Biomedical subjects

D Kocovic

Publications and source records attributed to D Kocovic.

7 recordsLinked to original sources

PubMed1998

Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction.

BACKGROUND: Patients with ventricular tachycardia (VT) after myocardial infarction often have multiple morphologies of inducible VT, which complicates mapping and is viewed by some as a relative contraindication to ablation. Attempting to identify and target a single "clinical" VT is often limited by inability to obtain 12-lead ECGs of VTs that are terminated emergently or by defibrillators. This study assesses the feasibility of ablation in patients selected without regard to the presence of multiple VTs by targeting all VTs that allow mapping. METHODS AND RESULTS: Radiofrequency catheter ablation targeting all inducible monomorphic VTs that allowed mapping was performed in 52 patients with prior myocardial infarction. Antiarrhythmic drug therapy had failed in 41 (79%) patients including amiodarone in 36 (69%) patients. An average of 3.6+/-2 morphologies of VT were induced per patient. More than 1 ablation session was required in 16 (31%) patients. Complications occurred in 5 (10%) patients, including 1 (2%) death caused by acute myocardial infarction. During follow-up 59% of patients continued to receive amiodarone; 23 (45%) had implantable defibrillators. During a mean follow-up of 18+/-15 months (range 0 to 51 months) 1 patient died suddenly, 2 died from uncontrollable VT, and 5 died from heart failure. Three-year survival rate was 70+/-10%, and rate for risk of VT recurrence was 33+/-7%. CONCLUSIONS: Radiofrequency catheter ablation controls VT that is sufficiently stable to allow mapping in 67% of patients despite failure of antiarrhythmic drug therapy and multiple inducible VTs. However, ablation was largely adjunctive to amiodarone and defibrillators in this referral population.

Adult↗

PubMed1997

Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping.

Ventricular tachycardia late after myocardial infarction is usually due to reentry in the infarct region. These reentry circuits can be large, complex and difficult to define, impeding study in the electrophysiology laboratory and making catheter ablation difficult. Pacing through the electrodes of the mapping catheter provides a new approach to mapping. When pacing stimuli capture the effects on the tachycardia depend on the location of the pacing site relative to the reentry circuit. The effects observed allow identification of various portions of the reentry circuit, without the need for locating the entire circuit. Isthmuses where relatively small lesions produced by radiofrequency catheter ablation can interrupt reentry can often be identified. A classification that divides reentry circuits into one or more functional components helps to conceptualize the reentry circuit and predicts the likelihood that heating with radiofrequency current will terminate tachycardia. These methods are helping to define human reentry circuits.

Cardiac Pacing, Artificial↗

PubMed1991

Epidural lead fracture caused by material processing fault.

Fracture of the epidural lead (Pisces Quad 3487) is documented in four out of eight patients with an implanted Itrel pacing system for treatment of peripheral vascular disease. In two patients, lead fracture was established during x-ray fluoroscopy. In the remaining two patients, x-ray examination did not reveal any fracture, due to proximity of the fragments. Microscopic examination of the extracted lead, however, confirmed lead fracture, as well as the presence of tissue fluid and thrombus between the two ends of the spiral shaped lead, but no insulation defect was observed. A cross-sectional area on the fracture line of the broken lead was examined using scanning electron microscopy. It was found, by tracing the radial marks to their point of convergence, that the initial microcrack started from a large inclusion of the calcium-silicon type at the lead surface. The initial microcrack was propagated by the fatigue mechanism. The presence of a large inclusion at the surface suggests that the main cause of the failure of the investigated epidural leads could be improper fabrication of the material. The high incidence of epidural lead fracture in our group suggests that this complication should be considered as a possible cause of epidural spinal electrical stimulation pacing system dysfunction.

Adult↗

PubMed1991

The etiology of syncope in pacemaker patients.

A total of 46 patients with syncopal episodes after VVI pacemaker implantation were studied. Of these, 92% had one to three syncopal episodes and 8% more than three. All underwent a thorough clinical examination, which included chest X ray, echocardiogram, neurological exam, and the following protocol: 24-hour Holter monitoring, EEG, blood pressure (BP) measurement in three positions, Doppler exam of the carotid vessels, fasting blood glucose, and head-up tilt table test (60 minutes, 60 degrees). Holter monitoring showed exit block in two patients (4.3%) and failed sensing in one (2.1%). In two patients there was unilateral slowing on EEG. Orthostatic hypotension was found in four patients (8.6%), and hypoglycemia in three insulin-dependent diabetics. An occlusive atherosclerotic plaque in the carotid artery was found in three patients (6.5%). Syncope was induced in 17 patients (36.9%) by the tilt table test, after a mean standing time of 47 +/- 11 minutes. The mean resting systolic BP of these patients was 140 +/- 24 mmHg, and fell to a mean level of 56 +/- 8 mmHg (mean systolic BP drop was 79 +/- 8 mmHg). Sixteen of these 17 patients with positive tilt table were being paced at the time of syncope and one had a spontaneous heart rate of 73 beats/min. In 14 cases (30.4%) the cause of syncopal episodes after this extensive workup remained unexplained. These results indicate that pacemaker dysfunction is not a major cause of syncopal episodes in pacemaker patients and that these are most often due to vasovagal syncope. Long-term follow-up is warranted to determine the prognostic significance of various types of syncope in pacemaker patients.

Blood Pressure↗

PubMed1989

Circadian variations of heart rate and STIM-T interval: adaptation for nighttime pacing.

In order to determine the optimal pacing rate for pacemaker patients at night, 150 normal subjects with regular sinus rhythm and free of manifest heart disease, were studied using 24-hour Holter monitoring. Minimum and average heart rates were analyzed on an hourly basis. The study group was divided into six age groups, 25 subjects each, ranging from 20-29 years to 60-69 years. The minimum heart rate during the night was found to be lower than 65 ppm for all groups. The youngest subjects showed the largest variation in the minimum heart rate. The results suggest that an automatic lowering of the pacing rate during the night would allow for longer periods of sinus rhythm, thereby improving hemodynamic performance and reducing pacemaker power consumption. Suitable sensors for automatic lowering of the pacing rate include inbuilt 24-hour clock systems and the QT interval that lengthens during sleep.

Adult↗

PubMed1988

Association between stimulated QT interval and ventricular rhythm disturbances: influence of autonomic nervous system.

To examine the association between ventricular rhythm disturbances and changes in the pacemaker-induced stimulated T interval (STIM-T interval), we compared findings from monitoring of two patient groups. The first group consisted of 15 patients with QTX microprocessor pacemakers and the second group consisted of 198 patients with documented ventricular rhythm disturbances and coronary artery disease (CAD). In the first group, which was free of ventricular rhythm disturbances and manifest coronary artery disease, the STIM-T interval was measured every 4 hours over a 36-hour period at four pacemaker frequency settings (70, 80, 90, and 100) in order to observe the circadian variation of the STIM-T interval as a function of changes in autonomic nervous system (ANS) tone. The second group was comprised of patients with CAD and over 30 VES/hrs (Lown grade classification 1-5), and taking no antiarrhythmic medication. These patients were followed using 24-hour Holter monitoring over a minimum of 23 hours and with less than 5% artifact/recording. Information regarding mean hourly heart rate, total number of VES, VES pairs, VT runs, and ischemic episodes in this group was compared with changes in the STIM-T interval in the first group. The STIM-T interval was found to be shorter during the day and longer at night at all heart rate settings. The total frequency of VES, of VES pairs, VT runs, and ischemic episodes in the second group varies in a similar circadian fashion. The greatest total number of VES, of VES pairs, VT runs, and ischemic episodes was recorded in the waking hours, at the same time when the STIM-T interval is the shortest, while this number was significantly lower during sleep, when the STIM-T interval of the first group is the longest. This coincidence of circadian variation pattern between STIM-T interval in group I, and ventricular arrhythmias and ischemic episodes in group II, suggests that alterations in ANS tone reflected in the STIM-T interval may be an important factor in the occurrence of these untoward events.

Adult↗

PubMed1986

Target lead--low threshold electrode.

Acute and chronic threshold measurements were compared for three different electrodes: the Medtronic Target Tip model 4011, the Medtronic Ring Tip Model 6971 and the Siemens-Elema Carbon Tip Model 412S. The results of this study show that acute thresholds are lower with the Target Tip lead as compared to the other two. This finding applies to chronic thresholds as well. The results of this study favor programming to lower output energies while maintaining adequate safety margins with this lead system.

Electrodes, Implanted↗