Beat by beat variations.
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Calcium Gluconate↗
Biomedical subjects
Polychronis Dilaveris
Publications and source records attributed to Polychronis Dilaveris.
Severe pulmonary hypertension due to pulmonary alveolar microlithiasis.
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Female↗
Exercise-induced left bundle branch block and propafenone administration.
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Aged↗
Upgrade to biventricular pacing in patients with pacing-induced heart failure: can resynchronization do the trick?
Dyssynchrony imposed on ventricular function by right ventricular (RV) apical pacing may lead in some cases to worsening or appearance of heart failure (HF) symptoms. This is a result of an altered pattern of activation, leading to several histological and functional adjustments of the left ventricle, including inhomogeneous thickening of the ventricular myocardium and myofibrillar disarray, fibrosis, disturbances in ion-handling protein expression, myocardial perfusion defects, alterations in sympathetic tone and mitral regurgitation. Studies of mid- and long-term effects of RV apical pacing on left ventricular (LV) function have demonstrated a progressive decline in ejection fraction and other indices of LV functional competence. Upgrading RV pacing systems to biventricular resynchronization modalities is a theoretically promising option for paced patients with worsening HF. The potentially favourable effect of upgrading on LV functional indices and patient clinical status has been demonstrated in few, non-randomized trials. Apart from the scantiness of existing clinical data, issues concerning technical aspects of the procedure and selection of eligible patients are raised. Is pacing-induced dyssynchrony equivalent to the indigenous dyssynchrony in unpaced patients with HF? What selection criteria should be applied in order to identify potential responders to cardiac resynchronization therapy in this patient population? Answers to these and more questions are still lacking.
Cardiac Pacing, Artificial↗
Torsades de pointes as a cause of sudden death in a patient with aortic stenosis and atrial fibrillation.
The occurrence of sudden cardiac death during Holter monitoring in patients with aortic stenosis has been reported previously. In the majority of the reported cases, the cause of death was a malignant ventricular tachyarrhythmia. The presence of a strong association between frequency and complexity of ventricular arrhythmias and sudden death in patients with aortic stenosis has been proposed. We report the case of a 77-year-old woman with aortic stenosis and atrial fibrillation who had an episode of torsades de pointes that degenerated into ventricular fibrillation during Holter monitoring. A short-long-short sequence, but not increased ventricular ectopics, precipitated torsades de pointes and sudden death in this case which is strongly indicative of triggered activity as the underlying mechanism of the lethal arrhythmia.
Aged↗
Heart rate lowering by inhibition of the pacemaker current: a new therapeutic perspective in cardiovascular disease.
Several studies have demonstrated that resting heart rate is an important correlate of cardiovascular and all-cause mortality and that the mortality benefit of some cardiovascular drugs seems to be related in part to their heart rate-lowering effects. Since the currently available classes of drugs with heart-rate lowering effect (e.g. beta-blockers and calcium channel antagonists) also exert multiple structural and functional actions on the cardiovascular system, which may be in some cases undesired, the introduction of a new class of agents exclusively affecting the pacemaker activity of the sinus node is of particular interest. The first molecule of this class - sinus node modulators or I(f)-current inhibitors - to reach clinical application is ivabradine. Cardiac pacemaker cells generate a spontaneous slow diastolic depolarisation that drives the membrane voltage away from a hyperpolarised level towards the threshold level for initiating a subsequent action potential, generating rhythmic action potentials that propagate through the heart and trigger myocardial contraction. The I(f) current is an inward ionic current that determines the slope of diastolic depolarisation, which in turn controls the heart beating rate. Extensive work has amply demonstrated its involvement in the generation of spontaneous activity. The molecular basis of the generation of the pacemaker current was landmarked by the cloning of hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels, which constitute the structural units of the f-channels. This review addresses the major basic properties of cardiac f-channels, with a focus on the mode of action of I(f)-current inhibitors and outlines the therapeutic implications of the existing research data.
Animals↗
Effects of thrombolysis on vectorcardiographic indices of ventricular repolarization: correlation with ST-segment resolution.
To investigate the effects of thrombolysis on vectorcardiographic (VCG) descriptors of ventricular repolarization in association with ST-segment resolution, 70 consecutively recruited patients with acute myocardial infarction underwent digital 12-lead electrocardiograms (ECGs) before and at 3 hours after thrombolysis. The alterations in the VCG descriptors spatial T amplitude and spatial QRS-T angle from the pre- to the post-thrombolysis ECG, as well as the ST-segment resolution, were calculated. Angiography revealed patency of the infarct-related coronary artery after thrombolysis in 52 (74%) patients (group A) and occlusion in 18 (26%) (group B). The spatial T amplitude was highly significantly reduced after thrombolysis in group A (P<.0001), but only marginally reduced in group B (P=.016). The spatial QRS-T angle was also significantly, although only marginally, reduced after thrombolysis in group A (P=.019), whereas it was not changed after thrombolysis in group B (P=.868). An ST-segment resolution of 60% and a 25% reduction in the spatial T amplitude after thrombolysis were able to identify patency of the infarct-related coronary artery with sensitivities of 90% and 77% and specificities of 94% and 74%, respectively. Both VCG descriptors were significantly affected by thrombolysis in patients with acute myocardial infarction, but constituted only moderate markers of thrombolysis efficacy, as evidenced by the presence of patency in the infarct-related coronary artery, compared with the ST-segment resolution.
Comorbidity↗
Conversion of recent-onset atrial fibrillation or flutter with amiodarone after ibutilide has failed: a rapid, efficient, and safe algorithm.
BACKGROUND: Ibutilide and amiodarone are used for the pharmacological conversion of atrial fibrillation (AF) or flutter (AFl), but their efficacy is rather moderate. METHODS: To test whether the use of ibutilide as a first-choice drug and of amiodarone as a second-line treatment provides a rapid, effective, and safe algorithm for conversion of recent-onset AF or AFl to sinus rhythm (SR), 85 consecutively recruited patients (59 women; mean age 69.7+/-0.9 years) with AF or AFl of recent onset received 1 or 2 mg of ibutilide infusion. In the case of ibutilide failure, amiodarone was given (6 mg/kg IV infusion over 60 minutes followed by 1200 mg IV infusion over 24 hours) 4 hours later. Ten patients with AF or AFl of recent onset were used as controls. The maximum rate-corrected QT interval was calculated in all patients and controls before the start of the study (baseline electrocardiogram (ECG)), 30 minutes later (30-min ECG), and 4 hours later (4-h ECG). RESULTS: Fifty-eight (68%) patients reversed to SR within the first 4 hours after the end of ibutilide infusion. In those 27 patients in whom ibutilide failed, amiodarone was given. Twenty-four of them (28%) were converted to SR during amiodarone infusion. Therefore, in total, 82 (96%) patients with recent-onset AF or AFl were converted to SR. The 10 controls were monitored for the same time period as the study patients and 5 (50%) out of them were spontaneously converted to SR (P<0.0001). No pro-arrhythmia or any other side effects were noticed in the study patients or in the controls. QTc was moderately decreased before the start of amiodarone infusion in patients group, while it did not differ among the three ECGs in controls. CONCLUSIONS: The combination of ibutilide as a first-choice drug and of amiodarone infusion in the case of ibutilide failure provides an effective, rapid, and safe algorithm for restoration of SR in patients with AF or AFl of recent onset.
Aged↗
The role of renin angiotensin system blockade in the treatment of atrial fibrillation.
Atrial fibrillation (AF) is the most common cardiac arrhythmia seen in clinical practice. The understanding of the pathophysiology of AF has changed drastically during the last several decades. Recent observations have challenged the concept of the multiple circuit reentry model in favor of single focus or single circuit reentry models. Atrial electrical dysfunction provides a favorable substrate and transmembrane ionic currents are key determinants. Recent research is focusing increasingly on the atrial structural remodeling, which underlies the development of AF in different pathological conditions. This has led to concepts about how interfering with the substrate might prevent AF development and recurrence. Particular interest has been generated in the role of renin angiotensin system (RAS) blockade in reversing the electrical and structural remodeling of diseased atria. The mechanisms for the preventive effect of angiotensin converting enzyme inhibitors (ACEi) or angiotensin-II (AT-II) type 1 receptor blockers (ARB) in AF are probably complex. They may comprise general haemodynamic changes leading to lower intra-atrial pressure and wall-stress, or reduce in atrial fibrosis, connexin43 over-expression and conduction delay. The promising results of several clinical trials concerning RAS blockade may herald a whole new era of AF treatment, where AF is prevented and treated by modifying its substrate rather than fighting it electrically. This review centers on the pathophysiology of the structural and electrical remodeling in AF, the possible mechanisms by which RAS blockade may reverse electrical and structural remodeling of diseased atria and on the role of ACEi or ARB blockers in AF prevention and treatment that has already been postulated both experimentally and clinically.
Angiotensin II Type 1 Receptor Blockers↗
Ibutilide-induced alterations in electrocardiographic and spatial vectorcardiographic descriptors of ventricular repolarization.
BACKGROUND: Ibutilide is used for the pharmacologic cardioversion of atrial fibrillation (AF) or flutter (AFl). Ibutilide-induced QT interval prolongation has been demonstrated previously. However, its effects on vectorcardiographic (VCG) descriptors of ventricular repolarization (VR) have not been studied so far. HYPOTHESIS: To evaluate the effects of ibutilide on electrocardiographic (ECG) and VCG descriptors of VR, one or two repeated 10-min infusions of 1 mg of ibutilide were given in 50 consecutively recruited patients (36 women, mean age 69.4 +/- 9.3 years) with AF or AFl of recent onset. METHODS: The maximum and the minimum QT intervals, QT dispersion, the rate-corrected QT maximum, and the spatial VCG descriptors, spatial T amplitude, and spatial QRS-T angle were calculated before (baseline ECG) and 30 min after the start of ibutilide infusion (postinfusion ECG). RESULTS: After ibutilide infusion, 40 (80%) patients were cardioverted to sinus rhythm (Group 1), while in the remaining 10 (Group 2) AF or AFl persisted. In both study groups, temporal measures of VR were significantly increased from baseline to the postinfusion ECG. In Group 1, spatial T amplitude and spatial QRS-T angle did not differ between those two ECGs, while in Group 2 spatial T amplitude was significantly increased (p = 0.005) and spatial QRS-T angle was significantly decreased (p = 0.002) post infusion compared with baseline ECG. CONCLUSIONS: While temporal measures of VR are significantly affected in all patients who receive ibutilide infusion for AF or AFl cardioversion, spatial VCG descriptors of VR are significantly altered only in those patients who fail to respond to the drug. A dose-related effect of ibutilide on the different aspects of VR should be suspected.
Aged↗
Exercise-induced prolongation of the infarct-related Q-waves as a marker of myocardial viability in the infarcted area.
OBJECTIVE: It is known that exercise-induced ischemia in patients with coronary artery disease (CAD) may produce QRS prolongation in the surface electrocardiogram (ECG). To investigate the presence of exercise-induced Q-wave prolongation in patients with single-vessel CAD and Q-wave myocardial infarction (MI), in association with the presence of reversible perfusion defects during thallium scintigraphy in the infarcted area. METHODS: 107 consecutive patients (89 males, mean age 56+/-8 years) were evaluated. All patients underwent coronary arteriography, maximal treadmill exercise testing and thallium-201 scintigraphy. Q-wave duration was measured both before exercise testing and during maximal heart rate from 12-lead ECGs recorded with a paper speed of 50 mm/s. RESULTS: Only 57 out of the 107 studied patients showed reversible perfusion defects in the infarcted area during thallium scintigraphy. Q-wave duration was significantly increased from the resting to the stress ECG (DeltaQ-wave duration) in patients with reversible perfusion defects in the infarcted areas (10+/-13 ms), but not in patients with fixed defects in the infarcted zone (-2.0+/-5 ms, p<0.01). The sensitivities and the specificities of Q-wave prolongation, ST segment elevation, and the combination of ST segment elevation with ST segment depression in the reciprocal leads for the detection of myocardial viability in the infarcted area were 82%, 48%, 29% and 88%, 50%, and 90%, respectively. CONCLUSIONS: Exercise-induced Q-wave prolongation is demonstrated in those patients with single-vessel CAD and a recent MI who show reversible perfusion defects in thallium scintigraphy. Exercise-induced Q-wave prolongation was found to be a sensitive and specific ECG marker for the detection of myocardial viability in the infarcted area.
Aged↗
Assessment of ventricular repolarization alterations in subjects with early repolarization.
BACKGROUND: Although the electrocardiographic (ECG) features of early repolarization (ER) have been studied extensively, no systematic quantification of ventricular repolarization in subjects with ER has been conducted so far. METHODS: The objective of the present study was to evaluate ECG and spatial vectorcardiographic (VCG) descriptors of ventricular repolarization in ER subjects and to associate them with the respective indices of ventricular depolarization. A digital 12-lead surface ECG was obtained from 108 young, healthy men with ER and 108 age-matched healthy controls. The maximum Q-onset-T-end interval (QT maximum), the maximum Q-onset-T-peak interval (QTp maximum), the respective QT dispersion values (QT maximum-QT minimum), the rate-corrected QTC maximum and QTpC maximum, the QRS duration, and the VCG markers spatial T amplitude, spatial QRS amplitude and spatial QRS-T angle, were evaluated in ER subjects and controls. RESULTS: QT maximum (P = 0.05) and QTp maximum (P = 0.003) were higher in ER subjects than in controls, while QTC maximum (P < 0.0001) and QTpC maximum (P = 0.002) were lower in ER subjects than in controls. The QRS duration (P = 0.013), as well as the spatial T amplitude, the spatial QRS amplitude, and the spatial QRS-T angle were higher in ER subjects than in controls (P < 0.0001). The spatial T amplitude was not associated with the indices of ventricular depolarization neither in ER subjects, nor in controls. CONCLUSIONS: Ventricular repolarization, as well as depolarization, is altered in young, healthy males with ER compared to age-matched healthy controls. Ventricular depolarization and repolarization indices in ER subjects are not associated to each other.
Adaptation, Physiological↗
Comparison between ventricular gradient and a new descriptor of the wavefront direction of ventricular activation and recovery.
BACKGROUND: Total R T cosine (TCRT) is a new descriptor of repolarization heterogeneity that quantifies the deviation between the directions of ventricular depolarization and repolarization. It revives the old concept of ventricular gradient (VG). HYPOTHESIS: Our goal was to examine whether TCRT and VG contain nonredundant information by comparing their reaction to autonomic tests, namely, postural changes and Valsalva maneuver. METHODS: Digital 12-lead electrocardiograms were recorded in 16 patients with cardiovascular syndrome X (SX, chest pain, exercise-induced ST-depression, normal coronary arteries, 3 men, age 60 +/- 9 years) and 40 healthy volunteers (31 men, age 33 +/- 7 years) during postural changes and Valsalva maneuver. The angle (VGA) [degrees] and magnitude (VGM) [ms.mV] of VG in reconstructed XYZ leads and TCRT (average cosine of the angles between the QRS and T vectors in mathematically reconstructed three-dimensional space) were calculated. RESULTS: (mean +/- standard of the mean): In healthy subjects, VGM and TCRT decreased, whereas VGA increased in the sitting and standing compared with supine position (TCRT: 0.61 +/- 0.05,0.47 +/- 0.06,0.29 +/- 0.08, supine, sitting, and standing, p < 0.05) and during phase II Valsalva (TCRT: 0.47 +/- 0.06 vs. 0.61 +/- 0.05, p < 0.01 in supine, 0.24 +/- 0.08 vs. 0.37 +/- 0.07, p < 0.01 in standing). In patients with SX, VGM decreased in the standing position, VGA did not change significantly, while TCRT decreased only in patients without T-wave abnormalities (n = 9) (TCRT in standing and supine: 0.55 +/- 0.09 vs. 0.68 +/- 0.08, p < 0.05). VG(M) increased during Valsalva in patients with SX. Total R T cosine correlated strongly with VGA (r = -0.84, p < 0.00001) and, unlike VGM, did not correlate with heart rate. CONCLUSIONS: Ventricular gradient and TCRT contain nonredundant information. In healthy subjects, they react sensitively to autonomic provocation. In patients with SX, their reaction is attenuated, which suggests disturbance of the autonomic control of repolarization.
Adult↗
QT-RR relationship in healthy subjects exhibits substantial intersubject variability and high intrasubject stability.
Recently, it was demonstrated that the QT-RR relationship pattern varies significantly among healthy individuals. We compared the intra- and interindividual variations of the QT-RR relationship. Twenty-four-hour 12-lead digital electrocardiograms (ECGs; SEER MC, GE Marquette; 10-s ECG recorded every 30 s) were obtained at baseline and after 24 h, 1 wk, and 1 mo in 75 healthy subjects (42 women, 33 men, age 27.9 +/- 9.6 vs. 26.8 +/- 7.5 yr, P = not significant). QT interval was measured automatically in each ECG by six different algorithms, and the mean of the six measurements was analyzed. In each recording of each individual, QT-RR relationship was assessed by 10 different regression models including linear (QT = beta + alpha x RR) and parabolic (QT = beta x RR(alpha)) models. Standard deviations (SDs) of regression parameters alpha and beta of consecutive recordings of each individual were compared with SD of the individual means. Intrasubject stability and interindividual variability were further tested by ANOVA. With all models, intraindividual SDs of the regression parameters were highly significantly smaller than SD of individual means (P < 10(-5)-10(-9)). The intrasubject stability was further confirmed by ANOVA (P < 10(-19)-10(-30)). The QT-RR relationship exhibits substantial intersubject variability as well as a high intrasubject stability. This has practical implications for a precise estimation of the heart rate-corrected QT interval in which optimized subject-specific rate correction formulas should be used.
Adolescent↗