  
Hypoxia Inducible Factor ◽  
Severe Heart Failure ◽  
Mtor Inhibitors ◽  
Left Ventricular ◽  
Close Monitoring ◽  
Cardiovascular Toxicity ◽  
Asymptomatic Patients

4610 Background: Almost all patients with advanced RCC are treated with therapies targeting the hypoxia inducible factor axis. The potential for these agents to cause cardiovascular (CV) toxicity has been increasingly recognized but the overall incidence and extent have not been well described. We sought to identify and characterize the incidence and severity of CV toxicity among RCC patients treated with targeted therapies. Methods: Between 2004 and 2011, all RCC patients treated with targeted therapies directed against the VEGF or mTOR axes were identified at our institution. The incidence of hypertension, left ventricular (LV) dysfunction, changes in serum markers of CV toxicity (e.g., troponin I, NT-proBNP) and heart failure were assessed and graded according to the Common Terminology Criteria for Adverse Events (CTCAE v.4.0). Results: Cardiovascular toxicity developed in 116 of 159 patients (73%). Excluding hypertension, 52 of 159 (33%) developed cardiovascular toxicity. Cardiac toxicity ranged from asymptomatic drops in LV ejection fraction (LVEF) to rises in NT-proBNP to severe heart failure. Asymptomatic cardiotoxicity as defined by decrease in LVEF or increase in NT-proBNP occurred in 43 patients (27%). Symptomatic heart failure (grade 2-3) and grade 3-4 decrease in LVEF each occurred in 4%. Sunitinib was the most frequently used and most common offending agent, with 66 of 101 sunitinib-treated patients (65%) developing a form of CV toxicity, or 32 of 101 (32%) excluding hypertension. However, it was notable that CV toxicity was observed in 68%, 66%, and 51% of patients treated with bevacizumab, sorafenib, and pazopanib as well. The mTOR inhibitors elicited significantly less CV toxicity, but sample sizes were small. Conclusions: Cardiovascular toxicity is an important adverse event related to targeted therapy administration. Close monitoring for the development of CV toxicity with the use of these agents should become standard of care as early detection of asymptomatic patients could preempt symptomatic toxicity and reduce treatment-related morbidity and mortality.

Serum neuron-specific enolase as an early predictor of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning

2017 ◽  
Vol 37 (3) ◽  
pp. 240-246 ◽  
Author(s):  
YS Cha ◽  
H Kim ◽  
HH Do ◽  
HI Kim ◽  
OH Kim ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Troponin I ◽  
Carbon Monoxide Poisoning ◽  
Neuropsychiatric Symptoms ◽  
Neuron Specific Enolase ◽  
Additional Parameter ◽  
Co Poisoning ◽  
Early Predictors ◽  
Delayed Neuropsychiatric Sequelae ◽  
Serum Neuron Specific Enolase

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). To date, there have been no studies on the utility of serum neuron-specific enolase (NSE), a marker of neuronal cell damage, as a predictive marker of DNS in acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 9-month period. Serum NSE was measured after emergency department arrival, and patients were divided into two groups. The DNS group comprised patients with delayed sequelae, while the non-DNS group included patients with none of these sequelae. A total of 98 patients with acute CO poisoning were enrolled in this study. DNS developed in eight patients. The median NSE value was significantly higher in the DNS group than in the non-DNS group. There was a statistical difference between the non-DNS group and the DNS group in terms of CO exposure time, Glasgow Coma Scale (GCS), loss of consciousness, creatinine kinase, and troponin I. GCS and NSE were the early predictors of development of DNS. The area under the curve according to the receiver operating characteristic curves of GCS, serum NSE, and GCS combined with serum NSE were 0.922, 0.836, and 0.969, respectively. In conclusion, initial GCS and NSE served as early predictors of development of DNS. Also, NSE might be a useful additional parameter that could improve the prediction accuracy of initial GCS.

Patterns of cardiac dysfunction after carbon monoxide poisoning

2020 ◽  
pp. 477-485
Author(s):  
Miguel Alvarez Villela ◽  
◽  
Omar Wever-Pinzon ◽  
Mona Parikh ◽  
Kayla Deru ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Cardiac Dysfunction ◽  
Carbon Monoxide Poisoning ◽  
Systolic Dysfunction ◽  
Tertiary Care ◽  
Acute Poisoning ◽  
Left Ventricular ◽  
Co Poisoning ◽  
Ventricular Systolic Dysfunction ◽  
Chronic Poisoning

Objective: To describe the structural sequelae of carbon monoxide (CO) poisoning on the heart assessed using stress cardiac MRI (CMR). CO poisoning is common. While acute cardiac injury is frequent among survivors, the mid- and long-term effects of CO on the myocardium are unclear. Methods: CMR studies performed between the years 2005 and 2014 for a primary diagnosis of CO poisoning at a tertiary care center were reviewed by an experienced cardiologist. Variables of interest were compared between patients with normal and abnormal studies to identify factors associated with cardiac dysfunction. Results: Eighty-eight patients underwent stress CMR, age 34 years (range 11-70); 49% were male, 74 had acute poisoning and 14 had chronic poisoning (CO exposure for longer than 24 hours). Time from CO poisoning to imaging was 24 months (1day-120 months). Patients were stratified into four categories, which included those with acute poisoning imaged: • ≤12 months; • 12-60 months; • >60 months from the event; and • those with chronic poisoning. Overall, 26 studies (30%) were abnormal. The most common findings were: left ventricular systolic dysfunction in 14 patients, right ventricular systolic dysfunction in nine, and LV dilatation in six. Abnormalities were mild in most cases and were equally prevalent in all four patient categories. Dyspnea at the time of follow-up was more frequent among those with abnormal studies. Conclusions: Mild alterations in ventricular structure and function are frequent in survivors of CO poisoning. Myocardial scarring is rare, suggesting that acute hypoxic injury may not fully explain these abnormalities.

Abstract 843: Restrictive Cardiomyopathy Linked cTnI Mutation (K178E) Causes Severe Heart Failure and Early Mortality

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Pierre-Yves Jean-Charles ◽  
Jianfeng Du ◽  
Yuejin Li ◽  
Nariman Gobara ◽  
Xupei Huang
Keyword(s):  
Heart Failure ◽  
Transgenic Mice ◽  
Diastolic Dysfunction ◽  
Troponin I ◽  
Severe Heart Failure ◽  
Restrictive Cardiomyopathy ◽  
Left Ventricular ◽  
Early Mortality ◽  
Cardiac Contraction ◽  
Actin Binding

Multiple mutations in cardiac troponin I (cTnI) have been linked to the development of restrictive cardiomyopathy (RCM) in human patients. Among them, K178E mutation has the worst clinical phenotype. K178E mutation may influence the inhibitory function through actin binding since previous studies have shown that amino acids number 173–181 bind to actin and increase the inhibitory effect of TnI. We modeled the mutation of lysine 178→glutamate (K178E) in human cTnI by cardiac specific expression of the mutated protein (cTnI 179Glu in mouse sequence) in transgenic mice. Multiple lines were generated with varying degrees of expression to establish a dose relationship. Increased resting tension in isolated cardiac myocytes and decreased myofibrillar compliance were the main manifestations in cellular function measurements. In vivo cardiac function measured by high-resolution ultrasonic imaging and Doppler echocardiography revealed a significant diastolic dysfunction characterized with decrease of left ventricular end diastolic dimension (LVEDD), decreased cardiac ejection fraction (EF) and left ventricular faction of shortening (FS) as well as a decreased cardiac output (CO). Doppler measurements showed a restrictive left ventricular filling pattern, i.e. reversed E/A ratio; decreased deceleration time (DT); decreased isovolumic relaxation time (IVRT). Enlarged left and right atria was a dramatic sign, which was observed in most of the transgenic mice, and was developed early and fast (at age of 2–3 weeks). Severely affected lines developed a pathology similar to that observed in human restrictive cardiomyopathy patients who carry the same mutation and with a high early mortality. Our data indicate the causality of this mutation for diastolic dysfunction and heart failure and provide a useful animal model for further understanding the thin filament structure-function relationships and the physiological function of triponin in cardiac contraction and relaxation. (Supported by NIH GM073621 and AHA0715116B) This research has received full or partial funding support from the American Heart Association, AHA Greater Southeast Affiliate (Alabama, Florida, Georgia, Louisiana, Mississippi, Puerto Rico & Tennessee).

The Evaluation of Myocardial Damage in 83 Young Adults with Carbon Monoxide Poisoning in the East Anatolia Region in Turkey

2006 ◽  
Vol 25 (8) ◽  
pp. 439-446 ◽  
Author(s):  
Sahin Aslan ◽  
Mustafa Uzkeser ◽  
Bedri Seven ◽  
Fuat Gundogdu ◽  
Hamit Acemoglu ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Young Adults ◽  
Troponin I ◽  
Complete Blood Count ◽  
Carbon Monoxide Poisoning ◽  
Photon Emission ◽  
Myocardial Damage ◽  
Cardiac Biomarkers ◽  
Emission Computed Tomography ◽  
Co Poisoning

Carbon monoxide (CO) poisoning is the leading cause of death from intoxication. In CO poisoning, it is important to know if there are any symptoms regarding myocardial damage, which are usually unobserved as a result of hypoxia. This study was planned to assess myocardial damage in young healthy patients with CO poisoning. Eighty-three young healthy cases who had been exposed to CO were included in this study. The demographic and clinical characteristics, the origin of CO gas and smoking habits of the patients were recorded. The evaluation of ECG, peripheral ABG, complete blood count and serial cardiac biomarkers (creatine kinase, creatine kinasemyocardial band and troponin I) measurements were performed in all cases. Additionally, echocardiogram (ECHO) and myocardial perfusion single-photon emission computed tomography (SPECT) were performed at the appropriate times in all cases. The mean age of the patients was 27.39 /10.9 years. The main complaint of the patients was loss of consciousness with a 62.7% rate. The average carboxyhaemoglobin level of the patients was 34.49 /15.9%. Sinus tachycardia was present in 26.5% of patients. Diagnostic ischaemic ECG changes were present in 14.4% of patients. In myocardial SPECT, myocardial ischaemic damage was observed in 9 cases, in 6 of whom ECHO findings were also confirmed. Myocar-dial damage due to CO poisoning should not be ignored. If patients are at risk in terms of myocardial damage, further studies, such as ECHO and scintigraphy are needed to determine myocardial damage resulting from CO poisoning. However, in the young adults of the risk group, if the baseline ECG and serial cardiac biomarkers are normal, further studies such as ECHO and scintigraphy, considering the length of exposure and the severity of poisoning, may not be necessary for the evaluation of myocardial damage due to CO poisoning.

523 Troponin I could stratify the patients with severe heart failure

2003 ◽  
Vol 2 (1) ◽  
pp. 108
Author(s):  
G DAN ◽  
A DAN ◽  
I DAHA ◽  
C STANESCU ◽  
V ILIE ◽  
...  
Keyword(s):  
Heart Failure ◽  
Troponin I ◽  
Severe Heart Failure

scholarly journals Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Qt Interval ◽  
Troponin I ◽  
Morphological Changes ◽  
Carbon Monoxide Poisoning ◽  
Myocardial Damage ◽  
Qt Dispersion ◽  
Ecg Changes ◽  
Corrected Qt Interval ◽  
Logistic Analysis

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

Cardiac mitofusin-1 is declined in non-responding patients with idiopathic dilated cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Hsiao ◽  
I Shimizu ◽  
T Wakasugi ◽  
S Jiao ◽  
T Watanabe ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Heart Failure ◽  
Ventricular Myocytes ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Heart Failure Patients ◽  
Underlying Mechanisms ◽  
Neonatal Rat Ventricular Myocytes ◽  
Mitofusin 1

Abstract Background/Introduction Mitochondria are dynamic regulators of cellular metabolism and homeostasis. The dysfunction of mitochondria has long been considered a major contributor to aging and age-related diseases. The prognosis of severe heart failure is still unacceptably poor and it is urgent to establish new therapies for this critical condition. Some patients with heart failure do not respond to established multidisciplinary treatment and they are classified as “non-responders”. The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Purpose Studies indicate mitochondrial dysfunction has causal roles for metabolic remodeling in the failing heart, but underlying mechanisms remain to be explored. This study tried to elucidate the role of Mitofusin-1 in a failing heart. Methods We examined twenty-two heart failure patients who underwent endomyocardial biopsy of intraventricular septum. Patients were classified as non-responders when their left-ventricular (LV) ejection fraction did not show more than 10% improvement at remote phase after biopsy. Fourteen patients were classified as responders, and eight as non-responders. Electron microscopy, quantitative PCR, and immunofluorescence studies were performed to explore the biological processes or molecules involved in failure to respond. In addition to studies with cardiac tissue specific knockout mice, we also conducted functional in-vitro studies with neonatal rat ventricular myocytes. Results Twenty-two patients with IDCM who underwent endomyocardial biopsy were enrolled in this study, including 14 responders and 8 non-responders. Transmission electron microscopy (EM) showed a significant reduction in mitochondrial size in cardiomyocytes of non-responders compared to responders. Quantitative PCR revealed that transcript of mitochondrial fusion protein, Mitofusin-1, was significantly reduced in non-responders. Studies with neonatal rat ventricular myocytes (NRVMs) indicated that the beta-1 adrenergic receptor-mediated signaling pathway negatively regulates Mitofusin-1 expression. Suppression of Mitofusin-1 resulted in a significant reduction in mitochondrial respiration of NRVMs. We generated left ventricular pressure overload model with thoracic aortic constriction (TAC) in cardiac specific Mitofusin-1 knockout model (c-Mfn1 KO). Systolic function was reduced in c-Mfn1 KO mice, and EM study showed an increase in dysfunctional mitochondria in the KO group subjected to TAC. Conclusions Mitofusin-1 becomes a biomarker for non-responders with heart failure. In addition, our results suggest that therapies targeting mitochondrial dynamics and homeostasis would become next generation therapy for severe heart failure patients. Funding Acknowledgement Type of funding source: None

Anaemia and heart failure

Open Medicine ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. 11-25
Author(s):  
Enrico Vizzardi ◽  
Tania Bordonali ◽  
Elena Tanghetti ◽  
Marco Metra ◽  
Livio Cas
Keyword(s):  
Heart Failure ◽  
Ventricular Dysfunction ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Favourable Effect ◽  
Heart Failure Trial ◽  
Patients With Heart Failure ◽  
Darbepoetin Alpha ◽  
Main Determinants ◽  
Independent Determinant

AbstractAnaemia is one of the most frequent co-morbidities in patients with heart failure. Its prevalence increases from 4% to7% in subjects with asymptomatic left ventricular dysfunction to >30% in patients with severe heart failure. Renal insufficiency, activation of inflammatory mediators and treatment with renin-angiotensin antagonists seem to be its main determinants. The results of many studies agree in providing evidence that anaemia is a powerful independent determinant of survival in patients with heart failure. However, the mechanisms of this relation are still not fully understood. Moreover a favourable effect of the correction of anaemia on prognosis has not yet been shown. Also In addition to this, controlled studies assessing its effects on exercise tolerance have yielded controversial results. Further research is needed to assess the effect of correcting anaemia in chronic heart failure (CHF) patients; ongoing reduction of events with RED-HF (Darbepoetin alpha in heart failure) trial will help define the role.

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