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Biomedical subjects

F Fabbiocchi

Publications and source records attributed to F Fabbiocchi.

46 records · Page 3Linked to original sources
PubMed1988

Coronary vasomotor and therapeutic influences of propranolol and nifedipine on the spontaneous component of mixed angina.

In 24 patients with spontaneous and effort-related angina (mixed angina), propranolol (80 mg q.i.d.) was significantly more beneficial than nifedipine (20 mg q.i.d.) on the number, duration and severity of the spontaneous manifestations. In some cases nifedipine elicited a paradoxical response. These patterns are unlikely to have resulted from different influences on the myocardial oxygen demands, since heart rate was steady before the occurrence of ischaemia and systemic arterial pressure was equally reduced in all patients. Sublingual nifedipine (10 mg) was tested in 12 patients and the residual lumen diameter of significant (greater than 50%) coronary stenoses (quantitative angiography) was unchanged in one, enhanced in seven and reduced in four of them. Lumen variations ranged from +1.59 to -1.2 mm and correlated closely with the results of oral nifedipine treatment. Propranolol (0.1 mg kg-1 i.v.) was tested in the other 12 cases and in none did variations of stenosis lumen diameter exceed 0.3 mm. These observations indicate that: in a number of lesions a portion of pliable wall may offer a compliant substrate for vasomotor influences; this may be the major factor whereby coronary obstructions cause spontaneous, besides effort-related angina; nifedipine is effective on the former manifestation provided that it does not promote stenosis constriction; propranolol may result in benefit through bradycardia facilitating coronary flow in diastole and reducing the baseline metabolic demands, to elevate the threshold of ischaemia during transient impedance to flow.

Administration, Sublingual↗
PubMed1988

Nifedipine and angina pectoris. Short-term changes in quantitative coronary angiography with nifedipine and clinical response to treatment in effort-induced, mixed, and spontaneous angina pectoris.

Changes induced by nifedipine (10 mg sublingually) in the residual luminal diameter of significant (greater than 50 percent) coronary lesions were assessed angiographically in 69 patients with effort-induced angina (group 1), in 22 patients with mixed angina (group 2), and in 14 patients with Prinzmetal's angina (group 3). These changes were related to the clinical response to treatment with the same drug, as evaluated through diary records and Holter monitoring in the mixed (spontaneous component) and Prinzmetal forms and through exercise testing in effort-induced and mixed (effort-associated component) angina. In groups 1 and 2, segments of stenotic vessels showed either an increase or decrease or no change in diameter with the calcium antagonist; in group 3, the majority of the lesions had compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (20 percent [14/69] unchanged; 19 percent [13/69] worsened) and mixed (41 percent [9/22] exacerbated) forms; 100 percent of the 14 patients with the Prinzmetal form had relief of the anginal episodes. In group 1, the response to exercise tests was dissociated from the short-term vasomotor pattern, and the pressure-rate product failed to explain the clinical results. Forty-five percent (ten) of the patients in group 2 showed significant short-term widening of critical stenoses, as well as obvious improvement; patients who did worse with treatment in this group had reacted to nifedipine with narrowing of critical stenoses. These data suggest that the response to nifedipine of classic effort-induced angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina, and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmetal form are quite sensitive to the relaxant action of calcium blockade, and this probably represents a background to the highly positive clinical response to treatment.

Angina Pectoris↗
PubMed1987

Increased cardiac electrical instability concomitant with pacing induced repolarisation abnormalities.

The relation between the occurrence of repolarisation abnormalities after right ventricular pacing and spontaneous arrhythmias was investigated in 16 patients in whom the sick sinus syndrome was suspected. All patients had normal QRS complexes and T waves in the electrocardiogram before pacing and required atrial stimulation and His bundle recording for diagnostic purposes. Patients were randomised into a study group or a control group. In the eight patients in the study group right ventricular pacing was performed for 12 hours, and was followed by inversion of the T wave in surface leads II, III, aVF, and V2-V5 and lengthening of the QTc interval. The frequency and complexity of ventricular arrhythmias increased after pacing in six patients who had ventricular extrasystoles in the baseline Holter recording. As the configuration of the T wave became normal the frequency of ventricular extrasystoles returned to baseline values. In the control group of eight patients ventricular pacing was not performed after the electrophysiological study and no changes were seen in T wave configuration and in the frequency of spontaneous arrhythmias. These results suggest that the post-pacing repolarisation abnormalities reflect abnormal electrical properties of the ventricle and that in some cases they lead to increased electrical instability.

Adult↗
PubMed1987

Analgesic and hemodynamic effects of buprenorphine in acute infarction of the heart.

The analgesic, hemodynamic and respiratory effects of buprenorphine (0.3 mg i.v.) were monitored in 15 coronary care unit-admitted patients presenting with myocardial infarction who were in functional class I according to the Killip classification. At the time of the study, 8 of them had unequivocal precordial pain (group 1); the remaining 7 were painfree (group 2). The agent showed a prompt and potent analgesic action. It also induced a slight decrease in mean aortic pressure associated with a reduction in systemic vascular resistance and an increase in cardiac index, a rise in the pulmonary arterial pressure and arteriolar resistance and right atrial pressure, a reduction in arterial pO2 and pH and an increase in pCO2. Tension-time-indices of the left and right ventricles varied in parallel with variations in aortic and pulmonary artery pressure, respectively. These responses were probably unrelated to analgesia since they were similar in groups 1 and 2. Changes in systemic circulation were such as to possibly decrease the contractile effort and the oxygen need of the left ventricle and the size of infarction. On the contrary, the rise in pulmonary arterial pressure imposes a hemodynamic burden on the right ventricle that, depending on the patient's condition, may assume clinical importance. It is felt that the use of buprenorphine in myocardial infarction should be restricted to uncomplicated and selected cases.

Buprenorphine↗
PubMed1984

Disparate unloading efficacy of the calcium channel blockers, verapamil and nifedipine, on the failing hypertensive left ventricle.

Calcium channel blockers reduce arterial smooth muscle tone and lower blood pressure. They may be regarded as left ventricular (LV) unloading agents. LV unloading efficacy of nifedipine (15 patients) and verapamil (14 patients) was tested in hypertensive decompensated patients, during a 1-month treatment period. Nifedipine persistently reduced systemic vascular resistance (SVR), mean arterial pressure, mean pulmonary wedge pressure (PWP), and LV diastolic diameter, and improved cardiac index and velocity of circumferential fiber shortening (Vcf). All of the patients had relief from dyspnea and reduction in heart size. The only side effect was ankle edema in six. Verapamil reduced SVR and mean arterial pressure and was not effective on PWP, LV diastolic diameter, and Vcf. The drug was discontinued in two patients who developed severe dyspnea at rest after 3 to 4 days of continuous oral treatment. Clinical symptoms and signs did not improve in the remaining patients despite persistent pressure reduction. A less potent vasodilating action of verapamil and a prominent depression in cardiac contractility may account for the differential results with the two compounds, in spite of a shared vasodilating antihypertensive effect. These findings indicate that functional changes in the failing hypertensive heart may differ from one calcium blocker to another as a result of interaction and relative preponderance of influence on afterload and contractility.

Cardiac Output↗
PubMed1983

Clinical use of calcium channel blockers as ventricular unloading agents.

Calcium channel blockers relax the arterial smooth vasculature and lower blood pressure when it is elevated because of excessive vasoconstriction. They may be regarded as ventricular unloading agents. Nifedipine (11 cases, Group 1) and verapamil (12 cases, Group 2) were tested in hypertensive patients with cardiac enlargement (LV diastolic diameter greater than or equal to 60 mm), ECG signs of LV strain, lung congestion and dyspnea at rest, in an acute (nifedipine 20 mg; verapamil 160 mg) and 1-month (nifedipine 20 mg q.i.d.; verapamil 160 mg t.i.d.) therapeutic evaluation. In the acute study nifedipine reduced systemic vascular resistance (SVR), mean arterial pressure (MAP), mean pulmonary wedge pressure (PWP) and LV diastolic diameter (DD) and improved cardiac index (CI) and Vcf. In Group 2 verapamil reduced SVR and MAP, improved CI and was not effective on PWP, LV DD and Vcf. Verapamil was discontinued in 2 patients who developed severe dyspnea at rest after 3-4 days of continued oral treatment. At the end of the trial Vcf, PWP and LV DD were unchanged in the remaining subjects in Group 2 despite persistent pressure reduction. In Group 1 all of the patients had relief of dyspnea and lung congestion, reduction of heart size, persistent decrease of MAP and PWP, and improvement in Vcf. The only side effect was ankle edema in 4 cases. A less potent vasodilating action of verapamil and a predominant depression in cardiac contractility may account for the different results with the two drugs, in spite of a shared antihypertensive effect. These findings prove that functional changes in the failing hypertensive heart may differ after nifedipine compared to verapamil as a result of interaction and relative preponderance of influences on afterload and contractility.

Adult↗