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Biomedical subjects

F Cucchini

Publications and source records attributed to F Cucchini.

At least 91 records · Page 5Linked to original sources
PubMed1976

[Aortic sinus aneurysm. The angiographic diagnosis (author's transl)].

Three cases of aortic sinus aneurysm and three cases of prolapse and regurgitation of the aortic valve associated with ventricular septal defect are discussed from an angiographic point of view. It is pointed out that aortic regurgitation into the left ventricle might be helpful for a correct diagnosis. Aortic regurgitation, in fact, is the result of an anatomically unsupported aortic valve that becomes gradually distorted by haemodynamic influences. This pathogenetic mechanism is often found in subpulmonar and infracrestal ventricular septal defect.

Adult↗
PubMed1976

[Myocardial "bridges". A new pathogenetic problem in angina without coronary obstruction (author's transl)].

Six patients showing at coronary angiography normal coronary arteries during dyastole, but a segmental constriction of the left anterior descending artery during systole, were studied. Four of these patients in which the degree of systolic artery narrowing was more evident had typical angina and positive stress test. In two of these cases, a probable idiopathic cardiac hypertrophy was present. The pathogenetic significance of the angiographic findings are discussed, on the basis of common knowledge of coronary physiology and of pathophysiology of angina with normal coronary arteries.

Adult↗
PubMedDate not supplied

Cardiovascular effects induced by the injection of a new nonionic contrast medium (Iopamidol): experimental study in dogs.

The hemodynamic effects induced by the injection in the pulmonary artery of the new nonionic water soluble contrast medium Iopamidol were compared with those obtained by the injection of two other currently used contrast media (meglumine diatrizoate and sodium iothalamate). The experiments were carried out in nine mongrel dogs. Hemodynamic variables were continuously measured prior to, during, and for 8 minutes after injection of the contrast media. Injections of iopamidol produced significantly smaller decreases in aortic pressure (p less than 0.01), contractile indices (p less than 0.01), and peripheral resistances (p less than 0.01), and changes in heart rate and in cardiac output were less pronounced. At 3-4 minutes after injection, an increase in Vmaxd was observed with all three contrast media, but it was significantly lower after injecting Iopamidol. The role of hyperosmolality in causing cardiovascular changes is discussed. The less significant changes induced by Iopamidol appear to be the result of its lower osmolality, which is about a third that of meglumine diatrizoate or sodium iothalamate.

Animals↗
PubMedDate not supplied

Hemodynamic effects of ibopamine in patients with idiopathic congestive cardiomyopathy.

We administered 150 mg of ibopamine orally to 10 patients suffering from idiopathic congestive cardiomyopathy. Hemodynamic function was evaluated by right heart catheterization and by measurement of cardiac output with the thermodilution technique. Ibopamine caused no significant change in heart rate or mean arterial pressure. Cardiac index, stroke volume index, and left ventricular work index all increased significantly by about 30%. Mean pulmonary arterial pressure decreased by about 30%, and systemic vascular resistance decreased by about 20%. The effects peaked at about 3 h and lasted 5-7 h. No side effects were noted. These findings with invasive techniques confirm those of others using noninvasive techniques, and suggest that ibopamine may be useful in the treatment of congestive heart failure.

Adult↗
PubMedDate not supplied

Effect of prenalterol on contractility, relaxation, and filling phase in coronary artery disease patients with previous myocardial infarction.

Twelve postmyocardial infarction patients, with angiographically proven asynergic areas, but without overt cardiac failure, were treated with prenalterol intravenously, (a new cardioselective inotropic agent) at a dose of 30 micrograms/kg. The aim of this study was to test the usefulness and safety of this new drug in postmyocardial infarction patients, monitoring systolic and diastolic acute hemodynamic changes. Significant improvement in cardiac contractility was demonstrated by the increase of ejection fraction (+23%), stroke volume index (+22%), cardiac output (+41%), positive dp/dt (+82%), and Vmaxd (+39%). Left ventricular systolic, mean aortic, and mean right atrial pressure remained unchanged; a slight decrease in end-diastolic volume index (-2%) occurred. A significant increase in heart rate (from 66 +/- 7 to 85 +/- 14 beats/min), without electrocardiographic changes or subjective complaints of angina pectoris, was observed. Segmental wall motion analysis showed an improved systolic shortening in normal (from 34 to 44%) and in asynergic areas (from 10 to 18%), whereas no changes were observed in dyskinetic areas. The relaxation and filling phase also improved, as tested by negative dp/dt (+39%), time constant of relaxation (-36%), and by indices of ventricular compliance. Side effects consisted of a slight feeling of tension in two patients and a short episode of ventricular tachycardia (5 beats) in another patients. No episode of angina pectoris was observed. These results, with special emphasis on lack of exacerbation of pre-existing ischemia (although obtained in patients without evident heart failure), suggest the potential usefulness of prenalterol in acute cardiac failure, as well as postmyocardial infarction low-output syndrome.

Adrenergic beta-Agonists↗
PubMedDate not supplied

[Cardiac injury in acute cerebral vasculopathy].

Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities, frequently occur following stroke and contribute to worsen the prognosis. Their clinical spectrum seems to be related to the type of cerebrovascular disease and its localization. Thus, the incidence of arrhythmias and pulmonary edema is significantly higher in subarachnoid hemorrhage than in ischemic stroke, and the lesions in the right insular cortex are a major risk for complex arrhythmias and sudden death. Elevated plasma norepinephrine levels are frequently associated with these events and strongly suggest an underlying sympathetically mediated mechanism. The autonomic and cardiovascular effects of stroke, however, are modulated by concomitant factors such as pre-existent cardiac diseases, electrolyte disorders and, probably, by genetic alterations in the ionic control of myocyte repolarization. Although beta-blockers have been reported to prevent myocardial damage following stroke, adequate clinical trials are lacking, and the widespread use of these drugs in acute cerebrovascular disease is not supported by evidence.

Aged↗