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S De Servi

Publications and source records attributed to S De Servi.

At least 37 records · Page 2Linked to original sources

[Evaluation of efficacy and mechanism of action of angioplasty and directed atherectomy assisted by intravascular ultrasonography].

Intravascular ultrasound (IVUS) is a unique method of coronary lumen visualization enabling also examination the structure of the artery wall. Aim of this study was to assess efficacy and mechanisms of action of balloon angioplasty (PTCA) and directional atherectomy by means of IVUS. IVUS examination was performed before and after mechanical revascularization procedure in 37 pts (DCA-19 pts, PTCA-18 pts). Both PTCA and DCA resulted in enlargement of the coronary artery lumen (2.29 +/- 1.19 mm2 vs 2.93 +/- 1.55 mm2) but, also external diameter of the vessel increased after the procedure (1.94 +/- 1.10 mm2 and 0.74 +/- 1.01 mm2 retrospectively). In 55.6% of cases after PTCA plaque rupture or artery wall dissection was observed, mainly in eccentric lesions (70%). IVUS allowed to recognize details of artery lumen and define efficiency of procedure. In about 15% cases decision to continue PTCA or DCA was made on the basis of IVUS images only. The mechanism in which PTCA modifies the artery lumen is diverse and depends on the structure of lesion. Factors possibly responsible for enlargement of the lumen are: stretching, squeezing and translocation of atheroma as well as cracking and dissections along the arterial wall. DCA effectiveness depends on the withdraw of the atheromatous deposit, however, in over one-half of cases also stretching has some effect.

Aged↗

Clinical and angiographic correlates of leukocyte activation in unstable angina.

OBJECTIVES: This study sought to evaluate the relation, if any, between clinical and angiographic findings in patients with unstable angina and monocyte and neutrophil CD11b/CD18 receptor density. The expression of HLA-DR molecules on T lymphocytes, an index of activation of these cells, was also investigated. BACKGROUND: Although activation of neutrophils and monocytes has recently been shown in unstable angina, no studies have correlated activation indexes with clinical and angiographic features of patients with this clinical condition. METHODS: Sixty patients underwent diagnostic coronary arteriography and simultaneous blood sampling from the aorta and coronary sinus before injection of contrast medium. Cell surface receptors were detected by direct immunofluorescence evaluated by flow cytometry using monoclonal antibodies tagged with fluorescent markers. RESULTS: In 38 patients with unstable angina, neutrophils and monocytes showed a significantly higher expression of CD11b/CD18 adhesion receptors in coronary sinus than aortic blood (p < 0.0001 and p < 0.001, respectively). When these patients were analyzed according to clinical characteristics or angiographic findings, no difference in CD11b/CD18 receptor expression in coronary sinus blood was found between the various subgroups, except for patients with at least one episode of chest pain at rest within 48 h of coronary arteriography and a higher neutrophil adhesion molecule density than patients who remained asymptomatic (p = 0.04). Lymphocytes in patients with stable and unstable angina showed a similar percent expression of CD2/CD19 and CD3/HLA-DR antigens, with no difference between aortic and coronary sinus blood. CONCLUSION: These results in a larger cohort confirm previous data that neutrophil and monocyte CD11b/CD18 adhesion molecules show a higher expression in the coronary sinus blood of patients with unstable angina. Among clinical and angiographic findings in patients with unstable angina, only the occurrence of chest pain within 48 h of coronary angiography was related to significantly higher values of neutrophil fluorescence intensity, suggesting that the degree of neutrophil activation is related to the proximity of rest angina episodes to blood sampling. Finally, our data do not support the concept of systemic or transcardiac lymphocyte activation in unstable angina.

Adult↗

Comparison of coronary lesions obtained by directional coronary atherectomy in unstable angina, stable angina, and restenosis after either atherectomy or angioplasty.

The present study investigated the incidence of the histopathologic lesions and of growth factor expression in a consecutive series of directional coronary atherectomy (DCA) samples from 40 unstable angina pectoris patients without prior acute myocardial infarction and compared the findings with those obtained in DCA samples from 18 patients with stable angina without previous infarction and 18 patients with restenosis. We investigated coronary thrombosis, neointimal hyperplasia, and inflammation. For unstable angina, we correlated the angiographic Ambrose plaque subtypes with the histopathologic findings. The immunophenotype of plaque cells and the growth factor expression were assessed with specific antibodies for cell characterization and for the expression of basic fibroblast and platelet-derived AA and AB growth factors and receptors. The incidence of coronary thrombosis was 35% in patients with unstable angina, 17% in those with stable angina, and 11% in patients with restenosis. Neointimal hyperplasia was found in 38% of unstable angina cases, in 17% of stable angina cases, and in 83% of restenosis cases. Inflammation without thrombus or accelerated progression occurred in 20% of unstable angina and 6% of stable angina samples. In 52% of unstable angina cases, inflammation coexisted with thrombosis and/or neointimal hyperplasia. In the unstable angina group, 71% of the plaques with thrombus had a corresponding angiographic pattern of complicated lesions. The growth factor expression, reported as percentage of cells immunostaining with different growth factor antibodies, was highest in restenosis, followed by unstable angina and stable angina lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Influence of plaque composition on luminal gain after balloon angioplasty, directional atherectomy, and coronary stenting.

This study was conducted to correlate the acute luminal enlargement achieved by three different nonsurgical revascularization procedures in 79 patients (32 treated by balloon angioplasty, 29 by directional atherectomy, and 18 by coronary stenting) with the morphologic characteristics of coronary plaques assessed by preprocedure intravascular ultrasound. The absolute luminal gain was 2.41 +/- 1.54 mm2 for balloon angioplasty, 3.17 +/- 1.8 mm2 for directional atherectomy, and 4.56 +/- 1.45 mm2 for coronary stenting (p = 0.00005). However, when luminal gain was corrected for the external vessel area (luminal gain index), such difference was no longer present (0.22 +/- 0.12 for balloon angioplasty, 0.24 +/- 0.15 for directional atherectomy, and 0.30 +/- 0.12 for coronary stenting, p = not significant). Concentric plaques treated by coronary stenting had a higher luminal gain index than eccentric plaques (p = 0.01). A comparison of the three devices showed that a similar luminal gain index was achieved in soft plaques, whereas coronary stenting was superior to directional atherectomy (0.41 +/- 0.10 vs 0.20 +/- 0.09, p = 0.002) and balloon angioplasty (0.41 +/- 0.10 vs 0.19 +/- 0.08, p = 0.0005) in concentric plaques. Coronary stenting also induced a greater luminal gain index than directional atherectomy in calcific plaques (0.30 +/- 0.11 vs 0.18 +/- 0.09, p = 0.04). In conclusion, these data show that plaque morphology assessed by preprocedure intracoronary ultrasound influences the acute luminal enlargement achieved by different coronary interventions. The knowledge of plaque composition may be useful in guiding the choice of the device to be used to obtain a larger acute luminal gain.

Adult↗

Influence of plaque morphology on the mechanism of luminal enlargement after directional coronary atherectomy and balloon angioplasty.

OBJECTIVE: To relate the mechanism of luminal gain after directional atherectomy and balloon angioplasty to the morphological characteristics of the coronary lesions, assessed by intravascular ultrasound imaging. DESIGN: Intravascular ultrasound imaging was performed before and after the revascularisation procedure to assess the contribution of wall stretching and plaque reduction in luminal gain. SUBJECTS: 32 patients undergoing balloon angioplasty and 29 undergoing directional coronary atherectomy. MAIN RESULTS: The main luminal area in vessels treated by balloon angioplasty increased from 1.51 (SD 0.30) to 3.91 (1.09) mm2 (P < 0.0001) with a concomitant increase in total vessel area from 11.44 (2.73) to 13.07 (2.83) mm2 (P < 0.0001). Therefore stretching of the vessel wall accounted for 68% of the luminal gain while plaque reduction accounted for the remaining 32%. This mechanism ranged from 45% in non-calcific plaques to 81% in echogenic plaques. The main luminal area in vessels treated by directional atherectomy increased from 1.49 (0.32) to 4.68 (1.73) mm2 (P < 0.0001), with a concomitant increase of total vessel area from 13.61 (4.67) to 15.2 (4.04) mm2 (P = 0.006). Thus stretching of the vessel wall accounted for 49% of the luminal area gain and plaque reduction for the remaining 51%. The presence of calcium influenced the relative contribution of these two mechanisms to the final luminal gain after directional atherectomy, since in calcific plaques stretching of the vessel wall accounted for only 9% of the luminal gain as compared to 56% in non-calcific plaques. After balloon angioplasty there was greater evidence of coronary dissections (32% v 3% after directional atherectomy, P < 0.01) and plaque fissure (60% v 0%, P < 0.01). Plaque fissure was more frequently seen in echolucent and concentric lesions, whereas dissections prevailed in echogenic and eccentric lesions. CONCLUSIONS: Intravascular ultrasound imaging may allow the assessment of acute changes in lumen and vessel wall after revascularisation procedures, and help in evaluating the potential effect of the structure and morphology of coronary lesions on the mechanism of luminal enlargement.

Adult↗

Effect of the increasing use of coronary angioplasty on outcome at one year in patients with unstable angina.

OBJECTIVE: To determine whether the increasing use of percutaneous transluminal angioplasty in patients with unstable angina has reduced the need for bypass surgery and whether this change in the choice of treatment affected the outcome at one year in patients with unstable angina who were admitted to hospital in two different periods of time. DESIGN: Retrospective analysis of consecutive patients with unstable angina (angina at rest with ST-T changes during pain) who underwent coronary arteriography in two different periods of time. PATIENTS: 158 patients were admitted to hospital between January 1988 and June 1989 (group 1) and 140 patients admitted between January 1992 and June 1993 (group 2). RESULTS: Coronary angioplasty procedures nearly doubled from 29% in group 1 to 56% in group 2 whereas bypass surgery decreased from 36% in group 1 to 23% in group 2 (P < 0.01). Coronary angioplasty increased and bypass surgery decreased in patients with one vessel disease (P < 0.01), two vessel disease (P < 0.05), and three vessel disease (P < 0.01). Coronary angioplasty also increased and bypass surgery decreased in refractory angina and in patients with ejection fraction < 0.50 (both P < 0.05). At 1-year follow up, 14 patients in group 1 (9%) and 10 in group 2 (7%) either died or had myocardial infarction (P = NS). Revascularisation procedures were needed in 16 group 1 patients (10%) and 27 group 2 patients (19%, P < 0.05). CONCLUSIONS: Coronary angioplasty became more widely used in patients with unstable angina. This reduced the need for bypass surgery in patients with multivessel disease, refractory angina, and depressed left ventricular function. This change in treatment did not affect 1-year mortality or the myocardial infarction rate. More patients in the more recent group in which angioplasty was the preferred treatment required a further revascularisation procedure than in the earlier group in which bypass grafting was more often used as the initial treatment.

Adult↗

[The evolution of the therapeutic choice in patients with the outcomes of non-Q myocardial infarct: 2 periods compared].

BACKGROUND: Over the last years there has been a tremendous increase in coronary angioplasty procedures (PTCA), due to the availability of better materials and to the refinement of operators skill. It is not known however if this "PTCA boom" has modified our approach to the patients with particular clinical situations, such as those with non-Q wave myocardial infarction. The purpose of this study was to verify, in patients undergoing coronary angiography for clinical reasons after a non-Q wave myocardial infarction, the clinical decision concerning the therapeutical choice in two different periods (101 patients in 1988 vs. 102 patients in 1992). METHODS AND RESULTS: Patients in the two groups had similar clinical manifestations whereas patients observed in 1992 had more frequently 2-vessel disease than single vessel disease as compared to patients studied in 1988 (p < 0.05). The distribution of patients with normal coronary arteries or with 3-vessel disease was similar in the two periods. In 1988 medical therapy was the most recommended treatment at discharge (47%), followed by aorto-coronary bypass (29%) and coronary angioplasty (24%). On the contrary, in 1992 PTCA was performed in 48% of patients, medical therapy was recommended in 28% while the incidence of coronary surgery was reduced to 24% (p < 0.01). From a clinical point of view a significant increase in PTCA procedures was seen in patients presenting with unstable angina after the non-Q wave myocardial infarction (54% of these patients undergoing PTCA in 1992 vs. 30% in 1988, p = 0.03) and in patients with effort angina and a positive exercise test at low workload (53% of these patients undergoing PTCA in 1992 vs. 22% in 1988, p < 0.05). Moreover, in 1992 PTCA procedures increased in patients with single vessel disease (64% in 1992 vs. 49% in 1988) and in patients with 2-vessel disease (64% in 1992 vs. 9% in 1988). Therefore, in these patients the need of aorto-coronary by pass was reduced from 39% in 1988 to 19% in 1992 (p < 0.05). The success rate of PTCA procedures was 98% in 1992 and 83% in 1988. No major complications were observed in the two study periods and no patients underwent urgent coronary surgery. CONCLUSIONS: These data show an increase in PTCA procedures over the last years in patients undergoing coronary angiography for clinical reasons after a non-Q wave myocardial infarction. The greater experience of operators allowed for improved results, thus reducing the need of coronary surgery in these patients.

Adult↗

[Different susceptibilities to the development of nitroglycerin tolerance in the human peripheral venous and arterial circulations].

Aim of the study was to assess the relative susceptibility to the development of nitroglycerin tolerance in the arterial and venous circulation in man and to evaluate the interactions between nitroglycerin and N-acetylcysteine. Twenty patients with coronary artery disease underwent a continuous 24-h nitroglycerin infusion followed by a bolus administration of N-acetylcysteine. Forearm blood flow (ml/100 ml/min) and venous volume (ml/100 ml) were measured by strain gauge plethysmography under control conditions, at the end of nitroglycerin titration, after 24 h of infusion and after N-acetylcysteine; vascular resistance was calculated as mean cuff blood pressure/flow. After 24 h of nitroglycerin infusion, the initial increase in venous volume was reduced by 48% (p < 0.01), while the acute effects on vascular resistance were not attenuated in the whole group. N-acetylcysteine restored nitroglycerin venodilator effects in all 10 patients who developed venous tolerance but did not change significantly vascular resistance in 5 patients in whom attenuation of the arterial effects was observed during the infusion period. In conclusion, the results indicate that the susceptibility to the development of nitrate tolerance in man is higher in the venous than in the arterial circulation and that the sulphydryl group donor N-acetylcysteine is more effective in reversing nitroglycerin tolerance in the venous than in the arterial circulation.

Acetylcysteine↗

Trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, reduces restenosis after percutaneous transluminal coronary angioplasty. Results of the randomized, double-blind STARC study. Studio Trapidil versus Aspirin nella Restenosi Coronarica.

BACKGROUND: Trapidil is an antiplatelet drug with specific platelet-derived growth factor antagonism and antiproliferative effects in the rat and rabbit models after balloon angioplasty. METHODS AND RESULTS: The Studio Trapidil versus Aspirin nella Restenosi Coronarica (STARC) is a multicentric, randomized, double-blind trial to assess the effects of trapidil in angiographic restenosis prevention after percutaneous transluminal coronary angioplasty (PTCA). Patients received either trapidil 100 mg TID or aspirin at the same dosage at least 3 days before angioplasty and for 6 months thereafter. Coronary angiograms before PTCA, after PTCA, and at 6-month follow-up were quantitatively analyzed with manual calipers. Of the initial 384 patients recruited, 254 were evaluable for restenosis analysis (128 trapidil, 126 aspirin). Restenosis, defined as a loss of initial percent gain after PTCA of at least 50% (primary end point), occurred in 24.2% of the trapidil group and 39.7% of the aspirin group (P < .01). A similar result was obtained when restenosis per vessel was considered (trapidil, 23.3%; aspirin, 36.9%; P = .018). Clinical events at follow-up were similar in the two groups except that recurrent angina was significantly more frequent in the aspirin group, 43.7% versus 25.8% in the trapidil group (P < .01). Trapidil was well tolerated: only 6 patients had to discontinue the drug because of side effects, which was not different from the aspirin group. CONCLUSIONS: Trapidil reduces restenosis after PTCA at the dosage of 100 mg TID and favorably influences the clinical outcome thereafter.

Aged↗

[Diagnostic and research potential of directional atherectomy].

Directional coronary atherectomy (DCA) is the sole technique for the in vivo study of coronary artery plaques which are responsible for myocardial ischemia. The technique confers the following advantages to the pathologic study of plaque samples: the brevity, in general, of the interval between acute myocardial ischemia and sampling of the guilty plaque; the absence in samples of autolytic phenomena (such as those that affect autopsy samples), an effect that enables the use of conventional histopathology, immunohistochemistry and molecular biology; the certainty with which the researcher can identify, and thus sample, the truly guilty lesions. The drawbacks of the technique are: the fragmentation of the plaque; the difficulty the pathologist has in correctly orientating the samples in the embedding phase, in distinguishing pre- from post-procedural lesions, and in providing a detailed description of the findings. Given the foregoing, the diagnostic information to which DCA sampling enables access is as follows: plaque derivation--the recognition of whether tissue removed with DCA originates from eccentric or concentric, atheromatous of fibrosclerotic, calcified or not calcified plaques; histopathology of coronary lesions that cause ischemia with regard to: evidence of acute events, such as thrombosis, ulceration and hemorrhage, thrombus composition, when it occurs, and definition of its age and presence of material deriving from the vascular wall that lies beyond the plaque; identification and immunophenotypical characterization of inflammatory infiltrates. As regards research, the main implications of DCA are for the study of the pathogenetic mechanisms that lead to plaque instability in acute ischemic syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Atherectomy, Coronary↗

[Coronary vasomotor response to acetylcholine correlates with plasma levels of cyclosporin and triglycerides in patients with heart transplantation].

BACKGROUND: Vasoconstriction of normal coronary arteries has been reported after intracoronary (i.c.) administration of acetylcholine (Ach) in cardiac transplant patients and has been related to early endothelial disfunction; the clinical correlates of this response are still unknown. METHODS: We infused graded i.c. concentrations of Ach in 32 pts with angiographically smooth coronary arteries 1 to 3 years after heart transplantation. Changes in diameters of the proximal and middle segments of the left anterior descending coronary artery were measured by quantitative coronary angiography (automatic edge detection). RESULTS: The response to Ach ranged from +44% to -58%; at linear regression analysis it was significantly related to the plasma levels of cyclosporine (r = -0.39, p < .05) and triglycerides (r = -0.42, p < .02) but not to vessel diameter, recipient and donor age, time after transplantation, hypertension, cholesterol levels, number of acute rejection episodes and previous cytomegalovirus infections. CONCLUSIONS: In heart transplant pts with angiographically normal coronary arteries i.c. Ach may reveal endothelial disfunction which is associated with high cyclosporine and triglycerides plasma levels. Whether this response may predict an earlier development of coronary disease remains to be elucidated.

Acetylcholine↗

Effects of coronary angioplasty on left ventricular function.

It is well known that myocardial revascularization after successful coronary bypass surgery results in improved left ventricular function. Coronary angioplasty also results in successful revascularization, favorably affecting both stunned and hibernating myocardium. We studied 22 patients with chronic stable angina who underwent successful angioplasty for an isolated narrowing of the proximal or midportion of the left anterior descending artery. These patients also performed isometric exercises before and after angioplasty, which can be used to characterize left ventricular function. Revascularization after angioplasty induced an immediate improvement in left ventricular function in those patients with dysfunction secondary to hibernating myocardium. Further studies are needed to assess the possibility of the myocardial stunning phenomenon occurring after angioplasty in those patients without left ventricular improvement.

Angioplasty, Balloon, Coronary↗

Morphologic changes induced by acetylcholine infusion in normal and atherosclerotic coronary arteries.

Low doses of acetylcholine induce "endothelium-dependent" dilatation in normal coronary arteries and constriction of diseased vessels. This study investigated morphologic changes induced by perfusion of normal and diseased coronary arteries with low and high doses of acetylcholine. Vessels were excised from a series of beating hearts explanted at transplantation for idiopathic dilated cardiomyopathy and coronary artery disease. Coronary arteries from other explanted hearts, perfused with saline solution under similar conditions were taken as controls. Samples were studied using conventional histopathologic and immunohistochemical methods. Coronary arteries were grouped according to presence or absence of histologically detectable structural modifications of any type and extent. Low doses of acetylcholine induced changes in all but 1 structurally diseased coronary artery, whereas no change was induced in any but 1 histologically normal coronary artery. High doses of acetylcholine induced contraction changes in both normal and diseased vessels. Changes observed in the wall of the contracted vessels were: (1) endothelial cell contraction with protruding nuclei and detachment of their intercellular junctions with exposure of subjacent collagen to flow, (2) contraction of plaque smooth muscle cells, (3) formation of cushions protruding into vessel lumens causing blunt microchannels. Contraction in both intimal and plaque cells occurred even in diseased vessel segments with intimal denudation. These effects seemed to be dose-dependent in structurally normal vessels because low doses of acetylcholine did not produce any morphologically detectable changes in histologically normal coronary arteries, while low doses of acetylcholine induced similar reactions in vessels affected by both atherosclerosis and subintimal fibrocellular thickening.

Acetylcholine↗

Influence of elastic recoil on restenosis after successful coronary angioplasty in unstable angina pectoris.

The elastic behavior of the dilated coronary vessel has been reported to affect the immediate results of coronary angioplasty. To determine whether elastic recoil may also influence the long-term restenosis process, 98 consecutive patients with unstable angina and 1-vessel disease were studied. An automated coronary quantitative program was used for the assessment of balloon and coronary luminal diameters. Elastic recoil was defined as the percent reduction between minimal balloon diameter at the highest inflation pressure and minimal lesion diameter immediately after coronary angioplasty. Follow-up coronary arteriography was performed 8 to 12 months after the procedure in all patients. The mean elastic recoil averaged 17.7 +/- 16% and was correlated to the degree of residual stenosis immediately after coronary angioplasty (r = 0.64; p < 0.001). Restenosis, defined as > 50% diameter stenosis at follow-up, developed in 53 patients (54%). There was no correlation between the degree of elastic recoil and the changes in minimal lesion diameter observed during follow-up, whereas a positive correlation between the amount of elastic recoil and the incidence of restenosis was documented (r = 0.84; p < 0.05). Thus, the elastic properties of the dilated vessel do not influence the active process of restenosis. However, because elastic recoil negatively influences the initial results of angioplasty, it is more likely that further reductions in lumen diameter during follow-up can reach a threshold of obstruction considered critical for a binary definition of restenosis.

Adult↗

Increased expression of neutrophil and monocyte adhesion molecules in unstable coronary artery disease.

BACKGROUND: A rapid increase in leukocyte adhesion to endothelial cells is one of the first events in the acute inflammatory response and in the pathogenesis of vascular diseases. A subgroup of cell surface glycoproteins (the CD11/CD18 complex) play a major role in the leukocyte adhesion process; in particular, the CD11b/CD18 receptor can be upregulated severalfold in response to chemotactic factors. The purpose of this study was to assess whether upmodulation of granulocyte and monocyte CD11b/CD18 receptors takes place during the passage of blood through the coronary tree of patients with clinical manifestations of ischemic heart disease. METHODS AND RESULTS: Thirty-nine patients who underwent diagnostic coronary arteriography were studied. Group 1 (15 patients) had a clinical diagnosis of unstable angina, group 2 (14 patients) had stable exertional angina, and group 3 (10 patients) had atypical chest pain. Simultaneous sampling from the coronary sinus and aorta was obtained before coronary arteriography. Cell surface receptors were detected by direct immunofluorescence evaluated by flow cytofluorimetry using monoclonal antibodies tagged with fluorescent markers. Leukocytes were stained in unseparated blood to avoid in vitro manipulation that could activate phagocytes. Group 1 and 2 patients had significant coronary artery disease (> 50% coronary narrowing in at least one major coronary vessel), whereas group 3 patients had normal coronary arteries. In group 1, granulocytes and monocytes showed a significantly higher expression of the CD11b/CD18 adhesion receptor in the coronary sinus than in the aorta (both P < .01), whereas no difference in CD11b/CD18 expression was seen in groups 2 and 3. CONCLUSIONS: Patients with unstable angina have an increased expression of granulocyte and monocyte CD11b/CD18 adhesion receptors, indicating that an inflammatory reaction takes place within their coronary tree. Activation of these leukocytes may induce coronary vasoconstriction, favor thrombotic processes, and further activate platelets, thus having potential implications on the pathogenesis of unstable coronary artery disease.

Adult↗

[Myocardial protection in the patient with angina: bases for a personalized treatment].

Secondary cardioprotection of patients with angina pectoris can be accomplished by selecting appropriate drugs for the specific clinical setting. Calcium-antagonists are the first choice drugs in patients with vasospastic angina or in those clinical situations in which vasoconstriction plays a significant pathogenetic role. On the contrary beta-blockers reduce mortality and the probability of myocardial infarction in patients with unstable angina. The beneficial effects of aspirin on survival of patients with unstable angina is also well known, whereas ACE-inhibitors reduce mortality as well as the incidence of unstable angina in patients with ischemic cardiomyopathy. Also nonpharmacologic treatments (physical exercise, preconditioning) may have beneficial effects although their role is not well established yet.

Adrenergic beta-Antagonists↗

[Coronary angioplasty in unstable angina].

Percutaneous transluminal coronary angioplasty is now largely applied either to stable or unstable patients suffering from angina pectoris. The procedural success rate and the incidence of acute complications are now comparable in the 2 population of patients. Very recent data have also shown that there is no difference in restenosis between patients with stable or unstable angina. Therefore, by now, in such unstable coronary syndromes the choice of surgical therapy is mainly determined by the presence of multivessel disease or by depressed left ventricular function. However, the possibility to obtain a complete revascularization by angioplasty or to stabilize the patients treating only the "culprit" vessel, may increase the number of unstable patients shifting from surgery to angioplasty.

Angina, Unstable↗