Impact of Medical Castration on Malignant Arrhythmias in Patients With Prostate Cancer

Background Medical castration, gonadotropin‐releasing hormone agonists, and antiandrogens have been widely applied as a treatment for prostate cancer. Sex steroid hormones influence cardiac ion channels. However, few studies have examined the proarrhythmic properties of medical castration. Methods and Results This study included 149 patients who underwent medical castration using gonadotropin‐releasing hormones with/without antiandrogen for prostate cancer. The changes in the ECG findings during the therapy and associations of the electrocardiographic findings with malignant arrhythmias were studied. The QT and corrected QT (QTc) intervals prolonged during the therapy compared with baseline (QT, 394±32 to 406±39 ms [ P <0.001]; QTc, 416±27 to 439±31 ms [ P <0.001]). The QTc interval was prolonged in 119 (79.9%) patients during the therapy compared with baseline. In 2 (1.3%) patients who had no structural heart disease, torsade de pointes (TdP) and ventricular fibrillation (VF) occurred ≥6 months after starting the therapy. In patients with TdP/VF, the increase in the QTc interval from the pretreatment value was >80 ms. However, in patients without TdP/VF, the prevalence of an increase in the QTc interval from the pretreatment value of >50 ms was 11%, and an increase in the QTc interval from the pretreatment value >80 ms was found in only 4 (3%) patients. Conclusions Medical castration prolongs the QT/QTc intervals in most patients with prostate cancer, and it could cause TdP/VFs even in patients with no risk of QT prolongation before the therapy. An increase in the QTc interval from the pretreatment value >50 ms might become a predictor of TdP/VF. Much attention should be paid to the QTc interval throughout all periods of medical castration to prevent malignant arrhythmias.

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P5641Impact of lethal arrhythmias on medical castration in patients with prostate cancer

European Heart Journal ◽

10.1093/eurheartj/ehz746.0584 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

K Hasegawa ◽

S Miyazaki ◽

K Kaseno ◽

K Hisazaki ◽

H Ito ◽

...

Keyword(s):

Prostate Cancer ◽

Heart Rate ◽

Hormonal Therapy ◽

Structural Heart Disease ◽

Torsades De Pointes ◽

Baseline Heart Rate ◽

Qtc Interval ◽

Interval Change ◽

Cardiac Ion Channels ◽

Qrs Duration

Abstract Background Prostate cancer is the most common non-cutaneous malignancy in men and has been steadily rising in an aging society. Medical castration had been widely applied as a treatment for prostate cancer. Sex steroid hormones regulate cardiac ion channels. However, the proarrhythmic properties of medical castration have not been reported. Methods This prospective observational study consisted of 149 patients (75±6 years) who underwent hormonal therapy using gonadotropin-releasing hormone with or without anti-androgen for prostate cancer. The changes of electrocardiogram (ECG) findings during the therapy and the associations of ECG findings with lethal arrhythmias were studied. Results QT (394±32 to 406±39 ms, p<0.001) and QTc intervals (416±27 to 439±31 ms, p<0.001) significantly prolonged during the therapy as compared to baseline. Heart rate significantly increased during the therapy as compared to baseline (68±11 to 71±14 / min, p=0.006). PQ interval and QRS duration were similar before and during the therapy. During the hormonal therapy, 2 patients (1.3%) presented with torsades de pointes and ventricular fibrillation. The first patient was 71 year-old and the second patient was 70 year-old. The period of the therapy was 6 and 45 months, respectively. Both patients had no structural heart disease. The magnitude of QTc interval change during the therapy as compared to baseline (Δ QTc interval) was significantly greater in patients with VF than those without (p<0.001), however the magnitude of Δ heart rate, Δ PQ interval, and Δ QRS duration were similar between the 2 groups. Conclusions Medical castration significantly prolonged QT/QTc interval and could be a trigger of lethal arrhythmias in patients with prostate cancer.

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Analysis of QTc Interval during Levofloxacin Prescription in Cardiac Patients with Pneumonia

Current Drug Safety ◽

10.2174/1574886315666200213112702 ◽

2020 ◽

Vol 15 (2) ◽

pp. 111-116 ◽

Cited By ~ 1

Author(s):

Lida Shojaei ◽

Mohammad Ruzbahani ◽

Shiva Khajavian ◽

Soodeh Shahsavari ◽

Negin Tamasoki ◽

...

Keyword(s):

Torsade De Pointes ◽

Cross Sectional Study ◽

Qt Prolongation ◽

Qtc Interval ◽

Cross Sectional ◽

Qtc Interval Prolongation ◽

Before And After ◽

The Mean ◽

General Wards ◽

Heart Hospital

Background: Medications induced QT prolongation could cause ventricular arrhythmia, torsade de pointes, and death. Objective: The purpose of this study was to evaluate the magnitude of QTc interval prolongation as a result of levofloxacin treatment in patients admitted to cardiology wards. Methods: This was a cross-sectional study conducted in the coronary care units and general wards of the Imam Ali Heart Hospital in Kermanshah, Iran. The QTc interval was determined at baseline and after 72 hours of levofloxacin administration. Changes in the QTc interval before and after the levofloxacin prescription were determined. Results: The mean age of recruited patients was 63.26 ± 14.56 years. More than 80% of patients who received levofloxacin experienced QTc prolongation. The QTc interval was increased significantly after levofloxacin administration (15.68 ± 26.84 milliseconds) (P<0.001). These changes remained significant after excluding medications with QTc lengthening properties (P<0.001). Conclusion: Treatment with levofloxacin in patients with heart disease increases the risk of QT prolongation.

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A Case of QT Prolongation Associated with Panhypopituitarism

Case Reports in Endocrinology ◽

10.1155/2013/989745 ◽

2013 ◽

Vol 2013 ◽

pp. 1-4

Author(s):

Dilek Arpaci ◽

Mustafa Volkan Demir ◽

Tayfun Garip ◽

Ali Tamer

Keyword(s):

Replacement Therapy ◽

Torsade De Pointes ◽

Qt Prolongation ◽

Long Qt ◽

Electrolyte Disturbances ◽

Plasma Electrolyte ◽

Qt Intervals ◽

Life Threatening ◽

Electrocardiographic Findings ◽

Symptoms And Signs

We describe a 37-year-old patient with panhypopituitarism who experienced symptoms and signs of hormonal insufficiency and QT prolongation on electrocardiogram without electrolyte disturbances. After hormonal (steroidal and thyroid) replacement therapy electrocardiographic findings were normalized. Hormonal disorders should be considered as a cause of long QT intervals which may lead to torsade de pointes, even if plasma electrolyte levels are normal, because life-threatening arrhythmia is treatable by supplementation of the hormone that is lacking.

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Thorough QT/QTc (TQT) study

International Journal of Basic & Clinical Pharmacology ◽

10.18203/2319-2003.ijbcp20212933 ◽

2021 ◽

Vol 10 (8) ◽

pp. 1019

Author(s):

Lakshmi Balasundaram ◽

Bharatraj Kidambi ◽

Surya Singaravelu

Keyword(s):

Structural Heart Disease ◽

Torsades De Pointes ◽

Qt Prolongation ◽

Electrolyte Imbalance ◽

Qtc Interval ◽

Cardiac Safety ◽

Drug Induced ◽

Exposure Response ◽

Response Modelling ◽

Current Guidelines

With a number of drugs entering the market, cardiac safety remains a cause of major concern for the regulatory authorities, before approval. The incidence of drug induced arrhythmia with non-cardiovascular drugs is low, however the result is fatal, hence much focus is being given to assess the pro-arrhythmic potential of a drug. The arrhythmogenic risk of the drug is higher if the patient is on polypharmacy or has other risk factors such as an electrolyte imbalance or an underlying structural heart disease. QT prolongation can be either due to congenital causes such as Long QT syndromes (LQTS) which include Romano-Ward syndrome, Jervell and Lange-Nielson syndrome or can be acquired, which is mainly due to drugs. Several drugs such as terfenadine, astemizole, cisapride and grepafloxacin have been withdrawn from the market due to QT prolongation and development of a fatal ventricular arrythmia - torsades de pointes (TdP). This has led to implementation of guidelines to assess cardiac safety. The pro-arrhythmic risk can be assessed using thorough QT/QTc studies or exposure response modelling of intensive ECGs. This article will give an overall view of the use of QT/QTc interval as a biomarker for cardiac safety and the current guidelines for thorough QT/QTc studies which are mainly done to assess the pro-arrhythmic potential of a non-anti-arrhythmic drug.

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Changes of QT interval in the acute phase after pulmonary vein isolation for paroxysmal atrial fibrillation

European Heart Journal ◽

10.1093/ehjci/ehaa946.0414 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

A Chikata ◽

T Kato ◽

K Ududa ◽

S Fujita ◽

K Otowa ◽

...

Keyword(s):

Atrial Fibrillation ◽

Pulmonary Vein ◽

Female Patient ◽

Pulmonary Vein Isolation ◽

Acute Phase ◽

Paroxysmal Atrial Fibrillation ◽

Qt Interval ◽

Qt Prolongation ◽

Qtc Interval ◽

The Impact

Abstract Introduction Pulmonary vein isolation (PVI) affects ganglionated plexi (GP) around the atrium, leading to a modification of the intrinsic cardiac autonomic system (ANS). In animal models, GP ablation has a potential risk of QT prolongation and ventricular arrhythmias. However, the impact of PVI on QT intervals in humans remains unclear. Purpose This study aims to evaluate the Impact of PVI on QT interval in patients with paroxysmal atrial fibrillation. Methods We analyzed consecutive 117 PAF patients for their first PVI procedures. 12-lead ECG was evaluated at baseline, 4 hr, day 1, 1 month, and 3 months after ablation. Only patients with sinus rhythm on 12-lead ECG at each evaluation point without antiarrhythmic drugs were included. Results Heart rate significantly increased at 4 hr, day 1, and 1 month. Raw QT interval prolonged at 4 hr (417.1±41.6 ms, P<0.001) but shortened at day 1 (376.4±34.1 ms, P<0.001), 1 month (382.2±31.5 ms, P<0.001), and 3 months (385.1±32.8 ms, P<0.001) compared to baseline (391.6±31.4 ms). Bazett- and Fridericia- corrected QTc intervals significantly prolonged at 4hr (Bazett: 430.8±27.9 ms, P<0.001; Fridericia: 425.8±27.4 ms, P<0.001), day1 (Bazett: 434.8±22.3 ms, P<0.001; Fridericia: 414.1±23.7 ms, P<0.001), 1M (Bazett: 434.8±22.3 ms, P<0.001; Fridericia: 408.2±21.0 ms, P<0.05), and 3M (Bazett: 420.1±21.8 ms, P<0.001; Fridericia: 407.8±21.1 ms, P<0.05) compared to baseline (Bazett: 404.9±25.2 ms; Fridericia: 400.0±22.6 ms). On the other hand, Framingham- and Hodges- corrected QTc interval significantly prolonged only at 4hr (Framingham: 424.1±26.6 ms, P<0.001; Hodges: 426.8±28.4 ms, P<0.001) and at day1 (Framingham: 412.3±29.3 ms, P<0.01; Hodges: 410.6±40.2 ms, P<0.05) compared to baseline (Framingham: 399.2±22.7 ms; Hodges: 400.7±22.8 ms). At 4 hr after ablation, raw QT and QTc of all formulas significantly prolonged than baseline. Raw QT and QTc prolongation at 4hr after ablation were more frequently observed in female patients. Multiple regression analysis revealed that female patient is a significant predictor of raw QT and QTc interval prolongation of all formulas 4hr after PVI. Conclusions Raw QT and QTc prolonged after PVI, especially in the acute phase. Female patient is a risk factor for QT prolongation in the acute phase after PVI. Funding Acknowledgement Type of funding source: None

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QT Prolongation in Dialysis Patients: An Epidemiological Study with a Focus on Malnutrition

Blood Purification ◽

10.1159/000512961 ◽

2021 ◽

pp. 1-8

Author(s):

Masanori Shibata ◽

Isao Ito ◽

Hisae Tawada ◽

Shinkichi Taniguchi

Keyword(s):

Risk Index ◽

Bioelectrical Impedance ◽

Impedance Analysis ◽

Serum Levels ◽

Qt Prolongation ◽

Fat Free Mass ◽

Nutritional Risk ◽

Diabetic Patients ◽

Qtc Interval ◽

Nutritional Risk Index

Background/Aims: QT prolongation is a known risk factor for ventricular fibrillation and ventricular tachycardia. Therefore, more refined management is necessary to reduce sudden cardiac death secondary to such arrhythmias. Methods: Electrocardiographic findings were reviewed in 224 patients, and the associations of QT prolongation with various clinical parameters were examined, including the nutritional state. Correlations were also examined between QT prolongation and body composition measurements determined by multifrequency bioelectrical impedance analysis. Results: Prolongation of the corrected QT (QTc) interval over 0.44 s was seen in 140 patients (62.5%). QT prolongation was independent of age and dialysis therapy duration and was more frequent in diabetics (70.1%) than in nondiabetics (54.2%, p = 0.014) and more frequent in women (78.8%) than in men (53.5%, p < 0.001). Serum levels of albumin (p < 0.001) and Cr (p < 0.001) and the Geriatric Nutritional Risk Index (GNRI, p < 0.001) were negatively correlated with QTc interval; no significant correlation was noted with total protein, urea nitrogen, or uric acid. Negative correlations with QTc interval were found for BMI(p < 0.01), percent total body water (%TBW; p < 0.05), and percent intracellular water (%ICW; p < 0.01) but not with the percent extracellular water/TBW ratio or edema ratio. The longer the QTc interval, the lower the fat-free mass (FFM; p < 0.01) and muscle mass (MM; p < 0.01), but there was no significant correlation with percent fat. Conclusion: These results suggest that QT prolongation is a common complication and is more frequent in women and diabetic patients. The decreases in serum albumin and Cr levels, GNRI, BMI, %TBW, %ICW, FFM, and MM together coincided with malnutrition and thus suggest a close relationship of QT prolongation with malnutrition. Management of QT prolongation may be achieved better in the future by understanding these biochemical and biophysical changes, particularly those regarding malnutrition.

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