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Biomedical subjects

M Tubaro

Publications and source records attributed to M Tubaro.

At least 37 records · Page 2Linked to original sources
PubMed1993

Dipyridamole echocardiography evaluation of acute inferior myocardial infarction with concomitant anterior ST segment depression.

The significance of anterior ST segment depression in inferior acute myocardial infarction (AMI) remains controversial. The aim of this study was to relate precordial ST segment depression to the topography of residual myocardial ischaemia, with myocardial mapping of the asynergic area and coronary anatomy. Twenty-five patients with first inferior AMI (15 patients with anterior ST segment depression: group A and 10 patients without anterior ST segment shift: group B), all underwent: (1) electrocardiographic evaluation on admission to the Coronary Care Unit and at 24 h intervals thereafter; (2) 2D-echocardiographic study within 3 h of CCU admission; (3) dipyridamole echocardiographic test (DET) (doses of dipyridamole up to 0.84 mg.kg-1 i.v. over 10 min) 4 days after AMI; (4) coronary arteriography within 14 days from AMI. To assess regional left ventricular wall motion, a 16 segment model was used and a wall motion score index (WMSI) was derived. The results of DET were correlated to the anatomy of the infarct-related vessel. Compared to group B, group A patients showed a significantly greater maximal ST segment elevation in inferior limb leads (lead III: 3.9 +/- 1.9 mm vs 2.2 +/- 1.1 mm, P < 0.05; aVF: 3.5 +/- 1.3 mm vs 1.7 +/- 0.8 mm, P < 0.001). Group A patients showed greater WMSI (1.35 +/- 0.22 vs 1.17 +/- 0.12, P < 0.05), with more frequent postero-lateral wall involvement (72% vs 20%, P < 0.05). No patient of either group showed asynergy of the anterior, anterolateral or anteroseptal segments. No differences in the distribution of coronary artery disease were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[The usefulness of the echo-dipyridamole test in the early period after an uncomplicated acute myocardial infarct].

OBJECTIVES: The aim of this study was to examine the ability of Dipyridamole Echocardiography Test (DET)--performed early after an acute myocardial infarction (AMI)--to assess: a) the presence of induced ischemia and its relation with coronary artery stenoses; b) the presence of myocardial viability and the comparison with late wall motion; c) the appearance of cardiac events during hospitalization and in the following period. METHODS: Ninety-five patients with AMI, subjected to thrombolytic therapy and without complications, underwent a DET on the 4th-5th day. All had a coronary angiography on the 8th-10th day; stenoses were deemed significative when > or = 70%. DET was carried out after drug discontinuance and following standard protocol; parietal kinesis was analyzed according to a 14 segment model. The myocardium was deemed viable when an improvement of a basal dyskinesis was noted; ischemia was considered when a new asynergy appeared or a basal dyskinesis worsened or enlarged; a wall motion score index (WMSI) was calculated. All 95 pts. had a clinical follow-up at 12 +/- 6 months (3-18); 62 pts. had a late echocardiographic examination at 6 +/- 3 months (3-15). RESULTS: Induced ischemia appeared in 59/95 pts. (62%): in 6/14 pts. (42%) without significative stenoses, in 29/49 pts. (59%) with a single vessel disease, and in 24/32 pts. (75%) with multivessel disease. In identifying multivessel disease, DET sensibility (SE) was 75% and specificity (SP) was 95-97%. In single or no vessel disease WMSI changed from 1.42 to 1.49 (p < 0.0001); in multivessel disease WMSI changed from 1.52 to 1.69 (p < 0.0001). As regards the assessment of diseased vessel(s), DET showed little accuracy when dyskinesis appeared in the basal segments of the inferior and lateral wall or in the mid-apical segments of the anterior and lateral wall; DET properly identified the culprit vessel when dyskinesis appeared in the remaining segments. Myocardial viability was noted in 26% of dyskinetic segments. In single or no vessel disease WMSI changed from 1.41 (basal--> B) to 1.35 (viability phase--> V) and was found 1.31 at the late echocardiography (L): p < 0.0001 between B and V, and between B and L. In multivessel disease WMSI changed from 1.5 (B) to 1.47 (V) and to 1.5 (L): p < 0.05 between B and V, NS between B and L. In comparison with late echocardiography, DET SE was 70%, SP 99%, positive predictive value (PPV) 97%, negative predictive value (NPV) 86%. As regards the prognostic value about cardiac events, DET SE was 80% and NPV was 78%; about only major cardiac events, the respective values are 91% and 97%. CONCLUSIONS: DET performed early after an AMI allows a better prognostic assessment, as it provides information about: a) the place and the severity of coronary artery stenoses; b) the presence and the extension of induced ischemia and of myocardial viability; c) the risk of subsequent cardiac events.

Adult↗
PubMed1992

Demonstration of the formation of hydroxyl radicals in acute myocardial infarction in man using salicylate as probe.

Dihydroxybenzoic acid (DHBA) derivatives of acetylsalicylic acid (ASA) are formed in vivo by the action of the hydroxyl radical (OH.). In order to evaluate the possible formation of OH(.) in acute myocardial infarction (AMI) in man, 9 consecutive patients with a first episode of AMI (8 males, 1 female, mean age 50.3 years), treated with rt-PA, and 8 healthy volunteers (7 males, 1 female, mean age 29.8 years) were studied. All subjects received 100 mg ASA p.o. daily; venous blood samples were taken 30 min after the first dose (time 0) and then at 3-, 6-, 12-, 24- and 48 h and 5 days. Serum was analyzed by HPLC and electrochemical detection for 2,3- and 2,5-DHBA contents. 2,3-DHBA was present in all subjects with AMI and undetectable in healthy volunteers at all time points studied. Serum levels of 2,5-DHBA did not show statistically significant differences between AMI patients and healthy volunteers. These data support the hypothesis that hydroxyl radicals are formed during AMI in man.

Aspirin↗
PubMed1992

Diastolic ventricular dysfunction in noncomplicated acute myocardial infarction: the influence of gallopamil.

The goal of this study was to assess the effect of gallopamil on left ventricular (LV) diastolic function early after acute myocardial infarction (AMI). Gallopamil was compared with placebo and atenolol in two different groups of patients. Study patients, 2 days after experiencing their first AMI, in Killip class I and stable sinus rhythm, were randomized in a crossover, double-blind sequence to receive (a) gallopamil (50 micrograms/kg over 5 min) or placebo (i.v. 10-ml bolus, with a time interval of 90 min); and (b) gallopamil (50 micrograms/kg over 5 min) or atenolol (5 mg over 5 min), with a time interval of 24 h. Group I and group II consisted of 28 patients (26 men and 2 women; mean age 55 +/- 9 years) and of 14 patients (13 men and 1 woman; mean age 56 +/- 10 years), respectively. All the patients were treated with thrombolysis within 6 h from the onset of symptoms. Doppler echocardiographic examinations were performed as follows: at baseline (B) and 15 min after administration of gallopamil bolus and placebo bolus, in group I; at baseline before gallopamil (BG) and atenolol (BA), and 15 min after each bolus in group II. The following echo-Doppler parameters were calculated, at each examination: the early and late transmitral peak velocity ratio (E/A), the early and late velocity integral ratio (Ei/Ai), the peak filling rate normalized to mitral stroke volume (nMPFR), and the LV isovolumic relaxation time (IVRT), which was normalized to an 800-ms R-R cycle length in the patients in group II. Mean blood pressure (MBP) and heart rate (HR) were also measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[The incidence and clinical implications of left ventricular thrombosis in 769 patients with acute myocardial infarct treated with antithrombotics and fibrinolytics].

Seven hundred sixty-nine patients (pts) admitted to the Coronary Care Unit (CCU) between January 1987 and January 1990 suffering from first acute myocardial infarction (AMI) were studied. The presence of left ventricular thrombosis (LVT) was evaluated by two-dimensional echocardiography (2D-echo). The relation of LVT to site, size and intra-CCU clinical outcome of AMI, in terms of systemic embolic events, Killip class and mortality, was also assessed. AMI was transmural in 707 pts (92%), anterior in 446 pts (58%) and inferior in 261 pts (34%), non-Q in 62 pts (8%). Two hundred sixty-one pts (34%) were treated with IV thrombolytic therapy followed by IV heparin 1000 IU/h over 12 hrs and then calcium heparin (CH) 12500 IU s.c. bid; 508 pts (66%) were given only antithrombotic therapy (CH 12500 IU s.c. bid). 2D-Echo was performed within 48 hours and on day 5-7 from the onset of AMI. In 41 pts (5.3%) LVT was observed: 39 had anterior AMI (8.7% of all anterior AMI pts), one had inferior AMI (0.4% of all inferior AMI pts), and one had non-Q AMI (1.6% of all non-Q AMI pts) [p less than 0.001 for anterior AMI vs inferior and non-Q AMI]. Pts with LVT had a greater infarct size (number of akinetic plus dyskinetic segments/total number of segments x 100) compared to pts without LVT (32.3 +/- 12.6% vs 16.4 +/- 5.7%, p less than 0.001). In pts treated with thrombolytic therapy, LVT incidence was not significantly different from that of pts treated with antithrombotic therapy (4.2% vs 5.9%) alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Chi-Square Distribution↗
PubMed1991

[Pharmacological effects on left diastolic ventricular function in acute myocardial infarct: comparison of gallopamil and atenolol].

The aim of the study was to assess the effects of gallopamil and atenolol administration on left ventricular (LV) relaxation and filling in patients (pts) with acute myocardial infarction (AMI), by pulsed Doppler echocardiography (PDE). Two days after first AMI, 14 pts aged 56 +/- 10 years in Killip class I and treated with thrombolysis were randomized to gallopamil (50 mcg/Kg over 5 min) or atenolol (5 mg over 5 min) IV 10 ml bolus, with a 24 hour time interval, in a cross-over double blind sequence. Four PDE were performed in each patient: at baseline, before gallopamil and atenolol IV bolus, and a 15 min after each bolus. The following Doppler parameters were calculated: early (E) and late (A) peak filling velocities and their ratios (E/A), early (Ei), late (Ai) and total (TVi) diastolic filling time velocity integrals; the ratio between Ei and Ai (Ei/Ai), the peak filling rate normalized to mitral stroke volume (calculated as E/TVi [nPRP]), the percentage of atrial contribution to total diastolic filling (%AC), and the isovolumic relaxation time (nTRIV) normalized to an 800msec RR cycle length. Compared to baseline PDE evaluation, gallopamil administration significantly shortened nTRIV (89 +/- 13 vs 116 +/- 13 msec), improved early LV filling parameters (E: 74.5 +/- 14.0 vs 58.1 +/- 14.6 cm/sec; E/A 1.2 +/- 0.4 vs 0.9 +/- 0.3; Ei: 11.2 +/- 1.8 vs 8.9 +/- 2.0 cm; Ei/Ai: 1.8 +/- 0.6 vs 1.3 +/- 0.6; nPRP: 3.9 +/- 1.0 vs 3.5 +/- 1.0 SV/sec), and reduced %AC (35.6 +/- 8.8 vs 44.6 +/- 10.6). A and Ai were not significantly changed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Endocavitary transcatheter electric fulguration as a therapeutic alternative in refractory ventricular tachycardia].

Three patients affected by dilated cardiomyopathy complicated by refractory ventricular tachycardia, with a high risk of sudden cardiac death, underwent transcatheter electric fulguration. The technique was applied transeptally, using the terminals of two catheter electrodes as cathode and anode. These were placed at the right and left ventricular apex, at septal level where the "critical" arrhythmia point had been identified by endocardial mapping. All patients had previously experienced more than one episode of cardiac arrest and had successfully taken several antiarrhythmic drugs. All patients presented variable morphology of ventricular tachycardia (whether spontaneous or induced). In all of them clinical tachycardia was considered as having a left bundle branch block morphology with an earlier activation at low septal level. After treatment, antiarrhythmic therapy (amiodarone 200 mg/day) was continued for all patients, although at a lower dose than before fulguration. One patient has been free from sustained ventricular tachycardia for more than two years after fulguration. In the other patients we observed an early and late arrhythmic recurrence (respectively within 1 and 8 months following fulguration) in spite of antiarrhythmic therapy. The second patient presented no further recurrence after permanent pacemaker implantation. The third patient showed an arrhythmic recurrence, with a different morphology from the previous one, concomitantly with a septic process. This technique does not appear dangerous and may be used, in highly specialized centres, on carefully selected patients as a therapeutic approach after pharmacological therapy and before automatic defibrillator implantation or surgical antiarrhythmic intervention.

Adult↗
PubMed1989

[Kinetics of intravenously administered flecainide in patients with acute myocardial infarct].

Flecainide (F) is a new antiarrhythmic agent recently introduced into clinical practice. The above study was aimed at evaluating its intravenous (iv) pharmacokinetics in patients (pts) with acute myocardial infarction (AMI) on 1st and 2nd day, complicated by complex ventricular premature beats (VPBs). 2 mg/kg F was given iv as bolus injection, followed by 300 mg/24 hrs iv infusion. Plasma F values were evaluated by HPLC. Plasma F levels increased progressively, in a non uniform but predictable manner: in pts with large AMI and cardiac failure, F plasma levels, although remaining within the therapeutic range, were greatly increased after the 2nd hour (P less than 0.05) in comparison with pts without cardiac insufficiency. Negative side effects, both cardiac and extracardiac, were not observed: F appeared a handy and effective agent in post-AMI arrhythmias, especially when plasma drug levels are controlled; plasma F level monitoring is anyway recommended in pts with cardiac failure, owing to the wide interindividual variations.

Adult↗
PubMed1989

Use of defibrotide in the treatment of acute myocardial infarction.

The results of this preliminary clinical trial confirm the thrombolytic effect of defibrotide demonstrated in preclinical models; demonstrate the positive influence of the product on the natural history of early AMI; suggest that the optimal dosage range should include not less than 1.6 gm of defibrotide during the first hour of treatment; and justify further commitment in the study of defibrotide also beyond the scope of treating AMI.

Dose-Response Relationship, Drug↗