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Biomedical subjects

A Lotto

Publications and source records attributed to A Lotto.

At least 55 records · Page 3Linked to original sources
PubMed1985

[Effects of intravenous diltiazem in acute myocardial infarction: hemodynamic evaluation].

The acute hemodynamic effects of intravenous Diltiazem were studied in 20 pts. with acute myocardial infarction, admitted to Coronary Care Unit within 24 hours from onset of Symptoms--19 men, 1 woman, aged from 46 to 83 years, 14 with anterior myocardial infarction, 6 with inferior myocardial infarction. All, but one, where at the time of their admission to CCU in first Forrester's hemodynamic subset (CI greater than 2.2 L/min/m2, WP less than 18 mmHg); in the last patient WP was 21 mmHg, CI 2.6 L/min/m2. Hemodynamic measurements were performed before (no drugs with hemodynamic effects were allowed during 4-6 hours before the study protocol) and after the administration of Diltiazem, 0,3 mg/kg i.v. administered in 2 min. (bolus) in 12 patients, Group A. In 8 pts--Group B--the bolus was followed by continuous infusion of Diltiazem at the rate of 5 mcg/Kg/min for three hours. The hemodynamic measurements were repeated: in Group A 2-5-30-60-120 min. after the end of the bolus; in the Group B at the same time as Group A, at the end of infusion (180 min) and 60 min after the end of infusion. Diltiazem induced no significant changes of HR, CVP, WP, CI, LVSWI and Triple product, in both groups of pts., at any time. Systolic and diastolic blood pressure decreased significantly (P less than 0.01) only 2 min. after Diltiazem administration (Group A: SBP 125.0 +/- 15.8----114.0 +/- 16.0 mmHg, DBP 85.4 +/- 6.5----76.6 +/- 10.5 mmHg; Group B: SBP 123.0 +/- 20.0----113.0 +/- 11.0 mmHg, DBP 78.1 +/- 7.0----75.0 +/- 4.9 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1984

Hemodynamic evaluation by M-mode echocardiography in acute myocardial infarction.

We assessed the relationship between echocardiographic and hemodynamic parameters in 28 patients with documented acute myocardial infarction (AMI), who underwent M-mode echocardiography and Swan-Ganz catheterization during the same hospitalization. Patients with valvular heart disease were excluded from the study. On mitral valve echogram, DE interval was measured and the area enclosed by mitral valve echogram during DE interval (DE subarea ) was calculated in each echocardiogram. DE subarea /DE interval ratio was computed for each measurement set. Hemodynamic parameters were obtained in the usual fashion. Patients with pulmonary artery wedge pressure (PWP) less than 18 mm Hg showed a DE interval markedly longer than patients with PWP greater than 18 mm Hg: 81.72 +/- 15.23 vs 55.12 +/- 9.85 msec (p less than 0.001). Patients with cardiac index greater than 2.2 L min-1 m-2 had a DE subarea /DE interval ratio greater than patients with cardiac index less than 2.2 L min-1 m-2: 0.169 +/- 0.035 vs 0.094 +/- 0.017 dm2 sec-1 (p less than 0.001). Echocardiographic and hemodynamic data were then correlated in the whole study group, and it was found that DE interval was significantly (p less than 0.001) and inversely correlated to PWP; stroke index more than cardiac index was correlated (p less than 0.005) both to DE subarea /DE interval ratio and to DE interval itself; DE interval was not affected by heart rate. We were able to categorize the patients into four subsets on the basis of echocardiographic measurements. Our findings suggest the possibility of providing, through M-mode echocardiography, a noninvasive and accurate evaluation of PWP and stroke index.

Adult↗
PubMed1984

[Hemodynamic effects of propafenone in acute myocardial infarct].

The hemodynamic effects of Propafenon were evaluated in 11 patients with acute myocardial infarction complicated by atrial and/or ventricular arrhythmias (atrial fibrillation in 4 cases, atrial premature beats in 3 cases, ventricular premature beats Class II-IVa in 4 and rapid sustained ventricular tachycardia in one case). Drug was administered as a bolus of 1-2 mg/kg in 5 min, followed by a 10-15 gamma/kg/min infusion for 24 hours in 7 patients. Serial measurements were taken of heart rate, systemic blood pressure, right atrial, pulmonary and capillary wedge pressure, cardiac output, cardiac index, total systemic resistances, left ventricular stroke work index, left ventricular ejection time and left ventricular mean ejection rate (LVMER) (8 cases) and PEP/LVET ratio (5 cases). After the intravenous bolus, a significant reduction of cardiac index (p less than 0.01) and LVMER (p less than 0.05) parallel to an increase of total systemic resistances and PEP/LVET ratio (p less than 0.01 and p less than 0.05 respectively); was observed no other parameter varied significantly. The peak hemodynamic effect was observed after 10 minutes and return to normal required from 30 minutes to 3-6 hours in the more severely affected patients. No late negative inotropic action was evident in 6 out of 7 patients who received long term infusion. Suppression or greater than 80% reduction of premature beats was evident in 9/12 cases. Sinus node function, atrioventricular and intraventricular conduction, and the QTc interval did not vary significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Hemodynamic effects of antiarrhythmic drugs in acute myocardial infarction.

The hemodynamic effects induced by an i.v. administration of Amiodarone (5 mg/Kg in 10 min + continuous infusion of 0.6 mg/min for 4-40 hrs), Propafenone (1-2 mg/Kg in 5 min + continuous infusion of 10-15 mcg/Kg/min for 24 hrs) and Mexiletine (250 mg in 15 min + 250 mg in 1 hr) have been evaluated in patients with acute myocardial infarction complicated by sinus tachycardia and hyperdynamic pattern, ventricular or supraventricular arrhythmias. The hemodynamic serial determinations have been comprehensive of: heart rate; systolic, diastolic and mean pressure; central venous pressure; arterial and wedge pulmonary pressure; cardiac output and cardiac index; vascular systemic resistences; left ventricular stroke work index; left ventricular mean ejection rate; double and triple product. In all of the three groups we observed: a reduction of cardiac index associated with an increase of left and right ventricular filling pressure and a reduction either of left ventricular stroke work index and left ventricular mean ejection rate; these hemodynamic changes were less significant after Mexiletine than after Amiodarone or Propafenone. These data confirm the negative inotropic effect of the three drugs; anyhow, these changes are usually well tolerated by patients affected by AMI with a sufficiently preserved ventricular function. The authors, however, reccommend an accurate hemodynamic monitoring of the effects of the drugs also to identify patients with a not overt ventricular failure which may become manifest after drug administration.

Amiodarone↗
PubMed1983

[Malignant ventricular hyperkinetic arrhythmia: role of permanent electric treatment].

While the technics of cardiac pacing have shown to have a precise role in the diagnosis and treatment of ventricular arrhythmias on a temporary basis, the role of permanent antiarrhythmic devices (PAD) in the treatment of these arrhythmias is still ill defined mainly because of the technological limits concerning the pacemakers and the frequent complications observed during the attempts to interrupt such tachycardias. On the basis of the available data and of theoretical considerations, three groups of pts susceptible of treatment with PAD can be selected: a) pts with brady-dependent arrhythmias where PAD is used as a prophylactic mean; b) pts with recurrent sustained ventricular tachycardia refractory to medical treatment, in whom PAD can be used to interrupt tachycardia; c) pts affected by ventricular fibrillation or rapidly deteriorating ventricular tachycardia (sudden death pts), refractory to conventional treatment, in whom the implantable defibrillator represents the only therapeutic possibility. Even if scanty, the data available seem to confirm that PAD does have a role in the treatment of malignant arrhythmias, although in selected cases and almost always together with drug treatment.

Arrhythmias, Cardiac↗
PubMed1982

[Hemodynamic effects of intravenous clonidine in patients with acute myocardial infarction].

To assess the hemodynamic effects of Clonidine in hypertensive patients (pts) with an acute myocardial infarction (AMI), we administered the drug to 12 such patients either in a single bolus (75--150 micrograms in 5 min - 8 pts) or by continuous infusion (0.4--5 micrograms/min - 4 pts). Hemodynamic measurements were obtained by means of a Swan-Ganz thermodilution catheter, before and 60 min after the administration of the drug. Clonidine did not significantly affected Heart Rate (from 80.5 +/- 3.9 to 78.4 +/- 5.9 beats/min), Mean Pulmonary Arterial Pressure (from 18.6 +/- 1.7 to 15.1 +/- 1 mmHg), Mean Pulmonary Wedge Pressure (from 12.5 +/- 1.1 to 10.6 +/- 0.7 mmHg), central Venous Pressure (from 4 +/- 0.8 to 3 +/- 0.9 mmHg), Cardiac Index (from 2.6 +/- 0.07 to 2.6 +/- 0.7 L/min/m2), Stroke Volume (from 65.2 +/- 2.8 to 68.5 +/- 5.5 ml/b). Conversely Mean Arterial Pressure fell significantly from 127 +/- 3.1 to 96.2 +/- 7.2 mmHg (P less than 0.001). Left Ventricular Systolic Work Index was reduced from 62.3 +/- 3.3 to 50.4 +/- 4.4 gm/beats/m2 (P less than 0.025), Total Systemic Resistances from 1888 +/- 50 to 1412 +/- 117 dyne sec cm-5 (P less than 0.005) and Tension Time Index from 3536 +/- 495 to 2389 +/- 385 x 10(3) mmHg x sec/min (p less than 0.05). Clonidine is a safe and useful drug to obtain a fall of high blood pressure often complicating AMI, without depressing left ventricular performance, as suggested by no significant changes of CI, WP and LVSWI. The reduction of TTI suggests a beneficial effect on the balance between myocardial oxygen delivery and demand. Clonidine is a hypotensive drug which can be safely used in patients with AMI, without depressing the left ventricular performance.

Adult↗
PubMed1982

[Electrophysiologic study of the intraventricular conduction disorders complicating acute myocardial infarct. Evaluation in the acute phase and follow-up].

In order to investigate the natural history and to evaluate the long-term risk of progression of the intraventricular (IV) conduction disturbances (CD) that complicate acute myocardial infarction (AMI), we prospectively followed the electrophysiological evolution of the IVCD in 47 patients admitted to our CCU in the years 1978-81 (34 anterior wall AMI, 13 inferior wall AMI; LAFB in 7, RBBB in 12, RBBB + LAFB in 13, RBBB + LPFB in 7, and LBBB in 8 cases). Only patients who acquired the IVCD after AMI and who did not develop 2 or 3 or 3 degrees degree AV blocks during the acute phase were considered. A His bundle recording (HBR) was obtained in every patient at the time of IVCD appearance. The HV interval was greater than 55 msec in 13 and less than or equal to 55 msec in 34. The study was repeated in 37 survivors after 3-20 months, mean 12. No significant change in infra His bundle conduction time was demonstrated at repeat HBR; the HV interval remained to be prolonged in all 8 patients with previously prolonged HV interval, and normal in all 29 patients with previously normal infra His bundle conduction time. The incidence of infra His bundle conduction delays was correlated with the degree of cardiac functional impairment, either during the acute phase or at follow-up. Late cardiac mortality rate was significantly higher for patients with HV prolongation during AMI (6/13 = 46%), compared to patients with normal HV interval (5/34 = 14%), (p less than 0.01). Two patients died suddenly during the follow-up period, both had had HV prolongation during AMI; all other deaths were due to reinfarction or to congestive heart failure. Our data indicate that patients who develop an IVCD, without advanced AV block, during AMI, do not exhibit late progressive deterioration of their infra His bundle conduction, whether it was normal or prolonged during AMI. The risk of late AV block seems to be negligible for patients with normal HV interval, while it cannot be overlooked in patients with prolonged HV interval during the acute phase of myocardial infarction.

Adult↗
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↗
PubMed1981

[Echocardiographic recognition of Valsalva aneurysm. A case report (author's transl)].

M-mode echocardiography has proved in these last years to be a reliable method for the recognition and evaluation of several cardiac diseases, both congenital and acquired. The following is a case we have examined in which M-mode echocardiography has allowed us to diagnose a Valsalva sinus aneurysm combined with a bicuspid aortic valve causing a valvular steno-insufficiency. We discuss the genesis of an echogram situated in the left ventricular outflow tract. A very similar image had been ascribed in the past to the rupture of an aneurysm into the interventricular septum, which caused a filling of the septum itself in diastole and therefore the echogram described above. On the basis of two-dimensional echocardiography, angiography and the autoptic report we could exclude this hypothesis in our case. We suggest that the image might be due to a prolapse of the valvular leaflet in the left ventricular outflow tract and/or to the prolapse of the aneurysm itself in the tract between the valvular leaflet and the interventricular septum.

Adult↗