scholarly journals The Effect of Passive Opium Smoking on Cardiovascular Indices of Rabbits with Normal and Ischemic Hearts

2010 ◽  
Vol 4 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Siyavash Joukar ◽  
Hamid Najafipour ◽  
Reza Malekpour-Afshar ◽  
Fatemeh Mirzaeipour ◽  
Hamid Reza Nasri
Keyword(s):  
Cardiovascular System ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ecg Changes ◽  
Short Term ◽  
Asian People ◽  
Cardiac Histopathology

Some Asian people believe that opium can protect the cardiovascular system. To assess this belief, we investigated the effect of passive opium smoking (POS) on cardiovascular indices in rabbits with ischemic and non-ischemic hearts. Rabbits (n = 43) were divided into control (CTL), short term opium (SO) and long term opium (LO) groups. SO and LO groups were exposed to opium smoking for 3 days and 4 weeks, respectively. ECG, blood pressure (BP), left ventricular pressure and cardiac troponin I levels were recorded. Isoproterenol (ISO) was injected to induce cardiac ischemia and after 4 h the above variables were measured along with cardiac histopathology assessment. All groups showed significant increments in troponin I level (P < 0.05) except the CTL group. This trend was more obvious in ISO-treated groups. Mean arterial pressure (MAP) significantly decreased in all groups (p< 0.05) except the LO group. Opium exposure attenuated ISO-induced myodegeneration but augmented tissue congestion and hemorrhage. In conclusion, higher troponin I serum level and ECG changes were found in passive opium smoking groups. This evidence is against the belief that opium can protect the cardiovascular system.

scholarly journals Effect of short-term microgravity and long-term hindlimb unloading on rat cardiac mass and function

2001 ◽  
Vol 91 (3) ◽  
pp. 1207-1213 ◽  
Author(s):  
Chester A. Ray ◽  
Marilyn Vasques ◽  
Todd A. Miller ◽  
M. Keith Wilkerson ◽  
Michael D. Delp
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Mass ◽  
Hindlimb Unloading ◽  
Sprague Dawley ◽  
Short Term ◽  
Cardiac Atrophy ◽  
Short Term Exposure ◽  
Heart Mass

The purpose of this study was to test the hypothesis that exposure to short-term microgravity or long-term hindlimb unloading induces cardiac atrophy in male Sprague-Dawley rats. For the microgravity study, rats were subdivided into four groups: preflight (PF, n = 12); flight (Fl, n = 7); flight cage simulation (Sim, n = 6), and vivarium control (Viv, n = 7). Animals in the Fl group were exposed to 7 days of microgravity during the Spacelab 3 mission. Animals in the hindlimb-unloading study were subdivided into three groups: control (Con, n = 20), 7-day hindlimb-unloaded (7HU, n = 10), and 28-day hindlimb-unloaded (28HU, n = 19). Heart mass was unchanged in adult animals exposed to 7 days of actual microgravity (PF 1.33 ± 0.03 g; Fl 1.32 ± 0.02 g; Sim 1.28 ± 0.04 g; Viv 1.35 ± 0.04 g). Similarly, heart mass was unaltered with hindlimb unloading (Con 1.40 ± 0.04 g; 7HU 1.35 ± 0.06 g; 28HU 1.42 ± 0.03 g). Hindlimb unloading also had no effect on the peak rate of rise in left ventricular pressure, an estimate of myocardial contractility (Con 8,055 ± 385 mmHg/s; 28HU 8,545 ± 755 mmHg/s). These data suggest that cardiac atrophy does not occur after short-term exposure to microgravity and that neither short- nor long-term simulated microgravity alters cardiac mass or function.

Short- and long-term biological variation of cardiac troponin I in healthy individuals, and patients with end-stage renal failure requiring haemodialysis or cardiomyopathy

2020 ◽  
Vol 58 (11) ◽  
pp. 1941-1949
Author(s):  
Nick S. R. Lan ◽  
Lan T. Nguyen ◽  
Samuel D. Vasikaran ◽  
Catherine Wilson ◽  
Jacqueline Jonsson ◽  
...  
Keyword(s):  
Renal Failure ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Biological Variation ◽  
Healthy Individuals ◽  
Short Term ◽  
End Stage Renal Failure ◽  
Short And Long Term ◽  
End Stage

AbstractObjectivesHigh-sensitivity (hs) cardiac troponin (cTn) assays can quantitate small fluctuations in cTn concentration. Determining biological variation allows calculation of reference change values (RCV), to define significant changes. We assessed the short- and long-term biological variation of cardiac troponin I (cTnI) in healthy individuals and patients with renal failure requiring haemodialysis or cardiomyopathy.MethodsPlasma samples were collected hourly for 4 h and weekly for seven further weeks from 20 healthy individuals, 9 renal failure patients and 20 cardiomyopathy patients. Pre- and post-haemodialysis samples were collected weekly for 7 weeks. Samples were analysed using a hs-cTnI assay (Abbott Alinity ci-series). Within-subject biological variation (CVI), analytical variation (CVA) and between-subject biological variation (CVG) was used to calculate RCVs and index of individuality (II).ResultsFor healthy individuals, CVI, CVA, CVG, RCV and II values were 8.8, 14.0, 43.1, 45.8% and 0.38 respectively for short-term, and 41.4, 14.0, 25.8, 121.0% and 1.69 for long-term. For renal failure patients, these were 2.6, 5.8, 50.5, 17.6% and 0.30 respectively for short-term, and 19.1, 5.8, 11.2, 55.2% and 1.78 for long-term. For cardiomyopathy patients, these were 4.2, 10.0, 65.9, 30.0% and 0.16 respectively for short-term, and 17.5, 10.0, 63.1, 55.8% and 0.32 for long-term. Mean cTnI concentration was lower post-haemodialysis (15.2 vs. 17.8 ng/L, p < 0.0001), with a 16.9% mean relative change.ConclusionsThe biological variation of cTnI is similar between end-stage renal failure and cardiomyopathy patients, but proportionately greater in well-selected healthy individuals with very low baseline cTnI concentrations.

Short-Term and Long-Term Changes of Left Ventricular Volumes During Rate-Adaptive and Single-Rate Pacing

1989 ◽  
Vol 12 (12) ◽  
pp. 1863-1868 ◽  
Author(s):  
MEREDITH I. SEDNEY ◽  
ERIC WEIJERS ◽  
ERNST E. WALL ◽  
JEEEREY D. ADIPRANOTO ◽  
JAN CAMPS ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Short Term ◽  
Ventricular Volumes ◽  
Long Term Changes ◽  
Rate Adaptive

scholarly journals Short- and Long-term Biologic Variability of Galectin-3 and Other Cardiac Biomarkers in Patients with Stable Heart Failure and Healthy Adults

2016 ◽  
Vol 62 (2) ◽  
pp. 360-366 ◽  
Author(s):  
Emily I Schindler ◽  
Jeffrey J Szymanski ◽  
Karl G Hock ◽  
Edward M Geltman ◽  
Mitchell G Scott
Keyword(s):  
Heart Failure ◽  
Troponin I ◽  
Prognostic Biomarker ◽  
High Sensitivity ◽  
Cardiac Biomarkers ◽  
Healthy Individuals ◽  
Short Term ◽  
Galectin 3 ◽  
Short And Long Term

Abstract BACKGROUND Galectin-3 (Gal-3) has been suggested as a prognostic biomarker in heart failure (HF) patients that may better reflect disease progression than traditional markers, including B-type natriuretic peptide (BNP) and cardiac troponins. To fully establish the utility of any biomarker in HF, its biologic variability must be characterized. METHODS To assess biologic variability, 59 patients were prospectively recruited, including 23 male and 16 female patients with stable HF and 10 male and 10 female healthy individuals. Gal-3, BNP, and high-sensitivity cardiac troponin I (hs-cTnI) were assayed at 5 time points within a 3-week period to assess short-term biologic variability. Long-term (3-month) biologic variability was assessed with samples collected at enrollment and after 4, 8, and 12 weeks. RESULTS Among healthy individuals, mean short-term biologic variability, expressed as intraindividual CV (CVI), was 4.5% for Gal-3, 29.0% for BNP, and 14.5% for hs-cTnI; long-term biologic variability was 5.5% for Gal-3, 34.7% for BNP, and 14.7% for hs-cTnI. In stable HF patients, mean short-term biologic variability was 7.1% for Gal-3, 22.5% for BNP, and 8.5% for hs-cTnI, and mean long-term biologic variability was 7.7% for Gal-3, 27.6% for BNP, and 9.6% for hs-cTnI. CONCLUSIONS The finding that Gal-3 has minimal intraindividual biological variability adds to its potential as a useful biomarker in HF patients.

Abstract 177: Overexpression of Cardiac Troponin I-Interacting Kinase, a Cardiac-Specific MAPKKK, Promotes Cardiac Dysfunction

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Hao Tang ◽  
Kunhong Xiao ◽  
Lan Mao ◽  
Howard A Rockman ◽  
Douglas A Marchuk
Keyword(s):  
Disease Progression ◽  
Cardiac Dysfunction ◽  
Cardiac Troponin ◽  
Kinase Activity ◽  
Troponin I ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Cardiac Response ◽  
Kinase Assay ◽  
Idiopathic Dilated Cardiomyopathy

Cardiac Troponin I-interacting kinase (TNNI3K) is a cardiac specific kinase whose biological function remains largely unknown. We have recently shown that TNNI3K expression greatly accelerates cardiac dysfunction in mouse models of cardiomyopathy, indicating an important role in modulating disease progression. To further investigate TNNI3K kinase activity in vivo, we have generated transgenic mice expressing both wild-type and kinase-dead versions of the human TNNI3K protein. Importantly, we show that the increased TNNI3K kinase activity induces mouse cardiac hypertrophy, and the kinase activity is required to accelerate disease progression in a left-ventricular pressure overload model of mouse cardiomyopathy. We demonstrate the clinical relevance of these observations by identifying two potential missense mutations near the kinase activation loop of TNNI3K in idiopathic dilated cardiomyopathy (DCM) human patients. Using an in vitro kinase assay and proteomics analysis, we show that TNNI3K is a dual-function kinase with Tyr and Ser/Thr kinase activity. Using antisera to TNNI3K, we show that TNNI3K protein is located at the sarcomere Z disc. These combined data suggest that TNNI3K mediates cell signaling to modulate cardiac response to stress. The essential role of the kinase activity makes TNNI3K a strong potential pharmaceutical target of kinase inhibitors for heart disease.

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
Keyword(s):  
Pregnant Women ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Normal Population ◽  
Laboratory Data ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Hypertensive Disorders Of Pregnancy ◽  
Ventricular Ejection Fraction ◽  
Hypertensive Disorders

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.

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