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Biomedical subjects

Georgios Giannopoulos

Publications and source records attributed to Georgios Giannopoulos.

6 recordsLinked to original sources
PubMed2006

Real-time three-dimensional dobutamine stress echocardiography for coronary artery disease diagnosis: validation with coronary angiography.

OBJECTIVE: To compare real-time three-dimensional echocardiography (RT3DE) with two-dimensional dobutamine stress echocardiography (2DE) for the detection of myocardial ischaemia, with angiographic validation of the results. METHODS: 56 patients (mean (SD) age 64.5 (6.2) years, 38 males), referred for coronary angiography, were examined by 2DE and RT3DE during the same dobutamine stress protocol. RESULTS: All 56 patients completed the stress protocol uneventfully. The mean (SD) acquisition time for the necessary views to evaluate all segments was 26.3 (2.5) s for RT3DE and 58.8 (3.7) s for 2DE (p<0.001). At peak stress, RT3DE had a higher wall-motion score index (1.25 (0.24) by 2DE, 1.30 (0.27) by RT3DE; p = 0.014). The regional wall-motion score for the four apical segments at peak stress was compared; it was 1.35 (0.55) by 2DE and 1.52 (0.69) by RT3DE (p = 0.003). The diagnostic parameters of 2DE versus RT3DE were: sensitivity 73% vs 78%, specificity 93% vs 89% and overall accuracy 86% vs 85%, respectively. In the left anterior descending artery territory, in particular, where RT3DE had higher regional wall-motion scores, it showed a tendency towards higher sensitivity (85% vs 78%), although this difference did not achieve statistical significance. CONCLUSION: RT3DE identifies wall-motion abnormalities more readily in the apical region than 2DE, which may explain the tendency towards higher sensitivity in the left anterior descending artery territory. RT3DE results were validated using angiography as reference and findings indicate diagnostic equivalence to 2DE, with the advantage of considerable shorter acquisition times.

Aged↗
PubMed2006

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↗
PubMed2006

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↗
PubMed2005

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↗