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Biomedical subjects

B Magnani

Publications and source records attributed to B Magnani.

At least 145 records · Page 8Linked to original sources
PubMed1990

[Lipoprotein (a) [Lp(a)] and ischemic cardiopathy: correlation between radial immunodiffusion (RID) and radioimmunoassay methods (RIA)].

The anomalous lipemic values are considered as a risk factor in coronarial pathology. We are separately studying different lipemic factors, Lp(a) in the present paper. May be our 38 clinical cases are still a too small number to demonstrate any correlation between Lp(a) haematic content and arterial pathology, and we will continue this study in the evolution of the pathology, eventually until the infarctus. For the moment, we established the significance of correlation between two methods in two laboratories of ours (in Pavia, Italy, and in Lisboa, Portugal). Correlation is more than 0.9. Assays were done on the same air mailed samples.

Coronary Disease↗
PubMed1990

[Determination of oxidative phenotype in a sample population and correlation with the pharmacokinetics of propafenone].

UNLABELLED: Propafenone, like other cardioactive drugs (metoprolol, propranolol, encainide) is submitted to oxidative metabolism, evaluable by assessment of debrisoquine oxidative capacity. Two phenotypes have been described: extensive and poor oxidizers, with interethnic differences in the prevalence of poor oxidizers. Aims of this study were: 1) to assess the oxidative phenotype in a sample of the Italian population and 2) to evaluate the relationships between oxidative capacity and propafenone pharmacokinetics or pharmacodynamics. The ratio between debrisoquine (D) and 4-hydroxy-debrisoquine (4-OH-D) in the urines after D administration (10 mg) was employed to characterize oxidative phenotype in 90 subjects (42 arrhythmia patients and 48 healthy volunteers). In 10 patients, extensive oxidizers of debrisoquine, we studied propafenone (P) and 5-hydroxy-propafenone (5-OH-P) kinetics after acute oral administration (450 mg) and chronic oral treatment (300 mg tid for 2 weeks), followed by wash out. RESULTS: 1) the prevalence of poor oxidizers (D/4-OH-D ratio greater than 12.6) in our population resulted to be 6.6%, like in other studies in Caucasians; 2) propafenone kinetics was strictly related to oxidative capacity since D/4-OH-D ratio strictly correlated with the ratio of P and 5-OH-P areas under curve in acute (r = 0.91) and in chronic administration (r = 0.90) and with P half-life in acute (r = 0.82) and in chronic administration (r = 0.82); 3) QRS widening both during chronic treatment and after acute administration correlated with oxidative capacity (r = -0.78 and -0.68 with D/4-OH-D ratio respectively) and with 5-OH-P areas under curve (r = 0.84 and 0.70 respectively); it did not correlate with P areas under curve. In conclusion both kinetics and electrophysiological effects of propafenone strictly correlate with oxidative capacity, even in extensive oxidizers. Thus even a small reduction in oxidative capacity may have relevant consequences during propafenone oral treatment.

Adult↗
PubMed1990

[Hyperkinetic ventricular arrhythmia during the treadmill test in chronic ischemic heart disease].

Aim of this study was to evaluate the pattern of onset and the characteristics of ventricular arrhythmias (VA) observed during treadmill test (TT) in patients with chronic ischemic heart disease (CIHD). Two groups of patients with CIHD were retrospectively compared: group A consisted of 120 consecutive patients with premature ventricular beats (PVBs) either isolated (greater than 2/min) or repetitive during exercise, or maximal exercise, or recovery; group B consisted of 140 consecutive patients without PVBs during TT. The two groups were comparable in mean age, male/female ratio, incidence of previous myocardial infarction, of previous coronary artery by-pass graft or of percutaneous transluminal coronary angioplasty. There were no significant differences between the two groups regarding the parameters evaluated during TT: duration of exercise, maximal heart rate, heart rate-systolic blood pressure product as well as in the percentage of positive tests for acute myocardial ischemia (51.6% vs 40.7%). In the two subgroups of patients who underwent coronary arteriography and left ventricular angiography (24/120 and 23/140 patients respectively) no differences were found in the number and distribution of critical coronary stenosis and of dyskinetic or akinetic areas. In both groups A and B the QTc interval at maximal exercise was significantly longer than its value at rest (p less than 0.001), but there was no relevant difference between the two groups. In group A patients with VA during maximal exercise (n = 60) showed a higher prevalence of complex VA (class Lown greater than or equal to 3) compared to the others (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

[Pseudoischemic T waves: a possible electrophysiologic mechanism].

An electrophysiologic study has been performed in 7 patients with giant stable inversion of the T waves in the precordial ECG leads and without any organic heart disease. The study was particularly directed to evaluate the specific properties of the conductive system. The main results of the study point out the presence of absolute (prolonged HV interval, delay of ventricular activation time) or relative (RRP of the left bundle branch greater than RRP of the right one) conduction delays already in basic conditions or occurring after ajmaline (1 mg/Kg iv). Moreover, repolarization normalized during repetitive high rate atrial extrastimuli in the beats where ventricular activation time shortened and not during regular pacing. On the other hand, repolarization worsened whenever an impairment of infra or intrahisian conduction occurred. During His bundle pacing an inversion of the T waves preceded a left bundle branch conduction delay. The present data make us to hypothesize that, in these patients with pseudoischemia, a delay of activation of the initial vectors of the QRS in the left side, by amplifying the electrical gradient between the 2 ventricles, can be the underlying mechanism causing the repolarization abnormalities.

Adult↗
PubMed1990

[Post-infarction rupture of the interventricular septum. Evaluation of the main clinical parameters and postoperative survival].

We reviewed 16 patients with ventricular septal rupture complicating myocardial infarction who underwent surgical repair between January 1984 and August 1987. Nine of them had anterior acute myocardial infarction (56%) and 7 inferior acute myocardial infarction (44%). The overall surgical mortality was 43.8%; in the group of patients with early treatment (less than 15 days after acute myocardial infarction) the mortality was 55%, while in the group with later treatment (16-30 days) the mortality was 28% (p-NS). Survival was unrelated to preoperative evidence of shock, magnitude of the shunt or the extent of coronary artery disease. We found a better in-hospital survival in the group of patients with ventricular septal rupture complicating anterior acute myocardial infarction (77%) vs inferior acute myocardial infarction (28%) with statistical significance (p less than 0.05). After a follow-up ranging from 1 to 40 months (mean: 17 months), 78% of the in-hospital survivors were alive and they were all in NYHA class II-III. We conclude that the major determinant of in-hospital survival in our patients was the anatomical site of acute myocardial infarction. Furthermore, we believe that the surgical repair of the ventricular septal defect is helpful in modifying the negative outcome of such an acute myocardial infarction complication.

Aged↗
PubMed1989

Clinical and hemodynamic effects of long-term administration of gallopamil in patients with coronary artery disease and normal or impaired left ventricular function.

The hemodynamic and clinical profiles of gallopamil, a new calcium antagonist, were evaluated in 20 patients with severe coronary artery disease in a placebo-controlled, single-blind study. The patients were divided into 2 groups depending on baseline ejection fraction (greater than 45 or less than or equal to 45%) and underwent nuclear ventriculography, both at rest and during bicycle exercise under electrocardiographic monitoring, after 3 weeks of therapy (50 mg 3 times daily) and the 1-week run in and washout placebo periods. The mean anginal weekly frequency per patient was significantly reduced, from 3.4 to 0.5 (p less than 0.001). The left ventricular ejection fraction, cardiac volumes, ejection and filling indexes at rest and for the same workload were not altered in the population as a whole or in each of the 2 groups. The rate pressure product during exercise was reduced for the same workload from 18.0 +/- 5.0 X 10(3) to 16.8 +/- 4.7 X 10(3), while the regional ejection fraction in ischemic regions was not significantly changed. Individual variations of ventriculographic parameters in both groups were not related to basal values. Gallopamil increased the total duration of exercise from 432 +/- 201 to 537 +/- 188 s (p less than 0.001). Six patients did not complain of angina and their exercise was interrupted because of muscular weakness. The hemodynamic and clinical responses did not differ when the results in the population as a whole and in each of the 2 groups were compared. Gallopamil was effective and well tolerated, even in patients with very depressed cardiac function.

Aged↗
PubMed1989

Tocainide and metoprolol: an efficacious therapeutic combination in the treatment of premature ventricular beats.

A double-blind crossover study was performed in 20 patients to verify the efficacy of tocainide plus metoprolol in patients with premature ventricular contractions (PVCs) class Lown greater than or equal to 2 (mean frequency greater than or equal to 30/h) judged as being "stable" by at least three basal 24-h Holter ECGs with PVC variation of less than +/- 25%. All 20 patients were submitted to a placebo period; and all were subsequently randomized to therapy with tocainide 1800 mg/day or metoprolol 200 mg/day for 15 days and then to tocainide 1800 mg + metoprolol 200 mg/day or tocainide 1200 mg + metoprolol 200 mg/day for 15 days, followed by a crossover of the two combination treatments. At steady state in every stage we controlled for plasma levels of the drugs, a 24-h Holter recording, and a 12-lead ECG. A modified Lown score was evaluated together with the Lown class. Tocainide (mean plasma level 3.3 +/- 0.7 micrograms/ml) was efficacious in 3 of 8 patients, the modified Lown score decreased from 63 +/- 32 (placebo period) to 42 +/- 27 (p less than 0.01) and Lown 4B arrhythmias were abolished in 3 of 4 patients. Metoprolol (mean plasma level 97.4 +/- 89.6 ng/ml) was efficacious in 2 of 10 patients; the modified Lown score and Lown classes did not change significantly. Administration of tocainide 1200 mg + metoprolol 200 mg obtained a positive response in 9 of 12 patients, the modified Lown score decreased significantly compared with placebo (from 53 +/- 31 to 32 +/- 30, p less than 0.01) and Lown 4B arrhythmias were abolished in 2 of 5 cases. Tocainide 1800 mg plus metoprolol 200 mg was scarcely tolerated owing to neurologic and gastroenteric side effects, and only three patients completed this stage with no better antiarrhythmic results compared to the lower dose. In conclusion, the combination of tocainide at 1200 mg and metoprolol 200 mg is well tolerated, efficacious in a high percentage of patients, and superior to single drug therapy in patients with stable PVCs.

Administration, Oral↗
PubMed1989

Peripheral hemodynamic and humoral effects of oral zofenopril calcium (SQ. 26,991) in patients with congestive heart failure.

In 14 patients with congestive heart failure (CHF) of various grade (NYHA class 2-4) the effects of zofenopril calcium (SQ 26,991) on blood pressure and forearm circulation were studied by venous occlusion plethysmography. Changes in plasma renin activity (PRA), aldosterone, Atrial natriuretic factor (ANF) and arginine-vasopressin (AVP) were also measured. Two hours after oral administration of 7.5 mg of zofenopril we observed a decrease in blood pressure, heart rate, and forearm vascular resistance along with an increase in venous distensibility. Zofenopril also decreased ANP levels in a manner directly related to peripheral venodilatation (r = .64; P less than .05) and modified arginine-vasopressin (AVP) proportionally to the fall in blood pressure observed in response to drug administration (%SBP/%AVP: r = .64, P less than .05; %DBP/%AVP: r = .67, P less than .05). Hemodynamic and humoral responses to zofenopril occurred without any significant unwanted adverse reaction, even in patients with greater pressor reduction. We conclude that oral acute zofenopril administration, in patients with congestive heart failure, causes an arterial and venous forearm vasodilatation which is probably involved in the acute changes in plasma levels of ANF and AVP observed after drug administration.

Administration, Oral↗
PubMed1989

Felodipine in severe chronic congestive heart failure: acute effects on central hemodynamics and regional blood flow distribution.

In order to assess the effect of felodipine, a new calcium antagonist with vascular selectivity, on regional blood flow distribution at rest in chronic congestive heart failure, ten patients were studied during an acute test. Right heart catheterization allowed the evaluation of hemodynamic parameters; renal blood flow was calculated using paraamino-hippuric acid clearance; hepatic blood flow measurement was based on indocyanine green clearance; and limb blood flow was assessed with venous occlusion plethysmography. Blood samples were collected for the analysis of plasma catecholamines, renin, and aldosterone. All parameters were recorded in duplicate under basal conditions and after felodipine infusion. The infusion of felodipine induced a significant increase in cardiac index, stroke work index, and limb blood flow. Systemic and pulmonary arterial blood pressure, pulmonary wedge pressure, and systemic resistance underwent a significant decrease. The heart rate, pulmonary resistance, renal blood flow, and hepatic blood flow were not changed. In conclusion, felodipine was of benefit in congestive heart failure at rest in an acute test, acting through a marked decrease in vascular resistance and a consequent improvement in cardiac output and limb blood flow. No changes in renal and hepatic blood flow were observed.

Adult↗
PubMed1989

Myocardial, coronary, and peripheral effects of xamoterol (ICI 118,587) in open-chest pigs.

The hemodynamic and coronary effects of increasing doses of xamoterol, a beta-adrenoceptor partial agonist, were assessed in an anesthetized pig preparation in which cardiovascular reflexes were abolished and sympathetic tone was modified by infusion of noradrenaline (NA). Xamoterol, in basal conditions, increased heart rate (HR) from 104 +/- 12 to 120 +/- 13 beats/min (p less than .001); systolic, diastolic, and mean blood pressure, respectively, from 77 +/- 8 to 103 +/- 17 mmHg (p less than .01), from 48 +/- 7 to 70 +/- 12 mmHg (p less than .01), and from 58 +/- 7 to 84 +/- 14 mmHg (p less than .01); left ventricular dP/dT max from 2098 +/- 564 to 4205 +/- 937 mmHg/sec (p less than .001); and systemic vascular resistance (SVR) from 1745 +/- 564 to 2270 +/- 739 dynes sec cm-5 (p less than .01). The increase in HR and dP/dT max brought about by xamoterol was about 37% and 56%, respectively, of the maximum increase produced by NA. At the highest level of sympathetic tone, xamoterol reduced HR from 148 +/- 11 to 122 +/- 11 beats/min (p less than .001) and no significant change was observed in dP/dT max. The increase in blood pressure and SVR induced by xamoterol was maintained at each level of sympathetic tone. On the contrary, SVR did not change after NA, as expected, since receptors were fully blocked. For a given inotropic effect, xamoterol and NA produced a similar increase in coronary blood flow and myocardial O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1989

Intravenous diltiazem in patients with paroxysmal re-entrant supraventricular tachycardia.

The electrophysiologic effects and efficacy of diltiazem were evaluated with programmed electrical stimulation of the heart in 12 patients with supraventricular re-entrant tachycardia (five with atrioventricular nodal tachycardia and seven with circus movement tachycardia the accessory pathway being concealed in 4). Diltiazem was infused over 1 minute at the dose of 0.25 mg/kg and the electrophysiologic parameters were evaluated at 5 and 30 minutes. Diltiazem prolonged the AH interval from 83.5 +/- 58 to 99 +/- 55 msec (P less than 0.05), effective and functional refractory periods of atrioventricular node from 244 +/- 40 to 268 +/- 56 msec (P less than 0.05) and from 432 +/- 124 to 468 +/- 130 msec (P less than 0.005) respectively, lowered the atrial pacing rate inducing second-degree atrioventricular block from 159 +/- 32 to 134 +/- 33 beats/min (P less than 0.005) and decreased systolic and diastolic blood pressure from 143.5 +/- 33 to 132.5 +/- 22 mm Hg (P less than 0.05) and from 90 +/- 15 to 82.5 +/- 9 (P less than 0.05), respectively. Diltiazem prevented the reinduction of the tachycardia in 4 of 5 patients with atrioventricular nodal tachycardia and in 4 of 7 with circus movement tachycardia. The mechanism of action of diltiazem consisted of depression of conduction in atrioventricular node in anterograde fashion while there were no effects on refractoriness of the accessory pathway. The drug was well tolerated with no adverse effects. Diltiazem, therefore, appears an effective and safe drug in the acute treatment of re-entrant supraventricular tachycardia.

Adolescent↗
PubMed1989

Radionuclide evaluation of ventricular function at rest and during exercise in double inlet ventricle.

We studied ventricular volumes and ejection fraction by radionuclide angiography (equilibrium technique) in 15 patients (aged 3-48 years) with double inlet ventricle not yet submitted to corrective surgery. The end-diastolic volume (measured in nine cases) ranged from 108 to 219 ml/m2 (156 +/- 32), being lower than the normal theoretical value (right plus left ventricle) in six cases. Ejection fraction ranged from 30 to 77% (56.4 +/- 13). The value was significantly higher in the subgroup of 10 patients with a dominant left ventricle as compared to the five cases with dominant right or indeterminate ventricular morphology (63.2 +/- 8.3 versus 42.8 +/- 9, P less than 0.01). In seven of the 15 patients, measurements were obtained both at rest and during dynamic exercise in the semi-upright position. The end-diastolic and end-systolic volumes, stroke volume, ejection fraction underwent a slight non-significant reduction (from 158 +/- 29 to 147 +/- 24 ml/m2, from 58 +/- 16 to 56 +/- 24 ml/m2, from 100 +/- 27 to 90 +/- 24 ml/m2, from 64% +/- 9 to 61% +/- 13). During exercise, ventricular volumes mostly behaved as follows: slight reduction of end-systolic volume, decrease of end-diastolic volume, no increase (no change or decrease) of ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Plasminogen Activator Italian Multicenter Study (PAIMS): comparison of intravenous recombinant single-chain human tissue-type plasminogen activator (rt-PA) with intravenous streptokinase in acute myocardial infarction.

A single chain preparation of recombinant tissue-type plasminogen activator (rt-PA) was compared with intravenous streptokinase to determine coronary thrombolytic efficacy in patients with acute myocardial infarction less than 3 h old. Eighty-six patients were randomly selected to receive the intravenous cumulative dose of 100 mg rt-PA and 85 patients to receive 1.5 million units streptokinase. At 240 min after initiation of the thrombolytic therapy noninvasive signs of sustained reperfusion occurred in 79% of patients in both groups (p = NS). Patency of the infarct-related vessel at follow-up angiography was observed in 81% of patients in the rt-PA group and 74% of patients in the streptokinase group (p = NS). At hospital discharge, compared with admission, echocardiographically determined left ventricular ejection fraction increased from 52 +/- 11% to 56 +/- 10% (p less than 0.01) in the rt-PA group; changes in the streptokinase group (50 +/- 9% to 51 +/- 11%) were not significant. A nadir value of less than 1 g/liter fibrinogen plasma level occurred in 6 patients (7%) receiving rt-PA versus 74 patients (87%) receiving streptokinase (p less than 0.0001). Plasma levels of fibrin(ogen) degradation products were more than doubled in the streptokinase group (p less than 0.01). One patient in the streptokinase group developed a fatal intracranial hemorrhage; five others showed a decline in hemoglobin greater than or equal to 5 g/dl. Other clinical events in the streptokinase-treated group included allergic reactions (four patients) and intrahospital reinfarction (two patients). None of these events occurred in the rt-PA group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Cardiac neurosis and psychopathology.

Psychiatric illness according to DSM-III-R criteria was investigated in 54 consecutive patients suffering from cardiac neurosis (neurocirculatory asthenia or Da Costa's syndrome). Thirty-seven of the 54 patients (68.5%) were found to suffer from a psychiatric disorder. Generalized anxiety disorder, social phobia and panic disorder accounted for most of the diagnoses. Panic disorder was frequently preceded by (and associated with) generalized anxiety, phobic avoidance and hypochondriasis. The results should alert the physician to inquire for symptoms of an anxiety disorder when a patient presents with cardiac neurosis.

Adult↗
PubMed1989

The role of infarct size in early and late mortality.

To evaluate the impact of infarct size on morbidity and mortality, blood samples were drawn for CPK-MB determination in 144 consecutive patients with first acute myocardial infarction. Enzymatically estimated infarct size was significantly higher in patients who developed in-hospital arrhythmias, congestive heart failure or mechanical complications, or died. After hospital discharge, infarct size was correlated with the extension score of resting thallium-201 perfusion defects. However, infarct size did not predict the occurrence of long-term complications. Thus, infarct size affects the short-term prognosis. The long-term follow-up is determined by the complex interaction of left ventricular dysfunction, residual ischemia, and arrhythmogenic potential.

Adult↗