PubMed Health⌕ Search

Biomedical subjects

G Novo

Publications and source records attributed to G Novo.

7 recordsLinked to original sources
PubMed2006

Changes of arterial hemodynamics in patients with type 2 diabetes mellitus or impaired glucose tolerance.

AIM: The aim of our study was to evaluate the arterial hemodynamics in patients with type 2 diabetes mellitus or impaired glucose tolerance without clinical or Doppler evidence of peripheral arterial disease, in order to early detect vascular damage. METHODS: We studied 20 subjects (12 men and 8 women, aged between 48 and 62 years) with type 2 diabetes mellitus (Group 1), 20 subjects (11 men and 9 women, aged between 49 and 61 years) with reduced glucose tolerance (Group 2), and 20 normal subjects (10 men and 10 women, aged between 48 and 62 years) (Group 3). Each subject underwent strain-gauge plethysmography and the following parameters were evaluated: rest flow (RF); peak flow (PF); PF/RF ratio; time to peak flow (tPF); half-time (t 1/2) and total time (tT) of hyperemic response; basal vascular resistances (BVR) and minimal vascular resistances (MVR). RESULTS: There was no difference among groups in RF, but maximal postischemic flow was reduced in patients with diabetes and with impaired glucose tolerance. The MVR showed a similar behavior, while the basal ones were increased only in the diabetic group. Finally, the t1/2 and the tT of the hyperemic response, that reflect arteriolar reactivity, were significantly reduced, if compared with controls. No significant differences between Group 1 and 2 were found. CONCLUSIONS: These results confirm the presence of hemodynamic modifications in the vascular bed of both diabetics and patients with impaired glucose tolerance, as compared with normal subjects.

Analysis of Variance↗
PubMed2006

Carotid and peripheral atherosclerosis in patients who underwent primary percutaneous coronary intervention and outcome associated with multifocal atherosclerosis.

AIM: The aim of our study was to determine if patients with multifocal atherosclerosis have a worse prognosis than patients with atherosclerosis only in the coronary bed. METHODS: We studied 45 subjects admitted to intensive coronary care unit of the Division of Cardiology with the diagnosis of acute myocardial infarction (AMI). Traditional cardiovascular risk factors were investigated and laboratory analysis included measurement of plasma lipids, glycemia, fibrinogen and high-sensitivity-C-reactive protein (hs-CRP). Each patient underwent coronary-angiography as well as carotid and peripheral arterial ultrasound examination. A follow-up of 13+/-2 months was performed. RESULTS: We found that the severity of coronary atherosclerosis is significantly associated with the presence of carotid (P<0.05) and peripheral atherosclerosis (P<0.005). Markers of inflammation, hs-CRP (P<0.005) and fibrinogen (P<0.05), were significantly associated with multifocal atherosclerosis. We have shown that an increased number of coronary vessels with atherosclerotic stenosis is associated with a higher value of carotid (P<0.0001) and peripheral intima media thickness (P<0.0001). During 13 months of follow-up the incidence of fatal or non fatal events was 18%. The multivariate analysis showed that the variables independently associated with fatal and non fatal events were: male sex (P<0.001), family history of cardiovascular disease (P<0.005), hypertension (P<0.01), diabetes mellitus (P<0.05), higher levels of total cholesterol (P<0.05), smoking habit (P<0.05), and multifocal atherosclerosis (P<0.05). CONCLUSIONS: The ultrasound examination of carotid and peripheral atherosclerotic lesions may be useful in placing patients with AMI in a category of higher risk of cerebrovascular and cardiovascular events. Moreover, the precocious identification of patients at risk can suggest a more aggressive pharmacological treatment and a more accurate follow-up in order to avoid future events.

Angioplasty, Balloon, Coronary↗
PubMed2005

TFPI antigen and activity levels in patients with asymptomatic atherosclerosis and target organ acute and chronic complications.

AIM: In patients with atherosclerosis there is an activation of the tissue factor mediated coagulation cascade. The aim of our study was to ascertain if there is a relationship between increased tissue factor pathway inhibitor (TFPI) antigen and activity plasma levels and atherosclerosis. METHODS DESIGN: case-control study. SETTING: Department of Internal Medicine and Cardiovascular Diseases, University of Palermo and Laboratory of Genetics and Molecular Biology, Mayo Clinic, Rochester, MN, USA. PATIENTS: 63 consecutive patients with asymptomatic atherosclerosis or with its acute or chronic complications, and 20 healthy volunteers. MEASUREMENTS: TFPI antigen was detected by an immunoenzimatic assay (Imunobind total TFPI ELISA kit, American Diagnostica Inc., USA). TFPI activity was evaluated by an activity assay (Actichrome TFPI activity assay, American Diagnostica Inc., USA). RESULTS: PATIENTS with chronic (P=0.0001 for TFPI Ag, P=0.006 for TFPI Ac) and acute (P=0.04 for TFPI Ag, P=0.01 for TFPI Ac) vascular disease and with asymptomatic carotid plaque (P=0.0019 for TFPI Ag, P<0.05 for TFPI Ac) had significantly increased TFPI antigen and activity plasma levels vs healthy volunteers. Moreover, patients with chronic vascular disease had higher TFPI Ag levels vs patients with asymptomatic atherosclerosis (P=0.0013). CONCLUSIONS: The originality of our study was the finding of increased TFPI levels, not only in patients with acute complication of atherosclerosis, but also in those with chronic vascular disease and with asymptomatic carotid plaque.

Adult↗
PubMed2001

Effects of drug therapy on cardiac arrhythmias and ischemia in hypertensives with LVH.

Left ventricular hypertrophy (LVH) in hypertensive subjects is associated with an increased prevalence of ventricular arrhythmias. To evaluate the effect of antihypertensive treatment on cardiac arrhythmias (CA) and transient episodes of myocardial ischemia (TEMI), we studied 46 hypertensive patients with LVH, divided into four groups randomly treated with enalapril, hydrochlorothiazide (HCTZ), atenolol, or verapamil (SR-V) for 6 months. Office blood pressure and office heart rate values were recorded, in basal conditions, after 1 and 6 months of treatment, and all patients underwent echocardiography, electrocardiographic Holter monitoring, and stress testing. All drugs significantly lowered blood pressure, whereas left ventricular mass index was reduced by atenolol, enalapril, and SR-V, but not by HCTZ. Treatment induced a significant reduction in the number of patients with supraventricular arrhythmias (35 v 15, P < .034, and 28 v 8, excluding patients treated with HCTZ, P < .008). The number of patients with ventricular arrhythmias was also reduced (32 v 16 considering all groups, P < .08, and 24 v 9, excluding patients treated with HCTZ, P < .04). The number of TEMI during Holter monitoring significantly decreased from 47 to 23 (P = .043) in all patients, and from 39 to 14 (P = .013) excluding patients treated with HCTZ. In all groups, irrespective of treatment, a reduction of blood pressure, heart rate, and systolic blood pressure/heart rate product measured by exercise stress test was observed. The present study shows that in hypertensive patients with LVH, antihypertensive treatment with atenolol, enalapril and SR-V reduces LVH and decreases the prevalence of CA and TEMI. Treatment with HCTZ during the 6-month study did not alter LVH and did not appear to reduce CA and TEMI.

Adult↗
PubMed1999

Increased plasma levels of fibrinogen in acute and chronic ischemic coronary syndromes.

BACKGROUND: The aim of this study was to evaluate the pathophysiological role of fibrinogen in patients with chronic or acute ischemic coronary syndromes on the basis of epidemiological and clinical evidences showing the importance of fibrinogen as a risk factor for cardiovascular diseases and atherosclerosis progression. METHODS: We evaluated the behavior of plasma fibrinogen in 310 hospitalized patients with 1) acute myocardial infarction (n = 98); 2) unstable angina (n = 87); 3) chronic ischemic heart disease (n = 75); and 4) in controls without myocardial ischemia (n = 50). Fibrinogen was evaluated, by using the Clauss method, on day 1 and 5 during in hospital-stay and at 6-month follow-up in patients suffering from acute myocardial infarction. RESULTS: Plasma levels of fibrinogen were higher in patients with chronic ischemic heart disease (335.3 +/- 81.2 mg/dl, p < 0.001) and especially in patients with acute myocardial infarction (454.72 +/- 69.5 mg/dl, p < 0.00001) and unstable angina (382.6 +/- 101.3 mg/dl, p < 0.00025) in comparison with controls (271.28 +/- 62.4 mg/dl). Q wave myocardial infarction showed higher levels of fibrinogen than non-Q wave (461.3 +/- 95.8 vs 422.5 +/- 71.3 mg/dl, p < 0.02). Patients with acute myocardial infarction showed a further increase in fibrinogen on day 5 in comparison with entry levels (525.88 +/- 87.3 vs 454.7 +/- 69.5 mg/dl, p < 0.00001) regardless of the fibrinolytic treatment. Patients who died (n = 6) or had severe arrhythmias (n = 4) during in-hospital stay as well as those with post-infarction angina (n = 20) showed higher fibrinogen levels. CONCLUSIONS: Our results confirm the role of fibrinogen as a risk factor for ischemic heart disease, especially in patients with unstable angina and acute myocardial infarction. In the latter, elevated fibrinogen values seem also to be associated with a worsen prognosis during hospitalization.

Acute Disease↗