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Biomedical subjects

A Bartorelli

Publications and source records attributed to A Bartorelli.

At least 37 records · Page 2Linked to original sources
PubMed1996

The primary structure of UK114 tumor antigen.

UK114 is a tumor antigen expressed by various malignant neoplasms. The complete amino acid sequence of UK114 purified from goat liver has been determined by automated Edman degradation of CNBr and endoproteinase Lys-C peptides. The protein contains 137 amino acid residues. which corresponds to a molecular mass of 14,229 Da. MALDI-TOF analysis resulted in a molecular weight of 14,290, suggesting that the N-terminal Met residue is acetylated. Sequence comparison shows that UK114 from goat liver (1) has 77% identity with a previously described 23 kDa protein from rat liver (Levy-Favatier et al. (1993) Eur. J. Biochem. 212, 665-673), (2) shares a very high degree of similarity with a family of prokaryotic and eukaryotic hypothetic proteins whose function have not yet been characterized, and (3) exhibits a significant similarity to a group of tumor-associated antigens which belongs to a superfamily of heat shock proteins, acting as possible targets for the host's antitumor immunity.

Amino Acid Sequence↗
PubMed1995

Spatial registration of echocardiographic and positron emission tomographic heart studies.

A method has been developed to match corresponding heart regions from functional echocardiographic (Echo) and metabolic fluorine-18-fluoro-2-deoxy-D-glucose ([18F]FDG) positron emission tomography (PET) studies in individual patients. Echo and PET images are spatially correlated by determining homologous anatomical landmarks (the two papillary muscles and the inferior junction of the right ventricle), identifiable in images obtained by both acquisition modalities. Echo-PET image registration is first performed in the plane identified by the three landmarks, using a rigid rotate-translate scale model. The registration parameters are then used to transform the whole PET volume. This allows a consistent Echo-PET regional analysis, according to a segmental subdivision of the heart. The technique was tested on patients. The overlay of Echo and PET registered images proved the reliability of realignment of the three markers and a good spatial correlation of myocardial walls. This approach to image registration could be applied to other acquisition modalities (such as magnetic resonance imaging and single-photon emission tomography), provided that the three anatomical landmarks are visualized.

Deoxyglucose↗
PubMed1995

[Circulatory support with Hemopump in cardiogenic shock secondary to papillary muscle rupture].

A 71-year-old woman submitted to multiple coronary artery bypass grafts suddenly developed in the third postoperatory day cardiogenic shock. Transesophageal echocardiography examination and color Doppler showed prolapse of the anterior mitral valve leaflet and detached anterolateral papillary muscle in the left atrial cavity with severe mitral valve regurgitation and increased left ventricular wall kynesis. Maximal inotropic and vasodilator support was not effective and a mechanical circulatory assistance was deemed necessary awaiting for mitral valve replacement not performed on emergency for unavailability of operatory rooms. Hemopump pump-cannula assembly was introduced through a femoral graft and the cannula was advanced in the aorta and positioned in the left ventricle across the aortic valve. Pump rate was set at the maximal speed and as an immediate result, mean arterial pressure increased and mean pulmonary pressure decreased. Global cardiac output during 190 min of assistance was 3.48 l/min at a mean arterial pressure of 81 mmHg. The Hemopump provided 3 l/min of flow with an effective left ventricle unloading. The patient subsequently underwent mitral valve replacement and her postoperative outcome was uneventful and free from complications.

Aged↗
PubMed1989

Comparison of coronary vasomotor responses to nifedipine in syndrome X and in Prinzmetal's angina pectoris.

To test whether calcium channel blockade plays a similar role in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal's angina pectoris (n = 12), quantitative angiography was used to evaluate the effect of nifedipine (10 mg, sublingually) on the lumen diameter of proximal, mid and distal thirds of normal epicardial branches. The main differences in the coronary vasomotor reaction were uniform vasodilatation in Prinzmetal's angina and a variable response to syndrome X, and a greater increase in the coronary lumen in patients with Prinzmetal's angina as compared with those with syndrome X who showed vasodilatation. The variable response in syndrome X was not related to changes in diastolic pressure and cardiac output. Patients showing coronary constriction were those who responded to nifedipine with a higher degree of tachycardia, which might suggest a neural participation in the paradoxic reaction to this drug. In the Prinzmetal group, on the contrary, at a similar heart rate increase the pattern was invariably vasodilatation. Thus, calcium ions appear to have a different role in the coronary smooth muscle contractility of the 2 series of patients; in fact, in Prinzmetal's angina nifedipine relaxed the coronary arteries to a greater degree and made them unresponsive to stimuli that were still able to cause vasoconstriction in patients with syndrome X.

Adult↗
PubMed1989

Different coronary vasomotor effects of nifedipine and therapeutic correlates in angina with spontaneous and effort components versus Prinzmetal angina.

Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis has been considered a trigger for the spontaneous component of angina occurring both on effort and at rest. To investigate more thoroughly this pathophysiologic aspect we evaluated (by means of quantitative coronary angiography) the acute vasomotor reaction to nifedipine (10 mg sublingually) of significant (greater than 50%) stenotic lesions in 22 patients with double-component angina. We also correlated this reaction with the clinical response (daily number of ischemic episodes evaluated by means of 48-hour Holter ambulatory monitoring) to treatment with nifedipine (20 mg four times a day); calcium channel blockade, in fact, is considered a specific remedy in cases of altered coronary vasomotility. Patients with Prinzmetal angina, who were known to have homogeneous coronary vasodilating reactions and favorable clinical responses to nifedipine, were studied by means of the same methods and served as the control group (14 patients). In double-component angina the residual lumen diameter of significant lesions was unchanged in two patients, enhanced in 10, and reduced in 10 after sublingual nifedipine; lumen variations from baseline values ranged from +1.29 to -1.56 mm. Acute changes in stenosis correlated closely with results obtained with oral treatment. In the group with Prinzmetal angina, coronary stenoses invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of baseline); 100% of the patients in this group responded favorably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Superior efficacy of propranolol versus nifedipine in double-component angina, as related to different influences on coronary vasomotility.

PURPOSE: In 24 patients with stable spontaneous and effort-related angina, ischemic episodes at rest were not preceded by changes in circulatory variables (heart rate, systemic and pulmonary arterial pressures) that may raise the myocardial oxygen consumption. We interpreted these episodes as caused by critical and reversible coronary flow reduction at the site of a stenotic lesion, and evaluated the clinical efficacy of nifedipine and propranolol in the treatment of this condition. PATIENTS AND METHODS: The study was randomized, placebo-controlled, and crossover in design. Nineteen of the 24 subjects were men (mean group age, 59 years; range, 47 to 65 years). The study consisted of four four-day periods. The first and the fourth periods, during which patients received placebo, were single-blind. The treatment consisted of 80 mg of propranolol or 20 mg of nifedipine administered four times daily. The second and the third periods, during which patients received propranolol or nifedipine crossing over to the alternative drug in the next period, were double-blind and separated by a 24-hour interval. RESULTS: Propranolol fully abolished or reduced the number of spontaneous ischemic episodes in a significantly larger proportion of patients than did nifedipine; it was also effective in several cases in which nifedipine had failed or had even caused a paradoxic effect. Quantitative angiographic evaluation of the influences of nifedipine (Group 1, 12 patients, 10 mg sublingually) and propranolol (Group 2, 12 patients, 0.1 mg/kg intravenously) on the residual lumen diameter of one significant coronary stenosis in each patient showed that (1) after nifedipine, the lumen was unchanged in one, augmented in seven, and reduced in four cases; (2) variations ranged between +1.59 and -1.2 mm, and their direction correlated closely with the influence of oral nifedipine on the episodes of spontaneous ischemia; and (3) in no case did treatment with propranolol vary the stenosis lumen by more than 0.3 mm. CONCLUSION: In this form of angina, a number of lesions seem to offer a compliant substrate for vasomotion and, possibly, for critical changes in flow. The vasomotor influences of nifedipine on these lesions are variable as well as the efficacy of the drug on the manifestations of ischemia at rest. Propranolol produces no important variations of the coronary stenotic lesions, causes a decrease of heart rate that facilitates coronary flow in diastole, and reduces the baseline metabolic demand of the heart so that the threshold of ischemia during critical reduction of coronary flow may become elevated.

Aged↗
PubMed1989

Different vasomotor action of nifedipine on dynamic coronary obstructions and therapeutic response in effort and prinzmetal angina.

Variations induced by nifedipine (10 mg sublingually) in the residual lumen diameter of significant (greater than 50%) coronary lesions were assessed angiographically in 58 patients with effort angina (group 1) and in 19 patients with Prinzmetal angina (group 2). A relationship was sought between these acute variations of the stenotic lumen and the clinical response to treatment with the same drug (20 mg four times daily). Treatment efficacy was evaluated with exercise testing in group 1 and Holter monitoring in group 2. In group 1 the residual segment of stenotic diameter showed an increase, decrease, or no change with the calcium antagonist. Nifedipine failed to improve 40% of the cases (21% unchanged and 19% worsened) in group 1. In the same group of patients, the responses to exercise tests were dissociated from the acute vasomotor pattern. Changes in the pressure-rate product also did not explain the clinical results. In group 2 the majority of lesions had compliant portions, which invariably reacted to nifedipine with dilatation. All patients with the Prinzmetal form had relief of the anginal episodes with treatment. These data suggest that the therapeutic efficacy of nifedipine in classic effort angina probably is the net result of influences on the myocardial oxygen consumption and supply, and the acute coronary vasomotor pattern does not allow to predict the clinical response. Stenotic lesions in the Prinzmetal form possess a distinct sensitivity to the relaxant action of calcium channel blockade, which reasonably explains the highly positive response to treatment.

Adult↗
PubMed1989

Elicitation of myocardial ischemia by nifedipine in a case of coronary artery fistula.

A 63-year-old woman had chest pain that worsened when nifedipine was given. She was found to have a right coronary-to-thorax angioma/fistula. Acute nifedipine administration elicited precordial symptoms, associated with ischemic changes in the inferior ECG leads and an obvious vasodilatation of the fistulous tract, suggesting that a nifedipine-induced "steal" phenomenon might be responsible for the paradoxic clinical response.

Coronary Disease↗
PubMed1989

[Activation and inhibition of adrenergic effects on the coronary vessels of patients with different forms of angina pectoris].

Experimental data in animals indicate that coronary vasoconstriction occurs following blockade of the beta-adrenergic receptors or alpha-receptors activation. The vasomotor effects of these maneuvers in man are unclear. Therefore we investigated whether and to which extent alpha-stimulation (cold pressor test: CPT) and beta-blockade (propranolol) cause coronary vasoconstriction; whether this effect involves the resistance arterioles as well as the large epicardial branches, and, within these, whether the normal and stenotic tracts are involved. Patterns in patients with effort angina were compared with those in patients with Prinzmetal angina. We studied 19 cases with classic and 15 cases with Prinzmetal angina. The systemic, pulmonary and coronary hemodynamics (pressure, flow and resistance) and the vasomotor pattern of normal and stenotic epicardial branches (quantitative angiography) were evaluated in the baseline condition, during CPT, after propranolol (5 mg iv) and during CPT repeated after propranolol. We observed that: changes of the coronary flow due to beta-blockade and to CPT are related to the variations of the myocardial oxygen consumption, induced by the inhibition and activation of adrenergic receptors and not to the concomitant vasomotor reaction of the stenotic vascular tract; beta-blockade does not affect homogeneously the lumen of the stenotic lesions in effort angina and invariably increases the lumen in the Prinzmetal form; influences of CPT, in the absence as well as in the presence of beta-receptor blockade, on the lumen diameter of both normal vessels and stenotic lesions are minimal in either form of angina.

Angina Pectoris↗
PubMed1989

[Various clinical and vasomotor coronary responses to calcium block in mixed angina and Prinzmetal's angina, expression of various physiopathologic mechanisms].

Impedance to flow due to coronary spasm is currently interpreted as the mechanism of Prinzmetal angina. Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis is also viewed as the trigger for the spontaneous component of mixed angina. The major question that we attempted to answer in this study was whether mixed angina may be considered a variant of the Prinzmetal form, or a particular manifestation of the classic effort form. For these purposes we investigated the acute vasomotor response to calcium channel blockade (nifedipine 10 mg sl) of both significant (greater than 50%) stenotic lesions and of normal coronary vessels in 22 patients with mixed angina and in 14 patients with Prinzmetal angina, and correlated it with the clinical response to treatment (nifedipine 20 mg qid). Calcium channel blockade, in fact, is considered as a specific remedy in the presence of an altered coronary vasomotility. The clinical response was evaluated through ambulatory Holter monitorings of 48 hour duration, while on placebo, nifedipine and placebo again. In mixed angina an angiographic evaluation showed that the residual lumen diameter of significant lesions was unchanged in 2, enhanced in 11 and reduced in 9 patients after sl nifedipine; lumen variations from base line ranged from +1.5 to -1.3 mm. Acute stenosis widening or narrowing correlated closely with the efficacy or not of the treatment. In the Prinzmetal group the vast majority of the lesions had compliant portions which invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of base line); 100% of patients in this group responded favourably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Comparison of the coronary vasomotor response to nifedipine in syndrome X and in Prinzmetal's angina].

In this study we tested whether Ca++ has a similar part in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal angina pectoris (n = 12). Through quantitative angiography we evaluated the influence of nifedipine (10 mg sl) on the lumen diameter of proximal, mid and distal thirds of normal epicardial branches. The main differences in the coronary vasomotor reaction were: uniform vasodilatation in Prinzmetal angina and a variable response in syndrome X; greater increase in the coronary lumen in patients in the former as compared to those in the latter group who showed vasodilatation. The variable response in syndrome X was not related to changes in diastolic pressure and cardiac output. Patients showing coronary constriction were those who responded to nifedipine with a higher degree of tachycardia; this might suggest a neural participation in the paradoxical reaction to this drug. In the Prinzmetal group, on the contrary, at similar heart rate increase the pattern was invariably vasodilatation. Thus, calcium ions appear to have a different role in the coronary smooth muscle contractility of the 2 series of patients; in fact, in Prinzmetal angina nifedipine relaxed the coronary arteries more potently and made them unresponsive to stimuli which were still able to cause vasoconstriction in syndrome X.

Adult↗
PubMed1988

Coronary vasomotor and clinical effects of nifedipine in effort, mixed and Prinzmental angina.

Changes induced by nifedipine (10 mg s.l.) in the residual lumen diameter of significant (greater than 50%) coronary lesions were assessed angiographically in 69 patients with effort angina (Group 1), in 22 patients with mixed angina (Group 2), and in 14 patients with Prinzmental angina (Group 3). These changes were related to the clinical response to treatment with the same drug (diary records, exercise testing, Holter monitoring). In Groups 1 and 2 segments of stenotic vessels showed either increase, decrease or no change in diameter with the calcium antagonist; in Group 3 the majority of the vessels showed compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (21% unchanged, 19% worsened) and mixed (41% exacerbated) forms; all patients with the Prinzmental form had relief of the anginal episodes. In Group 1, the response to exercise tests were dissociated from the acute vasomotor pattern and the pressure-rate product failed to explain the clinical results. Fifty-two percent of the patients in Group 2 showed significant acute widening of critical stenoses as well as obvious improvement; patients in this group who did worse with treatment had reacted to nifedipine with narrowing of their critical stenoses. These data suggest that: the response to nifedipine of classic effort angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmental form are quite sensitive to the relaxant action of calcium blockade and this probably represents a background to the highly positive clinical response to treatment.

Angina Pectoris↗
PubMed1988

Coronary vasomotor and therapeutic influences of propranolol and nifedipine on the spontaneous component of mixed angina.

In 24 patients with spontaneous and effort-related angina (mixed angina), propranolol (80 mg q.i.d.) was significantly more beneficial than nifedipine (20 mg q.i.d.) on the number, duration and severity of the spontaneous manifestations. In some cases nifedipine elicited a paradoxical response. These patterns are unlikely to have resulted from different influences on the myocardial oxygen demands, since heart rate was steady before the occurrence of ischaemia and systemic arterial pressure was equally reduced in all patients. Sublingual nifedipine (10 mg) was tested in 12 patients and the residual lumen diameter of significant (greater than 50%) coronary stenoses (quantitative angiography) was unchanged in one, enhanced in seven and reduced in four of them. Lumen variations ranged from +1.59 to -1.2 mm and correlated closely with the results of oral nifedipine treatment. Propranolol (0.1 mg kg-1 i.v.) was tested in the other 12 cases and in none did variations of stenosis lumen diameter exceed 0.3 mm. These observations indicate that: in a number of lesions a portion of pliable wall may offer a compliant substrate for vasomotor influences; this may be the major factor whereby coronary obstructions cause spontaneous, besides effort-related angina; nifedipine is effective on the former manifestation provided that it does not promote stenosis constriction; propranolol may result in benefit through bradycardia facilitating coronary flow in diastole and reducing the baseline metabolic demands, to elevate the threshold of ischaemia during transient impedance to flow.

Administration, Sublingual↗
PubMed1988

Nifedipine and angina pectoris. Short-term changes in quantitative coronary angiography with nifedipine and clinical response to treatment in effort-induced, mixed, and spontaneous angina pectoris.

Changes induced by nifedipine (10 mg sublingually) in the residual luminal diameter of significant (greater than 50 percent) coronary lesions were assessed angiographically in 69 patients with effort-induced angina (group 1), in 22 patients with mixed angina (group 2), and in 14 patients with Prinzmetal's angina (group 3). These changes were related to the clinical response to treatment with the same drug, as evaluated through diary records and Holter monitoring in the mixed (spontaneous component) and Prinzmetal forms and through exercise testing in effort-induced and mixed (effort-associated component) angina. In groups 1 and 2, segments of stenotic vessels showed either an increase or decrease or no change in diameter with the calcium antagonist; in group 3, the majority of the lesions had compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (20 percent [14/69] unchanged; 19 percent [13/69] worsened) and mixed (41 percent [9/22] exacerbated) forms; 100 percent of the 14 patients with the Prinzmetal form had relief of the anginal episodes. In group 1, the response to exercise tests was dissociated from the short-term vasomotor pattern, and the pressure-rate product failed to explain the clinical results. Forty-five percent (ten) of the patients in group 2 showed significant short-term widening of critical stenoses, as well as obvious improvement; patients who did worse with treatment in this group had reacted to nifedipine with narrowing of critical stenoses. These data suggest that the response to nifedipine of classic effort-induced angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina, and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmetal form are quite sensitive to the relaxant action of calcium blockade, and this probably represents a background to the highly positive clinical response to treatment.

Angina Pectoris↗
PubMed1987

Subaortic aneurysm of the left ventricle obstructing a coronary artery.

We report a subaortic aneurysm of the left ventricle causing compression of a coronary artery in a 52-year-old white man presenting with angina on effort. Endocarditis seemed to be implicated as the cause of this rare condition. To what extent coronary obstruction influenced the development of myocardial ischaemia was not defined since the patient also had aortic valvular disease. The clinical features, diagnostic studies and successful surgical treatment are described.

Angina Pectoris↗