Challenges of Management of Stunned Myocardium Associated with Acute Subarachnoid Hemorrhage: A Case Report

2018 ◽  
Vol 4 (2) ◽  
pp. 150-153
Author(s):  
Sirajee Shafiqul Islam ◽  
Kazi Mohibur Rahman ◽  
Sharif Uddin Khan ◽  
Dewan Md Elyas ◽  
Md Aminul Hasanat ◽  
...  

A 40 year old lady presented with headache and vomiting having no past history of hyper-tension, diabetes, smoking, alcohol or drug abuse. Computed Tomography (CT) scan of brain revealed sub-arachnoid haemorrhage in parasaggital frontal and lt. Sylvian fissure. Digital Subtraction Angiogram (DSA) was performed and revealed a small aneurysm (4x 2.5 x 2) mm in anterior communicating artery. After 12 hours of DSA patient complaints of sudden severe headache followed by unconsciousness. Repeat CT performed and revealed new onset rt. fronto-basal intra-cranial hematoma consistent with rebleed. On admission the patient was with normal Glasgow Coma Scale (GCS-15), Blood pressure (BP125/80mm/Hg), ECG & Echocardiogram. After rebleed patient developed low BP (50/35mmHg), GCS down gread (05), ECG showed sinus tachycardia with poor progression of R(V1-V3) wave, elevated cardiac Troponin –I(-4919.6 Pg). Then patient was given a regimen of ionotropic agent noradrenalin at dose 5mcg/kg/h. From day 3th of rebleed the patient was clinically improving, BP(120/84mmHg), GCS( 8), ECG normal, Cardiac Troponin-I- (790.8 Pg/dl). Then emergency endovascular ACOM coil embolization was done.Journal of National Institute of Neurosciences Bangladesh, 2018;4(2): 150-153

2018 ◽  
Vol 12 (1) ◽  
pp. 55-58 ◽  
Author(s):  
Rita Marinheiro ◽  
Pedro Amador ◽  
Leonor Parreira ◽  
Quitéria Rato ◽  
Rui Caria

Introduction: Since there are many manufacturers of cardiac troponin I assays, the true incidence of a false positive result is unknown. The authors report a case of an 18-year-old patient with previous history of recurrent myopericarditis and admitted to hospital twice again with a suspicious of myopericarditis. Conclusion: Troponin I was found to be a false positive and alkaline phosphatase interference was proved to have been the responsible for this.


2020 ◽  
Vol 66 (4) ◽  
pp. 567-578 ◽  
Author(s):  
Magnus Nakrem Lyngbakken ◽  
Erika Nerdrum Aagaard ◽  
Brede Kvisvik ◽  
Trygve Berge ◽  
Mohammad Osman Pervez ◽  
...  

Abstract Background Concentrations of cardiac troponin I (cTnI) and T (cTnT) are associated with clinical cardiac outcomes, but do not correlate closely in subjects recruited from the general population. Accordingly, we hypothesized that cTnI and cTnT concentrations would be influenced by different cardiovascular (CV) and non-CV risk factors and reflect different CV phenotypes. Methods We measured cTnI and cTnT with last generation assays in 1236 women and 1157 men with no known CV disease participating in the prospective observational Akershus Cardiac Examination 1950 Study. All study participants underwent extensive CV phenotyping at baseline, including detailed echocardiography. Results Concentrations of cTnI were measurable in 60.3% and cTnT in 72.5% of study participants (P < 0.001), and correlated moderately (r = 0.53; P < 0.001). cTnI was more strongly associated with male sex (P = 0.018), higher education (P < 0.001), history of hypertension (P < 0.001), and age (P < 0.001), whereas cTnT was more strongly associated with eGFR (P = 0.015). Both cTnI and cTnT were inversely associated with global longitudinal strain and positively associated with LV mass index (LVMI) in analyses adjusted for CV risk factors. The association between cTnI and LVMI was stronger than the association between cTnT and LVMI (P = 0.035). Concentrations of cTnI improved diagnostic accuracy for LV hypertrophy when added to established CV risk factors, but concentrations of cTnT did not improve these models further. Conclusions In a large community-based cohort examined with extensive echocardiography, concentrations of cTnI and cTnT are associated with subclinical LV hypertrophy and dysfunction. Concentrations of cTnI appear superior to cTnT in predicting subclinical LV hypertrophy.


2004 ◽  
Vol 287 (3) ◽  
pp. H1269-H1275 ◽  
Author(s):  
Brian S. Palmer ◽  
Paul F. Klawitter ◽  
Peter J. Reiser ◽  
Mark G. Angelos

Cardiac troponin I (cTnI) degradation has been noted in the stunned myocardium of rodents after ischemia and reperfusion and is one proposed mechanism for the decreased left ventricular (LV) contractility in postischemic hearts. cTnI degradation has been best described after reperfusion of the ischemic myocardium. The effect of ischemia, independent of reperfusion, on cTnI breakdown has not been well characterized. We tested the hypothesis that progressive cTnI degradation occurs with increasing durations of ischemia and that this ischemia-based degradation is, in part, oxidant mediated. Isolated perfused rat hearts underwent global ischemia of 15, 20, or 25 min with and without reperfusion. A second series of hearts was treated with the antioxidants tiron (10 mM) and N-acetylcysteine (4 mM) before 20 min of global ischemia without reperfusion. cTnI degradation was measured using a cTnI-specific antibody and Western blot analyses. A progressive increase in cTnI degradation was seen with increasing duration of ischemia (no reperfusion), which correlated with the return of LV developed pressure during reperfusion. The extent of cTnI degradation was increased in hearts pretreated with antioxidants, although the qualitative degradation pattern was not altered. We conclude that a time-dependent cTnI breakdown occurs during global ischemia that is independent of reperfusion. cTnI breakdown during ischemia is further increased in the presence of antioxidants, suggesting ROS generated during ischemia may play a cTnI protective role.


2018 ◽  
Vol 5 (3) ◽  
pp. 722
Author(s):  
Santosh Kumar ◽  
Sachin Patil

Background: The early mortality rate from AMI is 30% with about half of them occurring within 1hour of disability. Although the mortality rate after admission for AMI has declined by 30% over the past decades, approximately 1 of every 25 patients who survive the initial hospitalization die in the first year after AMI. The gold standard for diagnosis of MI has been an elevated serum level of creatinine kinase – myocardial band (CK- MB), the cardiac-specific isoenzyme of CK. However, elevated CK-MB may not detect all myocardial necrosis. In patients who die suddenly after severe or silent episodes of ischemia, autopsies frequently reveal micronecrosis that was not reflected in routine CK-MB measurements. The present study was undertaken to know that serum Cardiac Troponin-I is more sensitive marker than serum CPK-MB in early diagnosis of acute myocardial infarction (AMI).Methods: The study was carried out in tertiary care hospital in Gulbarga. The study was undertaken with an aim to study that serum cardiac troponin-I (cTnl) is more sensitive than serum CK-MB in early diagnosis of acute myocardial infarction (AMI). The study was conducted on patients admitted with history of chest pain suggestive of AMI as diagnosed by WHO criteria to medicine ward of Basaveshwar Teaching and General Hospital, Gulbarga. The period of study was from June 2012 to June 2014. The sample size included 100 patients with history of chest pain suggestive of AMI, selected by simple random method.Results: Our results revealed that cardiac troponin I was more sensitive (62%) than CK-MB in overall cases admitted in between 6-24 hrs from the onset of chest pain. Maximum number (41%) of AMI patients were affected on the anterior wall followed by Inferior wall of AMI. 11 percent were affected with Antero lateral wall wereas 5 to 6 percent were affected with anteroseptal and global acute and right ventricular AMI was seen among 2 percent of patients. Anterior wall AMI was the significantly affected site with AMI (ʎ2:12.5, P:0.0004). The maximum number of acute myocardial infarctions were ST elevation myocardial infarctions. 28% of cases where CKMB is normal, the cTnI detects the AMI cases indicating its sensitivity.Conclusions: Cardiac troponin-I (cTnI) was more sensitive serum marker than CKMB in the early diagnosis of acute myocardial infarction (AMI). Anterior wall was the most significantly affected site of AMI. In the future, further improvements in analytical performance may open additional diagnostic windows.


Author(s):  
Mayuri Gujrathi

A 35 years old male presented to the outpatient department with symptoms of chest pain (retrosternal), sweating/ uneasiness from 24 hours. The patient with these complaints first went to another practitioner and was diagnosed as ACS with following ECG.  PAST HISTORY: The patient has nil medical history. ADDICTION:  Smoker for 8 years and Alcohol intake daily for 10 years and also having h/o Tobacco consummation. CK-MB, TROPONIN-I is the cardiac-specific biomarker for myocardial injury. Cardiac Troponin-I is a protein found in the cells of the heart muscle. The level of cardiac Troponin-I can be measured by the health of the heart muscle. Can be detected in healthy asymptomatic individuals. Current risk stratification tools like Framingham, Euro score, Lipid Profile, hs CRP are not cardiac-specific and can be heavily influenced by age. Myoglobin is a sensitive marker for muscle injury, but, elevated myoglobin has low specificity for acute myocardial infarction. Troponin has more specificity than CK-MB in myocardial injury.


2020 ◽  
Vol 38 (10) ◽  
pp. 1948-1954
Author(s):  
Hella E.C. Muijsers ◽  
Dirk Westermann ◽  
Anna Birukov ◽  
Olivier W.H. van der Heijden ◽  
José T. Drost ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document