Prognostic Value of the QTc Interval after Cardiac Transplantation

Vrtovec, Bojan; Radovancevic, Rajko; Thomas, Cynthia D.; Yazdabakhsh, Aria P.; Smart, Frank W.; Radovančević, Branislav

doi:10.1016/j.healun.2005.05.004

Cited by 21 publications

(16 citation statements)

References 36 publications

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“…In a study involving 2,265 patients with left ventricular dysfunction (LVEF B40%), Padmanabhan et al [28] showed that patients with a QTc C450 ms had a significantly higher 5-year mortality rate (75%) compared to the remaining patients (52%, p \ 0.0001). Vrtovec et al [29] reviewed QTc intervals in 587 HTx recipients over a follow-up time of 17 years, and found an increase in QTc interval duration of C10% between the first and second post-transplant year to be a strong and independent predictor of long-term mortality. In this respect, it is of importance to assess the impact of ivabradine on myocardial metabolic energetics and electrophysiology in this particular patient population.…”

Section: Discussionmentioning

confidence: 99%

Lasting reduction of heart transplant tachycardia with ivabradine is effective and well tolerated: results of 48-month study

et al. 2012

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The safety and efficacy of ivabradine applied in heart transplant (HTx) recipients with permanent sinus tachycardia (PST) has been depicted in previous short-term follow-up studies. We sought to investigate the long-term impact of ivabradine in this patient population. From May to November 2006, 29 HTx recipients with PST, who exhibited either contraindications or intolerance of beta-blocker medication or insufficient heart rate (HR) reduction on beta-blocker treatment, first received oral ivabradine treatment (5 mg bid). Ivabradine treatment was discontinued in three patients due to adverse events within the first week. In the remaining 26 patients, resting HR was significantly lowered from 106.8 ± 9.2 at baseline to 83.2 ± 5.1 bpm after 3 months (p < 0.001). This effect remained stable in the long-term follow-up (82.1 ± 11.8 bpm after 4 years), whilst blood pressure was not affected. Apart from the corrected QT interval (QTc), there were no significant changes in ECG. The elongated QTc at baseline (469.4 ± 29.5 ms) decreased to 444.3 ± 33.1 ms after 3 months ivabradine treatment (p < 0.001). A decrease in QTc until month 9 was observed, followed by a partial increase to the upper limit of the normal value. Neither allograft rejection nor changes in left ventricular ejection fraction were observed over the follow-up period. In conclusion, ivabradine appears to be a safe and feasible long-term therapeutic option for HTx recipients with PST. It reduced the resting HR without impairment of blood pressure, myocardial contractility and cardiac conduction. The prognostic value of normalised QTc following ivabradine administration requires further observation.

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Section: Discussionmentioning

confidence: 99%

Lasting reduction of heart transplant tachycardia with ivabradine is effective and well tolerated: results of 48-month study

et al. 2012

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“…Over time, both sympathetic and parasympathetic reinnervation will occur, but the degree of reinnervation is incomplete, nonuniform, variable between patients, and heterogeneous within the same patient . Studies have correlated changes in the corrected QT interval to sympathetic reinnervation and have postulated that there may be a subset of patients with increased ventricular arrhythmia and mortality risk associated with heterogeneous reinnervation . Autonomic denervation may partially account for several unique electro‐physiological findings in HT patients, beginning with the low incidence of AF after HT.…”

Section: Mechanisms and Substratesmentioning

confidence: 99%

“…Those with progressive conduction system disease and bundle branch block have also been reported to have higher risk of SCD. Other risk factors noted in smaller studies include frequent rejection, older donor age, myocardial hypertrophy, and abnormally prolonged corrected QT interval in the donor heart . Patients with a history of syncope are also at higher risk and merit electrophysiological study, coronary angiography, and possible biopsy.…”

Section: Arrhythmias: Manifestations and Managementmentioning

confidence: 99%

“…17,18 Studies have correlated changes in the corrected QT interval to sympathetic reinnervation and have postulated that there may be a subset of patients with increased ventricular arrhythmia and mortality risk associated with heterogeneous reinnervation. 19,20 Autonomic denervation may partially account for several unique electrophysiological findings in HT patients, beginning with the low incidence of AF after HT. Denervation is also an intriguing possible factor in the lower incidence of ventricular fibrillation (VF) as the terminal rhythm among HT patients who have sudden cardiac death (SCD).…”

Section: Bicaval Versus Biatrial Anastomosismentioning

confidence: 99%

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Arrhythmias After Heart Transplantation: Mechanisms and Management

Thajudeen¹,

Stecker

Shehata³

et al. 2012

JAHA

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“…Long QT (>440msec) associated with high β-natriuretic peptide levels, were found to be an independent predictor of mortality in advanced CHF and in heart transplant patients [28, 29]. Additionally, QT duration and dispersion abnormalities were found to be significant predictors of cardiac mortality in the general population as well as in diabetics [30, 31] (Table 1 ).…”

Section: Mechanisms Of Long Qt Repolarization Abnormalities and Tdpmentioning

confidence: 99%

Iatrogenic QT Abnormalities and Fatal Arrhythmias: Mechanisms and Clinical Significance

Cubeddu

2009

CCR

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Severe and occasionally fatal arrhythmias, commonly presenting as Torsade de Pointes [TdP] have been reported with Class III-antiarrhythmics, but also with non-antiarrhythmic drugs. Most cases result from an action on K+ channels encoded by the HERG gene responsible for the IKr repolarizing current, leading to a long QT and repolarization abnormalities. The hydrophobic central cavity of the HERG-K+ channels, allows a large number of structurally unrelated drugs to bind and cause direct channel inhibition. Some examples are dofetilide, quinidine, sotalol, erythromycin, grepafloxacin, cisapride, dolasetron, thioridazine, haloperidol, droperidol and pimozide. Other drugs achieve channel inhibition indirectly by impairing channel traffic from the endoplasmic reticulum to the cell membrane, decreasing channel membrane density (pentamidine, geldalamicin, arsenic trioxide, digoxin, and probucol). Whereas, ketoconazole, fluoxetine and norfluoxetine induce both direct channel inhibition and impaired channel trafficking. Congenital long QT syndrome, subclinical ion-channel mutations, subjects and relatives of subjects with previous history of drug-induced long QT or TdP, dual drug effects on cardiac repolarization [long QT plus increased QT dispersion], increased transmural dispersion of repolarization and T wave abnormalities, use of high doses, metabolism inhibitors and/or combinations of QT prolonging drugs, hypokalemia, structural cardiac disease, sympathomimetics, bradycardia, women and older age, have been shown to increase the risk for developing drug-induced TdP. Because most of these reactions are preventable, careful evaluation of risk factors and increased knowledge of drugs use associated with repolarization abnormalities is strongly recommended. Future genetic testing and development of practical and simple provocation tests are in route to prevent iatrogenic TdP.

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Prognostic Value of the QTc Interval after Cardiac Transplantation

Cited by 21 publications

References 36 publications

Lasting reduction of heart transplant tachycardia with ivabradine is effective and well tolerated: results of 48-month study

Lasting reduction of heart transplant tachycardia with ivabradine is effective and well tolerated: results of 48-month study

Arrhythmias After Heart Transplantation: Mechanisms and Management

Iatrogenic QT Abnormalities and Fatal Arrhythmias: Mechanisms and Clinical Significance

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