Detection of abnormal high-frequency components in the QRS complex by the wavelet transform in patients with idiopathic dilated cardiomyopathy.
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In order to investigate whether increased fine, fractionated signals within the QRS complex can detect arrhythmogenic substrates and how these fine signals link with ventricular mechanical dysfunction, wavelet analysis was performed on averaged QRS complexes obtained from the left precordial lead in 26 patients with idiopatic dilated cardiomyopathy (IDCM) and in 12 normal subjects. The number of local maxima and the duration of the wavelet transform were significantly greater in patients with IDCM than in normal subjects; the number at 100 Hz was 8.8+/-3.1 vs 6.0+/-1.1 (p<0.01), and the duration at 100Hz was 93+/-15 vs 75+/-7ms (p<0.01). Both of these indices were greater in the patients with than in those without late potentials, repetitive ventricular premature beats or cardiac death. In addition, significant inverse curvilinear relationships were observed between the left ventricular ejection fraction and both the number of local maxima and the duration of the wavelet transform. In conclusion, fine fragmented signals in the QRS complex detected by wavelet analysis would be an important marker for potentially arrhythmogenic substrates and seemed to progress in parallel with left ventricular mechanical dysfunction in IDCM. (+info)
Correlation of ventricular mechanosensory neurite activity with myocardial sensory field deformation.
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The mechanosensory activity generated by ventricular epicardial sensory neurites associated with afferent axons in thoracic sympathetic nerves was correlated with sensory field deformation (long axis, short axis, and transmural dimension changes), regional intramyocardial pressure, and ventricular chamber pressure in anesthetized dogs. Ventricular mechanosensory neurites generated activity that correlated best with strain developed along either the long or short axis of their epicardial sensory fields in most instances. Activity did not correlate normally to local wall thickness or to regional wall or chamber pressure development in most cases. During premature ventricular contractions, the activity generated by these sensory neurites correlated best with maximum strain developed along at least one sensory field epicardial vector. Identified sensory neurites were also activated by local application of the chemical bradykinin (10 microM) or by local ischemia. These data indicate that the activity generated by most ischemia-sensitive ventricular epicardial sensory neurites associated with afferent axons in sympathetic nerves is dependent on not only their local chemical milieu but on local mechanical deformation along at least one epicardial vector of their sensory fields. (+info)
Possible theophylline toxicity during anesthesia.
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Asthmatic patients who undergo outpatient anesthesia are typically prescribed one or more drugs for treatment. Some of these agents have narrow therapeutic ranges and are associated with potentially serious adverse reactions, toxic effects, or drug interactions. Various clinical signs of toxicity may be first uncovered during routine monitoring of an office anesthetic. The case reported here demonstrates the need for proper understanding of the asthmatic patient's medical history and an appreciation for the medications used to control the disease. A sudden cardiovascular event possibly related to drug toxicity is witnessed and treated in an asthmatic patient during intravenous sedation. A possible drug interaction with a non-asthmatic medication taken concomitantly by the patient is implicated and discussed. In addition to the case report, the broad classification of drugs employed for bronchial asthma and their effects is reviewed. (+info)
Dental anesthetic management of a patient with ventricular arrhythmias.
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During routine deep sedation for endodontic therapy, a dentist-anesthesiologist observed premature ventricular contractions (PVCs) on a 62-yr-old woman's electrocardiogram (EKG) tracing. The dentist was able to complete the root canal procedure under intravenous (i.v.) sedation without any problems. The dentist-anesthesiologist referred the patient for medical evaluation. She was found to be free from ischemic cardiac disease with normal ventricular function. The patient was cleared to continue her dental treatment with deep sedation. She subsequently continued to undergo dental treatment with deep intravenous sedation without incident, although her EKG exhibited frequent PVCs, up to 20 per minute, including couplets and episodes of trigeminy. This article will review indications for medical intervention, antiarrhythmic medications, and anesthetic interventions for perioperative PVCs. (+info)
Unsuitability of corrected QT dispersion as a marker for ventricular arrhythmias and cardiac sudden death after acute myocardial infarction.
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The present study investigated whether corrected QT (QTc) dispersion could play a role as a marker of ventricular arrhythmias and sudden cardiac death after acute myocardial infarction (MI). The study included 76 males and 24 females with a mean age of 60+/-11 years. Standard 12-lead ECGs were recorded during the recovery phase (15+/-9 days) after the onset of MI. The QTc was calculated according to Bazett's formula and QTc dispersion was calculated as the difference between the maximum and minimum QTc intervals. Patients were divided into 2 groups: 21 patients (group A) had a QTc dispersion of > or =80ms, and the other 79 patients (group B) had a QTc dispersion of <80ms in the recovery stage (15+/-9 days). Clinical, angiographical, and Holter monitoring data, and prognosis (mean follow-up period 29+/-18 months) were compared between these 2 groups. The frequencies of early coronary reperfusion and recanalization of infarct-related vessels during the recovery phase were significantly higher in group B than group A. The left ventricular ejection fraction was also higher in group B than group A (51+/-12 vs 43+/-12%, p=0.0029). There were no significant differences in the number of premature ventricular contractions, the percentage of patients with repetitive ventricular arrhythmias, or in the frequency of sudden cardiac death during the follow-up period between the 2 groups. In summary, QTc dispersion in the recovery stage is not a useful marker for ventricular arrhythmias or sudden cardiac death after acute MI, although increased QTc dispersion may correlate with an ineffective early coronary reperfusion and with the degree of depressed left ventricular function. (+info)
Cyclic bursts of ventricular premature contractions of more than one minute intervals.
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Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs. (+info)
Pacing-induced delayed protection against arrhythmias is attenuated by aminoguanidine, an inhibitor of nitric oxide synthase.
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1. Cardiac pacing, in anaesthetized dogs, protects against ischaemia and reperfusion-induced ventricular arrhythmias when this is initiated 24 h after the pacing stimulus. Now we have examined whether this delayed cardioprotection afforded by cardiac pacing is mediated through nitric oxide. 2. Twenty-two dogs were paced (4 x 5 min periods at 220 beats min(-1)) by way of the right ventricle, 24 h prior to a 25 min period of coronary artery occlusion. Nine of these dogs were given the inhibitor of induced nitric oxide synthase, aminoguanidine (50 mg kg(-1) i.v.), 0.5 h prior to coronary artery occlusion. Sham-operated non-paced dogs with and without aminoguanidine treatment served as controls. 3. Pacing markedly (P<0. 05) reduced arrhythmia severity (ventricular fibrillation, VF, during occlusion 15%; survival from the combined ischaemia-reperfusion insult 62%) compared to control, sham-operated, unpaced dogs (VF during occlusion 58%; survival 17%). This protection was attenuated by the administration of aminoguanidine prior to coronary artery occlusion (survival from the combined ischaemia-reperfusion insult 11%, which was significantly (P<0.05) less than in the paced dogs not given aminoguanidine and similar to the controls). Aminoguanidine had no significant effects on coronary artery occlusion when given to dogs that had not been paced. In the dose used aminoguanadine transiently elevated systemic arterial pressure by a mean of 20 mmHg and reduced heart rate by a mean of 22 beats min(-1). 4. These results suggest that nitric oxide, probably derived from induced nitric oxide synthase, contributes significantly to the delayed cardioprotection afforded by cardiac pacing. (+info)
Heart rate variability analysis of patients with idiopathic left ventricular outflow tract tachycardia: role of triggered activity.
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There have been several reports with respect to idiopathic ventricular tachycardias (VTs) originating from the left ventricular outflow tract (LVOT). A previous report suggested that triggered activity plays a partial role in idiopathic LVOT tachycardia from the electrophysiological as well as the electropharmacological viewpoint. However, the exact role of triggered activity in this type of VT remains unknown. In the present study the relationship of the frequency of premature ventricular contractions (PVCs) and heart rate was examined and heart rate variability (HRV) was analyzed in 2 cases of LVOT tachycardia using 24-h Holter electrocardiographic (ECG) monitoring. The relation between the PVCs frequency and heart rate showed a persistently positive correlation, indicating frequent PVCs as heart rate increased. In HRV analysis, NN50(%), a time-domain variable of parasympathetic activity, showed no change prior to ventricular arrhythmias. In frequency-domain analysis of HRV, the high frequency (HF) component tended to fall prior to repetitive PVCs and VTs. The ratio of the low frequency to high frequency (LF/HF) components increased prior to single PVCs, repetitive PVCs and VTs. Sympathetic predominance predisposes the genesis of these kinds of arrhythmias originating from the LVOT and it is suggested that triggered activity plays an important role in LVOT tachycardia, at least in its initiation. (+info)