Recurrent Complete Atrioventricular Block During Cisplatin Infusion: A Case Report

Özcan, Türkay; Cirit, Abdullah; Kıykım, Ahmet

doi:10.4172/2155-9880.1000151

Cited by 9 publications

(6 citation statements)

References 9 publications

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“…Possible explanation for this cardiotoxic effect of cisplatin may be found in evidence for the deposition of cisplatin in the region of sinoatrial node [59] . It has been reported that cisplatin-induced bradicardia may be related to recurrent AV block [51] Also, negative chronotropic effect of cisplatin was observed after acute cisplatin application in isolated perfused rat heart [43] . However, NAC application in combination with cisplatin completely reversed cisplatin-induced negative chronotropic effect ( Fig.…”

Section: Discussionmentioning

confidence: 95%

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The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

et al. 2015

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The aim of this study was to estimate the protective effect of N-acetyl-l-cysteine (NAC) against cisplatin-induced cardiotoxicity under conditions of ischemic-reperfusion injury.Wistar albino rats were randomly divided into three groups (n = 8): control, cisplatin (5 mg/kg/w, i.p., 5 weeks) and cisplatin + NAC group (cisplatin – 5 mg/kg/w, i.p. and NAC – 500 mg/kg/w, i.p., 5 weeks). Isolated hearts were perfused according to the modified Langendorff technique at constant pressure (70 cmH2O). Following cardiodynamic parameters were measured: maximum rate of left ventricular pressure development, minimum rate of left ventricular pressure development, left ventricular systolic pressure (SLVP), left ventricular diastolic pressure and heart rate. The ischemic vasodilation episodes were induced by the complete interruption of coronary inflow for 30, 60 and 120 s. The samples of the coronary venous effluent (CVE) were continuously collected during the reperfusion period for determination of coronary flow (CF) rate and oxidative stress markers (H2O2, O2−, NO2− and thiobarbituric acid reactive substances – TBARS).Cisplatin reduced CF, heart rate and overflow (total, maximal and duration of overflow) during reperfusion, and increased SLVP (under basal conditions and after global ischemias). Cisplatin increased levels of H2O2 (under basal conditions), O2− and TBARS (under basal conditions and after ischemia), but decreased NO2− levels (during reperfusion) in CVE, and decreased superoxide dismutase and reduced glutathione in serum. NAC attenuated cisplatin-induced changes of cardiodynamic parameters (except CF under basal conditions) and oxidative stress parameters.Those results suggest that NAC, by decreasing oxidative stress, may be useful in cardioprotection during cisplatin therapy.

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Section: Discussionmentioning

confidence: 95%

“…Ischemia syndrome, palpitation and myocardial infarction can occur during treatment with cisplatin, or even as long-term consequences [57] . Treatment with cisplatin can be also associated with occasional complete atrioventricular block, hypotension [51] and recurrent sinus bradycardia [4] .…”

Section: Introductionmentioning

confidence: 99%

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

et al. 2015

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“…Recently, cardiac toxicity resulting from cisplatin treatment has been described (Pai and Nahata, 2000). Cisplatin-induced cardiotoxic effects have been reported to manifest through changes in electrocardiography (Al-Majed et al, 2006; Raja et al, 2013) and arrhythmias, which include ventricular arrhythmias, supraventricular tachycardia, atrial fibrillation, occasional sinus bradycardia and occasional complete atrioventricular block (Yavas et al, 2008; Guglin et al, 2009; Ozcan et al, 2011). Myocarditis, pericarditis, and angina have also been reported in cisplatin-induced cardiac toxicity (Khan et al, 2012; Bano et al, 2013).…”

Section: Clinical Manifestations Of Cisplatin-induced Cardiac Toximentioning

confidence: 99%

An integrative view of cisplatin-induced renal and cardiac toxicities: Molecular mechanisms, current treatment challenges and potential protective measures

2016

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Cisplatin is currently one of the most widely-used chemotherapeutic agents against various malignancies. Its clinical application is limited, however, by inherent renal and cardiac toxicities and other side effects, of which the underlying mechanisms are only partly understood. Experimental studies show cisplatin generates reactive oxygen species, which impair the cell’s antioxidant defense system, causing oxidative stress and potentiating injury, thereby culminating in kidney and heart failure. Understanding the molecular mechanisms of cisplatin-induced renal and cardiac toxicities may allow clinicians to prevent or treat this problem better and may also provide a model for investigating drug-induced organ toxicity in general. This review discusses some of the major molecular mechanisms of cisplatin-induced renal and cardiac toxicities including disruption of ionic homeostasis and energy status of the cell leading to cell injury and cell death. We highlight clinical manifestations of both toxicities as well as (novel)biomarkers such as kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-1 (TIMP-1) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). We also present some current treatment challenges and propose potential protective strategies with novel pharmacological compounds that might mitigate or prevent these toxicities, which include the use of hydrogen sulfide.

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“…CDDP-induced cardiotoxic effects have been observed through serious changes in electrocardiography and arrhythmias, which include ventricular arrhythmias, supraventricular tachycardia, atrial fibrillation, occasional sinus bradycardia, and occasional complete atrioventricular block ( 6 - 10 ). These cardiotoxic (and other potentially unknown) problems eventually lead to congestive heart failure and sudden cardiac death ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of curcumin and beta-carotene on cisplatin-induced cardiotoxicity: An experimental rat model

Bahadir

Ceyhan²,

Ö³

et al. 2018

Anatol J Cardiol

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ObjectiveCisplatin (CDDP) has been known to be an effective antineoplastic drug; however, it has a cardiotoxic effect. Curcumin (CMN) and beta-carotene (BC) have been suggested to protect biological systems against CDDP-induced damage. The current study was conducted to evaluate the possible protective roles of CMN and BC on CDDP-induced cardiotoxicity in rat cardiac tissues.MethodsA total of 49 adult femaleWistar albino rats were equally divided into seven groups as followscontrol (no medication), sesame oil (1 mg/kg), CDDP (single dose injection two times as once a week, 5 mg/kg/week), BC (100 mg/kg), CDDP+BC (pretreated BC for 30 min before CDDP injection), CMN (200 mg/kg), and CDDP+CMN (pretreated CMN for 30 min before CDDP injection). These treatments were applied intraperitoneally for CDDP and with gavage for CMN and BC. The oxidative/antioxidant indicators, inflammatory cytokines, and histopathological alterations were examined.ResultsThese alterations included a marked increase in malondialdehyde (MDA) level, significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities, and significant elevation of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6 in the CDDP group compared with the other groups. Histopathologically, CDDP-induced severe myocardial degenerative changes were observed. However, the CDDP-induced disturbances in the above-mentioned parameters significantly improved by treatment with BC and particularly CMN.ConclusionThis study indicated that CDDP treatment markedly caused cardiotoxicity; however, treatment with CMN or BC ameliorated this cardiotoxicity in rats. Furthermore, these findings revealed that treatment with CMN has a higher cardioprotective effect than that with BC against CDDP-induced cardiotoxicity in rat cardiac tissues.

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Recurrent Complete Atrioventricular Block During Cisplatin Infusion: A Case Report

Cited by 9 publications

References 9 publications

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

An integrative view of cisplatin-induced renal and cardiac toxicities: Molecular mechanisms, current treatment challenges and potential protective measures

Protective effects of curcumin and beta-carotene on cisplatin-induced cardiotoxicity: An experimental rat model

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