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Biomedical subjects

A Serradimigni

Publications and source records attributed to A Serradimigni.

At least 91 records · Page 5Linked to original sources

Evidence for isosorbide dinitrate (ISDN) promoting effect on prostacyclin release by the lung and prostacyclin implication in ISDN-induced inhibition of platelet aggregation in humans.

We investigated thromboxane B2 (TxB2), 6-keto-PGF1 alpha (6KPGF1 alpha reflecting prostacyclin), PGE2 and PGF2 alpha plasma levels; TxB2, PGE2 and PGF2 alpha platelet production and platelet aggregation response in ascending aorta (reflecting trans-pulmonary difference) and in venous coronary sinus (reflecting transcardiac difference) simultaneously in patients with ischemic heart disease, before and after right-atrial administration of 3 mg ISDN bolus. Transcardiac differences were scarce before as well as after ISDN administration. In aortic blood, ISDN administration into the right atria resulted in a significant increase in prostacyclin and PGF2 alpha plasma levels (472% and 242%, respectively), a decrease of both PGE2 plasma level (-173%) and PGE2 platelet production (-485%) and a marked lowering of platelet aggregation response to ADP, concomittantly. In contrast, TxB2-related features were poorly affected by ISDN. In coronary sinus blood, the aortic increase in 6KPGF1 alpha and PGF2 alpha plasma levels was detected to a lower extent whereas the characteristics of platelet aggregation had returned to control levels. By contrast, PGE2 plasma level (-191%) and PGE2 platelet production (-133%) were lower than prior ISDN administration. The results we report here, strongly support the view that ISDN promotes release of prostacyclin and PGF2 alpha from the lung and inhibit PGE2 production. These prostanoids may be responsible for the concomittant platelet reactivity lowering, thus providing a basis for understanding how ISDN might relieve myocardial ischemia favoring prostanoid mediated vasodilation and inhibition of platelet reactivity.

6-Ketoprostaglandin F1 alpha↗

[Detection of intracardiac thrombi by scintigraphy with indium111-labeled platelets. Correlation with 2-dimensional echography and cardiac scanning].

The aim of this study was to use scintigraphy with Indium III marked platelets to detect intracardiac thrombi. Platelet marking was performed with the patient's own platelets and Indium III oxinate. The date was recorded and treated with a gamma-camera-computer system. The results obtained in 45 patients (36 male, 9 female, aged 38 to 80 years, mean age 61 years) were compared with those of 2D echocardiography in all cases, and with CAT in 30 cases. Seventeen patients (13 myocardial infarcts, 2 cardiomyopathies with dilatation, 2 mitral stenoses) were considered to have intracardiac thrombi on platelet scintigraphy with foci of hyperfixation increasing with time, clearly distinguishable from circulating cardiac activity. Sixteen of these cases had appearances of thrombosis on 2D echo (14 left ventricle, and 2 left atrium) and 12 cases had a triple positive result (2D echo, CAT and platelet scintigraphy). One patient had positive platelet scintigraphy and negative 2D echo and CAT. In the 24 cases with negative platelets scintigraphy, an intracardiac thrombus was demonstrated by 2D echo and CAT scanning in 2 cases. Two out of 4 patients with transient hyperfixation had appearances of a large chronic thrombus on 2D echo and CAT. The efficacy of therapy was monitored in 3 patients on heparin and 4 patients on platelet antiaggregants. These results show that platelet scintigraphy is a highly specific method of detecting intracardiac thrombi. It is less sensitive than 2D echo because it depends on the haematological activity of the thrombus, making it a useful technique for assessing the efficacy of therapy.

Adult↗

[Genesis of myocardial infarction].

The causes of myocardial infarction (MI) are complex and multiple and may eventually be associated. Two main types of mechanism are thought to be implicated: Functional mechanisms: these are operative in prolonged angina: the difference between MI and angina pectoris is related to the duration of these phenomena and to the resistance of the myocardial cells to anoxia: unsatisfied increase in myocardial oxygen demand, as for example in exercise-induced myocardial infarction; sudden reduction in oxygen supply due to an excessive fall in coronary flow, inadequate vasodilatation, platelet aggregation or coronary spasm. Priviledged cases are presented to demonstrate the reality of these phenomena. These mechanisms can sometimes cause MI by themselves, even when the coronary arteries are normal (5% of cases), and nearly always complicate and aggravate obstruction due to an atheromatous plaque. Organic obstructive lesions: coronary obstruction observed in about 2/3 of cases, sometimes caused by rupture of an atheromatous plaque, is usually the result of coronary thrombosis. The predominance of this mechanism is an argument in favour of it being the principal cause of MI. However, other workers believe that thrombosis is a secondary phenomenon induced by stasis, functional mechanisms or severe stenosis. The clot itself would then cause obstruction even if the primary cause were to regress. Irrespective of the roles of each of these factors it would appear logical to treat the functional mechanisms assumed to be responsible and the coronary thrombosis before the myocardial cells are destroyed by the anoxia.

Coronary Circulation↗

[Esophageal spasm: a common cause of spontaneous precordial pain].

Fifty-eight consecutive patients were investigated for spontaneous chest pain without symptoms of effort angina, previous myocardial infarction or other signs of cardiac disease, to determine the incidence of oesophageal spasm. The character of the chest pain, its context and the results of resting ECGs were analysed. An ECG recorded during chest pain was available in 23 cases and exercise stress testing was performed in 43 cases. Coronary angiography was carried out in all patients. The coronary arteries were normal or showed little change in 44 patients. Further investigations were ordered: oesophageal manometry (42 cases), echocardiography 44 cases) and ergometrine provocation tests (44 cases). The patients were then divided into 4 groups: 23 patients (40 p. 100) with coronary artery disease; either atheroma (14 cases) or spasm (9 cases); 8 patients (13,5 p. 100) with non-coronary cardiac pathology (myocardial hypertrophy or mitral valve prolapse); 15 patients (26 p. 100) with oesophageal spasm alone; 12 patients (20,5 p. 100) with no obvious organic disease. Often simulating spontaneous angina, clinically and electrocardiographically, oesophageal spasm may sometimes be distinguished (6 out of 15 cases) by the finding of painful dysphagia on swallowing ice-cold liquid. The condition is confirmed by oesophageal manometry which shows abnormalities of oesophageal contraction. In addition, 13 out of 15 patients in our series had hypotonia of the gastro-oesophageal sphincter. Dyskinetic phenomena and this hypotonia should be taken into consideration in the treatment of this condition.

Adult↗

[Uni- and bidimensional echocardiography in the etiologic diagnosis of precordial pain].

The distinction between precordial pain of cardiac origin and pain of extra-cardiac origin is a daily problem. We wanted to study the value of echocardiography in this difficult diagnostic problem. In a series of 148 patients admitted to the unit in 1982 for chest pain. 104 were investigated by echocardiography and coronary angiography. In 36 per cent of patients, the echocardiogram was normal and was unable to predict the presence or absence of coronary artery disease. Further investigations seem to be justified in these cases. In 57 per cent of cases, the echocardiogram was abnormal, suggestive of a cardiac cause for the pain. The demonstration of a disorder of segmental kinetics in the left ventricle is suggestive of coronary artery disease, which is detected 82 per cent of cases and is a good indication for coronary angiography. The other abnormalities detected, mitral valve prolapse, hypertrophic cardiomyopathy and dilated cardiomyopathy are rarely associated with coronary artery disease, which was found in 0, 13 and 14 per cent of cases, respectively. Initially, these abnormalities may be sufficient to explain the symptomatology. Pericardial detachments are associated with coronary artery lesions in 50 per cent of cases and should be very carefully monitored.

Adult↗

[Phlebographic diagnosis of lower limb venous thrombosis].

Thrombosis of the veins of the lower limbs and of the inferior vena cava can be diagnosed by free flow phlebography completed by a technical device preventing puncture of the femoral veins. The thrombus shows as a lacuna or a cupshaped arrest of the contrast medium. This method can be used in most modern radiological centres and carries little risk in trained hands. Its field of application is limited in that the pelvic veins (iliac veins excepted) and the deep femoral vein are imperfectly explored or unexplored, but it is superior to other methods - such as labelled fibrinogen, Döppler ultrasonography or rheography - which are less sensitive, less specific and unable to localize precisely the site and extension of the thrombosis. However, these methods can be used at the patient's bedside and can be repeated at will, being painless. Whenever pulmonary thrombo-embolism is suspected on clinical grounds or on the results of other exploratory methods, phlebography should be systematically performed (except in pregnant women) as it helps to decide on the treatment. In contrast, it has no place in the routine detection and surveillance of the disease which are better carried out using non-invasive techniques.

Femoral Vein↗

[Plasma thromboxane B2 and capacity of the aorta to produce prostacyclin in arteriopathies of the lower extremities].

Plasma levels of thromboxane B2, and 6-Keto-PGF1 alpha, stable metabolites of thromboxane and of prostacyclin were determined by radioimmunoassay in 17 patients with arterial disease and 10 control subjects. The production of prostacyclin from incubates of aortic microsomal fractions of patients was also studied. There was a significant elevation of thromboxane B2 in the peripheral venous blood of patients with arterial lesions (142 +/- 152 pg/ml vs 22 +/- 2 pg/ml, p less than 0.005); levels of 6-KetoPGF1 alpha were equally low in controls and patients. Rate of production of prostacyclin, which was 450 +/- 24 pmol/50 mg of proteins in 10 minutes in controls, was reduced to 97 +/- 86 pmol/50 mg prot. 10 min (p less than 0.01) in patients. Co-existence of raised plasma thromboxane levels and a reduced capacity for prostacyclin synthesis in the same patients is supportive evidence of the thrombogenic theory of arterial disease.

6-Ketoprostaglandin F1 alpha↗

[Detection of left intraventricular thrombi in the acute phase of myocardial infarction by 2-dimensional echocardiography. Apropos of 103 cases].

Two-dimensional echocardiography (2D echo) was performed in 103 patients (94 men, 9 women, aged 35 to 76 years; mean 55,4 years) during the acute phase of primary myocardial infarction in order to detect left ventricular thrombi (LVT). This investigation was carried out between the 7th and 30th days with an 84 degrees phased array sector scanner. A total of 17 LVT were visualised, all at the apex of the left ventricle. There factors seemed to predispose to this condition: --the site of infarction: LVT were more common in anterior (16/56) than inferior infarcts (1/47) (p less than 0,001); --the extent of the necrosis: LVT occurred in 13/30 antérior infarcts when the akinesia involved at least two antero-apical segments, compared to only 3/26 when the necrosis was less extensive (p less than 0,05); --cardiac failure in anterior myocardial infarction: LVT were found in 11/21 cases with cardiac failure and in only 5/35 without cardiac failure (p less than 0,01). The outcome of 45 patients was assessed by 2D echo 3 to 12 months after the acute episode (mean 7,6 months). Control echo was unchanged in 35 patients (15 inferior, 20 anterior infarcts) without LVT. In 10 patients with LVT treated by oral VitK antagonists, the thrombus disappeared in 5 cases without embolism; it decreased in volume in 3 cases and persisted unchanged in 2 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Course of pulmonary embolism].

One hundred and fifty-five patients with a mean age of 59 years and suffering a recent pulmonary embolism (P.E.) underwent angiopneumography and phlebocavography before and after treatment. The P.E. was minimal in 42 cases (Muller less than 11) and severe in 113 cases (Muller greater than 11). There was an associated venous thrombosis (V.T.) in 134 cases (86%) affecting the iliac veins or vena cava in 44 cases (28%). Several types of treatment were used: heparin 66, SK 24, high dose UK 16, low dose UK + heparin 37, surgery 16. Fifty-two patients underwent a procedure to interrupt the I.V.C. Four patients received two types of treatment in succession. SK resulted in more rapid disappearance of the pulmonary clot than UK at the dose used but the results were comparable on the 15th day (SK = UK = H). With regard to V.T., the Marder index failed to reveal any significant difference between the types of treatment. However, SK resulted in the lowest therapeutic failure rate (19%) and it was the only agent which produced disobliteration of iliac or vena cava thromboses (6 cases out of 13), other types of treatment being ineffective (0 cases out of 28). The mortality rate was high (14%) but 86% of the patients who died had a massive P.E. (greater than 60%). The recurrence rate was less (6%) but recurrences were fatal in 6 cases out of 10. Sixty-four patients were seen again after a mean period of 20.7 months. Pulmonary sequelae were minor (CPC 4.6%, dyspnoea 18%). By contrast, one patient in two suffered from post-phlebitis syndrome. The latter was all the more common when obstruction of the proximal veins persisted after treatment. On the basis of these data, the authors emphasise the gravity of pulmonary thrombo-embolic disease: fatal in the early phase essentially as a result of recurrences, incapacitating in the late phase as a result of post-phlebitis syndrome. They note that proximal V.T. associated with P.E. is responsible for such complications. Such iliocaval disease must therefore be sought routinely by phlebocavography. Their presence justifies aggressive treatment designed to destroy them (SK) or protect against their consequences (I.V.C.I.).

Drug Therapy, Combination↗

[Outcome of vasospastic angina with normal or near-normal coronary arteries (author's transl)].

The outcome of vasospastic angina with normal or near-normal coronary arteries was investigated in 48 patients followed up for periods of 3 to 55 months (mean : 19.1 months). The course of the disease was unfavorable in 13 patients, of whom 3 died, 5 developed myocardial infarction and 5 refractory angina. It was favourable in 16 patients who remained asymptomatic for at least 6 months, and intermediate in 16 patients whose anginal attacks became less frequent. Three patients were lost sight of. Calcium antagonists were administered to 32 patients; they proved superior to beta-blockers but imperfectly controlled the course of the disease : the anginal attacks completely ceased in 12 patients, became less frequent in 11 and persisted or became worse in 5. A close correlation was found between long-term outcome and the results of provocation tests performed at the beginning of treatment, and it is proposed that these tests should be used as therapeutic guide-lines.

Adrenergic beta-Antagonists↗

[Disappearance of coronary collateral circulation during a crisis of spontaneous angina. The role of spasm].

Disappearance of the collateral coronary circulation was observed during an attack of spontaneous angina. During coronary angiography, the patient developed precordial pain, ST depression in Leads I, II, III, AVL, AVF, and V2 to V6. The two coronary arteries were opacified: there was no change in the left coronary tree but the collateral circulation arising from the right coronary artery and revascularising the obstructed left anterior descending artery the ECG reverted to its previous state and the collateral circulation reappeared. This case suggests that coronary artery spasm may lead to disappearance of the collateral circulation. It raises problems of methodology in the demonstration of spastic phenomena and emphasises the role of the collateral circulation in the genesis of ischaemia. It is another illustration of coronary artery spasm accompanied by ST depression.

Angina Pectoris, Variant↗

[Block of the autonomic nervous system in the study of sinus function].

Blockade of the autonomic nervous system by injection of propranolol (0,2 mg/Kg) and atropine (0,04 mg/Kg) was carried out in a series of 48 patients classified in 3 groups:--Group I:sinus bradycardia (22 cases)--Group II:suspected tachycardia-bradycardia syndrome (14 cases)--Group III:suspected sinus node dysfunction (12 cases). Two parameters were studied after autonomic blockade: observed intrinsic sinus node frequency (OIF) and corrected "adjusted" sinus node recovery time (CASRT). The results were compared with those obtained during basal electrophysiological investigation. The OIF was abnormal in 26 cases (54%) and junctional rhythm was observed 9 times (19%). Prolongation of the post-stimulation pause occurred in 32 cases (67%), transformation from a normal to a pathological pause in 15 cases and normalisation of a pathological pause in 4 cases (8%). Sinus node recovery time did not change significantly in the other cases. There was a good correlation between OIF and CASRT when the OIF was abnormal and mediocre (48%), when the OIF was normal. The following conclusions were made:--CASRT improves diagnosis of organic sinus node dysfunction which may escape detection by basal electrophysiological investigation and excludes functional abnormalities.--OIF is of good diagnostic value when pathological. However, the integrity of sinus node function cannot be affirmed when this parameter is normal.

Aged↗

[Determination of plasma catecholamine. Effects of glucagon administration].

Basal plasma dopamine (DA), Norépinephrine (NE) and Epinephrine (E) were determined in controls (n = 15) essential hypertension (n = 19) and Pheochromocytoma (n = 9). Plasma NE was significantly higher in essential hypertension than in control and in 5 cases, plasma NE or E was 3 SD above mean control values. In 8/9 pheochromocytomas DA, E or NE were significantly elevated. In 1 case, catecholamine levels were within normal range during normotensive period. When a provocative glucagon test (1 mg I.V) was performed in controls, there was no change in blood pressure DA and NE levels, but a significant increase in plasma E 2.5 and 5 min. after injection. Similar results were obtained in 8/10 cases of labile hypertension. However in 2 cases plasma NE or E increased significantly without elevation in blood pressure. In 3/4 pheochromocytomas under normotensive phase, blood pressure and plasma catecholamines increased significantly; however in 1 case, no change was observed.

Adrenal Gland Neoplasms↗

[Spasm, stenosis and thrombosis. Their role in the genesis of myocardial infarction].

A 42 year old patient underwent coronary angiography 3 hours after the onset of inferior myocardial infarction with the object of local thrombolysis therapy. Complete proximal obstruction of the right coronary artery was relieved mechanically by the catheter. This was associated with a return of the ST segment to the isoelectric line but Q waves persisted in Lead III and AVF. A second injection showed 70 p. 100 stenosis at the site of the obstruction and the radiolucent appearances of thrombus below it. This was followed by 4 successive periods of ST elevation as the right coronary artery reoccluded. These phenomena were relieved by injection of nitroglycerine suggesting a spastic mechanism. The radiolucent image of thrombus disappeared and was replaced by amputation of a distal branch of the right coronary artery. Further coronary opacification showed good run-off beyond the stenosis and reappearance of the distal branch. This case suggests that three factors played a role in the mechanism of infarction: stenosis accompanied by spasm and thrombosis.

Adult↗

[Phlebography in venous thrombosis of the lower limbs (author's transl)].

Phlebography is the best diagnostic technique for deep venous thromboses of the lower limbs. The authors use the "free flow" technique which they have modified by visualisation of the I. V. C. and I. V. A lacunar appearance or cupola-shaped interruption are indicative of a recent thrombosis, whilst the absence of a main venous trunk and a collateral circulation are more common in the presence of an old thrombosis. They emphasise the possible sources of error in interpretation and the difficulty in determining how long the thrombosis has been present. Despite its disadvantages, phlebography remains the essential examination in order to select treatment in patients in whom there is a suspicion of venous thrombosis or pulmonary embolism. Venous Doppler and rheoplethysmography, less sensitive and less specific, have a place in routine detection and the surveillance of treatment.

Diagnosis, Differential↗