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Biomedical subjects

D Bonaduce

Publications and source records attributed to D Bonaduce.

At least 73 records · Page 4Linked to original sources
PubMed1987

Role of increased cholinergic activity in reperfusion induced ventricular arrhythmias.

The effect of increased cholinergic activity on reperfusion induced ventricular arrhythmias was studied in alpha chloralose anaesthetised dogs by administering neostigmine during a 25 min occlusion of the anterior left descending coronary artery. The dogs were divided into five groups, each of 10 animals: the control group received only saline solution; group 1 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion (that is, 5 min before reperfusion); group 2 atropine 0.4 mg.kg-1 iv at 10 min of coronary occlusion and neostigmine 0.03 mg.kg-1 iv at 20 min; and group 3 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion and at the same time underwent atrial pacing at the same rate as that of the sinus node just before neostigmine administration. In group 4 heart rate was slowed (junctional rhythm) by destroying the sinus node at 20 min of coronary occlusion. The results obtained showed that ventricular tachycardia and fibrillation, which occur at the beginning of reperfusion, were significantly less frequent in group 1 (p less than 0.001) and in group 4 (p less than 0.001). The protective action of neostigmine was abolished by previous administration of atropine (group 2) and modified by preventing the decrease in the heart rate by atrial pacing (group 3). In group 3 ventricular tachycardia was more frequent but the incidence of ventricular fibrillation was reduced significantly compared with the control and atropine groups. Thus cholinergic activity has a protective role in reperfusion arrhythmias by decreasing the heart rate before release of the coronary occlusion and therefore reduces the incidence of ventricular fibrillation.

Animals↗
PubMed1986

Effect of nifedipine on dipyridamole thallium-201 myocardial scintigraphy.

The effect of a calcium antagonist drug, nifedipine, on dipyridamole thallium-201 images was assessed in 10 angina patients with positive dipyridamole test. Two dipyridamole thallium-201 tests were performed, the first in basal conditions, the second after administration of 20 mg nifedipine. After dipyridamole, heart rate and double product increased respectively from 68.0 +/- 8.2 to 94.7 +/- 11.5 beats/min (p less than 0.01) and from 9459.5 +/- 1800.2 to 12,770.0 +/- 1864.7 mmHg X beats/min (p less than 0.01). Dipyridamole when infused after nifedipine induced an increase in heart rate from 74.2 +/- 7.16 to 88.8 +/- 5.6 beats/min (p less than 0.01) and in double product from 9650.5 +/- 1348.0 to 11,399.0 +/- 1146 mmHg X beats/min (p less than 0.05). Systolic and diastolic blood pressures were unmodified during the two studies. Segment scores were comparable before and after nifedipine. Thus, nifedipine does not worsen thallium-201 myocardial images obtained during dipyridamole infusion, therefore, this test could provide an alternative to exercise thallium-201 in patients receiving calcium antagonist drugs.

Coronary Circulation↗
PubMed1986

Two-dimensional echocardiographic evaluation of ventricular asynergy induced by dipyridamole: correlation with thallium scanning.

Myocardial asynergies detected by two-dimensional echocardiography during intravenous administration of Dipyridamole (0.75 mg/kg) were evaluated in 54 patients referred for angiographic evaluation of chest pain. Technically adequate two-dimensional echocardiograms suitable for analysis were recorded in 42 of 54 (77.7%) patients studied. Thallium-201 myocardial perfusion scintigraphy, during dipyridamole test was performed in the same patients. Thirty of the 42 patients studied showed significant coronary narrowing at cardiac catheterization. Dipyridamole-induced wall motion abnormalities and myocardial perfusion defects were detected, respectively, in 19 (63.3%) and 21 (70%) of 30 patients with significant coronary artery disease. Wall by wall comparison of the distribution of dipyridamole-induced echocardiographic asynergy with reversible thallium-201 (201Tl) perfusion defects demonstrated complete correlation in 42 segments examined. Three segments with perfusion defects at thallium scanning did not show asynergy during the test while two segments showing wall motion abnormalities during dipyridamole infusion did not manifest perfusion defects. Our study demonstrates that two-dimensional echocardiography during dipyridamole testing is useful in detecting patients with coronary artery disease. Furthermore, ventricular asynergies detected during the test show a high correspondence with site of myocardial perfusion defects at thallium scanning.

Cardiac Catheterization↗
PubMed1986

[Involvement and function of the right ventricle in acute myocardial infarct. Hemodynamic, echocardiographic and angioscintigraphic correlations].

To assess the acute effects of myocardial infarction on right ventricular function 22 patients were studied utilizing right heart catheterization, radionuclide angiography and two dimensional echocardiography. Thirteen patients had inferior myocardial infarction (Group I) and 9 anteroseptal or anterior (Group II). Hemodynamic findings suggesting right ventricular infarction were present in 3 patients of Group I. Mean radionuclide right ventricular ejection fraction was lower in inferior myocardial patients (38.2 +/- 7.6-Group I vs 50.3 +/- 11.4-Group II, p less than 0.005), while left ventricular ejection fraction in anteroseptal, and anterior myocardial infarction patients (36.8 +/- 10.5-Group II vs 55.9 +/- 7.6-Group I, p less than 0.001). Six patients in Group I presented a depressed radionuclide right ventricular ejection fraction (less than 40%): moreover right ventricular ejection fraction correlated with left ventricular ejection fraction in Group II (r = 0.79, p less than 0.001) but not in Group I (r = 0.55, p = NS). By mean of 2 dimensional echocardiography Group I patients had an increased right ventricular end diastolic area (15.3 +/- 3.8 vs 12.1 +/- 1.2 cm2, p less than 0.05) while Group II an increased right ventricular free wall motion (47.3 +/- 10.7 vs 32.4 +/- 14.1%, p less than 0.005); right ventricular end diastolic area correlated with right ventricular ejection fraction only in Group I (r = 0.60, p less than 0.05). Five patients in Group I and no patients in Group II had an enlarged right ventricular end diastolic area. Therefore, radionuclide and echocardiographic evidence of right ventricular involvement were not always associated with abnormal hemodynamics. Thus, the damaged right ventricular chamber dilates to allow an adequate stroke volume in presence of low ejection fraction; hemodynamic significant right ventricular myocardial infarction becomes evident only in patients with more severe right ventricular compromise; the increase in right ventricular free wall motion in anterior myocardial infarction patients compensates the loss of contribution of interventricular septum contraction.

Adult↗
PubMed1986

[Prognostic evaluation of patients surviving acute myocardial infarct: univariate and multivariate analysis].

The relationship between 31 variables and survival after acute myocardial infarction was evaluated in 432 patients discharged from our Coronary Care Unit from 1975 to 1984. The patients were followed for 1 to 105 months and either univariate and multivariate analysis were performed. For end-point death the significant variables (p less than 0.05) selected by the univariate analysis were: age, diabetes, smoke, heart rate at recovery, supraventricular arrhythmias, cardiac failure and complex ventricular arrhythmias either during recovery, either after discharge and finally spontaneous angina after hospital discharge. Meanwhile, for the end-point cardiac death age, smoke and supraventricular arrhythmias were not yet significant while arterial pressure at recovery and effort angina after hospital discharge were. Multivariate analysis identified cardiac failure during recovery, diabetes, complex ventricular arrhythmias before and spontaneous angina after discharge as independent variables contributing to total mortality: effort angina was a further significant one relatively to cardiac death. Thus, our study points out the importance of multivariate survival analysis when evaluating the relationship between survival after discharge for the effect of other prognostic factors. Moreover, providing identification of high risk cohorts permits appropriate interventions designed to lessen risk.

Adult↗
PubMed1986

Effect of mexiletine on reperfusion-induced ventricular arrhythmias: comparison with lidocaine.

Thirty mongrel dogs underwent proximal occlusion of the left anterior descending coronary artery to evaluate the comparative action of mexiletine and lidocaine on ventricular arrhythmias during myocardial reperfusion. Heart rate, arterial blood pressure, left ventricular end-diastolic pressure and dp/dt max were evaluated before and at the 20th and 25th min after coronary occlusion; at the 25th min coronary occlusion was removed. Dogs were randomly assigned to one of the following groups of 10: 1) control group; 2) dogs given i.v. mexiletine; 3) dogs given i.v. lidocaine. As expected, during ischemia, myocardial contractility decreased after mexiletine or lidocaine administration more than in the control group. Ventricular arrhythmias during myocardial reperfusion occurred in 9 dogs of the control group (ventricular tachycardia in 2 cases and ventricular fibrillation in 7 cases). Among dogs given mexiletine only 1 had ventricular fibrillation (p less than 0.001 vs control). Six of the 10 dogs given lidocaine had ventricular arrhythmias (ventricular tachycardia in 5 cases and ventricular fibrillation in 1 case) (p = ns vs control group; p less than 0.05 vs mexiletine group). Thus mexiletine and lidocaine had similar effects on cardiac function during myocardial ischemia and only mexiletine showed a protective effect against reperfusion ventricular arrhythmias.

Animals↗
PubMed1985

[Ventricular tachycardia].

Various electrocardiographic forms of ventricular tachycardia are described. After a discussion of the different pathogenetic mechanisms about this arrhythmia, the various types of pharmacological and electrical treatment are examined.

Amiodarone↗
PubMed1985

24-hour blood pressure recording in patients with orthostatic hypotension.

Continuous intra-arterial blood pressure measurement and electrocardiograms were obtained in two ambulatory patients with orthostatic hypotension due to autonomic dysfunction. Systolic and diastolic arterial pressure presented marked variations which took place mainly during the day and were related to several physical activities; however, marked falls in blood pressure were also observed during sleep and at the moment of arousal. A peak incidence of hypotensive events was found in the afternoon, mainly in the hours following the afternoon meal. Recording was repeated after 3 weeks of treatment with propranolol, 40 mg t.i.d. In patient 1, beta blockade drastically reduced the number and severity of hypotensive episodes, while propranolol failed to control blood pressure in patient 2, who experienced a higher number of hypotensive events during treatment. Findings of this study may be relevant to the management of patients with orthostatic hypotension and should contribute to a more accurate characterization of blood pressure profile in autonomic dysfunction.

Blood Pressure↗
PubMed1985

Efficacy of a new antihypertensive agent (indenolol) assessed by ambulatory blood pressure monitoring.

The effects of two-week treatment periods with indenolol (I) and metoprolol (M) were examined by 24-hour mean blood pressure (BP) monitoring in control conditions and during exercise stress test in 7 patients with essential hypertension, using the Oxford method. Both drugs induced a significant reduction in mean BP and heart rate (HR) as compared to pretreatment values (mean BP: from 117 +/- 3 mmHg to 106 +/- 4 after I, p less than 0.05 and to 102 +/- 3 after M, p less than 0.01; HR: from 78 +/- 2 bpm to 66 +/- 2 after I, p less than 0.01 and to 67 +/- 2 after M, p less than 0.01). I and M induced a significant reduction in systolic and diastolic BP throughout the day and most of the night. During bicycle ergometer the basal and peak values of systolic and diastolic BP were significantly lower after both treatments as compared to the pretreatment values (both p less than 0.01). Our data suggest that I once a day possesses a substantial and consistent antihypertensive action, effective over most of the 24 hours.

Adrenergic beta-Antagonists↗
PubMed1984

Inhibition of IgE-mediated histamine release from human basophils and mast cells by fenoterol.

Fenoterol, a beta 2-adrenergic agonist recently introduced to treat asthmatic disorders, inhibits antigen-induced histamine release from human basophil leukocytes and lung mast cells in a dose-dependent fashion. The dose-response inhibition curve is paralleled by a fenoterol-induced increase in the cAMP levels of human leukocyte preparations. The relationship between the effect of fenoterol and cAMP level is supported by the finding that the beta 2-adrenergic agonist only inhibits the first stage of antigen-induced histamine release and not the release caused by the Ca2+ ionophore, A23187. Propranolol, a competitive antagonist of beta 2-adrenergic receptor, blocks the inhibition of release and the cAMP accumulation caused by fenoterol. Finally, theophylline, a cAMP phosphodiesterase inhibitor, synergistically potentiates the inhibitory effect of fenoterol on histamine release and the accumulation of cAMP. These data suggest that fenoterol may modulate the in vivo release of the mediators of immediate hypersensitivity reactions via the activation of beta 2-adrenergic receptor linked to adenylate cyclase on human basophils and mast cells.

Adolescent↗
PubMed1984

Effect of beta-blockade on thallium-201 dipyridamole myocardial scintigraphy.

The effect of beta-blockade on dipyridamole thallium-201 images was assessed in 8 patients with coronary artery disease and positive dipyridamole test. Three dipyridamole thallium-201 tests were performed, the first in basal conditions, the second 30' after propranolol and the third with propranolol and atrial pacing. After dipyridamole heart rate and double product increased respectively from 75 +/- 7 to 98 +/- 15 b/min (p less than 0.01 vs starting values) and from 10 551 +/- 1255 to 11 740 +/- 4542 mmHg X b/min (p less than 0.05 vs starting values). Propranolol reduced heart rate to 64 +/- 6 b/min (p less than 0.05 vs basal conditions), systolic blood pressure to 136 +/- 13 and double product to 8733 +/- 1248 (p less than 0.05 vs basal conditions). Dipyridamole when infused after propranolol, induced an increase in heart rate to 70 +/- 5 b/min (p less than 0.05 vs starting values) while double product was 9133 +/- 1189 mmHg X b/min (p = NS vs starting values). Atrial pacing prevented the fall in heart rate and double product induced by propranolol so during dipyridamole infusion double product increased to 13 271 +/- 1868 (p less than 0.05 vs propranolol treatment; p less than 0.05 vs starting values). Segmental score calculated after dipyridamole was 5.2 +/- 2.0 in basal conditions, 5.1 +/- 1.3 after propranolol (p = NS) and 4.8 +/- 1.3 after propranolol plus atrial pacing (p = NS). Thus the results of the study show that beta-blockade does not worsen dipyridamole thallium-201 images. Furthermore the steal phenomenon seems to be the main mechanism of the dipyridamole induced ischemia. In fact, also when the increase, oxygen consumption is blunted with beta-blockade the disparity in myocardial blood flow resulted unaffected.

Blood Pressure↗
PubMed1984

[Relation between the QT interval and the severity of ventricular arrhythmias in the early phases of myocardial infarct].

The purpose of our research was to evaluate the relationship between the severity of ventricular arrhythmias in the first hours of myocardial infarction and the duration of electrical systole (QT). Twelve-lead resting electrocardiograms (ECGs) of 66 non-consecutive patients admitted to our Coronary Care Unit for myocardial infarction were retrospectively evaluated. Criteria for retrospective selection of patients were the following: 1) admission to the coronary care unit within 12 hours from the onset of myocardial infarction symptoms; 2) appropriate ECG changes suggesting acute transmural infarction (pathologic Q waves, envolving ST changes) and diagnostic elevation of serum enzymes activity; 3) good-quality ECG recordings with sinus rhythm and no conduction defects, recorded before the beginning of therapy and within the first hours after the onset of symptoms. After this first selection, the following criteria of exclusion were applied: 1) abnormal values of serum Ca++ and K+; 2) historical and/or electrocardiographic findings of a previous myocardial infarction; 3) chronic treatment with antiarrhythmic or beta-blocking drugs, digitalis or other drugs affecting the QT interval; 4) administration of drugs affecting the QT interval before admission; 5) clinical signs of left ventricular failure or cardiogenic shock at admission or during the hospitalization; 6) development of severe ventricular arrhythmias after 24 hours from the onset of symptoms. Three subgroups were individuated : group A: 39 patients with non life-threatening ventricular arrhythmias; group B: 12 patients with episodes of ventricular tachycardia within the first 12 hours of myocardial infarction; group C: 15 patients with episodes of ventricular fibrillation within the first 12 hours of myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗