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Biomedical subjects

R Valentini

Publications and source records attributed to R Valentini.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Early and late prognosis in acute myocardial infarct. A retrospective study in patients admitted to the coronary care unit in the past 10 years].

The prognostic evaluation of the patient with an acute myocardial infarction is one of the most interesting unanswered problems. This is both because of its complexity and its implications in terms of secondary prevention. Several clinical studies have emphasized the reliability of the prognostic evaluation based on data collected during the first 24 hours. We therefore evaluated the prognostic relevance of 26 variables measured in the coronary care unit in 1914 patients admitted to our Unit as a result of acute myocardial infarction during the past 10 years. Twenty-four patients were lost to follow-up so that the evaluation refers to 1,890 patients, 1,506 of whom are males aged between 22 and 99 years (mean 58.1) and 384 are females aged between 29 and 88 years (mean 67.1); thus there is a greater prevalence of males. The sex-related difference in the age distribution is statistically significant. In-hospital mortality was analyzed using univariate and multivariate statistical methods (chi-squared test, multiple logistic regression analysis). The prognostic relevance of the considered variables in relation to the survival was analysed using the logrank test and using Cox's model. The variables associated with a greater risk of in-hospital death were found to be: age, presence of diabetes, anterior location of the infarct, arterial hypotension at admission, Killip class III and IV and the presence of ventricular tachyarrhithmias. In contrast, smokers had a lower in-hospital death risk. As to mortality during the follow-up, there was an association with age, female sex, pre-existent coronary disease, presence of high heart rate on admission, low peripheral tissue perfusion, x-ray documented pulmonary congestion, supraventricular tachiarrhythmias and intraventricular block. In contrast, the presence of obesity was associated with a reduced death risk during the follow-up. During the follow-up the most frequent cause of death was re-infarction, followed by sudden death, death from non-cardiac causes and heart failure.

Adult↗
PubMed1987

Controlled study of the haemodynamic effects of isosorbide 5-mononitrate in acute myocardial infarction.

In view of the favourable results of the short-term therapy of acute myocardial infarction (AMI) with glyceryl-trinitrate (GTN) infusion, we undertook a randomized study to test the hypothesis whether the administration of a single dose of isosorbide 5-mononitrate (IS 5-MN) given orally would have the same favourable haemodynamic effect as observed with GTN infusion. For this purpose we evaluated the haemodynamic effects of IS 5-MN compared to isosorbide dinitrate (ISDN), observed in the same group of patients. 10 patients (8 males, 2 females) aged 50-76 years (mean 63) with AMI (7 anterior, 3 inferior) admitted to the coronary care unit within 48 h from onset of symptoms were entered into this single-blind randomized study; at the time of study entry, 8 patients were in Killip class I, and 2 patients in Killip class II. All drugs with haemodynamic effects were withdrawn 12 h before the study started. Both the haemodynamic profile and the clinical status were stable in all patients. Haemodynamic parameters were recorded with a Swan-Ganz thermodilution catheter, cardiac output was measured by the thermodilution method, and the left ventricular ejection time was calculated according to the Weissler method. The echo left ventricular end-diastolic diameter was measured by evaluation of the M-mode echocardiographic recording.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1986

Long-term prognostic significance and electrophysiological evolution of intraventricular conduction disturbances complicating acute myocardial infarction.

Fifty-nine patients with post-infarctional, isolated intraventricular conduction disturbances (IVCD) who survived the acute stage of myocardial infarction were followed up after hospital discharge for a mean period of 11.4 +/- 4.8 months. Fourteen patients (24%) had HV interval prolongation (greater than 55 ms) during AMI (group A), and 45 patients had normal HV intervals (76%, group B). His bundle recordings were repeated during follow-up in 48 survivors after a mean period of 7.2 +/- 0.7 months. Infranodal conduction delay in the acute stage of infarction was correlated with a higher incidence of heart failure during AMI (78% of patients in group A vs 22% in group B, p less than 0.001), and with higher rate of cardiac mortality during follow-up (50% in group A vs 13% in group B, p less than 0.01). Survivors of group A showed a higher functional NYHA class, a higher incidence of CHF, and a higher prevalence of complex ventricular arrhythmias at Holter monitoring. No statistically significant difference in late sudden death was evident between the two groups of patients, and the global incidence of late AV block was 2%. At repeat His bundle recording no significant change (greater than 5 ms) in HV interval could be demonstrated in comparison to the acute phase recording, neither in patients with prolonged nor in patients with normal HV time. We conclude that HV prolongation in patients with isolated, post-infarctional IVCD is correlated with a worse prognosis, both during acute infarction and during the follow-up period, which presumably reflects wider anatomic damage in comparison to patients with normal HV time. The low incidence of late AV block and the electrophysiological demonstration of the stability of infranodal conduction several months after AMI indicate that these patients do not require permanent prophylactic pacing after acute myocardial infarction.

Adult↗
PubMed1986

[Use of amrinone in refractory cardiac insufficiency: clinical and hemodynamic evaluation].

UNLABELLED: Amrinone is a nonadrenergic, nonglycosidic agent with combined positive inotropic and vasodilator properties. To determine its clinical and hemodynamic effects we treated 14 patients (12 men and 2 women ranging in age from 36 to 78 years, mean 56) with severe chronic heart failure (New York Heart Association functional class IIIa or IVa) not controlled by conventional therapy. Drug administration: 1 mg/Kg intravenous bolus followed by infusion of 10 mcg/Kg/min over 24 hours; in 11 patients, upon termination of long term infusion, oral therapy was begun (100 mg tid) for a period of four weeks. After bolus and during infusion dyspnea, pulmonary and jugular vein congestion, hepatomegaly rapidly improved, and increase of diuresis was noted. All patients responded with a substantial reduction in central venous pressure (CVP 9.64 +/- 5.96----4.79 +/- 5.66 mmHg, P less than 0.01), wedge pressure (WP 26.3 +/- 4.6----19.00 +/- 4.66 mmHg, P less than 0.01), pulmonary and systemic vascular resistances (PVR 212.07 +/- 121.08----127.64 +/- 50.37 dyne. sec. cm-5; SVR 1687 +/- 301----1297 +/- 357 dyne. sec. cm-5; P less than 0.01); these changes were accompanied by an increase of cardiac index (CI 1.96 +/- 0.38----2.84 +/- 0.83 L/Min/m2; P less than 0.01), stroke index (SI 23.43 +/- 5.85----31.64 +/- 8.86; P less than 0.01) and left ventricular stroke index (LVSWI 22.36 +/- 8.45----34.50 +/- 12.29 g.m/b/m2; P less than 0.01). These positive clinical and hemodynamic effects were not maintained in long term therapy. Moreover we observed adverse effects: fever, nausea and vomiting, thrombocytopenia, liver enzyme elevation, tachycardia and ventricular arrhythmias. CONCLUSIONS: good efficacy and tolerability during short term intravenous therapy in emergency conditions; no clinical improvement and sometimes adverse effects in oral long term therapy.

Administration, Oral↗
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↗
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↗
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↗
PubMed1977

Circulatory reflexes from carotid and extracarotid baroreceptor areas in man.

The carotid sinus baroreceptor reflex was studied in 11 normotensive subjects, using a variable pressure neck chamber and correcting for imperfect pressure transmission to the carotid sinus. Decreased carotid baroreceptor stimulation caused a sustaineded rise in arterial pressure, and increased carotid baroreceptor stimulation caused a sustain fall. The responses were in linear relation to the stimulus, and, after reaching the steady state, greater for the reduced than for the increased baroreceptor stimulation. Thus the carotid sinus baroreceptor reflex of the normotensive man is an effective antihypotensive and antihypertensive feedback system, though the former function may have more sensitivity. The increased and decreased baroreceptor stimulation by the neck chamber also caused bradycardia and tachycardia which were modest in magnitude and often transient. In eight subjects the reflex changes in heart rate induced by the neck chamber were compared with those induced by altering transmural pressure not merely at the carotid sinus but throughout the arterial tree (injection of phenylephrine and trinitroglycerin). The slopes of these relations were 3 times as great in the latter circumstance. Thus the carotid baroreceptors play a lesser role in heart rate control than do extracarotid baroreceptors.

Adult↗
PubMed1976

Carotid baroreceptor reflex in normotensive and hypertensive subjects.

1. A graded decrease and increase in carotid baroreceptor activity (induced by a varying pressure in a neck chamber) caused a linearly related increase and decrease in arterial blood pressure. This occurred in both normotensive and hypertensive subjects. 2. Decrease of carotid baroreceptor activity caused a greater increase of blood pressure in normotensive than in hypertensive subjects. Increasing the activity caused changes of similar magnitude in the two groups. 3. Decrease of baroreceptor activity also caused an increase in heart rate although increasing the activity of the reflex had little effect on heart rate, particularly in normotensive subjects. Thus the carotid baroreceptor effect on blood pressure does not always reflect that on heart rate and inference of one reflex response from measurement of the other may be in error.

Blood Pressure↗