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F Crea

Publications and source records attributed to F Crea.

At least 37 records · Page 2Linked to original sources
PubMed2004

Diagnostic and prognostic value of ST segment depression limited to the recovery phase of exercise stress test.

OBJECTIVES: To investigate the diagnostic and prognostic value of ST segment depression limited to the recovery phase of an exercise stress test, as compared with that of ST segment depression appearing during exercise. SETTING: Exercise stress test laboratory of a university hospital. PATIENTS AND DESIGN: Clinical and angiographic data were compared for 574 consecutive patients who developed ST segment depression during the active phase of an exercise test (group 1) and for 79 patients who developed ST segment depression only during the recovery phase of the exercise test (group 2). RESULTS: There were no differences between the two groups in major clinical features. Significant coronary artery stenoses were found in 488 group 1 patients (85%) and in 62 group 2 patients (78%, p = 0.14). Three vessel or left main disease was found in 166 (29%) group 1 and in 14 (18%) group 2 patients (p = 0.045). At a median follow up of 55.3 months of 321 group 1 and 54 group 2 patients, there were no significant differences in major cardiac events between the groups (univariate relative risk 0.81, 95% confidence interval 0.25 to 2.68, p = 0.72). CONCLUSION: The diagnostic and prognostic power of ST segment depression limited to the recovery phase of an exercise test is largely similar to that of ST segment depression induced during effort; thus, assessing ST segment depression during recovery can significantly improve the clinical information derived from exercise stress tests.

Blood Pressure↗
PubMed2004

Surviving acute myocardial infarction: survivin expression in viable cardiomyocytes after infarction.

BACKGROUND: Apoptosis is a key feature in postinfarction remodelling leading to progressive myocyte loss. Both proapoptotic and antiapoptotic factors contribute to the delicate balance between death and survival. The survivin pathway has emerged as essential in the control of apoptosis, although its role in heart disease is unknown. AIM: To evaluate survivin expression after acute myocardial infarction (AMI). METHODS: Survivin expression was assessed immunohistochemically in the peri-infarct and remote viable myocardium in 17 consecutive patients who died 1-30 weeks after AMI and in four control hearts. RESULTS: Survivin was expressed by myocytes in the peri-infarct area in eight patients and in the remote region in 13 patients. The rate of survivin expression after AMI was significantly higher in the remote versus peri-infarct regions and compared with control hearts. Its expression was inversely associated with the presence of dilated cardiopathy and of apoptosis, independently from the gross pathology infarct size. CONCLUSIONS: Survivin myocardial expression after AMI may be associated with the survival of at risk myocardium and may be indicative of more favourable remodelling after AMI. These findings identify a potential new target for the treatment of postinfarction remodelling.

Apoptosis↗
PubMed2004

Preoperative shift from glibenclamide to insulin is cardioprotective in diabetic patients undergoing coronary artery bypass surgery.

AIM: The cardioprotective effects afforded by volatile anesthetics, i.e. isoflurane, during heart surgery may be due to preconditioning of the myocardium through the activation of KATP channels. The aims of this study were to establish whether glibenclamide prevents the isoflurane-induced cardioprotection in diabetic patients undergoing coronary surgery (CABG) and whether this cardioprotective effect can be restored by preoperative shift from glibenclamide to insulin therapy. METHODS: We enrolled 60 patients undergoing CABG. Twenty consecutive non-diabetic patients were randomized to receive conventional anesthesia (CA) or conventional anesthesia plus isoflurane (ISO) (added to the inspired oxygen before starting cardiopulmonary bypass); 40 consecutive diabetic patients in chronic treatment with oral glibenclamide were randomized to conventional anesthesia (G-CA), conventional anesthesia plus isoflurane (G-ISO), conventional anesthesia after shifting to insulin (I-CA) or conventional anesthesia plus isoflurane after shifting to insulin (I-ISO). Serum levels of cardiac troponin I (CTnI) and CK-MB, as markers of ischemic injury, were obtained 1, 24, 48 and 96 hours, postoperatively. RESULTS: Postoperative peak levels of CTnI and CK-MB were lower in ISO than in CA (0.5+/-0.3 vs 2.8+/-2.2 ng/ml, p<0.05 and 61+/-27 vs 79+/-28 U/L, p<0.05, respectively), as well as in I-CA and I-ISO than G-CA and G-ISO groups (0.5+/-0.7 and 0.7+/-0.9 vs 3.5+/-3 and 2.7+/-2.5 ng/ml, p<0.05; 47+/-7 and 41+/-5 vs 85+/-28 and 50+/-23 U/L, p<0.05, respectively). No significant differences were detected in postoperative hemodynamic variables or in-hospital outcome. CONCLUSION: This prospective randomized study shows a cardioprotective effect of preoperative administration of isoflurane during CABG. Such an effect is prevented by glibenclamide, but can be restored in diabetic patients by preoperative shift from glibenclamide to insulin.

Aged↗
PubMed2003

Temporal evolution and functional outcome of no reflow: sustained and spontaneously reversible patterns following successful coronary recanalisation.

OBJECTIVE: To identify in humans the temporal patterns of no reflow and their functional implications. METHODS: 24 patients with first acute myocardial infarction and successful coronary recanalisation by recombinant tissue-type plasminogen activator (n = 15) or primary percutaneous transluminal coronary angioplasty (n = 9) were studied by myocardial contrast echocardiography within 24 hours of recanalisation and at one month's follow up. Myocardial contrast echocardiography was performed by intermittent harmonic power Doppler and intravenous Levovist. The regional contrast score index (CSI) was calculated within dysfunctioning myocardium. Videointensity was measured (dB) within risk and control areas and their ratio was calculated. RESULTS: In 8 patients reflow was observed at 24 hours and persisted at one month. Conversely in 16 patients areas of no reflow were detectable at 24 hours. At one month, no reflow was spontaneously reversible in 9 patients (mean (SD) CSI and videointensity ratio improved from 2.5 (0.5) to 1.4 (0.6) and from 0.6 (0.1) to 0.7 (0.1), respectively; p < 0.05) and was sustained in the remaining 7 patients (CSI and videointensity ratio remained unchanged from 2.6 (0.6) to 2.6 (0.5) and from 0.5 (0.2) to 0.5 (0.2), respectively; NS). Left ventricular function improved significantly in patients with reflow and reversible no reflow. Volumes were enlarged only in patients with sustained no reflow. CONCLUSIONS: No reflow detected at 24 hours may be sustained or spontaneously reversible at one month. Such reversibility of the phenomenon is associated with preserved left ventricular volumes and function. Clarification of the mechanisms of delayed reversibility may lead to tailored treatment of no reflow even in the subacute phase of myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed2003

Quality of life in young diabetic patients.

AIM: To assess the health-related quality of life (HRQoL) in young diabetic patients. MATERIAL AND METHODS: We studied 30 consecutive (16 male, 14 female; mean age 15.8 years) out-patients affected by Type 1 diabetes mellitus (T1DM). We used validated clinical, metabolic (HbA1c) and patient-oriented (Short Form-36) measurements. RESULTS: Patient-oriented physical scores were significantly related to several clinical and habit features (daily glycaemia and number of insulin administration, dosage of HbA1c, number of snacks). Interestingly, the number of snacks is associated with better social functioning; furthermore, the mother's educational level is related with physical and mental aspects of the patient's quality of life. DISCUSSION: The patient-oriented measure provides an important perspective of the severity of the disease and suggests new interpretations to conventional biological measurements. This multidimensional study shows that HRQoL is influenced by the metabolic picture. During adolescence a "constant attendance" of the disease, through strict self-control and the high number of therapy administrations, can deteriorate the patient's quality of life. Interestingly, this study indicates the mother's crucial role in the management of the disease during adolescence: the higher the mother's educational level the better the patient's HRQoL probably because she is able to help the child to manage and accept the disease.

Adolescent↗
PubMed2002

Inflammatory gene polymorphisms and ischaemic heart disease: review of population association studies.

Inflammation and genetics are both prominent mechanisms in the pathogenesis of atherosclerosis and arterial thrombosis. Accordingly, a number of population studies have explored the association of ischaemic heart disease with gene polymorphisms of the inflammatory molecules tumour necrosis factors (TNF) alpha and beta, transforming growth factors (TGF) beta1 and 2, interleukin (IL) 1 and its receptor antagonist (IL 1ra), CD14 (the receptor for lipopolysaccharide), P and E selectins, and platelet endothelial cell adhesion molecule (PECAM) 1. Although they are very preliminary and partly conflicting, the data provide some evidence that alterations in the genetics of the inflammatory system may modify the risk of ischaemic heart disease.

Adult↗
PubMed2001

Coronary artero-venous gradient of endogenous urokinase.

Experimental data indicate that urokinase-type plasminogen activator (u-PA) contributes significantly to endogenous fibrinolysis and vascular remodeling in proportion to its local concentrations. In humans, however, it is not known whether u-PA levels vary at different sites and across specific vascular beds. We investigated possible regional and artero-venous differences in plasma u-PA concentrations in 15 patients undergoing cardiac catheterization. Three pairs of simultaneous samples were taken from: (1) the ascending aorta and coronary sinus; (2) left ventricle and right atrium; (3) femoral artery and femoral vein. Single-chain urokinase-type plasminogen activator (scu-PA) was measured by bioimmunoassay, and total u-PA antigen (including scu-Pa and two-chain urokinase-type plasminogen activator complexed with inhibitors (tcu-PA)) by enzyme-linked immunosorbent assay. Scu-PA represented, on average, 51+/-15% of total u-PA concentrations. Scu-PA and total u-PA levels were correlated (r=.72, P<.0001) and did not differ significantly among the arterial or venous locations. There was a small but consistent increase in mean (+/-standard deviation (S.D.)) scu-PA concentrations from all arterial to all venous samples (1.5+/-0.6 vs. 1.6+/-0.5 ng/ml, P=.038) and from ascending aorta to coronary sinus (1.6+/-0.5 vs. 1.7+/-0.6 ng/ml, P=.046). Similarly, total u-PA levels increased from femoral artery to femoral vein (2.9+/-0.7 vs. 3.0+/-0.8 ng/ml, P<.001). In contrast, across the lungs, no significant concentration-gradient was seen in either scu-PA or total u-PA. The changes in total u-PA roughly followed those of scu-PA. These data identify an artero-venous gradient in human plasma u-PA across the coronary and peripheral beds, but not across the lungs, suggesting differences in u-PA kinetics according to vascular location.

Aged↗
PubMed2001

Unstable angina and elevated c-reactive protein levels predict enhanced vasoreactivity of the culprit lesion.

BACKGROUND: Because plaque inflammation may modulate coronary vasomotion, the association between systemic levels of C-reactive protein (CRP) and coronary vasoreactivity was assessed in patients with stable or unstable angina. METHODS AND RESULTS: In 31 patients with stable angina and 23 patients with unstable angina undergoing coronary angiography, minimal luminal diameter (MLD) of the culprit lesion was measured by quantitative coronary angiography at baseline, during the cold pressor test (CPT), and after intracoronary administration of nitroglycerin (NTG) and expressed as percent change from baseline. MLD of patients with unstable angina exhibited a greater reduction during CPT and a greater increase after NTG than did patients with stable angina (-17+/-14% versus -5+/-12%, P=0.0013, and 34+/-25% versus 8+/-20%, P<0.001, respectively). According to preprocedural serum levels of CRP, 36 patients had normal (</=0.5 mg/dL) and 18 patients had elevated CRP levels. MLD of patients with elevated CRP levels exhibited a greater reduction during CPT and a greater increase after NTG than of patients with normal CRP levels (-15+/-12% versus -7+/-14%, P=0.037, and 31+/-23% versus 13+/-25%, P=0.011, respectively). Both unstable angina and elevated CRP levels resulted in independent predictors of enhanced vasoreactivity at the multivariate analysis. CONCLUSIONS: This study confirms enhanced vasoreactivity of the culprit lesion in patients with unstable angina compared with those with stable angina. More importantly, it demonstrates that inflammatory mechanisms play a key role in modulating the reactivity of coronary atherosclerotic plaques and may partially account for the enhanced vasoreactivity of the unstable plaques.

Adult↗
PubMed2001

Autoantibodies against oxidized low density lipoproteins in patients with stable angina, unstable angina or peripheral vascular disease; pathophysiological implications.

BACKGROUND: Antibody antioxidized low density lipoproteins (oxLDL) might play a role both in atherogenesis and in the pathogenesis of acute coronary syndromes. METHODS AND RESULTS: Antibody titres to oxLDL and levels of C-reactive protein were compared in unstable angina, stable angina or peripheral artery disease. Antibody titres to LDL oxidated by CuSO(4)for 2, 4 and 18 h (Cu-oxLDL-Ab(2-4-18)) or by peroxidase (HRP-oxLDL-Ab) were assessed by ELISA. Cu-oxLDL-Ab(2-4-18)were consistently higher in peripheral artery disease than in unstable angina (P<0.001, P<0.001, P=0.01, respectively) or in stable angina (P<0.001, P=0.01, P=ns) but similar in unstable and stable angina. Accordingly, HRP-oxLDL-Ab were higher in peripheral artery disease than in unstable angina (P<0.001) or stable angina (P=0.04) but similar in unstable and stable angina. The number of arterial stenoses was higher in peripheral artery disease than unstable and stable angina (P<0.01). Cu-oxLDL-Ab and HRP-oxLDL-Ab correlated with the severity of atherosclerosis (P<0.01, R=0.4;P=0.02, R=0.3 respectively). Conversely, C-reactive protein levels were higher in unstable than in stable angina (P<0.001) or in peripheral artery disease (P<0.03) but similar in stable angina and peripheral artery disease and did not correlate with the severity of atherosclerosis. CONCLUSION: The autoimmune response to oxLDL is likely to play an important role in atherogenesis but not in precipitating acute coronary syndromes.

Aged↗
PubMed2001

Coronary microvascular endothelial dysfunction in transplanted children.

AIMS: To assess the response of the coronary microcirculation to acetylcholine (endothelium-dependent vasodilator) and of adenosine (endothelium-independent vasodilator) in children after heart transplantation and to verify whether endothelial dysfunction is time-dependent. METHODS AND RESULTS: We studied the endothelial function of 26 asymptomatic children previously submitted to heart transplantation, with normal transplanted hearts and epicardial coronary arteries. Ten untransplanted children served as controls. The response of coronary blood flow velocity to intracoronary infusion of acetylcholine (1.8 microg x min(-1)) and adenosine (270 microg x min(-1)) was assessed using a Doppler wire positioned in an epicardial coronary branch. In the study group, coronary blood flow velocity increased slightly during acetylcholine infusion (peak/baseline ratio=1.17+/-0.22). The ratio was inversely correlated with the length of follow-up (r=-0.50;P=0.0078). The peak/baseline ratio in control children was 1.76+/-0.73 (P<0.0002 vs. study group). After adenosine infusion, the coronary blood flow velocity peak/baseline ratio was 3.75+/-1.54 in transplanted children and 3.72+/-1.34 in controls (P=ns). CONCLUSIONS: Endothelial dysfunction in paediatric transplanted patients becomes more evident in patients with longer follow-up. This finding could prove useful in the prevention of accelerated arteriosclerosis.

Acetylcholine↗
PubMed2001

Platelet aggregability in cardiac syndrome X.

AIMS: To assess platelet aggregability at rest and in response to exercise in patients with cardiac syndrome X (anginal chest pain, ST-segment depression on exercise, angiographically normal coronary arteries). METHODS AND RESULTS: We performed a symptom/sign-limited exercise test in 31 patients with syndrome X, 25 patients with coronary artery disease and 29 healthy subjects. Platelet aggregability was measured in flowing whole blood at baseline, at peak exercise, and after 30 and 120 min, as the time to occlude a collagen/adenosine diphosphate coated ring (aggregation time). Resting aggregation time was shorter in syndrome X patients (83.2+/-12 s), compared to patients with coronary disease (94.0+/-18 s, P<0.01) and to healthy subjects (96.4+/-21 s, P<0.01). With exercise, aggregation time did not change in healthy controls, decreased in patients with coronary disease (-13.8 s at peak; 95% CI, -10.2, -17.3 s;P<0.001), but increased in syndrome X (+17.4 s 30 min after exercise; 95% CI, +10.4, +24.4 s;P<0.0001). The intravenous administration of an adenosine antagonist (theophylline) prevented the exercise-induced prolongation of aggregation time in syndrome X patients (n=11), but had no effect in healthy controls (n=11). CONCLUSION: Platelet aggregability at rest was increased in syndrome X patients, compared to patients with coronary artery disease and healthy subjects. In contrast to patients with coronary disease, however, platelet aggregability was reduced by exercise. This response was prevented by theophylline, strongly suggesting the involvement of adenosine.

Aged↗
PubMed2001

Coronary risk factors: new perspectives.

The predisposing and precipitating causes of acute myocardial infarction (MI) are multiple; furthermore, different individuals may have different susceptibility, to a large extent genetically determined, to each of them. In spite of the complex aetiology of MI and of our limited knowledge of the causes responsible for the formation of persistent occlusive thrombosis in epicardial coronary arteries, the achievements obtained by controlling traditional risk factors are remarkable. Traditional risk factors, however, have a limited sensitivity among subjects with low/moderate levels of risk. Furthermore, in particular among subjects at medium risk, current preventive strategies are limited by the low incidence of preventable events which makes it necessary to also treat the vast majority of subjects who would not develop cardiac events even without any treatment. An improvement in preventive strategies for IHD can be achieved with the identification of: (1) new risk factors; (2) genotypes enhancing the susceptibility to specific risk factors; (3) phenotypes and genotypes making patients susceptible to specific preventive strategies; (4) genotypes protecting from risk factors. Although a word of caution is necessary as a number of recent studies on genetic markers, on new risk factors and on the interaction between genetic markers and environment have failed to withstand the rigour of population-based studies, the early findings available to date suggest that cost-effective preventive strategies based on individual susceptibility to specific predisposing and precipitating causes of MI may become a reality in the foreseeable future.

Biomarkers↗
PubMed2001

Spinal cord stimulation in patients with refractory anginal pain and normal coronary arteries.

BACKGROUND: Spinal cord stimulation (SCS) has been shown to be effective in patients with refractory angina and coronary artery disease. No previous study assessed the clinical effects of SCS in patients with refractory angina who present angiographically normal coronary arteries. METHODS: SCS was performed in 7 patients (4 men, 3 women, mean age 59.3 +/- 11 years) with refractory angina and normal coronary arteries. Clinical status was assessed 1 month after SCS device implantation and at a mean follow-up of 11 months (range 2-17 months) by: 1) an estimate of the number of anginal attacks and nitrate consumption in the 2 weeks prior to implantation and to follow-up visits; 2) a score of quality of life by a visual analogic scale; 3) a five-item questionnaire assessing effort angina and satisfaction with treatment; 4) treadmill exercise testing. RESULTS: At the last follow-up the number of anginal episodes (p < 0.001) and nitrate consumption (p < 0.004) were both reduced by SCS. Visual analogic scale score improved from 2.1 +/- 0.98 to 9.0 +/- 0.9 (p < 0.001) at 1 month and to 6.4 +/- 2.3 (p < 0.01) at the last follow-up. Questionnaire analysis showed that mild (p = 0.006) and moderate (p = 0.000) physical activity, as well as patient satisfaction with anginal status (p = 0.000) and with current treatment (p = 0.000) all improved by SCS. Finally, time to 1 mm ST segment depression, time to angina, and exercise duration were all prolonged by SCS. CONCLUSIONS: Our data point out that SCS may considerably improve anginal symptoms and exercise tolerance in a significant number of patients with refractory angina and normal coronary arteries and therefore it should be considered as a valuable treatment option in this group of patients.

Electric Stimulation Therapy↗