scholarly journals Electrocardiographic Changes Associated With Ibrutinib Exposure

2020 ◽  
Vol 27 (1) ◽  
pp. 107327482093180
Author(s):  
Michael G. Fradley ◽  
Allan Welter-Frost ◽  
Matthew Gliksman ◽  
Josephine Emole ◽  
Federico Viganego ◽  
...  

Although ibrutinib-associated atrial and ventricular arrhythmias have been well described, there is little information about ibrutinib’s effects on other electrocardiographic parameters, particularly the QT interval. Using our database of 137 patients treated with ibrutinib, we retrospectively identified 21 patients in whom an electrocardiogram (ECG) was obtained both prior to and after ibrutinib exposure. All traditional ECG parameters as well as QT dispersion were manually measured by an electrophysiologist. Compared to baseline ECGs, post ibrutinib ECGs demonstrated QT interval shortening from 386 ms to 356 ms ( P = .007), corrected QT interval shortening using Bazett’s formula from 446 ms to 437 ms ( P = .04), and corrected QT interval shortening using Fridericia’s formula from 425 ms to 407 ms ( P = .003). QT dispersion also increased post ibrutinib exposure compared to baseline (39.8 ms vs 57.3 ms, P = .002). There was no significant change in other ECG parameters. In conclusion, both the absolute and corrected QT intervals significantly shortened after ibrutinib exposure, while there was a significant increase in QT dispersion. These findings may point to a common underlying electrophysiologic mechanism of ibrutinib-associated arrhythmias.

2012 ◽  
Vol 81 (4) ◽  
pp. 409-414 ◽  
Author(s):  
Carlos Fernando Agudelo Ramírez ◽  
Peter Scheer ◽  
Jaroslava Tomenendálová

The effect of enrofloxacin on the QT interval of the electrocardiogram was studied in 30 hospitalized dogs. The experimental group (n = 15) received enrofloxacin parenterally (subcutaneously) at a dose of 5 mg/kg twice daily and amoxicillin-clavulanate intravenously at a dose of 22 mg/kg three times daily. The control group (n = 15) received only amoxicillin-clavulanate. Electrocardiography was carried out for 5 min once daily for 6 days. The QT interval was corrected by four different formulae. No differences were found between the two groups or within each group for the duration of the study. On the last day of the study the average QT interval for the control and experimental groups was 213.2 ms and 202.9 ms, respectively. Enrofloxacin did not cause prolongation of the QT or corrected QT intervals. We can conclude that the parenteral administration of enrofloxacin in non-cardiac dogs does not adversely affect the electrocardiographic indicators (no prolongation of the QT or corrected QT interval) and does not induce ventricular arrhythmias. Parenteral use of enrofloxacin is thus safe and effective in non-cardiac dogs.


2013 ◽  
Vol 94 (2) ◽  
pp. 176-180
Author(s):  
I V Logacheva ◽  
N G Barantseva

Aim. To study the change of the main parameters of 24-hour EKG monitoring over time in patients with myocardial infarction associated with ventricular arrhythmias of different grades. Methods. The change of the echocardiography parameters, heart rhythm variability, corrected QT interval duration and dispersion, late ventricular potentials, heart rhythm turbulence were examined in 70 adult men (mean age 52.6±1.3 years) with primary Q-wave myocardial infarction on 10-14th day of the disease and after 6 months. Patients were assigned into 3 groups depending on ventricular arrhythmias severity (according to Lown classification modified by Ryan): А1 (n=29) - grade 1-2, А2 (n=23) - grade 3-4, А3 (n=18) - patients with paroxysmal ventricular tachycardia. Results. Presence of late ventricular potentials and pathologic heart rhythm turbulence in patients in acute period of myocardial infarction suggested high grade of ventricular arrhythmia. Ventricular arrhythmias were associated with severe sympathicotonia, prolongation of corrected QT interval and QT dispersion. 6 months after Q-wave myocardial infarction an autonomic imbalance increased and no positive changes of myocardial homogenicity parameters, late ventricular potentials and pathologic heart rhythm turbulence were observed with increasing ventricular arrhythmia grading and heart rate frequency. A relationship between left ventricle ejection fraction, myocardium mass and myocardial electric non-stability values was revealed. In patients with Q-wave myocardial infarction ventricular arrhythmias are mediated by several mechanisms: systolic and autonomic disorder, repolarization abnormalities, late ventricular potentials pathologic heart rhythm turbulence. The severity of abnormalities is marked by the ventricular arrhythmias grade. Conclusion. 6 months after myocardial infarction (in healing stage) the significant positive changes are found only in patients with 1-2 grades ventricular arrhythmias. The significant non-homogeneity of myocardial electrophysiological features still persists in patients with life-threatening ventricular arrhythmias.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.


Open Medicine ◽  
2008 ◽  
Vol 3 (2) ◽  
pp. 179-182 ◽  
Author(s):  
Mohammad Ostovan ◽  
Shahdad Khosropanah ◽  
Shohreh Hooshmand

AbstractThe 12-lead surface electrocardiogram adjacent QTc dispersion, which is the maximum difference of corrected QT interval between two adjacent leads, is a simple method to determine regional variation in repolarization and refractoriness. The aim of this study is to evaluate adjacent QTc dispersion as a marker of susceptibility to ventricular arrhythmias after myocardial infarction. A total of 135 consecutive patients with acute myocardial infarction were enrolled in the study. Adjacent QTc, measured by lens magnifier, was calculated on the first, second and third days after acute myocardial infarction. On the second day after acute myocardial infarction, adjacent QTc dispersion was significantly greater in patients with ventricular arrhythmias (P < 0.001). Adjacent QTc dispersion on the first and fifth day after acute myocardial infarction was not associated with development of ventricular arrhythmias. On the second day after acute myocardial infarction, adjacent QTc dispersion is a simple and feasible method for prediction of ventricular arrhythmias.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Mohamed Farhan Nasser ◽  
Ahmad Jabri ◽  
Saima Karim ◽  
Elizabeth Kaufman

Introduction: QT prolongation is associated with increased risk of ventricular arrhythmias.As many patients with COVID19 may be started on QT prolonging drugs, measuring and monitoring QT is imperative to prevent fatal ventricular arrhythmias. However, we need to limit exposure of staff to patients with confirmed COVID19 and judiciously use personal protective equipment. Thus, it is important to find alternatives to doing frequent 12-lead ECGs. Hypothesis: We hypothesize that the QT interval measured from telemetry is similar to the QT interval on 12-lead ECG. Methods: Telemetry recordings and 12-lead ECGs were obtained from 15 patients at the same time and identical heart rates. Patients were from two different inpatient units with the same telemetry monitoring service. QT intervals were measured manually using calipers with the tangent method, excluding U waves. Telemetry recordings included lead I and II or a precordial lead. QT from telemetry was compared to the corresponding leads and to the longest QT on the 12-lead ECG. In cases of atrial fibrillation (AF), the QT from all the complexes was averaged. Results: Of 15 patients, 2 were in AF and 2 had RBBB. One patient had abnormal T-wave morphology and QT prolongation (abnormal repolarization). In all patients, QT intervals from the same leads as telemetry matched the QT measured from 12-lead. In 14 of 15 patients, telemetry QT matched the longest QT on the 12-lead ECG. However, in the patient with abnormal repolarization, maximum QT on 12-lead ECG was substantially longer than telemetry QT (Figure 1). Conclusion: When using the same lead, QT intervals were identical on telemetry and 12-lead ECG. However, in the patient with abnormal repolarization, the longest QT on 12-lead ECG was not represented on telemetry. In patients with abnormal repolarization on 12-lead ECG, we recommend serial 12-lead ECGs while on QT-prolonging drugs. Telemetry may suffice as a surrogate for 12-lead ECG to follow QT intervals in most patients.


2019 ◽  
Author(s):  
Pierre Delanaye ◽  
François Krzesinski ◽  
Bernard E Dubois ◽  
Alexandre Delcour ◽  
Sébastien Robinet ◽  
...  

Abstract Background Sudden death is frequent in haemodialysis (HD) patients. Both hyperkalaemia and change of plasma potassium (K) concentrations induced by HD could explain this. The impact of increasing dialysate K by 1 mEq/L on plasma K concentrations and electrocardiogram (ECG) results before and after HD sessions was studied. Methods Patients with pre-dialysis K >5.5 mEq/L were excluded. ECG and K measurements were obtained before and after the first session of the week for 2 weeks. Then, K in the dialysate was increased (from 1 or 3 to 2 or 4 mEq/L, respectively). Blood and ECG measurements were repeated after 2 weeks of this change. Results Twenty-seven prevalent HD patients were included. As expected, a significant decrease in K concentrations was observed after the dialysis session, but this decrease was significantly lower after the switch to an increased dialysate K. The pre-dialysis K concentrations were not different after changing, but post-dialysis K concentrations were higher after switching (P < 0.0001), with a lower incidence of post-dialysis hypokalaemia. Regarding ECG, before switching, the QT interval (QT) dispersion increased during the session, whereas no difference was observed after switching. One week after switching, post-dialysis QT dispersion [38 (34–42) ms] was lower than post-dialysis QT dispersion 2 weeks and 1 week before switching [42 (38–57) ms, P = 0.0004; and 40 (35–50) ms, P = 0.0002]. Conclusions A simple increase of 1 mEq/L of K in the dialysate is associated with a lower risk of hypokalaemia and a lower QT dispersion after the dialysis session. Further study is needed to determine if such a strategy is associated with a lower risk of sudden death.


2002 ◽  
Vol 36 (7-8) ◽  
pp. 1156-1161 ◽  
Author(s):  
A Scott Mathis ◽  
Ashesh J Gandhi

OBJECTIVE: To establish a relationship between serum quinidine concentrations (SQCs) and QT interval dispersion, compared with corresponding QT intervals, in order to identify a reason why many reports describe torsade de pointes as occurring at subtherapeutic concentrations. DESIGN: Retrospective study. SETTING: University teaching hospital. PARTICIPANTS: Eleven patients with atrial arrhythmias managed with quinidine therapy. MAIN OUTCOME MEASURES: Patients with subtherapeutic (<2 μg/mL) and therapeutic (2–5 μg/mL) SQCs with corresponding 12-lead electrocardiograms (ECGs) (25 mm/sec) and baseline ECG were evaluated for QT interval dispersion, calculated as the maximum minus the minimum QT interval on the 12-lead ECG. RESULTS: Mean ± SD subtherapeutic and therapeutic SQCs were 1.48 ± 0.39 μg/mL and 3.78 ± 0.88 μg/mL (p < 0.001). Baseline values for QT/QTc intervals were 376.4 ± 59.2/429.5 ± 57.3 msec. At subtherapeutic and therapeutic SQCs, mean QT/QTc intervals were 403.6 ± 59.9/450.5 ± 38.5 msec and 439.1 ± 48.9/472.4 ± 44.6 msec, respectively. Mean QT dispersion was 47 ± 16.2 msec at baseline, 98.2 ± 27.5 msec at subtherapeutic SQC, and 70.9 ± 33.9 msec at therapeutic SQCs (p = 0.001 for overall analysis; p < 0.001 for baseline vs. subtherapeutic concentrations; p = NS for therapeutic vs. subtherapeutic in post hoc comparison). CONCLUSIONS: Despite QT interval lengthening with increasing SQCs, QT dispersion was numerically greatest at subtherapeutic SQCs. Further study is required to determine the value of QT dispersion as a tool for identifying proarrhythmic risk with drugs that prolong the QT interval.


2015 ◽  
Vol 93 (9) ◽  
pp. 765-772 ◽  
Author(s):  
Andrea Orosz ◽  
István Baczkó ◽  
Viktória Nagy ◽  
Henriette Gavallér ◽  
Miklós Csanády ◽  
...  

Stratification models for the prediction of sudden cardiac death (SCD) are inappropriate in patients with hypertrophic cardiomyopathy (HCM). We investigated conventional electrocardiogram (ECG) repolarization parameters and the beat-to-beat short-term QT interval variability (QT-STV), a new parameter of proarrhythmic risk, in 37 patients with HCM (21 males, average age 48 ± 15 years). Resting ECGs were recorded for 5 min and the frequency corrected QT interval (QTc), QT dispersion (QTd), beat-to-beat short-term variability of QT interval (QT-STV), and the duration of terminal part of T waves (Tpeak–Tend) were calculated. While all repolarization parameters were significantly increased in patients with HCM compared with the controls (QTc, 488 ± 61 vs. 434 ± 23 ms, p < 0.0001; QT-STV, 4.5 ± 2 vs. 3.2 ± 1 ms, p = 0.0002; Tpeak–Tend duration, 107 ± 27 vs. 91 ± 10 ms, p = 0.0015; QTd, 47 ± 17 vs. 34 ± 9 ms, p = 0.0002), QT-STV had the highest relative increase (+41%). QT-STV also showed the best correlation with indices of left ventricular (LV) hypertrophy, i.e., maximal LV wall thickness normalized for body surface area (BSA; r = 0.461, p = 0.004) or LV mass (determined by cardiac magnetic resonance imaging) normalized for BSA (r = 0.455, p = 0.015). In summary, beat-to-beat QT-STV showed the most marked increase in patients with HCM and may represent a novel marker that merits further testing for increased SCD risk in HCM.


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