Prolongation of the Frequency-Corrected QT Dispersion following Cerebral Strokes with Involvement of the Insula of Reil

Eckardt, Michael J.; Gerlach, Lauren B.; Welter, Friederike

doi:10.1159/000008105

Cited by 42 publications

(31 citation statements)

References 9 publications

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“…From our experiments, ventricular ectopy was a most frequently observed malignant arrhythmia. Previous studies have shown the presence of either inverted T waves or severe QTc prolongation had a sensitivity of 100% and a specificity of 81% for predicting left ventricular dysfunction [26,27]. The QT intervals were significantly longer in cerebral ischemic rats (Figure 2B), which significantly indicated that cardiac conduction had slowed [28] and affected ventricular repolarization of cardiac myocytes in cerebral ischemic rats.…”

Section: Discussionmentioning

confidence: 72%

Aberration of L-type Calcium Channel in Cardiac Myocytes is One of the Mechanisms of Arrhythmia Induced by Cerebral Ischemia

Sun

Zhang

et al. 2008

Cell Physiol Biochem

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We have examined whether there is a close link between cerebral ischemia and arrhythmogenesis in rats as well as its possible electrophysiological mechanisms. Cerebral ischemic model was made by middle cerebral artery occlusion (MCAO). The incidence of electrocardiographic (ECG) abnormality was as high as 75.71% and the myocardium was severely damaged after MCAO 2 h. The normalized peak currents of I_Ca,L in ventricular myocytes investigated by whole-cell patch clamp were larger in cerebral ischemic rats with arrhythmias than those in sham-operated rats. The steady-state inactivation curve of I_Ca,L was shifted to more positive potentials and recovery of I_Ca,L from inactivation was accelerated significantly, but the activation of I_Ca,L was not influenced in cerebral ischemic rats with arrhythmias compared with control. Meanwhile the action potential duration (APD) of ventricular myocytes was prolonged obviously. The [Ca²⁺]_i induced by KCL in ventricular myocytes was also significantly increased by scanning confocal microscopy. Additionally, the mRNA and protein expression of α_1C/Ca_V1.2 detected by RT-PCR and immunohistochemistry analysis was also increased in myocardium of cerebral ischemic rats with arrhythmias. We conclude that the up-regulation in function and expression of L-type Ca²⁺ channel as well as [Ca²⁺]_i increasing in cardiac myocytes of cerebral ischemic rats may provide mechanisms of arrhythmogenesis.

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Section: Discussionmentioning

confidence: 72%

Aberration of L-type Calcium Channel in Cardiac Myocytes is One of the Mechanisms of Arrhythmia Induced by Cerebral Ischemia

Sun

Zhang

et al. 2008

Cell Physiol Biochem

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“…As an example, cerebrovascular disease involving the insular cortex leads to significantly increased QT D [10, 11], perhaps because of increased sympathetic activity that is observed (particularly after involvement of right insular cortex [12]). In fact, QT D measurements were recommended in cases of acute stroke [11].…”

Section: Introductionmentioning

confidence: 99%

Cardiac Repolarization Indices in Epilepsy Patients

Neufeld¹,

Lazar²,

Chari³

et al. 2009

Cardiology

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Objectives: Although epilepsy may be associated with an increased risk for sudden cardiac death, its effects on Q-T intervals has not been established. Methods: To determine whether changes in Q-T interval duration (QT_{max c}, QT_{min c}) and dispersion (QT_{D c}) occur in epileptic patients, we retrospectively studied 40 consecutive patients (age: 36.1 ± 22.2 years) who have had a seizure disorder for 14.0 ± 12.2 years and were seen in the Epilepsy Monitoring Unit, and 60 age-matched non-epileptic controls (age: 38.0 ± 15.6 years). Q-T intervals were calculated from a single 12-lead ECG. Results: QT_{max c} (425 ± 30 vs. 410 ± 36 ms, p = 0.040) and QT_{D c} (63.1 ± 22.4 vs. 31.0 ± 17.2 ms, p = 0.000) were higher, and QT_{min c} (362 ± 36 vs. 379 ± 33 ms, p = 0.040) was lower in epilepsy patients. QT_{max c} was significantly correlated with disease duration (r = –0.35, p = 0.028) before, but not after age correction (r = –0.31, p = 0.053). Neither age nor reported recent seizure frequency was correlated with any repolarization index. Conclusions: QT_{max c} and QT_{D c} are higher in epilepsy patients as compared to control subjects. While Q-T interval appears to be related to disease duration, particularly over the early history of disease, it is unrelated to patient age or recent reported seizure frequency.

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“…Regarding repolarization inhomogeneity, QT dispersion is increased after acute stroke compared to age-matched hospitalized controls, both groups without history or clinical evidence of cardiac disease [15]. Since this was noted only within 24 hours of stroke onset, it strengthens the association and interestingly, was noted specifically with insular infarcts [16]. Further insular association arises from the linkage between right insular stroke and AV block, QTc prolongation, T wave inversion and ventricular ectopy, (these not observed with strokes in other locations) and with increased mortality at 3 months [17,18].…”

Section: Strokementioning

confidence: 75%

Cerebrogenic cardiopathy

Oppenheimer¹

2017

Blood Heart Circ

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Hypereosinophilic Syndrome (HES) is a condition related to helminthiasis, allergies, vasculitis, adverse reactions to drugs or malignant neoplasms. We report a case of a boy, 7 years old, presenting abdominal pain, vomiting, tachidispnea and leukocytosis with predominance of eosinophils. Bone marrow biopsy revealed intense granulocytic hypercellularity characterized by eosinophilia, as well as immature lymphoid cells in the interstitium, associated with trabecular bone infiltration. The immunohistochemical study revealed positivity for CD79a and TDT. Peripheral blood flow cytometry demonstrated 6.5% of lymphoid blasts. The diagnosis was Lymphoproliferative Disease associated with Hypereosinophilia: Acute Lymphoblastic Leukemia. The association presented is infrequent and its aggressiveness is determined by the physiological limitations imposed by the damages secondary to eosinophilia.

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Prolongation of the Frequency-Corrected QT Dispersion following Cerebral Strokes with Involvement of the Insula of Reil

Cited by 42 publications

References 9 publications

Aberration of L-type Calcium Channel in Cardiac Myocytes is One of the Mechanisms of Arrhythmia Induced by Cerebral Ischemia

Aberration of L-type Calcium Channel in Cardiac Myocytes is One of the Mechanisms of Arrhythmia Induced by Cerebral Ischemia

Cardiac Repolarization Indices in Epilepsy Patients

Cerebrogenic cardiopathy

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