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Biomedical subjects

F Bonechi

Publications and source records attributed to F Bonechi.

12 recordsLinked to original sources
PubMed1992

Automated blood pressure determination during exercise test. Clinical evaluation of a new automated device.

The accuracy and reproducibility of a new automatic device (P) specially designed for noninvasive blood pressure monitoring during the exercise stress test were evaluated in 50 consecutive subjects (34 normotensives and 16 hypertensives). Automatic measurements were compared with those taken by a sphygmomanometer (RR). A good agreement between systolic pressure values obtained by the two methods was found (RR 159 +/- 30 mmHg, P 158 +/- 28 mmHg, mean difference = -1.53 +/- 13 mmHg, p = 0.166, ns). On the contrary the new device significantly underestimated diastolic pressure values (RR 89.3 +/- 13 mmHg; P 84 +/- 13 mmHg, mean difference -5.37 +/- 9.3, p < 0.001). In conclusion the new device seems able to measure systolic but underestimates diastolic blood pressure both in hypertensives and in normotensives during the effort test.

Adult↗
PubMed1992

[Efficacy of intravenous and per os propafenone in the ambulatory treatment of recent-onset atrial fibrillation].

Propafenone efficacy in conversion of atrial fibrillation to sinus rhythm has been well documented. In this study we considered propafenone efficacy according to a graduated protocol of administration. Forty-two patients with recent-onset atrial fibrillation, without left ventricular failure, ischemic symptoms and in absence of antiarrhythmical treatment, were treated according to the following protocol: propafenone 1 mg/kg i.v. (5 min) followed, in the non-responder patient group, by a second dose, 0.5 mg/kg i.v. (15 min). Patients with persistent atrial fibrillation received 900 mg/daily of propafenone per os, at home for two days. Thereafter, patients still not restored to sinus rhythm were considered non-responders. Patients who were converted to sinus rhythm received 450 mg daily of the drug (oral administration), at home, as antiarrhythmical prophylaxis, for three months. Thirty-nine patients were converted to sinus rhythm (92.8%), 24 of them after intravenous propafenone (57.2%), and the other 15 (35.6%) after oral administration of the drug. The average heart rate in patients not converted to sinus rhythm with intravenous propafenone was significantly reduced after drug administration, compared to basal values (from 136.4 +/- 18.1 to 107.1 +/- 17.6, p < 0.01), allowing home treatment. No major cardiac effects were observed after infusion, nor after oral administration of propafenone. During a three-month follow-up we observed 3 cases of relapsed atrial fibrillation and 2 discontinued treatments due to minor gastroenteric side effects. In conclusion, propafenone therapy in ambulatory regimen is safe and effective in patients with recent-onset atrial fibrillation. In many patients refractory to IV treatment, further therapeutic success may be achieved following oral propafenone administration.

Administration, Oral↗
PubMed1991

Diagnostic accuracy of peak exercise echocardiography in coronary artery disease: comparison with thallium-201 myocardial scintigraphy.

To evaluate the accuracy of exercise two-dimensional echocardiography for the recognition of coronary artery disease, 53 patients (46 men and 7 women, age range 35 to 69 years) without either previous myocardial infarction or resting wall motion abnormalities, were studied. According to coronary angiography 26 had normal coronary arteries, 14 had one-vessel, seven had two-vessel, and six had three-vessel disease. After withdrawal of any therapy, all patients underwent a single exercise stress test with a stress table during which cine-loop digitized echocardiography was acquired and 74 MBq of thallium-201 (TI-201) were injected. Echocardiographic images were evaluated at rest and at peak exercise. Three-view planar scintigraphic images were collected immediately after exercise and 4 hours later. For the overall recognition of coronary artery disease, exercise electrocardiography had 77.8% sensitivity and 65.4% specificity; myocardial scintigraphy had 100% sensitivity and 92.3% specificity; and exercise echocardiography had 92.6% sensitivity and 96.2% specificity (both NS versus myocardial scintigraphy). Global accuracy was 71.7% for exercise electrocardiography, 94.3% for stress echocardiography, and 96.2% for myocardial scintigraphy. For the classification of the individual involved coronary arteries, the sensitivity of myocardial scintigraphy was 84.8% and that of exercise echocardiography was 63% (p less than 0.01); the related specificities were 98% and 98.2% respectively (NS). It may be concluded that exercise echocardiography is highly accurate for the recognition of coronary artery disease, whereas it appears less sensitive in the identification of the involved vessels, particularly in patients with multivessel disease.

Adult↗
PubMed1991

[Changes in the wall motion of left ventricle in dipyridamole-induced ischemic cardiopathy studied by nuclear magnetic resonance. A comparison with myocardial scintigraphy with 99mTc MIBI].

To investigate whether magnetic resonance imaging (NMR) can detect alterations in LV contractility during myocardial ischemia, ten patients aged 32-72 with coronary artery disease underwent ECG gated NMR performed at 0.5 Tesla after intravenous infusion of high dose dipyridamole (DP) (0.7 mg/Kg) over 5 minutes. LV contraction in planes similar to echo short axis projection was imaged under condition, 3' and 15-20' after infusion of DP by fast multiphasic imaging (FMI), multiple angulated cine-NMR sequence with a temporal resolution of 50 m/sec. Entity and size of perfusion defects after DP were determined by Tc 99m MIBI myocardial scintigraphy. In all patients changes in LV contractility appeared at NMR in the same site of perfusion impairments revealed with MIBI. In 8 patients the alterations lasted even more than 20' after the first NMR scan. NMR provides the opportunity of performing long-lasting assessment of ventricular wall contractility and enables to exactly localize the site and extension of kinetic changes as well as their time of onset and time duration.

Contrast Media↗
PubMed1991

Anaerobic threshold in patients with exercise-induced myocardial ischemia.

The aim of the present study was to investigate the ventilatory anaerobic threshold in patients with exercise-induced myocardial ischemia. Ventilatory volumes and gas exchanges were measured during treadmill stress testing in 36 patients (11 with previous myocardial infarction) with electrocardiographic criteria of myocardial ischemia during the test and in 23 healthy, untrained control subjects of equivalent age. The anaerobic threshold was detected in 32 of 36 patients (89%) and in 22 of 23 control subjects (96%). The anaerobic threshold was significantly lower in patients than in control subjects (13.5 +/- 1.9 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). In the 21 patients without previous myocardial infarction, the anaerobic threshold was also significantly lower than in the control subjects (13.9 +/- 1.6 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). Among the 21 patients without previous myocardial infarction, the 12 with a low ischemic threshold, which occurred during the first three steps of the modified Bruce protocol, had an anaerobic threshold significantly lower than the other nine patients (13.1 +/- 1.5 versus 14.9 +/- 1.0 ml/kg per minute VO2, p less than 0.01). However, even in the patients with a moderate to high ischemic threshold, the anaerobic threshold was significantly lower than in the control subjects (p less than 0.001). These data show that the anaerobic threshold can be measured in the great majority of patients with exercise-induced myocardial ischemia. The low anaerobic threshold level indicates a relevant functional impairment in these patients.

Adult↗
PubMed1990

Defective coronary prostaglandin modulation in anginal patients.

In order to investigate whether coronary vasodilating prostaglandins (PGI2 and PGE2) have a role in the pathophysiology of myocardial ischemia, 26 patients with angina pectoris and 23 control subjects (nonischemic patients) were studied by assessing coronary hemodynamics and prostaglandin formation in relation to sympathetic stimulation. Following a cold pressor test (CPT), coronary prostaglandin output markedly increased (p less than 0.001) and coronary vascular resistance (CVR) decreased (p less than 0.001) in all control subjects. In contrast, in anginal patients prostaglandins in the coronary sinus were undetectable and after CPT prostaglandin output did not increase, whereas CVR paradoxically increased (p less than 0.001). In control subjects the inhibition of coronary prostaglandin formation (by ketoprofen [1 mg/kg intravenously] or by aspirin [15 mg/kg intravenously]) caused a paradoxical increase of CVR following CPT (p less than 0.001). In anginal patients the inhibition of prostaglandins further exaggerated the increase of CVR after CPT (p less than 0.001). These results indicate that coronary vasodilating prostaglandin PGI2 and PGE2 play a role in modulating coronary vascular response to sympathetic stimulation induced by CPT. Their defective production in anginal patients may be responsible for the paradoxical increase in CVR following sympathetic stimulation.

Adult↗
PubMed1990

Physiologic role of coronary PGI2 and PGE2 in modulating coronary vascular response to sympathetic stimulation.

To investigate a physiologic role of coronary prostacyclin (PGI2) and prostaglandin E2 (PGE2) 30 patients who were not affected by coronary heart disease were evaluated for coronary hemodynamics and coronary PGI2 and PGE2 production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p less than 0.001) and decreases in coronary vascular resistance (p less than 0.001) without changes in cardiac oxygen extraction and with consequent increases in calculated myocardial oxygen consumption. Simultaneously, a marked increase in coronary PGI2 (as 6-keto-PGF1 alpha) and PGE2 formation was observed (p less than 0.001). Both ketoprofen (1 mg/kg) and aspirin (15 mg/kg) administration completely abolished PGI2 and PGE2 formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p less than 0.02; aspirin: p less than 0.05). The results of this study support a physiologic role for the coronary prostaglandins in modulating coronary vascular response to sympathetic stimulation in nonischemic patients.

Adult↗
PubMed1990

Low-dose heparin as an antithrombotic agent.

Heparin, after subcutaneous administration, has been found to be able to bind to endothelial receptors both in rabbits and in humans. N-sulphonate 35S-heparin remains bound in rabbits for at least 24 h and is able to enhance the inactivation process of thrombin and factor Xa. Heparin subcutaneously (200 U/kg) injected for 2 weeks resulted in an enhanced inactivation of thrombin and factor Xa by the endothelium. The antithrombin-enhancing activity persists longer than the anti-Xa activity. In man, daily subcutaneous administration of heparin (12,500 U/day) for 2 weeks significantly reduces the increased fibrinopeptide A plasma levels and normalizes the increased 125I-fibrinogen turnover. The present work indicates that heparin administration at a low dose represents a treatment able to remarkably enhance the antithrombotic properties of the vessel wall, independently of the presence of detectable heparin levels in the circulating blood.

Animals↗
PubMed1990

Thrombolytic versus fibrinogenolytic activity of rt-PA and streptokinase in patients with acute myocardial infarction.

In this study the concentration of plasma breakdown products of cross-linked fibrin (XDP), serum fibrinogen-fibrin degradation products (FDP), and plasma fibrinogen were measured before and at the end of the administration of single-chain recombinant tissue-type plasminogen activator (rt-PA, 100 mg IV over three hours) or streptokinase (1.5 million units over one hour), respectively, in two groups, each composed of 22 patients with acute myocardial infarction. The XDP concentration was not statistically different between the two groups at the end of thrombolytic treatment, whereas FDP and fibrinogen concentrations were significantly different (FDP: streptokinase 396 +/- 287 vs rt-PA 177 +/- 222 micrograms/mL, p less than 0.01; fibrinogen: streptokinase 71 +/- 43 vs rt-PA 181 +/- 49 mg/dL, p less than 0.001). These results indicate that the two drugs have equipotent thrombolytic activity at this administration regimen but that rt-PA causes a markedly more selective lysis of fibrin in comparison with streptokinase.

Adult↗
PubMed1989

Blood clotting active drugs in long-term post-myocardial infarction treatment.

Oral anticoagulants have been used for over three decades in long-term post-myocardial infarction treatment. The cumulated results of the early clinical trials showed a reduction of general mortality of 20%. The reduction reached 60% when trials with adequate anti-coagulant treatment were considered. The most recent study (Sixty Plus Study 1980), a very well designed and conducted study with optimal anticoagulant dosage, reported a 2-year reduction in total mortality of 43% (p less than 0.017 vs. controls) and a reduction of reinfarction of 64.1% (p less than 0.0002). However, the incidence of major hemorrhagic episodes (27 vs. 3) and of definite intracranial hemorrhages (8 vs. 1) was very high in the treatment group with 6 deaths vs. 1 due to hemorrhage. An alternative way for controlling blood clotting activation and thrombin generation appears to be low-dose heparin treatment. In a randomized controlled clinical trial heparin administered in low doses (12,500 i.u. daily by subcutaneous route) reduced the reinfarction rate by 63% (p less than 0.05 vs. controls) and general mortality by 47% (p less than 0.05) over 2 years. Even the frequency of the fatalities attributable to thromboembolic events was significantly decreased. No hemorrhagic complication occurred in any patients. Oral anticoagulants and low-dose heparin appears to be equally effective in secondary prevention of myocardial infarction. However, low-dose heparin treatment appears to be free from the elevated risk of major hemorrhages related to oral anticoagulants and does not require any blood clotting check.

Anticoagulants↗
PubMed1988

Decrease in frequency of anginal episodes by control of thrombin generation with low-dose heparin: a controlled cross-over randomized study.

Increased thrombin generation is frequently associated with an increase in anginal activity. A cross-over, single-blind, completely randomized study was planned in order to evaluate whether the control of thrombin generation affected the increase in anginal activity. After discharge from the hospital, 24 patients (18 men and 6 women, aged 40 to 69 years) suffering from spontaneous angina were followed up to 12 months and were alternatively treated during two consecutive 6-month periods with calcium heparin, 12,500 IU by the subcutaneous route, or with placebo by the intramuscular route, in addition to the usual antianginal medications. Thrombin generation and clinical activity of angina were assessed every 15 days by measuring fibrinopeptide A (FPA) plasma levels and by grading in three classes (symptomless, mildly symptomatic, and severely symptomatic) the anginal activity on the basis of the number and the time concentration of the ischemic attacks and ECG changes. Low-dose heparin treatment significantly reduced both the FPA plasma level (from 4.1 +/- 3.7 to 2.3 +/- 1.8 ng/ml, p less than 0.001) and the clinical activity of angina. During heparin treatment, the frequency of the observations in the severely and mildly symptomatic classes decreased, respectively, by 53% and by 30%, whereas that in the symptomless class increased by 23% (p less than 0.001) in comparison with the period on placebo. Present results indicate that the control of thrombin generation obtained by low-dose heparin treatment favorably affects the degree of anginal activity in patients with spontaneous angina.

Aged↗