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Results for “EXTRASYSTOLE”

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At least 469 records · Page 26Linked to original sources
PubMed2002

[Effect of post-extrasystole potentiation on blood pressure and heart rate regulation].

Noninvasive finger arterial blood pressure and ECG were recorded for 30 min in patients with idiopathic dilated cardiomyopathy (IDC) and healthy control subjects (CON) for the investigation of blood pressure and heart rate regulation following a premature ventricular complex (PVC). The potentiation of blood pressure amplitude of the postextrasystolic beat was fivefold increased in IDC compared with CON (48.7 +/- 32.6% vs. 9.8 +/- 5.4%, p < 0.01). PVC starts a baroreflex response, which last about 10 s in physiological regulation. In contrast, the baroreflex response in IDC is immediately suppressed by the augmented potentiation of the blood pressure amplitude from the first postextrasystolic beat. Thus, the regulation after PVC is determined by the PVC itself and postextrasystic potentiation.

Baroreflex↗
PubMed1978

Changes in fetal supraventricular extrasystoles during uterine contractions in labour.

The electrocardiogram and phonocardiogram were recorded from a fetus exhibiting supraventricular ectopic beats during labour. The ectopic beats showed increased amplitude of the first heart sound (S1) compared to sinus and postectopic beats; the R-S1 interval was prolonged and the mechanical systole, measured as the S1-S2 interval, shortened. During uterine contractions these parameters were measured every 10 sec. The S1 amplitude of the ectopic beats decreased; simultaneously the R-S1 interval increased and the S1-S2 interval shortened. The changes were delayed compared to the amniotic pressure curve. The changes found can be explained by a shift of blood between the fetus and placenta, caused by uterine contraction.

Adult↗
PubMed2001

[Radiofrequency catheter ablation of symptomatic isolated ventricular extrasystole in patients with a normal heart].

INTRODUCTION: Premature ventricular depolarizations (PVDs) in patients without heart disease, are a frequent clinical problem that can cause important symptoms. Most commonly, this benign arrhythmia responds to treatment with antiarrhythmic drugs. However, occasionally PVDs are refractory to pharmacological treatment but they can be eliminated with radiofrequency catheter ablation. AIM: To show our experience with four patients in whom we used this method. MATERIAL AND METHOD: We studied three men and a woman, twelve to forty six years old. All of them were symptomatic, their EKG and echocardiogram were normal and they had been treated with several drugs without response. In three of them the PVDs had left bundle-branch block morphology with inferior axis; the other patient had right bundle-branch block morphology with superior axis. The origin of the PVDs was determined using pace mapping. RESULTS: Two of the patients had spontaneous PVDs; in the other two isoproterenol infusion was used to induce them. In three patients the origin of the PVDs was located in right ventricular outflow and in the other in the anterolateral region of the left ventricle. None had sustained atrial or ventricular arrhythmia. In all of them PVDs were eliminated. A patient presented a second morphology that could not be treated. None of the patients had complications and they were discharged within the next 24 hours. Three noted symptomatic improvement and after 18 months, only one had a probable recurrence of the arrhythmia. CONCLUSIONS: Radiofrequency catheter ablation can be successfully used to eliminate PVDs in severely symptomatic and drug-resistant patients.

Adult↗
PubMedDate not supplied

[Anisotropy of stationary rates and delays in extrasystolic waves in the dog heart].

Excitation propagation in the ventricle and auricle bands of the dog's myocardium has been studied. The anisotropy of stationary valocities and delays of the initiation of extrasistole exciation has been shown: along the fibres the velocity is higher and the delay smaller than across the fibres. The levels of anisotropy of velocities and delays are almost equal in each structure. The strongest anisotropy of delays and velocities (-4,5) is observed in the ventricle muscle layer; the weakest (1,7)-in a specialized layer. The anisotropy of velocities and delays is the greater, the greater is the electrotone anisotropy. A new mechanism of extrasistole initiation (reentry) in the system homogenous by the membrane properties, but with anisotropy of intercellular bonds is considered.

Animals↗