scholarly journals Use of drugs with potential cardiac effect in the setting of SARS-CoV-2 infection

2020 ◽  
Vol 113 (5) ◽  
pp. 293-296 ◽  
Author(s):  
Frederic Sacher ◽  
Laurent Fauchier ◽  
Serge Boveda ◽  
Christian de Chillou ◽  
Pascal Defaye ◽  
...  
Keyword(s):  
Cardiac Effect

scholarly journals Terbufos-sulfone exacerbates cardiac lesions in diabetic rats: a sub-acute toxicity study

2016 ◽  
Vol 67 (2) ◽  
pp. 126-135 ◽  
Author(s):  
Syed M. Nurulain ◽  
Mohamed Shafiullah ◽  
Javed Yasin ◽  
Abdu Adem ◽  
Juma Al Kaabi ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Organophosphorus Compounds ◽  
Lethal Dose ◽  
Density Lipoprotein ◽  
Cardiac Effect ◽  
Diabetic Rats ◽  
Ultrastructural Changes ◽  
Biochemical Tests ◽  
Wide Range ◽  
Cardiac Lesions

AbstractOrganophosphorus compounds (OPCs) have a wide range of applications, from agriculture to warfare. Exposure to these brings forward a varied kind of health issues globally. Terbufos is one of the leading OPCs used worldwide. The present study investigates the cardiac effect of no observable dose of a metabolite of terbufos, terbufos-sulfone (TS), under non-diabetic and streptozotocin-induced diabetic condition. One hundred nanomoles per rat (1/20 of LD50) was administered intraperitoneally to adult male Wister rats daily for fifteen days. The left ventricle was collected for ultrastructural changes by transmission electron microscopy. The blood samples were collected for biochemical tests including RBC acetylcholinesterase, creatinine kinase (CK), lactate dehydrogenase (LDH), cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), triglycerides, ALT, AST, and GGT. The study revealed about 10 % inhibition of RBC-AChE in two weeks of TS treatment in non-diabetic rats whereas RBC-AChE activity was significantly decreased in diabetic TS treated rats. CK, LDH, and triglycerides were significantly higher in diabetic TS treated rats. Electron microscopy of the heart showed derangement and lesions of the mitochondria of cardiomyocytes in the TS treated groups. The present study concludes that a non-lethal dose of TS causes cardiac lesions which exacerbate under diabetic condition. Biochemical tests confirmed the ultrastructural changes. It is concluded that a non-lethal dose of TS may be a risk factor for a cardiovascular disease, which may be fatal under diabetic condition.

Abstract 076: Lapatinib Reduced Cardiac Hypertrophy Induced By Combined Use Of A Pi3k-mtor Dual Inhibitor And Doxorubicin

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Xinhua Yan ◽  
Yongyao Yang ◽  
Juyong Lee ◽  
Jillian Onufrak ◽  
John Fuseler ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Effect ◽  
Mtor Pathway ◽  
Dual Inhibitor ◽  
Cardiac Side Effects ◽  
Compound C ◽  
Transmission Electron ◽  
Combined Use ◽  
Cardioprotective Effects ◽  
Lapatinib Treatment

The HER2-PI3K-mTOR pathway is pivotal for regulating the physiological function of the heart. Currently, drugs targeting the HER2-PI3K-mTOR pathway are either approved or being tested in clinical trials for cancer therapy. It is, therefore, important to evaluate the cardiac effects of using these drugs. In addition, it is necessary to develop countermeasures to prevent the cardiac side effects if any. Methods: Three-month old female FVB/n mice were treated with lapatinib (an HER2 inhibitor) or BEZ235 (BEZ, a PI3K-mTOR dual inhibitor), alone or with doxorubicin (DOX). Cardiac function was monitored by echocardiography and hemodynamic measurements. Cardiac morphology was assessed by confocal microscopy and transmission electron microscopy. The activation of signaling molecules were measured by Western blot analysis. Results: BEZ alone induced cardiac hypertrophy and subsequent heart failure and lapatinib alone induced cardiac failure, in a course of 17 months, respectively. Combination of BEZ with DOX, either concurrently or sequentially, induced cardiac hypertrophy which was associated with higher mortality rate compared to DOX alone. Neuregulin1, a HER receptor ligand worsened, while Lapatinib alleviated, cardiac hypertrophy in these mice. Lapatinib increased the activation of AMPK in DOX+BEZ treated hearts. The cardiac effect of lapatinib was blocked by Compound C, an AMPK inhibitor. Metformin, an AMPK activator, alleviated DOX+BEZ induced cardiac hypertrophy. Conclusions: BEZ or lapatinib treatment alone induced irreversible cardiac dysfunction in mice. Combined use of BEZ and DOX induced cardiac hypertrophy and early mortality, which were prevented by lapatinib. The cardioprotective effects of lapatinib may rely on activating AMPK in the heart.

Determinants of cardiac fibrosis in experimental hypermineralocorticoid states

1995 ◽  
Vol 269 (4) ◽  
pp. E657-E662 ◽  
Author(s):  
M. Young ◽  
G. Head ◽  
J. Funder
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Fibrosis ◽  
Cardiac Effect ◽  
Mineralocorticoid Receptor Antagonist ◽  
Salt Loading ◽  
Blood Pressure Elevation ◽  
Intracerebroventricular Infusion ◽  
Ru 28318 ◽  
Primary Action ◽  
Drinking Solution

Uninephrectomized rats maintained on 1.0% NaCl to drink and infused with aldosterone (0.75 microgram/h) for 8 wk have previously been shown to develop hypertension, cardiac hypertrophy, and cardiac fibrosis. In the present study we have shown that K+ supplementation (1.0% NaCl plus 0.4% KCl drinking solution) alters neither the interstitial nor the perivascular fibrotic response to mineralocorticoid treatment. Second, rats receiving 0.75 microgram/h 9 alpha-fluorocortisol, a mineralocorticoid and glucocorticoid agonist, respond with hypertension and cardiac fibrosis without cardiac hypertrophy. Finally, intracerebroventricular infusion of the mineralocorticoid receptor antagonist RU-28318 blocks blood pressure elevation, but not cardiac hypertrophy or fibrosis, when aldosterone is coinfused peripherally. We conclude that the myocardial fibrosis observed in response to chronic mineralocorticoid elevation and salt loading is a humorally mediated event independent of hypokalemia, hypertension, and cardiac hypertrophy. It remains to be determined whether the fibrosis observed in the presence of excess salt represents a direct (e.g., cardiac) effect of mineralocorticoid hormones or one mediated via a primary action on classical epithelial aldosterone target tissues (e.g., kidney).

scholarly journals Preclinical cardiac organ damage during statin treatment in patients with inflammatory joint diseases: the RORA-AS statin intervention study

Rheumatology ◽  
2020 ◽  
Vol 59 (12) ◽  
pp. 3700-3708
Author(s):  
Hanna A Os ◽  
Silvia Rollefstad ◽  
Eva Gerdts ◽  
Ester Kringeland ◽  
Eirik Ikdahl ◽  
...  
Keyword(s):  
Organ Damage ◽  
Statin Treatment ◽  
Cardiac Effect ◽  
Left Ventricular ◽  
Baseline Body Mass Index ◽  
Joint Diseases ◽  
Biologic Dmards ◽  
Inflammatory Joint Diseases ◽  
Concentric Geometry

Abstract Objective Statin treatment has been associated with reduction in blood pressure and arterial stiffness in patients with inflammatory joint diseases (IJD). We tested whether statin treatment also was associated with regression of preclinical cardiac organ damage in IJD patients. Methods Echocardiography was performed in 84 IJD patients (52 RA, 20 ankylosing spondylitis, 12 psoriatric arthritis, mean age 61 (9) years, 63% women) without known cardiovascular disease before and after 18 months of rosuvastatin treatment. Preclinical cardiac organ damage was identified by echocardiography as presence of left ventricular (LV) hypertrophy, LV concentric geometry, increased LV chamber size and/or dilated left atrium. Results At baseline, hypertension was present in 63%, and 36% used biologic DMARDs (bDMARDs). Preclinical cardiac organ damage was not influenced by rosuvastatin treatment (44% at baseline vs 50% at follow-up, P = 0.42). In uni- and multivariable logistic regression analyses, risk of preclinical cardiac organ damage at follow-up was increased by higher baseline body mass index [odds ratio (OR) 1.3, 95% CI: 1.1, 1.5, P = 0.01] and presence of preclinical cardiac organ damage at baseline (OR 6.4, 95% CI: 2.2, 18.5, P = 0.001) and reduced by use of bDMARDs at follow-up (OR 0.3, 95% CI: 0.1, 0.9, P = 0.03). Conclusion Rosuvastatin treatment was not associated with a reduction in preclinical cardiac organ damage in IJD patients after 18 months of treatment. However, use of bDMARDS at follow-up was associated with lower risk of preclinical cardiac organ damage at study end, pointing to a possible protective cardiac effect of bDMARDs in IJD patients. ClinicalTrials.gov https://clinicaltrials.gov/NCT01389388

Electrocardiographic manifestations and the cardiac effect of drugs in vitamin B1 deficiency in rats

1938 ◽  
Vol 15 (2) ◽  
pp. 206-220 ◽  
Author(s):  
Soma Weiss ◽  
Florence W. Haynes ◽  
Paul M. Zoll
Keyword(s):  
Vitamin B1 ◽  
Cardiac Effect ◽  
Vitamin B1 Deficiency

Cardiac effect of piroxicam and DFU in rat fetuses

2013 ◽  
Vol 41 ◽  
pp. 33
Author(s):  
F. Burdan ◽  
J. Kobylinska ◽  
J. Szumiło ◽  
R. Klepacz
Keyword(s):  
Cardiac Effect ◽  
Rat Fetuses

Cardiac effect of halofantrine

The Lancet ◽  
1993 ◽  
Vol 342 (8869) ◽  
pp. 501 ◽  
Author(s):  
J Karbwang ◽  
K.Na Bangchang ◽  
D Bunnag ◽  
T Harinasuta ◽  
P Laothavorn
Keyword(s):  
Cardiac Effect

scholarly journals Serial Assessment of Cardiac Function during and following Mitoxantrone Infusion in 30 Consecutive Patients with Multiple Sclerosis

2010 ◽  
Vol 2010 ◽  
pp. 1-4
Author(s):  
Damian Franzen ◽  
Angelika Haus ◽  
Martin Hellmich
Keyword(s):  
Multiple Sclerosis ◽  
Heart Failure ◽  
Cardiac Function ◽  
Low Dose ◽  
Therapeutic Option ◽  
Clinical Signs ◽  
Cardiac Effect ◽  
Left Ventricular ◽  
History Taking ◽  
Dose Dependent

Immunosuppressive therapy is an established therapeutic option in patients suffering from multiple sclerosis (MS). In an open nonrandomized study we serially assessed cardiac function in 30 consecutive patients with MS before, during, and after mitoxantrone therapy. Mitoxantrone (12 mg/m2) was administered intravenously at 3-month intervals. Before each infusion, cardiac function was assessed by history taking, resting electrocardiogram, and echocardiography. Whereas no patient experienced clinical signs of heart failure, left ventricular pump function decreased continuously during mitoxantrone therapy and did not recover after cessation. The presented data suggest a dose-dependent and long-lasting toxic cardiac effect of low-dose mitoxantrone therapy in MS.

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