The protective effect of thiamine pyrophosphate, but not thiamine, against cardiotoxicity induced with cisplatin in rats.

This study investigated the effect of thiamine pyrophosphate on oxidative damage associated with cardiotoxicity caused by cisplatin (CIS), an antineoplastic agent, in rats, and compared this with thiamine. Animals used in the study were divided into four groups of 6 rats each. These represented a control group receiving 5 mg/kg of CIS, study groups receiving 20 mg/kg of thiamine pyrophosphate plus 5 mg/kg of cisplatin (CTPG) or 20 mg/kg of thiamine plus 5 mg/kg of cisplatin and a healthy (H) group. All doses were administered intraperitoneally once a day for 14 days. Malondialdehyde, total glutathione and products of DNA injury results were similar in the CTPG and H groups (p > 0.05). Creatinine kinase, creatine kinase MB and troponin 1 levels were similar in the CTPG and H groups (p > 0.05). Thiamine pyrophosphate prevented CIS-associated oxidative stress and heart injury, whereas thiamine did not prevent these.

Evaluation of aortic stiffness by echocardiography in tympanosclerosis patients.

BACKGROUND AND AIMS: Tympanosclerosis (TS) is a scarring process that may occur during otitis media. Aortic stiffness (AS) is a significant predictor for the development of heart diseases due to its close relationship with atherosclerosis. Similar pathophysiological processes based on inflammation may explain both TS and AS formation. This study aimed to determine echocardiographically whether aortic elasticity is impaired in TS-detected patients and to correlate blood inflammatory parameters with TS and aortic elasticity. METHODS: Ninety-eight participants diagnosed with chronic otitis media were enrolled in the study. TS-detected 42 participants were assigned to the study group, while 56 without TS constituted the control group. The two groups' demographic, clinical, echocardiographic, and laboratory characteristics were comparable. RESULTS: Demographic, clinical, and laboratory parameter differences were insignificant. Hs-CRP, neutrophil-to-lymphocyte ratio, and systemic immune-inflammation index were significantly higher in the study group than in the control group (P=0.018, P=0.003, P=0.019, respectively). The study group had significantly lower aortic strain (11.80 ± 4.84 vs. 16.30 ± 3.91; P<0.001) and distensibility (5.23 ± 2.68 vs. 7.24 ± 2.89; P=0.001) values than the control group. The AS index was significantly higher in the study group than in the control group (4.81 ± 2.41 vs. 3.12 ± 1.02; P<0.001). CONCLUSION: In TS-detected patients, AS parameters were found to be impaired. Aortic elasticity parameters measured by echocardiography, a non-invasive and easily accessible method, may signify early cardiovascular involvement in TS-developed patients.

Protective effect of adenosine triphosphate and benidipine separately or together against cardiotoxicity caused by bevacizumab.

Bevacizumab is a recombinant humanized monoclonal antibody whose adverse effects include cardiotoxicity. We investigated whether using adenosine triphosphate (ATP) or benidipine either separately or together protects against cardiac damage induced by bevacizumab in rats. Forty Wistar albino male rats were allocated to five groups of eight: bevacizumab (Bv), ATP + bevacizumab (ABv), benidipine + bevacizumab (BBv), ATP + benidipine + bevacizumab (ABBv) and untreated controls. Rats in the ABv group were injected intraperitoneally (i.p.) with 2 mg/kg ATP. The BBv group was given 4 mg/kg benidipine by oral gavage. The ABBv group was injected i.p. with 2 mg/kg ATP and simultaneously administered 4 mg/kg benidipine orally. One hour after administration of ATP, benidipine or normal saline, the Bv, ABv, BBv and ABBv groups were injected i.p. with 10 mg/kg bevacizumab. Malondialdehyde (MDA) and total glutathione (tGSH) levels were measured in cardiac tissue, and troponin I (TP I) and creatine kinase MB (CK-MB) levels were measured in blood samples. Tissue samples were examined for histopathology. We found the lowest TP I, CK-MB and MDA levels and the highest tGSH level in the ABBv group; these results were similar to the control group. Nuclei of cardiomyocytes in the BV group were misshapen and shrunken, and myofibers were disrupted; we also observed eosinophilic degeneration and interstitial edema. Blood capillaries were dilated and congested. We observed amelioration of these findings in the ABBv group. We found that ATP and benidipine alone or in combination reduced cardiac damage associated with the use of bevacizumab. ATP + benidipine combined therapy produced the most favorable results.

Myringosclerosis as a predictor of the requirement for a permanent pacemaker in patients with drug-related atrioventricular block.

AIMS: Drug-related atrioventricular block (DR-AVB) may develop in patients with underlying latent degenerative conduction disorders, especially with antiarrhythmics and antihypertensives. Although, according to the current guidelines, reversal is achieved with cessation of the inducing agent, this is not the case for nearly half of the patients. The pathophysiological processes of DR-AVB and myringosclerosis include systemic inflammation and degeneration. This study investigated the role of myringosclerosis in predicting irreversible high-grade DR-AVB despite drug cessation. METHODS: This observational, non-randomized, prospective study involved 152 patients with high-grade DR-AVB, 72 of whom had reversible DR-AVB and 80 had irreversible DR-AVB and required permanent pacemakers. The patients' demographic, clinical, echocardiographic, and laboratory characteristics were recorded. Otoscopic tympanic membrane examinations for myringosclerosis were performed. RESULTS: There were no major differences in demographic, echocardiographic or laboratory characteristics between the two groups or previous medications. The median monitoring time with a temporary pacemaker was significantly longer in the irreversible than in the reversible group (5 [4-7] days vs. 2 [1-5] days; P<0.001). The incidence of myringosclerosis was significantly higher in the irreversible than in the reversible group (61.3% vs. 22.2%; P=0.001). Multivariate logistic regression analysis showed that myringosclerosis was an independent predictor of irreversible DR-AVB (odds ratio: 1.703, 95% confidence interval: 1.194-3.058; P=0.01). CONCLUSION: Myringosclerosis is a readily available, inexpensive, and non-invasive assessment and is a marker of inflammation and degeneration that can predict irreversible DR-AVB.

Role of the coronary and non-coronary cardiovascular findings on non-cardiac gated thoracic CT in predicting mortality in SARS-CoV-2 infection.

BACKGROUND: The potential effects of cardiovascular comorbidities on the clinical outcomes in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection remain unclear. Identification of the coronary and non-coronary cardiovascular findings may help to stratify the patients' prognosis. Therefore, we aimed to evaluate the prognostic impact of the coronary and the non-coronary cardiovascular findings in SARS-CoV-2 patients. METHODS: We studied a total of 594 SARS-CoV-2 patients who were hospitalized and performed a non-cardiac gated thoracic computed tomography. Two blinded radiologists assessed the coronary artery calcification segment involvement score (CACSIS) and non-coronary atherosclerosis cardiovascular findings (NCACVF). The baseline characteristics of the patients and CT findings were evaluated according to survival status. Logistic regression analyses were performed to identify the independent predictors of mortality. RESULTS: At a mean follow-up of 8 (4-12.5) days, 44 deaths occurred (7.4%). Compared to survivors, non-survivors had increased CACSIS [27.3% (CACSIS = 0) vs 25% (CACSIS 1-5) vs 47.7% (CACSIS >5), p < 0.001]. Similarly, on NCACVF, non-survivors had much more major findings compared to survivors (29.5% vs. 2.7%, respectively, p < 0.001). At multivariable analysis, age (p = 0.009), creatinine (p < 0.001), hs-cTnI (p = 0.004) and NCACVF (HR 1.789; 95% CI 1.053-3.037; p = 0.031) maintained a significant independent association with in-hospital mortality. CONCLUSION: Our study shows that coronary and non-coronary cardiovascular findings on non-cardiac gated thoracic CT may help to predict mortality in patients with SARS-CoV-2 infection.

The Relationship between Coronary Artery Calcium Score and Monocyte to High-Density Lipoprotein Cholesterol Ratio in Patients with Stable Angina Pectoris.

OBJECTIVE: Coronary artery calcification is a cornerstone marker for coronary atherosclerosis. Therefore, the calculation of the coronary artery calcium score has become a routine method in diagnosing coronary artery disease in recent years. Monocyte to high-density lipoprotein cholesterol ratio reflects proatherogenic and antiatherogenic balance, and this ratio is associated with coronary atherosclerosis and cardiovascular events. This study aimed to investigate the value of monocyte to high-densitylipoprotein cholesterol ratio in predicting coronary atherosclerosis, which coronary artery calcium score determines. METHODS: A total of 276 patients with chest pain who underwent coronary computed tomography angiography were enrolled in the study. The patients were divided into 3 groups according to coronary artery calcium score [coronary artery calcium score=0 for very low risk (n=121), coronary artery calcium score=1-99 for low risk (n=100), coronary artery calcium score ≥ 100 for moderate-high risk (n=55)]. The monocyte to high-density lipoprotein cholesterol ratio, neutrophil-to-lymphocyte ratio, systemic immune-inflammation index, and plateletto-lymphocyte ratio were calculated from venous blood samples. RESULTS: Monocyte to high-density lipoprotein cholesterol ratio values were significantly higher in patients with moderate-high coronary artery calcium score (1.29 ± 0.59 vs 1.41 ± 0.56 vs 1.56 ± 0.58, P =.009). However, there were no differences between the groups in terms of other inflammatory markers (neutrophil-to-lymphocyte ratio, systemic immune-inflammation index, and platelet-to-lymphocyte ratio). Age (odds ratio: 1.178; 95% CI: 1.107-1.253; P < .001), dyslipidemia (odds ratio: 14.252; 95% CI: 5.459-37.211; P <.001), smoking (odds ratio: 2.893; 95% CI: 1.317-6.358; P=.008), and monocyte to high-density lipoprotein cholesterol ratio (odds ratio: 2.082 per 1-point increase; 95% CI: 1.016-4.268; P=.045) were independent predictors of coronary artery calcium score in multivariate analysis. CONCLUSION: Our data showed that high monocyte to high-density lipoprotein cholesterol ratio is significantly associated with increased coronary artery calcium score. Monocyte to highdensity lipoprotein cholesterol ratio indicates that it can be applied easily and swiftly in clinics to help predicting the coronary artery disease.

Predictors of left atrial remodeling in newly diagnosed hypertensive patients: a speckle-tracking echocardiographic study.

Endothelial dysfunction, oxidative stress, and increased inflammatory activity are the main pathophysiological mechanisms responsible for cardiac remodeling secondary to hypertension. Bilirubin has anti-oxidant, anti-inflammatory, and anti-fibrotic functions. This report's objectives are to determine whether Query identifiers of left atrial (LA) remodeling, total atrial conduction time (TACT) and LA reservoir strain (LARS), are associated with serum total bilirubin levels, and to identify the possible predictors of LA remodeling in newly diagnosed hypertensive subjects. One hundred thirty-four subjects were enrolled in this study. TACT was evaluated by tissue Doppler imaging, and LARS was calculated by speckle-tracking echocardiography. Laboratory parameters were recorded. The subjects were classified into two separate groups according to the median value of TACT and LARS. In patients with supramedian TACT, LA volume index (LAVI) and epicardial adipose tissue (EAT) thickness were higher, while LARS and LVGLS were lower. In subjects with inframedian LARS, TACT was longer, LAVI and EAT thickness were higher, and LVGLS was lower. Patients with supramedian TACT and inframedian LARS were older and had lower total bilirubin. Total bilirubin, EAT thickness, and age were predictors of TACT and LARS. Serum bilirubin levels may have a protective effect on the LA remodeling process in newly diagnosed hypertensive subjects.

The preventive effect of exogenous adenosine triphosphate on methanol-induced cardiotoxicity in rats

Abstract Exposure to methanol can cause serious consequences such as permanent visual disturbances and death. The heart tissue is highly vulnerable to ATP deficiency. Our study aimed to investigate whether exogenous ATP administration may alleviate methanol-induced ATP deficiency and subsequent oxidative damage in rat heart tissue. A total of 30 rats were divided into equal five groups; Healthy Group (HG), Methotrexate (MXG), Methanol (MeOH), Methotrexate+Methanol (MXM), and Methotrexate+Methanol+ATP (MMA) groups. We inhibited tetrahydrofolate synthesis by methotrexate to induce methanol toxicity. Methotrexate was administered to MXG, MXM, and MMA group animals for seven days with a catheter directly to the stomach at a 0,3 mg/kg dose per day. At the end of this period, % 20 methanol at a dose of 3 g/kg was administered to MeOH, MMA and MXM group animals. Immediately after methanol application, MMA group animals were injected with ATP at a 4 mg/kg dose intraperitoneally. Blood samples and heart tissues were used for biochemical analysis and histopathological examination. Co-exposure to methanol and methotrexate substantially exacerbated cardiac damage, indicating the potent cardiotoxic effects of methanol. However, the administration of exogenous ATP to MMA group animals brought biochemical oxidative damage parameters and histopathological findings closer to HG.

The effects of ketamine and thiopental used alone or in combination on the brain, heart, and bronchial tissues of rats.

INTRODUCTION: We compared the side effects of ketamine and thiopental used alone and of a ketamine/thiopental combination dose on the brain,heart, and bronchial tissues of rats. MATERIAL AND METHODS: Three groups received intraperitoneal injections of 30 mg/kg ketamine (K-30); 15 mg/kg thiopental (T-15); or of both in combination (KTSA). These doses were doubled in another set of study groups (K-60, T-30, and KTA groups, respectively). Optimal anesthesia duration was examined in all groups. RESULTS: Anesthesia did not occur with 30 mg/kg ketamine or 15 mg/kg thiopental. However, when used alone ketamine and thiopental led to oxidative stress in the striatum, heart, and bronchial tissues. Conversely, combined administration of anesthetics and subanesthetic doses were found not to create oxidative stress in any of these areas. The highest level of adrenaline in blood samples collected from the tail veins was measured in the KTA-60, and the lowest amount in the T-30. Creatine kinase activity was highest in the KTA-60 group (p < 0.001). When we compared for all 5 groups to untreated control group; the creatine kinase-MB activities were significiantly different in K-30, T-15 and T-30 (p < 0.001). CONCLUSIONS: The studied doses of ketamine led to oxidative stress by increasing the amount of adrenaline. Thiopental increased oxidative stress with decreases in adrenaline. A longer anesthetic effect with minimal adverse events may be achieved by ketamine and thiopental in combination.

The preventive effect of taxifolin on acrylamide-induced heart damage in rats / O efeito preventivo da taxifolina em danos cardíacos induzidos por acrilamida em ratos

ABSTRACT Objective Acrylamide is a toxic compound widely used in industrial sectors. Acrylamide causes reactive oxygen species formation and the subsequent lipid peroxidation reaction, which plays an important role in the pathogenesis of oxidative damage. Taxifolin is a flavonoid with antioxidant properties that inhibit reactive oxygen species formation. In this study, we aimed to investigate the preventive effect of taxifolin on acrylamide-induced oxidative heart damage. Methods The rats were divided into three groups: Acrylamide, Acrylamide+Taxifolin , and Healthy group. Water and food intake and body weight alterations were recorded daily. Malondialdehyde, total glutathione, nuclear factor kappa-B, total oxidant status, and total antioxidant status levels were analyzed from the heart tissue. Troponin-I levels, the parameter known as a cardiac biomarker, were analyzed from the blood sample. The cardiac histopathologic examination was also performed. Results In the Acrylamide group animals, the malondialdehyde, nuclear factor kappa-B, total oxidant status, and troponin-I levels were significantly higher compared to the ones of Acrylamide+Taxifolin and Healthy groups. The levels of total glutathione and total antioxidant status were significantly lower compared to Acrylamide+Taxifolin and Healthy groups'. Additionally, in the Acrylamide group, body weight gain, food and water intake, significantly declined compared to the Acrylamide+Taxifolin and Healthy groups. However, in the Acrylamide+Taxifolin group, taxifolin supplementation brought these values close to Healthy group ones. Furthermore, taxifolin treatment ameliorated structural myocardial damage signs induced by acrylamide. Conclusion Acrylamide exposure significantly induced oxidative damage to rat heart tissue. Taxifolin was able to improve the toxic consequences of acrylamide biochemically and histopathologically, possibly due to its antioxidant properties.

RESUMO Objetivo A acrilamida é um composto tóxico amplamente utilizado em setores industriais. Ela causa a formação de reativas de oxigênio e subsequente reação de peroxidação lipídica, que desempenham um papel importante na patogênese do dano oxidativo. A taxifolina é um flavonóide com propriedades antioxidantes que inibe a formação de reativas de oxigênio. Neste estudo, o objetivo foi investigar o efeito preventivo da taxifolina no dano cardíaco oxidativo induzido por acrilamida. Métodos Os ratos foram divididos em três grupos: Acrilamida, Acrilamida+Taxifolina e grupo Saudável. Ingestão de água e comida e alterações de peso corporal dos animais foram registradas diariamente. Malondialdeído, glutationa total, fator nuclear kappa-B, estado oxidante total e estado antioxidante total foram analisados no tecido cardíaco dos ratos. Os níveis de troponina-I, - parâmetro conhecido como biomarcador cardíaco, foram analisados a partir de amostra de sangue. Um exame histopatológico cardíaco também foi realizado. Resultados Nos animais do grupo Acrilamida, os níveis de malondialdeído, fator nuclear kappa-B, estado oxidante total e troponina-I foram significativamente maiores em comparação com os do grupo Acrilamida+Taxifolina e Saudável. Os níveis de glutationa total e estado antioxidante total foram significativamente mais baixos em comparação com grupos Acrilamida+Taxifolina e Saudável. Além disso, no grupo Acrilamida, o ganho de peso corporal e a ingestão de alimentos e água diminuíram significativamente em comparação com os animais dos grupos Acrilamida+Taxifolina e Saudável. No entanto, no grupo Acrilamida+Taxifolina, a suplementação com taxifolina aproximou esses valores aos do grupo Saudável. Além disso, o tratamento com taxifolina melhorou os sinais de dano miocárdico estrutural induzidos pela acrilamida. Conclusão A exposição à acrilamida induziu significativamente o dano oxidativo do tecido cardíaco dos ratos. A taxifolina foi capaz de melhorar as consequências tóxicas da acrilamida bioquímica e histopatologicamente, possivelmente devido às suas propriedades antioxidantes.

Effect of disulfiram on ketamine-induced cardiotoxicity in rats.

It is known that ketamine increases the production of catecholamines, causing oxidative damage to the heart. Suppression of the production of catecholamines by disulfiram, a drug with antioxidant properties, indicates that disulfiram may decrease ketamine-induced cardiotoxicity. The objective of the present study was to investigate the effect of disulfiram on ketamine-induced cardiotoxicity in rats. Disulfiram was administered by oral gavage in doses of 25 mg/kg to rats in the DK-25 group and 50 mg/kg to rats in the DK-50 group. Distilled water was applied in the ketamine control (KC) and healthy (HG) rat groups. At one hour after drug administration and subsequently at ten-minute intervals, a 60 mg/kg dose of ketamine was intraperitoneally injected in the rats in all groups other than HG, and anesthesia was maintained for three hours. Disulfiram prevented both increase in the levels of parameters indicating oxidative and myocardial damage and decrease of antioxidant levels in the heart tissue with ketamine in a dose-dependent manner. Disulfiram better prevented occurrence of cardiotoxicity with ketamine in the 50 mg/kg dose than in the 25 mg/kg dose. It is concluded that disulfiram may usefully be applied in clinical practice in the prevention of cardiotoxicity as observed during anesthesia with ketamine.

Comparative Investigation of Protective Effects of Metyrosine and Metoprolol Against Ketamine Cardiotoxicity in Rats.

This study investigated the effect of metyrosine against ketamine-induced cardiotoxicity in rats and compared the results with the effect of metoprolol. In this study, rats were divided into groups A, B and C. In group A, we investigated the effects of a single dose of metyrosine (150 mg/kg) and metoprolol (20 mg/kg) on single dose ketamine (60 mg/kg)-induced cardiotoxicity. In group B, we investigated the effect of metyrosine and metoprolol, which were given together with ketamine for 30 days. In group C, we investigated the effect of metyrosine and metoprolol given 15 days before ketamine and 30 days together with ketamine on ketamine cardiotoxicity. By the end of this process, we evaluated the effects of the levels of oxidant-antioxidant parameters such as MDA, MPO, 8-OHGua, tGSH, and SOD in addition to CK-MB and TP I on cardiotoxicity in rat heart tissue. The experimental results show that metyrosine prevented ketamine cardiotoxicity in groups A, B and C and metoprolol prevented it in only group C.