PubMed Health⌕ Search

Biomedical subjects

L Sernesi

Publications and source records attributed to L Sernesi.

7 recordsLinked to original sources
PubMed1992

[Ventricular stimulation triggered by esophageal atriogram: a new technique of temporary physiologic stimulation in the course of acute myocardial infarct complicated by atrioventricular block and low cardiac output].

Advanced atrio-ventricular (AV) block during acute myocardial infarction (AMI) is considered a complicating dysrhythmia as the well as mechanism responsible for occurrence of life-threatening hemodynamic changes. Often, simple VVI pacing can result insufficient in improving the decreased cardiac output. VDD pacing, which preserves atrial contribution, should represent the most effective electrical approach; therefore, it requires intracavitary placement of 2 catheters. In 10 pts (6M, 4F, mean age of 63.8 +/- 6.6 years) with advanced AV block due to AMI (4 inferior, 6 anterior) and without sinus node dysfunction, we performed stable VDD stimulation (mean 16.6 +/- 20.6 hours) using only one catheter positioned in the right ventricle while the atrial impulse, filtered (50-70 Hz) and amplified through a special device, was derived from the esophagus. Such technique is rapid and reliable, avoiding problems associated with atrial sensing and catheterization.

Aged↗
PubMed1981

[The permanent electrostimulation with ventricular programmable pacemaker (author's transl)].

The purpose of this study is to evaluate the directions, reliability and long-term results of ventricular programmable pacemakers (PPM's). One hundred and ten PPM's, types Cordis and Medtronic, were implanted in 60 patients (pts) with intermittent or paroxysmal 2 degrees, 3 degrees a-v block and in 50 pts with S.S.S., mostly symptomatics, with a follow-up of 45 months. We did not observe either spontaneous or wrong reprogrammations nor circuit failure. In 92% of pts with Omni-Stanicor Cordis PM's, the stimulation was effective at the "lower" current amplitude, hence a longer life of the generator. Eighteen pts (16.3%) needed to raise ventricular rate (average 65 bpm): 6 pts for dizziness, syncopes or cardiac failure; 2 pts to control ventricular arrhythmias; 10 pts for a stable bradycardia lower than 50 bpm. In 11 pts with bradyarrhythmia due to S.S.S., cardiac output (CO) was measured both with thermodilution and echocardiography ("mitral valve echogram", being "r" of the two methods = 0.92), in spontaneous rhythm (63.3 +/- 3.13 bpm) and increasing artificially heart rate to 74.8 +/- 3.0 bpm; CO decreased from 4.65 +/- 0.13 l/min to 3.58 +/- 0.09 l/min, likely for the loss of atrial pumping. Similar results were obtained in other pts evaluated only with echocardiographic method after PM implantation: some of these underwent a further echocardiographic haemodynamic evaluation after 15 days of constant ventricular pacing at a mean rate of 75 bpm, with a different behaviour among them. This emphasizes the utility of PPM's in preserving spontaneous rhythm until bradycardia reaches dangerous levels and also the usefulness of echocardiography to evaluate, haemodinamically, the paced patient's ventricular performance.

Adult↗
PubMed1980

Serum myoglobin, total CK and MB CK isoenzyme after D.C. cardioversion and during the early phase of acute myocardial infarction.

Myoglobin, total CK and MB CK isoenzyme were determined in the sera of 6 patients admitted with arrhythmias and treated with D.C. countershock and also in 37 patients with acute myocardial infarction or anginal syndrome. All the three tests were increased in patients with myocardial infarction. Serum myoglobin seems sufficiently sensitive and specific but the time required for the assay is a limiting factor for practical use in emergencies. After electrical cardioversion, myoglobin and CPK remain normal, although MB isoenzyme was increased in two of six patients. These results suggest that electrical cardioversion in itself does not influence serum levels of myoglobin. The occasional increase of MB CK observed after cardioversion seems to be the consequence of an easier release of the enzyme due to a myocardial injury.

Adult↗
PubMed1978

Relationship between the hypotensive and renin-stimulating actions of diuretic therapy in hypertensive patients.

1. The pressor role of renin stimulated by chronic diuretic therapy has been assessed in 31 patients with essential hypertension by infusing the angiotensin II antagonist, saralasin, immediately before and at the end of 2 weeks' treatment with the diuretic, chlorthalidone. 2. Under diuretic therapy the change in blood pressure caused by saralasin was found to be correlated to plasma renin activity values, in such a way that small pressor responses were again observed in patients whose renin was mildly stimulated by the diuretic, whereas a marked depressor response occurred in patients whose renin was markedly increased. 3. On the other hand, the hypotensive effect of chlorthalidone was correlated to values of plasma renin activity under diuretic therapy in an opposite direction: indeed little or no decrease and sometimes an increase in blood pressure were observed in patients with marked renin activation by diuretic therapy. 4. It is concluded that stimulation of renin release by chronic diuretic therapy can be considered a factor limiting the hypotensive activity of diuretic drugs.

Adult↗