Long QT: Good, bad or indifferent?

Surawicz, Borys; Knoebel, Suzanne B.

doi:10.1016/s0735-1097(84)80232-6

Cited by 230 publications

(58 citation statements)

References 113 publications

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“…Max=maximum, Min=minimum, QTc=corrected QT, OTd=OT dispersion, OTcd=corrected OT dispersion arrhythmia [9,10]. Elongation of the repolarization time increases the risk of arrhythmia but not always cause ventricular arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Can QT dispersion predict multi-vessel coronary artery disease in patients with acute coronary syndrome?

Akgumus¹,

Karaagac²,

Peker³

et al. 2016

Eur Res J

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Objectives. This study was planned to evaluate the relation between QT dispersion (QTd) and multi-vessel coronary artery disease in acute coronary syndrome. Methods. Two hundreds and twenty-five consecutive patients with a diagnosis of non-ST segment elevation acute coronary syndrome were included. Three groups were defined as a single vessel, two vessels, and three vessels. Echocardiographic, biochemical and electrocardiographic parameters of the groups were compared. Results. QTd, corrected QT dispersion (QTcd) and corrected QT max values significantly increased in patients with the three-vessel disease compared to the patients in the single-vessel disease group (60±27 vs. 45±28 ms, 68±32 vs. 50±32 ms and 471±52 vs. 443±48 ms; p=0.002, p=0.001, and p=0.001, respectively). Also, QTd and QTcd were statistically more increased in patients with the two vessels disease than single-vessel disease group (57±29 vs. 45±28 ms; p=0. 045, and 63±32 vs. 50±32 ms; p=0.046, respectively). Conclusion. In a patient with acute coronary syndrome and diffuse vessel disease, changes in the myocardial cells due to ischemia cause more of the QT dispersion in the patients with a multi-vessel disease than those with single-vessel disease.Eur Res J 2016;2(1):12-15

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Section: Discussionmentioning

confidence: 99%

Can QT dispersion predict multi-vessel coronary artery disease in patients with acute coronary syndrome?

Akgumus¹,

Karaagac²,

Peker³

et al. 2016

Eur Res J

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“…However, it should be noted that this study did not have the appropriate design to establish these correlations for the following reasons: QTc max is known to vary between and within individuals, and the QTc dispersion (i.e. the distribution of repolarization on the heart) rather than the absolute value of QTc max may be considered as a risk factor for the occurrence of arrhythmias (Surawicz and Knoebel, 1984). Moreover, in our study patients were not randomized for the different S9788 dose levels.…”

Section: Discussionmentioning

confidence: 99%

“…This might be explained by the abovementioned reasons, and/or by the fact that other doses and schedules of S9788 were used. Although a predictive value of QTc lengthening for the occurrence of severe arrhythmias has never been established for values < 600 ms (Surawicz and Knoebel, 1984), the study was terminated after the occurrence of severe cardiac arrhythmias (torsade de pointe with syncope) in another ongoing study with S9788 given over 6 h (Terret et al, 1996). Such a risk would preclude the routine use of S9788.…”

Section: Discussionmentioning

confidence: 99%

Phase IB study of doxorubicin in combination with the multidrug resistance reversing agent S9788 in advanced colorectal and renal cell cancer

Punt

Voest²,

Tueni³

et al. 1997

Br J Cancer

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Summary S9788 is a new triazineaminopiperidine derivate capable of reversing multidrug resistance (MDR) in cells resistant to chemotherapeutic agents such as doxorubicin. It does not belong to a known class of MDR revertants, but its action involves the binding of P-glycoprotein. Thirty-eight evaluable patients with advanced colorectal or renal cell cancer were treated with doxorubicin alone (16 patients) followed after disease progression with combination treatment of doxorubicin plus S9788 (12 patients) or upfront with the combination of doxorubicin plus S9788 (22 patients). S9788 was given i.v. as a loading dose of 56 mg m-2 over 30 min followed by doxorubicin given at 50 mg m-2 as a bolus infusion. Thereafter, a 2-h infusion of S9788 was administered at escalating doses ranging from 24 to 120 mg m-2 in subsequent cohorts of 4-10 patients. Pharmacokinetic analysis demonstrated that concentrations of S9788 that are known to reverse MDR in vitro were achieved in patients at non-toxic doses. Compared with treatment with doxorubicin alone, treatment with the combination of doxorubicin and S9788 produced a significant increase in the occurrence of WHO grade 3-4 granulocytopenia. Treatment with S9788 was cardiotoxic as it caused a dose-dependent and reversible increase in corrected QT intervals as well as clinically non-significant arrhythmias on 24-or 48-h Holter recordings. Although clinically relevant cardiac toxicities did not occur, the study was terminated as higher doses of S9788 may increase the risk of severe cardiac arrhythmias. Twenty-nine patients treated with S9788 plus doxorubicin were evaluable for response, and one patient, who progressed after treatment with doxorubicin alone, achieved a partial response. We conclude that S9788 administered at the doses and schedule used in this study results administered in combination with doxorubicin.Inherent or acquired multidrug resistance (MDR) is an important cause of failure of cancer chemotherapy. Several mechanisms responsible for MDR have been described, and the most extensively investigated is the expression of the product of the MDRJ gene, P-glycoprotein (P-gp) or P-170 (Roninson, 1992). This protein acts as an efflux pump for a number of commonly used cytotoxic agents, e.g. doxorubicin, vincristine, vinblastine and actinomycin D. Different compounds have been shown to reverse P-gp-mediated MDR, including calcium channel antagonists (verapamil), calmodulin inhibitors (quinine, quinidine), oestrogen receptor antagonists (tamoxifen), steroids and immunomodulators (cyclosporin A). The mechanisms by which these drugs influence MDR have not always been identified. The clinical use of these MDR modulators is hampered by the toxic side-effects that occur when the suprapharmacological doses required to achieve significant reversal of MDR are used (Pennock et al, 1991;Raderer and Scheithauer, 1993

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“…These three functions (CQT, NDIFF, and PROD) are shown in figure 4-4. The function CQT was based on the clinical finding that in most people, the length of the QT interval (beginning of QRS complex to the end of the T-wave) is proportional to the inverse square root of the preceding RR interval (Surawicz 1984). Therefore, dividing RR 1 by sqrt(RR 2 ) provided a measure of where the beat B 1 fell with respect to the normalized QT interval of B 2 .…”

Section: ________________________________________ ___________________mentioning

confidence: 99%

A stochastic characterization of chronic ventricular ectopic activity

Albrecht

Cohen

Mark

1988

IEEE Trans. Biomed. Eng.

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Ventricular ectopic beats are clinically important because of their association with the problem of sudden cardiac death. Ventricular ectopic activity (VEA) is most commonly evaluated using long-term ambulatory electrocardiographic (ECG) recordings. The results of these recordings are usually summarized in the form of hourly counts of VEA events.Although such hourly counts are useful, they are a nonspecific measure which, in effect, treats VEA generation as an unpredictable process.This thesis develops a new means for characterizing the activity of the VEA-generating mechanism using the beat type and timing information of the long-term ECG. The approach is founded on the hypothesis that the VEA mechanism is often stable over time, although its activity may be modulated by physiologic influences and by the timing of the sino-atrial node impulses.This hypothesis implies that there should be some relationship between the beat type and timing of preceding beats and the subsequent generation of ectopic beats.The VEA generation was characterized by a multi-dimensional conditional distribution which gives the probability that an ectopic beat will follow a specific conditioning sequence of beat types and intervals. Using this approach a three part study was performed. The first step examined the conditional distributions and tested the null hypothesis that the generation of ectopic beats is unpredictable.Using a database of half-hour ECG tapes from 66 patients, the null hypothesis was rejected at p=0.005 in 80% of the tapes.The second step developed a means of displaying the multidimensional distributions. By an appropriate transformation of the conditioning variables, the distributions could be represented as one-dimensional distributions. The resulting distributions were useful for. separating patients into groups and for finding characteristic, VEA-related events in the ECG data.The third step examined the reproducibility of the onedimensional distributions over time. Using ten-hour ECG tapes, it was found that in 7 of 10 patients the patient-specific distribution, although modulated in amplitude, maintained a similar shape over the ten hours.The VEA characterization which has been developed goes significantly beyond the simple counting of ectopic beats. The distributions can be considered a kind of "fingerprint" of the VEA-generating mechanism -a "fingerprint" which may be useful in the selection and evaluation of therapy.

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Long QT: Good, bad or indifferent?

Cited by 230 publications

References 113 publications

Can QT dispersion predict multi-vessel coronary artery disease in patients with acute coronary syndrome?

Can QT dispersion predict multi-vessel coronary artery disease in patients with acute coronary syndrome?

Phase IB study of doxorubicin in combination with the multidrug resistance reversing agent S9788 in advanced colorectal and renal cell cancer

A stochastic characterization of chronic ventricular ectopic activity

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