Beat by beat variations.
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Calcium Gluconate↗
Biomedical subjects
Andreas Synetos
Publications and source records attributed to Andreas Synetos.
Large recesses associated with left ventricular noncompaction: an unusual presentation of the disease.
Left ventricular noncompaction (LVNC) represents an arrest of myocardial morphogenesis, resulting in persistence of multiple prominent ventricular trabeculations and deep intertrabecular recesses. We report a case of a 30-year-old patient who was referred to our hospital due to familial history of cardiomyopathy. The patient underwent transthoracic echocardiography, cardiac catheterization and contrast ventriculography and cardiac magnetic resonance imaging. All imaging techniques showed the characteristic pattern of noncompaction together with two unusually large recesses in the inferior wall of myocardium. This unusual form of LVNC may have an impact on the clinical course of the disease and may require anticoagulation therapy.
Adult↗
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↗
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↗
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↗
Blood pressure course in acute ischaemic stroke in relation to stroke subtype.
OBJECTIVES: Blood pressure (BP) management in acute stroke remains a matter of little consensus. Data on BP changes during the first hours of ictus are lacking. We aimed to evaluate the early spontaneous time course of BP in different ischaemic stroke (IS) subtypes. METHODS: Twenty-four h BP monitoring was performed in 200 first-ever hyper-acute IS patients. The recording was initiated and terminated at 3 h and 27 h of ictus respectively. All IS patients were classified on admission into the following subgroups of different etiology: large artery atherosclerotic stroke (LAA), cardio-embolic stroke (CE), lacunar stroke (LAC) and infarct of undetermined cause (IUC). Statistical comparisons between stroke subgroups were performed using one-way ANOVA and linear regression analyses were used to evaluate the influence of different factors in BP course. RESULTS: Although there were no significant differences in 24 h systolic (SBP) and diastolic (DBP) BP values between IS subgroups, a distinctly different SBP course was observed. The SBP dropped sharply in the LAA and LAC subgroups, while a more gradual decrease was monitored in the CE subgroup. Throughout the BP-recording, a SBP decrease of 10.1% (95% CI: 8.6-11.5) and 10.4% (95% CI: 9.0-11.8) was documented in patients with LAA and LAC respectively, while a milder drop was recorded in CE (3.7%, 95% CI: 2.4-5.0) and IUC (5.5%, 95% CI: 4.1-6.8). Increasing stroke severity (p<0.001) and brain oedema (p=0.013) was independently associated with a milder spontaneous SBP reduction. CONCLUSIONS: Spontaneous SBP course varies in acute ischaemic stroke subtypes of different etiology. This may have implications in the optimal management of post-stroke hypertension.
Acute Disease↗
Association between 24-h blood pressure monitoring variables and brain oedema in patients with hyperacute stroke.
OBJECTIVE: To assess the effects of blood pressure (BP) values on oedema formation following hyperacute stroke. DESIGN: Prospective observational study. SETTING AND PATIENTS: Acute stroke-unit in University hospital. A total of 240 consecutive first-ever ischaemic or haemorrhagic stroke patients were recruited within 3 h of ictus. METHODS Casual and 24-h BP values were measured. Known stroke risk factors and clinical findings on admission were documented. Patients were imaged with computed tomography (CT) scan within 24 h from stroke onset and 5 days later in order to determine the presence of brain oedema. Patients who received antihypertensive medication during the BP monitoring were excluded. RESULTS: The main outcome measure was brain oedema formation, which was present in 78 (32.5%) patients. The 24-h systolic (SBP), diastolic (DBP) and mean BP values, 24-h pulse pressure and heart rate values were significantly higher in patients with brain oedema than in the reference group (stroke patients without brain swelling). On multiple variable analysis, containing clinical, demographic and BP monitoring variables, 24-h SBP remained significantly (P = 0.019) associated with brain oedema. The odds ratio for oedema formation associated with each 10-mmHg increase in 24 h SBP was 1.25 (95% confidence intervals: 1.04-1.51). During the first 27 h after onset SBP course showed a spontaneous decline in the reference group, which was not documented in patients with brain oedema. CONCLUSION: Elevated 24-h SBP values in the acute stroke period are associated with subsequent brain oedema formation.
Aged↗
Two-peak temporal distribution of stroke onset in Greek patients. a hospital-based study.
A circadian distribution with a single peak of stroke onset in the morning hours has been described in various countries. Analysis of the temporal pattern of symptom onset in a series of 1253 Greek first-ever stroke patients revealed a circadian distribution with two incidence peaks between 08.00 and 10.00 h, and between 16.00 and 18.00 h. Considering the different etiopathogenic types of stroke, the same two-peak time pattern was evaluated in all stroke subgroups with the only exception of lacunar stroke, which seems to predominantly occur during night and sleep. A secondary stroke onset peak in the late afternoon has not been previously described in such detail. A relation between the second, however lower, frequency peak and the traditional Greek habit of afternoon sleep (siesta) could be assumed and deserves further investigation.
Adult↗