Biomedical subjects

G Corbucci

Publications and source records attributed to G Corbucci.

5 recordsLinked to original sources

PubMed2002

Computationally inexpensive methods for intra-cardiac atrial bipolar electrogram compression.

AIM: This paper reports studies of mathematical algorithms for intra-cardiac atrial bipolar electrogram compression suitable with implementation on implantable devices. PATIENTS AND METHODS: Bipolar intra-cardiac electrograms (IEGMs) of high right atrium were obtained from 20 patients who underwent electrophysiological studies for arrhythmias. Four thousand seven hundred and eighty-two seconds of IEGM were collected and divided into three rhythm groups: sinus rhythm (SR), atrial fibrillation (AF) and atrial flutter (AFL). Since mathematical algorithms suitable for use with implantable devices demand low computational cost, we employed piecemeal linear approximation methods (ZOP--Zero Order Prediction and SAPA--Scan Along Polygonal Approximation), and beat detection method (Peak) both or which need small numbers of operations to perform electrogram compression. Compression ratio (CR) and percent root mean square difference (PRD) were used to compare the three methods, with statistical analyses performed using paired t-test. RESULTS AND CONCLUSION: The best performance was obtained using the Peak method which reaches an average CR of 10.6 in the case of SR group, 2.8 for AF, and 3.6 for AFL groups, respectively, while PRD lies below 2% for SR and AFL groups and 6% for the AF group. Results show that, for bipolar electrograms, the Peak method reaches statistically significant better performance (P<0.001) in all cases except for Peak vs SAPA applied to AF (P=0.2). The number of operations necessary to compress the data indicate that time consumption can be reduced to be suitable for real time compression in implantable devices. The Peak method, which was assumed to receive the instant of occurrence of each recognized beat, from the hardware of the device, requires fewer operations than ZOP and SAPA. Increasing the length of electrograms recorded in pacemakers will enhance the amount of information provided by the implantable device, allowing more detailed characterization of the intra-cardiac activity and leading to new perspectives in arrhythmia diagnosis and therapy.

Adult↗

PubMed2000

Automatic atrial tachyarrhythmia detection from intracardiac electrograms.

BACKGROUND: Automatic atrial tachyarrhythmia recognition is crucial in order to allow a correct switching-mode function of dual-chamber pacemakers and to avoid inappropriate shocks of ventricular implantable cardioverter-defibrillators. In this paper we considered three algorithms suitable for implantable devices. The first was based on the atrial cycle length; the others analyze different morphologic characteristics of atrial signals. METHODS: Intracardiac bipolar electrogram recordings were obtained from the high right atrium during electrophysiological study. Twenty patients were considered, some of them presenting with different types of cardiac rhythm at different intervals of the study. Cardiac rhythms were divided into three groups: sinus rhythm consisting of 2,196 s obtained from 12 subjects, atrial fibrillation consisting of 771 s obtained from 7 subjects, and atrial flutter consisting of 1,793 s obtained from 7 subjects. The automatic detection was performed on each electrogram segment lasting 1 or 4 s. Atrial segments were separated into two subgroups: the first for the training of the algorithm and the second for testing and validation of results. We considered two types of statistical analysis: comparison between pairs of rhythm (paired classification), and classification among the three different groups (direct classification). RESULTS: The combination of the cycle length algorithm with a morphological method achieved the best performance for both statistical analyses. Paired classification resulted in the following: atrial fibrillation vs sinus rhythm was detected with no error; atrial flutter vs sinus rhythm with a total accuracy of 99.3% (sensitivity 99.4%, specificity 99.2%); atrial fibrillation vs atrial flutter with a total accuracy of 99.1% (sensitivity 98.5%, specificity 99.4%). The total accuracy achieved for the direct classification was 98.6% (average sensitivity 98.5%, specificity 98.8%). CONCLUSIONS: Our results support the association of algorithms for future enhancement of atrial tachyarrhythmia detection in dual-chamber devices, thanks to the limited computational effort.

Algorithms↗

PubMed1997

Detecting incipient vasovagal syncope: intraventricular acceleration.

The peak endocardial acceleration (PEA) caused by ventricular isometric contraction can be measured with an implantable microaccelerometer located inside the tip of a normal unipolar pacing lead. It has been shown that PEA correlates with myocardial contractility and the maximum rate of rise of ventricular pressure (peak dP/dt) of the left ventricle. A PEA measuring system was temporarily inserted into the apex of the right ventricle in seven patients affected by syncope of uncertain origin. Each patient subsequently underwent 60 degrees tilt testing with three different protocols: without pharmacological challenge (baseline); potentiated with sublingual trinitroglycerin (at a dose of 0.3 mg); and with isoproterenol infusion (at a dose of 3 micrograms/min). Each phase lasted 20 minutes. Syncope was induced in 1 patient during the baseline phase, in 3 patients during the trinitrin phase, and in 4 patients during the isoproterenol phase. Six patients had a negative response during the baseline phase and served as a control group. From the beginning of upright posture to the time of maximum heart rate, PEA increased by about the same amount in both positive and negative patients, but absolute values were from two- to three fold higher with isoproterenol (from 1.2 +/- 0.5 G to 1.6 +/- 0.8 G, from 0.8 +/- 0.2 G to 1.2 +/- 0.4 G, and from 2.8 +/- 1.8 G to 3.6 +/- 1.8 G, respectively, for negative, positive baseline or trinitrin, and positive isoproterenol tests). At the time of syncope, PEA values fell to baseline values. PEA changes were inversely correlated with blood pressure changes and directly correlated with heart rate changes. Thus, tilt induced syncope occurred both at low and high levels of left ventricular contractility. Whether spontaneous syncopes occur at low or high PEA behavior remains to be established. Since heart rate correlates well with changes in PEA and is far easier to measure, it is unlikely that a PEA measurement system or, in general, a contractility-based system, might become an ideal sensing parameter for the introduction of devices to combat vasovagal syncope.

Acceleration↗

PubMed1996

An implantable intracardiac accelerometer for monitoring myocardial contractility. The Multicenter PEA Study Group.

As the myocardium contracts isometrically, it generates vibrations that are transmitted throughout the heart. These vibrations can be measured with an implantable microaccelerometer located inside the tip of an otherwise conventional unipolar pacing lead. These vibrations are, in their audible component, responsible for the first heart sound. The aim of this study was to evaluate, in man, the clinical feasibility and reliability of intracavity sampling of Peak Endocardial Acceleration (PEA) of the first heart sound vibrations using an implantable tip mounted accelerometer. We used a unidirectional accelerometer located inside the stimulating tip of a standard unipolar pacing lead: the sensor has a frequency response of DC to 1 kHz and a sensitivity of 5 mV/G (G = 9.81 m/s-2). The lead was connected to an external signal amplifier with a frequency range of 0.05-1,000 Hz and to a peak-to-peak detector synchronized with the endocardial R wave scanning the isovolumetric contraction phase. Following standard electrophysiological studies, sensor equipped leads were temporarily inserted in the RV of 15 patients (68 +/- 15 years), with normal regional and global ventricular function, to record PEA at rest, during AAI pacing, during VVI pacing, and during dobutamine infusion (up to 20 micrograms/kg per min). PEA at baseline was 1.1 G +/- 0.5 (heart rate = 75 +/- 14 beats/min) and increased to 1.3 G +/- 0.9 (P = NS vs baseline) during AAI pacing (heart rate = 140 beats/min) and to 1.4 G +/- 0.5 (P = NS vs baseline) during VVI pacing (heart rate = 140 beats/min). Dobutamine infusion increased PEA to 3.7 G +/- 1.1 (P < 0.001 vs baseline), with a heart rate of 121 +/- 13 beats/min. In a subset of three patients, simultaneous hemodynamic RV monitoring was performed to obtain RV dP/dtmax, whose changes during dobutamine and pacing were linearly related to changes in PEA (r = 0.9; P < 0.001). In conclusion, the PEA recording can be consistently and safely obtained with an implantable device. Pharmacological inotropic stimulation, but not pacing induced chronotropic stimulation, increases PEA amplitude, in keeping with experimental studies, suggesting that PEA is an index of myocardial contractility. Acute variations in PEA are closely paralleled by changes in RV dP/dtmax, but are mainly determined by LV events. The clinical applicability of the method using RV endocardial leads and an implantable device offers potential for diagnostic applications in the long-term monitoring of myocardial function in man.

Acceleration↗

PubMedDate not supplied

Neuroendocrine control of basal insulin secretion in man: a study with bromocriptine, clonidine and naloxone.

The effects of bromocriptine (CB-154, 2.5 mg po), clonidine (0.05 mg im) and naloxone (0.4 mg im), as well as the interaction between naloxone and CB-154 or clonidine on basal insulin secretion were studied in 6 normal men. Clonidine, naloxone and CB-154 plus naloxone lowered insulin plasma levels; CB-154 alone caused only a slight reduction, whereas clonidine plus naloxone did not affect insulin secretion. These results prove the existence of a complex neuroendocrine control of basal insulin secretion through dopaminergic, adrenergic and opiate mechanisms; they also suggest that the opiate inhibitory control of insulin release may be dissociated from the dopaminergic one, but may interact with the adrenergic one.

Adult↗