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Biomedical subjects

G Botti

Publications and source records attributed to G Botti.

At least 127 records · Page 7Linked to original sources
PubMed1981

[Selective coronary scintiscanning].

30 patients, undergoing coronary angiography for diagnostic and/or bypass surgery evaluation, have been studied also by intracoronary scintigraphy (IS). Scintigraphic and angiographic data have been compared: --21 cases had concordant results: normal in 2 patients (quite normal coronary system); pathological in 19, accounting for a damage both of the principal coronary artery branches and the arteriolar-capillary system: --6 cases had a pathological angiography with a normal IS: an indication of a normal myocardial perfusion; --in 3 cases a normal angiography was coupled with a pathological IS, pointing out a damage of the arteriolar-capillary system. On the basis of these results and of the literature, the AA. emphasize that the IS, allowing an exact evaluation of the myocardial perfusion, complete the essential morphological informations of the coronary angiography and it is specifically useful: --in the candidates to bypass coronary surgery; a viable myocardium is important both for surgery indication and results; --in bypassed patients to assess patency and the actual blood delivery (also for the low reliability of e.v. Thallium); --in patients with typical angina and positive stress test but with normal coronary angiography, to establish an organic lesion of the arteriolar-capillary system.

Adult↗
PubMed1981

[Treatment of acute myocardial infarction with verapamil. Hemodynamic effects and electrical changes studied by body surface maps (author's transl)].

The effects of Verapamil on main haemodinamic parameters and on Max sigma pos., sigma Q15, Max sigma pos./Max sigma neg. and sigma ST, studied by automatic recording of thoracic maps, were evaluated in 11 patients with acute myocardial infarction within 6 hours from pain onset. Verapamil was given at the dose of 0.1 mg/Kg followed by infusion of 0.035 mg/min. Hemodynamic measurements were made before and 15 minutes after Verapamil; the maps were recorded before and 5, 15 and 30 minutes after Verapamil. Heart rate and sistolic arterial pressure were reduced, though not significantly: right atrial pressure, pulmonary pressures and capillary pulmonary pressure remained unchanged. On the contrary, the reduction of diastolic arterial pressure (from 94 +/- 4.2 to 88 +/- 4.5 mmHg; P less than 0.05) and of cardiac index (from 3.1 +/- 0.11 to 3 +/- 0.11; P less than 0.05) was important. Max sigma pos. increased after 15 minutes from 11619 +/- 1970 to 12349 +/- 2151 microV (P less than 0.01), but il decreased after 30 minutes to 11037 +/- 2042 microV (P less than 0.05). Max sigma pos./Max sigma neg. ratio increased significantly after 5 and 15 minutes. Sigma Q15 increased significantly only after 30 minutes (from 7198 +/- 1643 to 8688 +/- 1541 microV; P less than 0.05). Sigma ST showed a transient, non significant increase after 5 minutes, but decreased significantly after 30 minutes (from 76664 +/- 19505 to 67157 +/- 18581 microV; P less than 0.05). The results show that Verapamil does not cause worsening of main haemodinamic parameters during acute, non complicated myocardial infarction and reduces significantly ST segment elevation. The Authors discuss also a possible electrophysiological effect of Verapamil on action potential of ischemic cells, responsible for early increase of sigma ST observed in some patients.

Aged↗
PubMed1980

[Changes on release of MB isoenzyme of creatine kinase by propranolol in acute myocardial infarction (author's transl)].

MB isoenzyme of creatine kinase was measured every 3 hours during the first 24 hours of admission to C.C.U. and successively every 4-6 hours in the next 24-48 hours in 42 patients with acute transmural myocardial infarction. The pain-C.C.U. admission time interval was less than 6 hours in all cases. 22 patients were treated by propranolol (2 mg bolus followed by 0.1 mg/Kg/die for the next 48 hours in continuous i.v. infusion), 20 patients served as a control. Cumulated activity, peak plasma value, rate of release and total duration of release of MB-CK did not differ significantly between the two groups. In patients treated within 3 hours from pain onset (n = 12) cumulated activity, peak plasma value and rate of release of MB-CK were significantly inferior than control group. In patients treated between the 3rd and 6th hour from pain onset (n = 10) the total duration of release of isoenzyme was significantly prolonged. No treated patients developed clinical or radiologic signs of cardiac insufficiency. The incidence of ventricular arrhythmias was 17% in the treated group vs. 62% in the control group (P < 0.05). The data show that propranolol, if started early in the course of acute myocardial infarction, reduces significantly infarct size and slows down the evolution of necrotic process.

Clinical Trials as Topic↗
PubMed1980

[Ischemic and non ischemic electrophysiologic changes during selective coronary arteriography. Their role in the pathogenesis of the electrocardiographic changes and arrhythmias (author's transl)].

The results of a study made in mae recording the right ventricular monophasic action potential (RV MAP) by suction electrocatheter during coronary arteriography (35 cases) are reported. Normally, when no coronary spasm is present, coronary arteriography provokes a prolongation of MAP of the myocardial diffusion of the contrast medium. On the contrary in five cases, in which right coronary spasm occurred, modifications of a clear ischemic pattern were seen: a shortening of the RV MAP phase 2 in two cases; a reduction of the amplitude and rate of the RV MAP phase 0 in one case; both shortening of total duration of RV MAP and changes of its 0 phase in other two cases. The Authors compare these clinical observations with the experimental data and discuss the role of these different electrophysiological alterations in the pathogenesis of the electrocardiographic changes and arrhythmias.

Adult↗
PubMed1979

Preliminary report on electrophysiological effectiveness of creatinol O-phosphate (COP) in human subjects.

N-Methyl-N-(beta-hydroxyethyl) guanidine O-phosphate (creatinol O-phosphate, COP), in previous pharmacological and clinical research showed useful effects on both normal and ischemic heart. These effects can be reconduced to a protective action of COP on cell membrane. In this investigation the possible electrophysiological effects of COP were ascertained in 6 patients, some of whom were free of excitation-conduction disturbances, while others were suffering from sinusal automaticity of A-V conduction alterations. When the nodal A-V conduction was slowed by iatrogenic or functional factors, COP as well as atropine improved it. Thus both COP and atropine act in the non-organic component of the conduction disturbances. The organic component was not affected by both the drugs. The effect of atropine was more evident than that of COP. All the electrophysiological parameters were not affected by COP. This fact allows COP to be administered with absolute safety even in the presence of alterations in the formation and conduction of the stimuli.

Aged↗
PubMed1979

[Recording of monophasic action potentials of the right ventricle in a case of long QT and isolated alternation of the U wave].

Monophasic action potentials (MAP) of the right ventricle were recorded with suction electrodes in a case of long QTU, electrical alternans of the U wave and "torsades de pointe" by hypocalcaemia. Two electrophysiological features were observed:--a notable difference in the duration of MAPs of different zones of the right ventricle;--a change in the length and appearances of phase 3 of the longest MAPs with an inconstant bulge (delayed repolarisation) in the terminal portion of these same MAPs. These changes, which favourise focal reentry phenomena and/or reciprocal conduction are the probable explanation of the pathogenesis of episodes of "torsades de pointe". A reduction in the conductance of potassium associated or related to hypocalcaemia probably explains the second of the two changes.

Aged↗
PubMed1978

[Acute myocardial infarction in a case of obstructive cardiomyopathy of the left ventricle (author's transl)].

A case of acute myocardial infarction in 64 year old man with idiopathic hypertrophic obstructive cardiomyopathy of left ventricle is described. The Authors emphasize the rarity of association and that the diagnosis of obstructive cardiomyopathy in the elderly is always almost misinterpreted. This depends on the poor specificity of clinical and phonocardiographic findings, both basal and under pharmacological tests. The Authors point out that in adult patients with left ventricular idiopathic obstructive cardiomyopathy who must be operated also selective coronary angiography should be performed.

Cardiomyopathy, Hypertrophic↗
PubMed1977

[Origin of the left circumflex coronary artery from the right Valsalva sinus. Two cases with clinical and instrumental signs of coronary insufficiency (author's transl)].

Two cases of isolated anomalous origin of the left circumflex coronary artery from the right Valsalva sinus are described. In contrast with all the cases reported in the literature, both our female patients had typical angina; in one case, moreover, in coincidence with the precordial pain there were significant alterations of the repolarization, also caused by stress testing with the bicycle ergometer. On the basis of these findings, the authors believe that in patients with this anomaly the angina might be produced through a sharp decrease in the circumflex coronary artery blood flow correlated with caliber changes of the aorta.

Coronary Angiography↗
PubMed1976

[Effects of Bunaphtine on right atrial and ventricular monophasic action potentials in man. Preliminary note (author's transl)].

Effects of Bunaphtine on right atrial and ventricular monophasic action potentials were investigated in 6 patients using the technique of endocavitary recording with a suction electrode. The authors found that the drug, given intravenously in the usual therapeutic dosages, increases the total duration of MAP both atrial and ventricular, together with quite a proportional ERP prolongation. At ventricular level MAP's increase in correlated to a prevailing and strong increase of phase 3. However, the variations of the MAP's amplitude, its O dv/dt phase and the cardiac specific conduction's alterations (noted only at higher dosages) have been inconstant and poor on the whole. On the basis of these results, the mechanism of the action of the drug is discussed.

Action Potentials↗
PubMed1976

[A study of the mechanism of the action of Bunaphtine recording the myocardial monophasic action potentials in man. Conclusive report (author's transl)].

In this paper the authors conclude their study of the mechanism of the action of Bunaphtine. Both atrial and ventricular MAP were recorded by a suction electrode in 13 patients before and after Bunaphtine (1.5-2 and 2.5 mg/Kg i.v.). With the lower dosages, the drug acts specifically on repolarization: it greatly increases the duration of MAP, together with a proportional ERP prolongation; the ERP/MAP ratio is not changed. With the higher dosages, there is a greater effect on the depolarization velocity (decrease of the O dv/dt phase of MAP) and on the conduction, this last being less evident. At the atrial level there is a conspicous ERP prolongation, with a remarkable increase of ERP/MAP ratio. There is full agreement between these results and those obtained experimentally on the dog and in vitro. Bunaphtine has therefore unquestionable antiarrhythmic properties and it can have a double action mechanism; with higher dosages its action-quinidine-like-is predominant at the atrial level.

Action Potentials↗