PubMed Health⌕ Search

Biomedical subjects

A Manzoli

Publications and source records attributed to A Manzoli.

At least 19 recordsLinked to original sources
PubMed2003

Eccentric atherosclerotic plaques with positive remodelling have a pericardial distribution: a permissive role of epicardial fat? A three-dimensional intravascular ultrasound study of left anterior descending artery lesions.

AIMS: The transversal distribution of coronary atherosclerotic plaques (AP) (myocardial vs pericardial) affects vessel remodelling. The aim of this study was to define the impact of transversal lesion distribution on vessel remodelling in proximal and distal coronary segments using a 3D intravascular ultrasound (IVUS) reconstruction. METHODS: The study group included 70 lesions located in the left anterior descending artery within 5mm of the septal take-off, and imaged using 3D-IVUS. The take-off of the septal branch was used to divide the plaque into a myocardial and pericardial surface. The IVUS index of vessel remodelling was calculated as: [narrowest external elastic membrane (EEM) site cross-sectional area (CSA)-reference EEM CSA)/reference EEM CSAx100]. The lesions with an intermediate vessel remodelling index (between -25% and +15%) were excluded from analysis. RESULTS: Of the 38 APs with a pericardial distribution, 34 (89%) showed positive remodelling (P<0.001). The distal lesions had a positive vessel remodelling index regardless of transversal plaque distribution. At multivariate analysis, pericardial distribution and the distal location of AP were the only independent variables predictive of positive remodelling. CONCLUSIONS: The transversal distribution of atherosclerotic plaque affects vessel remodelling in left anterior descending coronary lesions, probably because of an extravascular splinting effect. Distal lesions usually show positive remodelling regardless of transversal plaque distribution.

Adipose Tissue↗
PubMed2002

Increased prevalence of the G20210A prothrombin gene variant in acute coronary syndromes without metabolic or acquired risk factors or with limited extent of disease.

AIMS: To investigate the prevalence of the G20210A prothrombin and G1691A factor V gene variants in patients with acute coronary syndrome stratified according to risk factor profile and to extent of coronary disease, in comparison with matched healthy controls. METHODS AND RESULTS: The 20210 prothrombin and the 1691 factor V loci were genotyped in 247 patients < or =65 years of age (190 myocardial infarction and 57 unstable angina as first presentation of disease) and in 247 healthy age- and sex-matched controls. The prevalence of the 1691A factor V allele was similar in cases and controls. The frequency of heterozygotes for the 20210A prothrombin allele was 6.5% among patients and 2.8% among controls (OR 2.4, 95% CI 1.0-5.9), increasing to 8.7% in patients with a family history of myocardial infarction (OR 3.3, 95% CI 1.2-9.1), to 9.9% in patients (n=81) with < or =1 vessel disease (OR 3.8, 95% CI 1.3-10.8), and to 13.0% in patients who were normocholesterolaemic, non-diabetic, normotensive and non-smokers (OR 5.1, 95% CI 1.2-21.4). CONCLUSIONS: These findings suggest that the 20210A prothrombin allele represents an inherited risk factor for acute coronary syndrome among patients who have limited extent of coronary disease at angiography or who lack major metabolic and acquired risk factors.

Acute Disease↗
PubMed2000

Early and long-term results of stenting of diffuse coronary artery disease.

Diffuse coronary artery disease (CAD) is considered unfavorable for interventional procedures; however, the results of stenting of diffuse CAD have not been completely characterized. We performed stenting in 100 consecutive patients with diffuse CAD, defined as significant stenosis >20 mm (n = 59 patients), multiple significant stenoses in the same artery (n = 23 patients), or significant narrowing involving the whole length of the coronary artery (n = 18 patients). Angiographic success was achieved in 103 arteries (100%) and clinical success was obtained in all 100 patients. There were no deaths; no patient had stent closure, acute myocardial infarction, or required emergency coronary artery bypass surgery. All 100 patients had >6 months follow-up (mean 18 +/- 7 months, range 7 to 31); 77 (77%) remained asymptomatic, and 5 (5%) had acute myocardial infarction, of whom 2 died (2%). In-stent restenosis was observed in 12 patients (12%) and repeat angioplasty was performed in 10. Including those patients who underwent repeat angioplasty, 89 (89%) maintained clinical improvement and 95 (95%) were alive and free of bypass surgery during follow-up. Life-table analysis showed 86% freedom from death, myocardial infarction, and target lesion revascularization at 28 months. Thus, selected patients with diffuse CAD may be treated with satisfactory acute and long-term results by stent implantation.

Angioplasty, Balloon, Coronary↗
PubMed2000

Homocysteine and risk of cardiovascular disease.

This pictorial introduction to homocysteine illustrates at a glance the nature of homocysteine and its role in cardiovascular disease by means of eight simple figures and an essential bibliography. Homocysteine is a sulfur-containing metabolite of methionine. Conversion back to methionine or transsulfuration to cysteine are the two major metabolic pathways that reduce total homocysteine (tHcy) concentrations in cells and blood. B vitamins are essential cofactors in homocysteine metabolism. Median fasting total homocysteine levels in adult males are approximately 10 micromol/L. Increased plasma tHcy concentrations are found with methionine-rich diets, low vitamin B intake, male gender, age, impaired renal function, and genetically determined defects of the enzymes involved in homocysteine metabolism. An inverse relation exists between plasma tHcy and circulating folate or vitamin B(6) concentrations, and folic acid supplements of 0.5 mg/d can reduce tHcy levels by approximately 25%. Homocystinuric patients, who have severe hyperhomocysteinemia, die prematurely of atherothrombotic disease. Many (but not all) cross-sectional and prospective studies indicate, on average, that plasma tHcy levels <.10 micromol/L are associated with, or predict the development of, coronary, cerebral, and peripheral vascular disease. The risk conferred by hyperhomocysteinemia is graded and is independent of traditional risk factors, with an estimated odds ratio for ischemic heart disease of 1.4 for every 5 micromol/L increase in plasma tHcy. In vitro and in vivo, tHcy has been found to impair endothelial function. It is now well established that tHcy represents a marker of current or subsequent ischemic vascular disease. However, irrefutable proof that hyperhomocysteinemia actually causes atherothrombosis will come only if interventions to lower plasma tHcy will produce concomitant reductions in cardiovascular events.

Arteriosclerosis↗
PubMed2000

Vascular and haemostatic gene polymorphisms associated with non-fatal myocardial infarction: a critical review.

The importance of genetics to the pathogenesis of myocardial infarction is suggested by the frequent familial clustering of premature disease. Yet, studies associating myocardial infarction with gene polymorphisms of vascular proteins (angiotensinogen, angiotensin converting enzyme, angiotensin II type 1 receptor, endothelial nitric oxide synthase) and haemostatic factors (fibrinogen, coagulation factors II, V, VII and XIII, plasminogen activator inhibitor-1, tissue-type plasminogen activator, platelet glycoproteins IIb/IIIa, Ia/IIa and Ib-IX-V, or methylenetetrahydrofolate reductase) have revealed conflicting results. This is hardly surprising, given: 1) the multigenic nature of myocardial infarction, whereby single polymorphisms are bound to play at best only a limited role in the global risk of disease; 2) the multiple pathogenetic mechanisms of infarction (e.g., atheromatous obstruction, plaque rupture, thrombosis, vasospasm), each of which is likely influenced by a number of genes and by several environmental factors. The simultaneous investigation of a set of polymorphisms--and of their interactions with environmental factors--in extremely homogeneous sets of patients should offer a better understanding of the contribution of specific genes to the risk of myocardial infarction.

Angiotensinogen↗
PubMed1999

Improvement of myocardial ischemia by subclavian stent implantation in patients with internal mammary grafts: a case report and review of the literature.

In patients with coronary bypass which utilizes left (LIMA) or right internal mammary artery (RIMA), recurrent ischemia is often due to stenosis of the distal anastomoses of the grafts. However, occasionally, ischemia may be due to extracoronary causes, such as subclavian disease proximal to the internal mammary artery origins. This case report describes such clinical situation emphasizing the need for careful patient evaluation, and discusses therapeutic interventional options, in particular, safety and effectiveness of self expanding subclavian stent implantation. A review of the literature is also presented.

Humans↗
PubMed1999

Homocysteine and arterial occlusive disease: a concise review.

Many cross-sectional and prospective studies have shown that raised serum/plasma levels of total homocysteine increase the risk of coronary, cerebral, and peripheral artery disease. The risk associated with hyperhomocysteinemia appears to be concentration-dependent and not attributable to traditional risk factors. The odds ratio for ischemic heart disease has been estimated to be 1.4 for every 5 mumol/l increase of total plasma homocysteine. Median fasting total plasma homocysteine in adult males is approximately 10 mumol/l. Mild hyperhomocysteinemia is estimated to occur in 5-10% of the general population. Plasma concentrations are increased as a result of age, male gender, impaired renal function, low vitamin B intake, and genetically-determined defects of the enzymes involved in homocysteine metabolism. Folate supplements can reduce total homocysteine levels by approximately 25%. Studies in vitro and in vivo indicate that homocysteine can impair endothelial function. Despite increasing recognition of hyperhomocysteinemia as a risk factor for arterial occlusive disease, irrefutable proof that mild hyperhomocysteinemia contributes directly to the pathogenesis of atherothrombosis will come if interventions to lower total homocysteine reduce cardiovascular events. Family studies may also provide evidence of causality if genetic causes of hyperhomocysteinemia are found to segregate with disease.

Arterial Occlusive Diseases↗
PubMed1999

Internal mammary artery grafts and competitive flow. Controversies persist.

We report one case in which chronic native competitive flow from an almost normal target coronary artery did not influence IMA graft patency. This patient underwent control postoperative angiography 11 months after surgery and the mammary artery-left anterior descending graft was found to be normofunctioning despite the fact that the coronary artery showed no residual stenosis.

Coronary Angiography↗
PubMed1999

Allelic polymorphism of the interleukin-1 receptor antagonist gene in patients with acute or stable presentation of ischemic heart disease.

BACKGROUND: One of the most potent pro-inflammatory mediators is the early-acting cytokine interleukin (IL)-1, whose actions are regulated by the structurally related IL-1 receptor antagonist (IL-1 Ra). IL-1 Ra is a competitive IL-1 inhibitor and a powerful anti-inflammatory agent. Several autoimmune and inflammatory diseases have been associated with an allelic polymorphism of the IL-1 Ra gene. METHODS: We investigated the frequency of allele 2 of an intron 2 polymorphism of the IL-1 Ra gene in 115 consecutive patients with ischemic heart disease -74 of which had a previous myocardial infarction (48 +/- 11 years), 21 chronic stable angina (54 +/- 10 years), and 20 unstable angina (54 +/- 9 years)--and in 80 healthy controls, matched for age and sex to patients with myocardial infarction (47 +/- 10 years). An 86 base pair variable tandem repeat in intron 2 of the IL-1 Ra gene was determined by a polymerase chain reaction-based method. RESULTS: The frequency of allele 2 was 15% in controls (carriage rate 25%) and 17% in ischemic heart disease patients (carriage rate 28%; p = 0.70). The allele 2 frequency did not differ significantly among the three patient groups. Among patients with myocardial infarction, the allele 2 frequency tended to be higher in patients with myocardial infarction < 40 years compared to those > or = 40 years (20 vs 11%, p = 0.20, OR 1.85, 95% CI 0.70-4.90), and in patients with C-reactive protein levels > or = 3 mg/l compared to those with values < 3 mg/l (31 vs 16%, p = 0.15, OR 2.38, 95% CI 0.64-9.25). CONCLUSIONS: These data do not show a clear-cut association between the allele 2 of this IL-1 Ra gene polymorphism and ischemic heart disease. Among patients with myocardial infarction, the increased allele 2 frequency in those of younger age and with higher levels of C-reactive protein merits further investigation.

Adult↗
PubMed1997

Ischemic-like ST-segment changes during Holter monitoring in patients with angina pectoris and normal coronary arteries but negative exercise testing.

To evaluate whether Holter electrocardiographic monitoring may improve the detection of ST-segment depression in patients with anginal chest pain and normal coronary arteries, we performed symptom-limited exercise testing and 24-hour Holter monitoring in a group of 38 such patients (27 women, age 54 +/- 8 years). Patients were divided into 2 groups:group X1 included 28 patients with and group X2 10 patients without significant ST-segment depression during exercise testing. There were no significant differences between the 2 groups in age, gender, characteristics of chest pain, exercise duration, heart rate (HR), and blood pressure at peak exercise, but anginal pain during exercise testing was reported by 10 patients of group X1 (36%) and 9 of group X2 (90%) (p <0.01). Episodes of ST-segment depression on Holter monitoring were found in 17 patients of group X1 (61%) and in 5 patients of group X2 (50%) (p = NS). There were no differences between the 2 groups in daily number of ST episodes (3.6 +/- 4 vs 2.8 +/- 5 episodes per patient), symptomatic episodes (8% vs 18%), and duration of the episodes. On average, HR increased significantly, in a similar way, from 15 minutes before ST-segment depression to 1-mm ST in both groups, and its value at the onset of ischemia was similar in the 2 groups (102 +/- 22 vs 109 +/- 18 beats/min, p = NS). Finally, HR at 1-mm ST during Holter monitoring was significantly lower than that observed at 1-mm ST during exercise testing (127 +/- 16 beats/min, p < or = 0.01) in group X1, and it was also lower than that observed at peak exercise (136 +/- 22 beats/min, p < or = 0.01) in group X2. In conclusion, Holter monitoring can significantly increase the detection of ST-segment depression in patients with anginal pain and normal coronary arteries, indicating a cardiac, although not necessarily ischemic, origin of the pain. Indeed, 50% of our patients with negative symptom-limited exercise testing showed spontaneous ST changes, compatible with transient myocardial ischemia, during daily activities. Differences in the response of coronary microvascular tone to exercise testing and to stimuli operating during daily life are likely to play a significant role in determining these findings.

Activities of Daily Living↗
PubMed1995

Circadian variation of ischemic threshold in syndrome X.

To evaluate whether the ischemic threshold has a circadian rhythm in patients with syndrome X, we analyzed 90 episodes of ST depression detected on 24-hour Holter recordings of 12 such patients. Ischemic threshold was considered as heart rate (HR) at 1 mm ST depression. To correct for differences in basal HR among patients, however, the ischemic threshold was also calculated as a normalized index of HR at 1 mm ST depression: [(HR at 1 mm ST-24-hour modal HR)/24-hour modal HR]-100. Mean hourly values of both absolute and normalized HRs at 1 mm ST depression were obtained by grouping and averaging respective values of all episodes detected in every hour of the day in all patients. Chronobiologic analysis was performed by single cosinor method. A significant circadian rhythm was found for HR (mesor 76 beats/min, amplitude 10 beats/min, acrophase at 2:16 P.M., p < 0.001), number of episodes of ST depression (mesor 3.75, amplitude 2.9, acrophase at 2:45 P.M., p < 0.001) and cumulative time of ischemia, with a high correlation of distributions. Episodes of ST depression showed a double peak initially in the morning, and again in the afternoon. Both raw and normalized values of HR at 1 mm ST depression also had a significant circadian variation in ischemic threshold, which was lower in the night and early morning hours, progressively increased until the first afternoon hours, and subsequently decreased in the evening.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Electrophysiologic effects of amlodipine vs. diltiazem in patients with coronary artery disease and beta-blocking therapy.

This study compares the electrophysiologic effects of amlodipine and diltiazem in patients with coronary artery disease concomitantly treated with background beta-blocking therapy. Thirty patients were included in an open-label parallel study in two phases. During phase 1, patients were screened and placed on maintenance atenolol therapy at 50 or 100 mg/day, while phase 2 consisted of right-sided catheterization and randomization of patients to either amlodipine (10 mg i.v.) or diltiazem (10 mg i.v.). Following treatment with amlodipine, no significant alteration in markers of electrophysiological activity was observed. Treatment with diltiazem resulted in a significant lengthening of sinus cycle length (SCL, p < 0.04), AH interval (p < 0.02), and Wenckebach CL (WCL, p < 0.001), and a trend towards an increase in sinus node recovery time (SNRT, p = 0.057). No effects were observed with regard to HV interval and corrected SNRT. The results of this study indicate that 10 mg intravenous amlodipine has no significant electrophysiological action on sinus or AV node function in patients receiving beta-blocker therapy with atenolol, suggesting that amlodipine can be added to beta-blockers to treat patients with myocardial ischemia and/or hypertension without any significant increase in the risk of bradyarrhythmias.

Adult↗
PubMed1994

Acute effects of nitrates on exercise testing in patients with syndrome X. Clinical and pathophysiological implications.

BACKGROUND: Sublingual nitrates are much more effective in relieving angina pectoris in patients with coronary artery disease than in patients with syndrome X, but it is not known whether their effect on exercise tolerance is also different in these two groups of patients. METHODS AND RESULTS: Treadmill exercise testing was performed before and after administration of sublingual isosorbide dinitrate (ISDN, 5 mg) in 18 patients with syndrome X (effort angina and normal coronaries, group X) and in 33 patients with documented coronary artery disease (group C). As a selection criterion, all patients had ST-segment depression > or = 1 mm on the control exercise test. Compared with the control test, the main differences in the two groups observed during the exercise test after administration of ISDN were (1) heart rate at 1-mm ST-segment depression was higher (126 +/- 25 versus 104 +/- 15 beats per minute [bpm], P < .01) in group C, whereas it was not different (125 +/- 15 versus 126 +/- 16 beats per minute) in group X; (2) the rate-pressure product at 1-mm ST-segment depression, the time to 1-mm ST-segment depression, and the exercise duration were significantly improved in group C (P < .01 for all) but were worsened in group X (18,047 +/- 4159 versus 20,535 +/- 4507 bpm . mm Hg, P = .014; 268 +/- 312 versus 429 +/- 214 seconds, P < .01; 494 +/- 279 versus 622 +/- 194 seconds, P = .013, respectively); (3) a normalization of the ECG (no ST-segment depression) was obtained in 10 patients (30%) of group C but in only 1 (5%) of group X (P < .01); (4) angina was prevented in 10 of 19 patients of group C but in no patient of group X (P < .01). CONCLUSIONS: In patients presenting with anginal chest pain, the effects of sublingual nitrates on exercise testing appear to be clinically useful to distinguish patients with coronary artery stenoses from patients with syndrome X. Indeed, worsening of exercise tolerance is highly predictive of normal coronary arteries. Furthermore, the failure of nitrates to improve exercise tolerance in patients with syndrome X suggests that a deficiency in coronary prearteriolar nitric oxide production is unlikely to play a key role in the pathophysiology of the syndrome.

Aged↗
PubMed1994

[Neurovegetative changes before and during episodes of silent ischemia in variant angina].

In order to evaluate whether variations in autonomic nervous tone have a significant role in the induction of coronary arterial spasm in variant angina, we analyzed the changes in heart rate variability (HRV) related to spontaneous episodes of ST-segment elevation, recorded during 24-hour ambulatory ECG monitoring, in 13 patients with variant angina (9 men and 4 women, aged 63 +/- 12 years). In order to obtain an accurate analysis of HRV changes, we only included ischemic episodes characterized by silent ST-segment elevation, lasting at least 3 min and without any ST change in the previous 30 min. HRV indexes in the time domain (RR interval, standard deviation of RR intervals [SD], pNN50, r-MSSD) and in the frequency domain (LF = 0.04-0.15 Hz, HF = 0.15-0.40 HZ, LF/HF ratio) were calculated on 2 min intervals, centered at 15 min before (15B), 5 min before ed 1 min before (1B) the appearance of ST elevation, as well as at peak of ST-segment elevation. Of 161 ischemic episodes found on 24-hour Holter recordings, 60 (37%) fulfilled the inclusion criteria for analysis (4.6 +/- 3.5 episodes/patient, range 1-12). The duration of the selected episodes was 6 +/- 2.5 min and ST elevation was 2.2 +/- 1.0 mm. Heart rate (HR) did not have any change before ST elevation, whereas it showed a small, but significant increase at peak ST (73 +/- 12 versus 67 +/- 11 b/min at 15B, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Results of surgical treatment in supraventricular tachycardias].

From May 1989 to May 1992, 44 patients (mean age 41 years, range 15-66) underwent surgery for supraventricular tachycardias: in 35 patients with atrioventricular reentrant tachycardia or atrial fibrillation associated with accessory pathway and refractory to medical treatment, the epicardial approach was used; in 8 with atrioventricular nodal reentrant tachycardia, a perinodal cryosurgery of the atrioventricular node was used, and in 1 patient with atrial flutter a cryosurgical ablation around the orifice of the coronary sinus and surrounding tissues was performed. All 38 accessory pathways were successfully ablated in 35 patients and no recurrences of delta wave or tachycardia were observed during a mean follow-up of 17 +/- 10 months. Atrial perforation during surgery and pericarditis were the only complications observed. All 8 patients with atrioventricular nodal reentrant tachycardia were successfully treated: in 2 patients dual pathways persisted after surgery but tachycardia was no longer inducible. No recurrences were observed during a mean follow-up of 15 +/- 4 months. Since surgery (15 months), the patient with atrial flutter has been free of recurrent episodes of atrial flutter. In conclusion, surgical treatment of supraventricular tachycardias is highly successful, with no mortality and very low morbidity. Should transcatheter ablation fail, surgery should be the treatment of choice in patients with frequent and symptomatic supraventricular tachycardias.

Adolescent↗