Abstract P234: Hypertensive Disorders Of Pregnancy And Increased Levels Of Cardiac Troponin I After Delivery

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Takao Kato ◽  
Eri Muta ◽  
Moriaki Inoko

Background: Cardiovascular functions and hemodynamics dramatically change during pregnancy such as cardiac output, expanded blood volume, reduced systematic vascular resistance, and heart chamber enlargement. Hypertensive disorders of pregnancy (HDP) may affect the cardiac load during pregnancy; however, the data about plasma concentration of cardiac troponin in pregnant women with HDP is very limited. Methods: We prospectively collected data of 751 pregnant women between 2012 and 2013 in Japanese general hospital. We analyzed laboratory data and echocardiographic findings after delivery. The elevated cTnI was defined as >0.015 ng/mL because the normal population have serum cTnI of less than 0.015 ng/mL in this assay. Results: The HDP were observed in 32 patients; the elevated cTnI was observed 40 patients. The age of patients with HDP (33.7 ±4.3 years) was not different from that of those without HDP (33.3 ± 5.0 years). The brain natriuretic peptides levels were not different between those with and without HDP. The proportion of elevated cTnI was higher in those with HDP (21.8%) than those without (3.6%, P<0.0001). After adjusting for confounders, the risk of elevated cTnI in those with HDP relative to those without HDP remained significant (odds ratio 4.52, 95% confidence interval 1.45-14.5). There were no women with reduced left ventricular ejection fraction. Conclusions: HDP was associated with elevated cTni, suggesting myocardial microinjury might occur more frequently in those with HDP.

2019 ◽  
Vol 12 (1) ◽  
pp. 24-29
Author(s):  
Mohammad Jakir Hossain ◽  
Khondoker Asaduzzaman ◽  
Solaiman Hossain ◽  
Muhammad Badrul Alam ◽  
Nur Hossain

Background: In the diagnosis of acute coronary syndrome, cardiac troponin I is highly reliable and widely available biomarker. Serum level of cardiac troponin I is related to amount of myocardial damage and also closely relates to infarct size. Our aim of the study is to find out the relationship between cardiac troponin I and left ventricular systolic function after acute coronary syndrome. Methods: Total of 132 acute coronary syndrome patients were included in this study after admission in coronary care unit of Sir Salimullah Medical College, Mitford Hospital. Troponin I level was measured at admission and left ventricular ejection fraction (LVEF) was measured by echocardiography between 12-48 hours of onset of chest pain. Results: There was negative correlation between Troponin I at 12 to 48 hours of chest pain with LVEF in these study patients. With a cutoff value of troponin I e”6.8 ng/ml in STEMI patients there is a significant negative relation between 12 to 48 hrs troponin I and LVEF (p<0.001). Sensitivity of troponin I e” 6.8 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% in STEMI was 93.75% and specificity was 77.78%. In NSTEMI sensitivity of troponin I e” 4.5 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% was 65% and specificity was 54.05%. Conclusion: Serum troponin I level had a strong negative correlation with left ventricular ejection fraction after acute coronary syndrome and hence can be used to predict the LVEF in this setting. Cardiovasc. j. 2019; 12(1): 24-29


2002 ◽  
Vol 12 (6) ◽  
pp. 519-523 ◽  
Author(s):  
Richard V. Williams ◽  
L. LuAnn Minich ◽  
Robert E. Shaddy ◽  
L. George Veasy ◽  
Lloyd Y. Tani

Despite pathologic evidence of myocardial inflammation, the significance of myocarditis in children with acute rheumatic carditis remains controversial. Elevations in cardiac troponin I have been demonstrated in other forms of myocarditis. The purpose of our study was to determine if levels of cardiac troponin I are elevated, suggesting myocardial injury, in patients with acute rheumatic carditis. We identified all those patients with acute rheumatic fever, presenting between July 1998 and December 2000, who had clinical evidence of carditis, such as a new murmur of mitral or aortic regurgitation, and who had an echocardiogram, measurements of levels of cardiac troponin I, erythrocyte sedimentation rate, and/or C-reactive protein performed at the time of presentation. Their charts were reviewed for demographic and clinical data. Echocardiograms were reviewed for severity of aortic and mitral regurgitation, and measurements made of left ventricular ejection fraction, fractional shortening, and end-diastolic dimension. We found 16 patients with acute rheumatic carditis, ranging in age from 2.0 to 16.1 years, with just over one-third having symptoms of congestive heart failure. All patients had evidence of acute inflammation. There was a significant relationship between symptoms and severity of mitral regurgitation. No patient had elevated levels of cardiac troponin I level. The fact that levels of cardiac troponin I are not elevated in the serum of children with acute rheumatic carditis suggests that there is minimal myocytic necrosis in this setting. This supports the concept that acute valvar regurgitation is the major hemodynamic abnormality in these patients.


2021 ◽  
Vol 16 (1) ◽  
pp. 34-38
Author(s):  
Kamal Uddin Ahmed ◽  
Mst Rabeya Bilkis ◽  
AKM Monwarul Islam ◽  
Gias Uddin Ahmed ◽  
Syed Md Romel ◽  
...  

Myocardial infarction is one of the leading cause of death globally and following acute myocardial infarction prognosis depends on extent of myocardial damage. This study was aimed to correlate cardiac troponin I level with the left ventricular systolic function in patients with acute ST-elevated myocardial infarction. A total of 104 patients of acute ST-segment elevated myocardial infarction receiving streptokinase therapy within 12 hours of onset of chest pain were studied. Cardiac troponin I concentration was measured by immunometric assay and echocardiographic left ventricular ejection fraction was calculated by modified biplane Simpson's method. Left ventricular ejection fraction (LVEF) was compared with serum cardiac troponin I concentration. Study subjects were divided into two groups on the basis of LVEF. In group I, there were 54 patients with LVEF < 50% and in group II, there were 50 patients with LVEF >_ 50%. The mean cTnI within 12 hours of onset was 129 ± 8.7 ng/ml in group I and11 ± 2.1 ng/ml group II and the difference was statistically significant (p<0.001). Serum cardiac troponin I concentration has a strong negative correlation with left ventricular ejection fraction after first acute myocardial infarction. A level of serum cardiac troponin I >_ 6.6 ng/ml provided a good indication for LVEF <50% and this can be used to detect patients with higher risk. Faridpur Med. Coll. J. 2021;16(1):34-38


2021 ◽  
Author(s):  
Hiroshi Yamaguchi ◽  
Hiroyuki Awano ◽  
Tetsushi Yamamoto ◽  
Masafumi Matsuo ◽  
Kazumoto Iijima

Abstract Background: Cardiac troponin I (cTnI), uniquely expressed in the myocardium, is a marker for acute myocardial injury. Its clinical significance in Duchenne and Becker muscular dystrophy (DMD and BMD) and its relation to alpha-actinin-3 (ACTN3) genotype as a genetic modifier of cardiomyopathy are still unknown.Methods and Results: Overall, 529 and 131 serum cTnI values of 127 DMD and 47 BMD patients, respectively, were reviewed. cTnI elevation was generally observed in the second decade of life. Both cTnI levels and the proportion of abnormal cTnI levels were significantly higher in DMD patients than in BMD patients (age range: 1< years ≤10 and 10< years ≤18 and 10< years ≤18, respectively). Decreased left ventricular ejection fraction was observed after cTnI elevation in both populations. cTnI levels by age in DMD patients with ACTN3 null genotype tended to increase highly and early.Conclusions: Myocardial injury indicated by cTnI was more common and severe in DMD patients than in BMD patients. cTnI elevation preceding cardiac dysfunction may represent an early phase of cardiomyopathy progression and may be a biomarker for early detection of cardiomyopathy in DMD and BMD patients. The ACTN3 null genotype may be a risk factor for early myocardial injury.


2020 ◽  
Vol 72 (1) ◽  
Author(s):  
Ahmed Ayuna ◽  
Nik Abidin

Abstract Background Anthracycline-induced cardiotoxicity has been classified based on its onset into acute, early, and late. It may have a significant burden on the quality and quantity of life of those exposed to this class of medication. Currently, there are several ongoing debates on the role of different measures in the primary prevention of cardiotoxicity in cancer survivors. Our article aims to focus on the role of neurohormonal blockers in the primary prevention of anthracycline-induced cardiotoxicity, whether it is acute, early, or late onset. Main body of the abstract PubMed and Google Scholar database were searched for the relevant articles; we reviewed and appraised 15 RCTs, and we found that angiotensin-converting enzyme inhibitors (ACEI) and B-blockers were the most commonly used agents. Angiotensin II receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRAs) were used in a few other trials. The follow-up period was on the range of 1–156 weeks (mode 26 weeks). Left ventricular ejection fraction (LVEF), left ventricular diameters, and diastolic function were assessed by either echocardiogram or occasionally by cardiac magnetic resonance imaging (MRI). The occurrence of myocardial injury was assessed by troponin I. It was obvious that neurohormonal blockers reduced the occurrence of LVEF and myocardial injury in 14/15 RCTs. Short conclusion Beta-blockers, especially carvedilol and ACEI, especially enalapril, should be considered for the primary prevention of acute- and early-onset cardiotoxicity. ARB and MRA are suitable alternatives when patients are intolerant to ACE-I and B-blockers. We recommend further studies to explore and establish the role of neurohormonal blockers in the primary prevention of the acute-, early-, and late-onset cardiotoxicity.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dan Zhu ◽  
Weiyu Chen ◽  
Yuchen Pan ◽  
Tingcui Li ◽  
Ming Cui ◽  
...  

AbstractTo evaluate the effect of age and parity on maternal cardiac diastolic function in second trimester among pregnant women with normal left ventricular ejection fraction. To analyze the correlation between impaired diastolic function and pre-eclampsia. It had been suggested that maternal cardiac adaptations during pregnancy differed between nulliparous and primiparous women and also varied according to age. Impaired cardiac function may precede pre-eclampsia. Therefore, we examined the effects of parity and age on cardiac diastolic function during pregnancy and whether impaired diastolic function during the second trimester correlates with pre-eclampsia. Women with singleton pregnancies at 13 + 0 to 27 + 6 weeks’ gestation and left ventricular ejection fraction (LVEF) ≥ 50% were retrospectively identified. Diastolic function parameters were assessed using transthoracic echocardiography. Pre-eclampsia was identified from medical records. The effect of age and parity on maternal cardiac diastolic function as well as the correlation between impaired diastolic function and occurrence rate of pre-eclampsia were examined. 376 pregnant women were included (median age: 30 years; median gestational age: 14 weeks; 171 primiparous women). LVEF was 66%. Impaired cardiac diastolic function was seen in 7.8% of pregnant women < 35 years compared with 28.6% of those ≥ 35 years (p = 0.000). ROC curve showed women with maternal age over 32 began to have a higher rate of impaired cardiac diastolic function (AUC = 0.704, p = 0.000, sensitivity = 54.5%, specificity = 75.3%). There was no difference in diastolic function indices between maternal women grouped by parity. Higher maternal age was an independent risk factor of declining Em (p < 0.05). Em < 13 cm/s was significantly associated with pre-eclampsia occurrence (HR 8.56; 95% CI 3.40–21.57) after being adjusted for confounders. Maternal age is an independent risk factor for diastolic function decline. There is no difference in cardiac diastolic function between nulliparous women and primiparous women. Pre-eclampsia occurrence is significantly higher in patients with impaired diastolic function at mid-gestation. The application of risk grading using diastolic function at mid-gestation may improve the survival outcomes of pregnant women.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rachel Ruckdeschel Smith ◽  
Isotta Chimenti ◽  
Eduardo Marbán

Cardiosphere-derived cells (CDCs), a naturally heterogeneous mixture of cell sub-populations, were grown from percutaneous endomyocardial adult human biopsy specimens (n=6). c-Kit + and CD90 + CDCs were selected using magnetic-activated cell sorting with excellent purity as determined by flow cytometry. Immunostaining revealed that ~30% of c-Kit + CDCs expressed Nkx2.5, ~100% of CD90 + CDCs expressed procollagen type I, and ~100% of both sub-populations expressed CD105. When placed in co-culture with neonatal myocytes and fibroblasts, c-Kit + CDCs expressed cardiac troponin I, while CD90 + CDCs expressed vimentin. In order to assess the therapeutic potential of purified CDCs, acute myocardial infarcts (MIs) were created in immunodeficient mice and c-Kit + (n=16), CD90 + (n=14), or CD105 + (n=3) CDCs were injected into the border zone. Echocardiograms were performed 3 weeks post-MI to measure left ventricular ejection fraction (LVEF). CD105-injected mice were comparable to an historical control group of mixed CDC-injected mice (LVEF = 41.3±2.9% CD105 vs. 42.8±10.4% CDC [n=11], p=0.60), indicating that the sorting process did not itself impair the therapeutic potential of CDCs. c-Kit- and CD90-injected mice were indistinguishable from one another (LVEF=31.7±8.2% c-Kit vs. 32.1±11.8% CD90, p=0.92), and both groups were significantly outperformed by the CD105-injected mice (p=0.01 and p=0.03, respectively). All groups were then compared to two other historical control groups, mice treated with normal human dermal fibroblasts (NHDFs [n=7]) and mice treated with phosphate-buffered saline (PBS [n=11]). c-Kit-injected mice did significantly outperform both NHDF- (p=0.04) and PBS-injected mice (p=0.03), while more variability in the CD90-injected group resulted in nearly significant comparisons with the NHDF (p=0.08) and PBS groups (p=0.08). While the therapeutic mechanisms of action of these two distinct sub-populations are undoubtedly different, both offer similar global functional benefits in the setting of acute MI. We conclude that the spontaneously-emerging unselected CDC population serves as a therapeutic cell cocktail, and that no functional advantage is conferred by the extra step of sorting for c-Kit + or CD90 + sub-populations.


2010 ◽  
Vol 28 (25) ◽  
pp. 3910-3916 ◽  
Author(s):  
Daniela Cardinale ◽  
Alessandro Colombo ◽  
Rosalba Torrisi ◽  
Maria T. Sandri ◽  
Maurizio Civelli ◽  
...  

Purpose Treatment of breast cancer with trastuzumab is complicated by cardiotoxicity in up to 34% of the patients. In most patients, trastuzumab-induced cardiotoxicity (TIC) is reversible: left ventricular ejection fraction (LVEF) improves after trastuzumab withdrawal and with, or sometimes without, initiation of heart failure (HF) therapy. The reversibility of TIC, however, is not foreseeable, and identification of patients at risk and of those who will not recover from cardiac dysfunction is crucial. The usefulness of troponin I (TNI) in the identification of patients at risk for TIC and in the prediction of LVEF recovery has never been investigated. Patients and Methods In total, 251 women were enrolled. TNI was measured before and after each trastuzumab cycle. LVEF was evaluated at baseline, every 3 months during trastuzumab therapy, and every 6 months afterward. In case of TIC, trastuzumab was discontinued, and HF treatment with enalapril and carvedilol was initiated. TIC was defined as LVEF decrease of > 10 units and below 50%. Recovery from TIC was defined as LVEF increase above 50%. Results TIC occurred in 42 patients (17%) and was more frequent in patients with TNI elevation (TNI+; 62% v 5%; P < .001). Twenty-five patients (60%) recovered from TIC. LVEF recovery occurred less frequently in TNI+ patients (35% v 100%; P < .001). At multivariate analysis, TNI+ was the only independent predictor of TIC (hazard ratio [HR], 22.9; 95% CI, 11.6 to 45.5; P < .001) and of lack of LVEF recovery (HR, 2.88; 95% CI,1.78 to 4.65; P < .001). Conclusion TNI+ identifies trastuzumab-treated patients who are at risk for cardiotoxicity and are unlikely to recover from cardiac dysfunction despite HF therapy.


2018 ◽  
Vol 56 (4) ◽  
pp. 250-256 ◽  
Author(s):  
Zeynep Yildiz ◽  
Abdulkadir Koçer ◽  
Şahin Avşar ◽  
Göksel Cinier

Abstract Background and purpose. Cardiac troponin I (cTnI) is a reliable marker to diagnose acute myocardial infarction, but the pathophysiological explanation for the increase in cTnI levels in patients with acute ischemic stroke (IS) remains unknown. To overcome this question, we aimed to compare serum cTnI levels in acute coronary syndrome (ACS) concomitant with and without stroke. By doing like this, we thought that we could demonstrate the effect of stroke on TrpI level. Methods. Serum cTnI levels of 41 patients having ACS with acute IS during hospitalization were compared with 97 control patients having only ACS. Cranial CT was performed to evaluate the lesions. The severity of IS was evaluated objectively by national institutes of health stroke scale. Results. cTnI levels were found to be similar in both groups. Presence of diabetes mellitus, coronary artery disease and previous myocardial infarction were more frequent in patients with acute IS. The cTnI levels in the patients with the cranial lesion in the anterior circulation was higher (p = 0.039). Presence of acute IS, cTnI level higher than 20 ng/mL and left ventricular ejection fraction < 40% were found to be independent risk factors for mortality (p < 0.05). Conclusions. We found that abnormal troponin levels were more likely to be due to cardiac causes than cerebral ones in this first study evaluating the cTnI levels in patients with ACS concomitant with acute IS. The severity of IS, lesion location in the anterior circulation and higher troponin levels were associated with mortality.


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