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Biomedical subjects

E Bramucci

Publications and source records attributed to E Bramucci.

At least 19 recordsLinked to original sources
PubMed1992

Similar antiischemic effects of intracoronary atenolol and nifedipine during brief coronary occlusions in humans.

To compare the antiischemic effects of intracoronary administration of a beta blocker, atenolol, and of a calcium antagonist, nifedipine, on the clinical and electrocardiographic signs of myocardial ischemia induced by balloon occlusion of the coronary artery, we studied 32 consecutive patients undergoing routine PTCA. In each patient at least three balloon inflations were performed: the first served to verify the occurrence of ischemia (ST segment depression/elevation greater than 1.5 mm); the second was used as a control occlusion; the third was performed after the patients were assigned to receive either atenolol 1.0 mg IC (group 1, N = 16) or nifedipine V = 0.2 mg IC (group 2, N = 16). In a control population of 10 patients, the time to return to baseline of the ECG tended to be progressively shorter during the three consecutive inflations, but the other clinical and ECG parameters did not change significantly. In group 1 and group 2, two patients did not show ECG signs of ischemia at the third inflation; the time to ischemia increased in group 1 (+76%, p less than .001) and group 2 (+85%, p less than .01; NS group 1 versus group 2); ST segment displacement at 30 seconds decreased in group 1 (-38%, p less than .01) and group 2 (-36%, p less than .01; NS group 1 versus group 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Abnormal coronary vasoconstriction as a predictor of restenosis after successful coronary angioplasty in patients with unstable angina pectoris.

BACKGROUND: High rates of restenosis after coronary angioplasty have been reported in patients with vasospastic angina. This study was designed to determine whether the occurrence of abnormal coronary vasoconstriction, detected by means of hyperventilation testing before angioplasty, influences the risk of restenosis after successful dilation. METHODS: Hyperventilation testing was performed 0 to 4 days before coronary angioplasty in 106 consecutive patients with unstable angina and single-vessel coronary artery disease. Abnormal coronary vasoconstriction was considered present if hyperventilation-induced myocardial ischemia occurred during the recovery phase of the test. All patients had follow-up angiography 8 to 12 months after angioplasty. RESULTS: Abnormal coronary vasoconstriction was observed in 48 patients (group 1), whereas 58 patients (group 2) had either a negative response throughout the test or a positive response only during the overbreathing phase of the hyperventilation test. Angioplasty was successful in 40 patients in group 1 and 51 in group 2. Restenosis was documented in 29 patients (73 percent) in group 1 and 13 (25 percent) in group 2 (relative risk of restenosis, 2.84; 95 percent confidence interval, 1.69 to 4.28; P less than 0.001). In a multivariate analysis, the following three characteristics were independently related to the risk of restenosis (in descending order of importance): ST-segment elevation during spontaneous ischemic attacks (P less than 0.001), hyperventilation-induced abnormal coronary vasoconstriction (P less than 0.001), and the presence of a lesion more than 10 mm long in the left anterior descending coronary artery (P less than 0.05). CONCLUSIONS: In patients with unstable angina and single-vessel coronary artery disease who have been selected for coronary angioplasty, the presence of hyperventilation-induced abnormal coronary vasoconstriction identifies a subgroup at high risk for restenosis.

Angina, Unstable↗
PubMed1991

Coronary atherosclerotic plaques with and without thrombus in ischemic heart syndromes: a morphologic, immunohistochemical, and biochemical study.

We investigated incidence, severity, and distribution of coronary atherosclerosis, acute thrombosis, and plaque fissuring in ischemic heart disease (both unstable-acute syndromes and chronic ischemia) and in nonischemic controls. We also studied the structural, immunohistochemical, and biochemical profile of plaques, with and without thrombus, including morphometry, immunophenotyping of inflammatory infiltrates, cytokine presence, and ultrastructural features. Critical coronary stenosis was almost the rule in both acute and chronic ischemic series (greater than 90%) whereas it reached 50% in control subjects. Thrombosis was principally characteristic of unstable-acute ischemic syndromes (unstable angina, 32%; acute myocardial infarction, 52%; cardiac sudden death, 26%) but was also found in chronic ischemia (stable angina, 12%; ischemic cardiomyopathy, 14%) and in control subjects (4%). Plaque fissuring without thrombus occurred in low percentages in lipid-rich, severe eccentric plaques in most series. Major differences were found between pultaceous-rich versus fibrous plaques rather than between plaques with or without thrombus. Pultaceous-rich plaques were frequent in sites of critical stenosis, thrombosis, and ulceration. Inflammatory infiltrates, i.e., T cells, macrophages, and a few beta cells, mostly occurred in lipid-rich, plaques unrelated to thrombus. In adventitia, infiltrates were a common finding unrelated to any syndrome. Necrotizing cytokines such as alpha-TNF were immunohistochemically detected in macrophages, smooth muscle, and intimal cells and detected by immunoblotting in 67% of pultaceous-rich plaques, either with or without thrombus. Immune response mediators such as IL-2 were also expressed in analogous plaques but in a minor percentage (50%-40%). Media were extensively damaged in severely diseased vessels with and without thrombus. Ultrastructural study showed that the fibrous cap was either highly cellular or densely fibrillar. Intimal injury with collagen exposure was often associated with platelet adhesion, whereas foamy cell exposure was not. In conclusion, investigated parameters were essentially similar in plaques, both with and without thrombus, whereas major differences were found between pultaceous-rich and fibrous plaques. Since platelets adhere to exposed collagen and not to foam cells, the type of exposed substrates could play a major role in thrombosis.

Adult↗
PubMed1991

Transcardiac release of leukotriene C4 by neutrophils in patients with coronary artery disease.

Leukotriene C4 is a potent constrictor of smooth muscle in vitro and may induce coronary vasoconstriction in vivo. To study leukotriene C4 release by neutrophils in patients with coronary artery disease, neutrophils were separated from blood samples taken from the coronary sinus and aorta in 20 patients with stable exertional angina and angiographically documented coronary artery narrowings (group I). Eight patients with normal coronary arteries were also studied (group II). To assess leukotriene C4 generation, neutrophils were incubated with calcium ionophore A 23187 (0.25 microM) and the supernatants obtained after centrifugation were analyzed for leukotriene C4 by radioimmunoassay. Patients in group I had a significantly lower release of leukotriene C4 from neutrophils separated from the coronary sinus blood than from those separated from aortic blood (4.33 +/- 0.69 versus 5.92 +/- 0.54 ng/ml, p less than 0.025), whereas patients in group II had a similar release of leukotriene C4 by the neutrophils separated from coronary sinus blood and from aortic blood (6.0 +/- 0.72 versus 6.4 +/- 0.66 ng/ml, p = NS). Moreover, in group I patients, a significant correlation was found (p less than 0.01) between the extent of coronary artery disease (expressed by the Leaman coronary score) and the percent reduction in leukotriene C4 released from neutrophils separated from coronary sinus blood as compared with leukotriene C4 produced by neutrophils separated from aortic blood. These data show that neutrophils from patients with coronary artery disease have a reduced ability to produce leukotriene C4 after stimulation by calcium ionophore A 23187.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Protection against ischemic damage during percutaneous coronary angioplasty].

Minimizing ischemia during percutaneous transluminal coronary angioplasty (PTCA) may lower the risks of the procedure and enhance the short- and long-term success rates of the procedure. However we have to remember that the effects of pharmacological and mechanical interventions during PTCA may be influenced by the functional status of the myocardium. In man the myocardium supplied by a stenotic coronary artery may have a normal metabolic condition or may be stunned, hibernated or even preconditioned by previous ischemic episodes, while the procedure itself may provoke stunning or preconditioning. Many different drugs have been tested for their efficacy under this clinical setting but we recognize that the prolongation of balloon inflation time, though statistically significant, has never proved to be so large to be clinically relevant. Mechanical antegrade coronary infusion (with either blood or oxygenated fluorocarbons) offers the most reliable method for prolonged periods of myocardial protection during PTCA.

Adrenergic beta-Antagonists↗
PubMed1991

[Doppler estimation of the stenotic mitral valve area. Direct application of the continuity equation to the flow convergence region].

The continuity equation, applied to the flow convergence region (FCR), fournishes a simple alternative to calculate stenotic valve area. The flow rate in the FCR can be calculated by multiplying the hemispheric isovelocity surface area by the velocity of the isovelocity surface. Since according to the continuity principle the flow rate through any isovelocity surface equals the flow rate through the stenotic orifice, the stenotic orifice area can be calculated as: 2 pi r2Vr/Vm, where 2 pi r2 is the hemispheric isovelocity area, Vr is the velocity at the radial distance r from the orifice and Vm is the peak jet velocity. This study was designed to analyze the validity of application of the continuity equation to the FCR for estimating mitral orifice area by Dopler ultrasound. We studied 35 consecutive patients with rheumatic mitral stenosis. Three patients were excluded; the final study population consisted of 32 patients (8 men and 24 women; mean age 56 years). Nine patients were in normal sinus rhythm and 23 in atrial fibrillation. Doppler examination was performed from the apical approach within 24 hours of cardiac catheterization. On color Doppler image Vr was defined as the first aliasing limit (lowered to 38 cm/s to increase FCR r); r represented the maximal early diastolic distance between the first alias and the stenotic orifice in a direction parallel to that of the transducer; Vm was the early diastolic peak jet velocity by continuous wave Doppler.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Granulocyte activation after coronary angioplasty in humans.

To determine whether percutaneous transluminal coronary angioplasty (PTCA) would lead to neutrophil activation with subsequent discharge of proteolytic enzymes, like elastase, and oxygen free radicals, like superoxide anion, blood samples were taken from the coronary sinus and aorta in 14 patients with stable angina and one-vessel disease who underwent PTCA. Neutrophils were separated by means of the Ficoll-Hypaque system and were stimulated to detect release of elastase and generation of superoxide anion. Plasma levels of elastase were also measured by an immunoenzymatic method. PTCA was successful in all patients. Plasma elastase levels increased significantly at the end of the procedure compared with pre-PTCA values both in the coronary sinus (from 129.2 +/- 16.6 to 286.6 +/- 39.7 micrograms/l, p less than 0.005) and in the aorta (from 117.4 +/- 13.6 to 258.1 +/- 41.3 micrograms/l, p less than 0.005). On the other hand, superoxide anion released in the supernatants after neutrophil stimulation by phorbol-myristate-acetate decreased after PTCA in the coronary sinus (before PTCA, 60.1 +/- 7.1; after PTCA, 40.7 +/- 6.8 nmol 1 x 10(7) granulocytes/ml/15 min, p less than 0.05), whereas a mild but not significant decrease was observed in the aorta (from 58.3 +/- 10.9 to 55.3 +/- 8.6 nmol 1 x 10(7) granulocytes/ml/15 min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Coronary arterial spasm as a cause of exercise-induced ST-segment elevation in patients with variant angina.

Four patients with variant angina pectoris exhibited reproducible exercise-induced chest pain and ST-segment elevation. Coronary arterial spasm was documented with arteriography during exercise-induced ST-segment elevation (three patients) or after intravenous administration of ergonovine maleate (one patient). Our observations show that in patients with variant angina exercise can trigger coronary arterial spasm, thus inducing anginal pain and ST-segment elevation.

Adult↗
PubMed1979

[Clinical and angiographic study and pathogenic mechanism of Prinzmetal's angina. Apropos of 31 cases].

31 patients presenting with Prinzmetal variant angina were divided into three groups according to their angiographic appearances. Group I comprised 9 patients with normal or coronary arteries with lesions less than 50% narrowing. Group II comprised 12 patients with single vessel disease. Group III comprised the other 10 patients with significant lesions on two or all three principal arteries. No clinical or electrocardiographical differences were found between the groups as to age, sex or the clinicapresentation of the chest pain. Most patients with normal or nearly normal coronary arteries had normal electrol cardiogrammes between attacjs (8 out of 9) and electrical changes mainly over the inferior wall (8 out of 9). Exercise electrocardiography reproduced ST elevation in 4 of the 9 patients but, in contrast to the patients in the other two groups, never ST depression. However, these features are not specific for patients in Group I as they were observed in 4 patients in the other two groups. Spontaneous or induced coronary spasm were observed in 27 patients, confirming its role as the mechanism of Prinzmetal angina, whatever the anatomical appearance of the coronary tree.

Adult↗
PubMed1978

[Liberation of inorganic phosphates in the coronary sinus as an indicator of human myocardial ischemia].

The effects of atrial pacing (A.P.) on the myocardial balance of inorganic phosphate (Pi) were studied in 11 patients with coronary atherosclerosis and pacing-induced angina (Group C) and in 5 normal subjects (Group N). During A.P. in group C 64% of patients had myocardial loss of Pi, statistically significant (p less than 0,025) always with concomitant reduced myocardial extraction or production of lactate, but only 70% of patients with reduced myocardial extraction or production of lactate had myocardial loss of Pi. In only 1 p. of group N myocardial loss of Pi with normal lactate extraction was observed. These data show that during pacing-induced ischemia there is a negative myocardial balance of Pi, that can be used as a metabolic indicator of ischemia, but less reliable than lactate reduced extraction or production.

Cardiac Pacing, Artificial↗
PubMed1978

[Coronary spasm on exercise. Demonstration of a case by coronary angiography].

We have seen a case with spasm of the right coronary artery coming on during exercise ergometry in the course of a coronary arteriogram. The patient had angina pectoris spontaneously and on exercise. Bicycle ergometry was repeated four times by the same method, and was positive in three; in two of these there was angina and ST elevation in II, III, aVF, and ST depression in I, aVL and V2 to V5. On one occasion the test was negative, the patient having taken a trinitrin tablet one hour before the test. Repeating the exercise test during coronary arteriography showed spasm of the right coronary artery and elevation of the segment ST in II, III and aVF; this disappeared after trinitrin treatment.

Adult↗
PubMed1978

[Reproducibility of the clinical, electrocardiographic and coronarographic aspects of spontaneous coronary spasm with the use of ergonovine maleate].

Five patients affected by angina pectoris showed a spontaneous attack of myocardial ischemia in the course of coronary arteriography examination. During the ischemic episode it was shown a severe coronary arterial spasm promptly relieved by nitroglycerin. In these patients the administration of ergonovine maleate induced the same clinical, electrocardiographic and coronariographic patterns of spontaneous ischemic episodes. These data support the hypotesis that the ergonovine maleate administration is a suitable test for detection of the vasospastic pathogenesis in acute myocardial ischemia.

Adult↗
PubMed1978

Spontaneous and provoked coronary artery spasm: are they the same?

A 44-yr-old man suffering fro exertional, emotional and spontaneous angina underwent coronary arteriography. During the examination he had a spontaneous attack of angina with ST elevation in the anterior leads. Injection of a contrast medium in the left coronary artery during pain showed marked spasm with anterior descending artery occlusion. The spasm was quickly relieved by nitroglycerin. Intravenous administration of 0.4 mg of ergonovine maleate reproduced the anginal episode with pain, ST elevation in the anterior leads and coronarographic patterns of a spasm occluding the anterior descending artery at the same level. After nitroglycerin, the pain disappeared and the electrocardiographic and coronarographic findings returned to basal conditions.

Adult↗