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Biomedical subjects

L Angoli

Publications and source records attributed to L Angoli.

At least 55 records · Page 3Linked to original sources

Increased neutrophil aggregability in coronary artery disease.

The purpose of this investigation was to study neutrophil (PMN) aggregation in the aorta and coronary sinus of 20 patients with angiographically documented coronary artery disease (group I) compared with eight patients with normal coronary arteries (group II). PMNs were separated from the other blood components and their aggregation response to Ca2+ ionophore A 23187 l x 10(-5) M (final concentration) was measured. Group I patients had higher aggregating activity in the coronary sinus than in the aorta (24.9 +/- 3.7 vs 18.7 +/- 3.4 average maximum delta T, P less than 0.01), while no difference was found in group II (coronary sinus 16.7 +/- 3.5; aorta 16.3 +/- 2.4 average maximum delta T P = NS). Among group I patients, smokers had a significantly higher aggregating activity than non-smokers, whereas no correlation was found between aggregation response and blood cholesterol values. These data suggest that the presence of atherosclerotic plaques in coronary vessels may prime PMNs so that they show greater aggregating response to subsequent stimulation.

Aorta↗

Granulocyte activation after coronary angioplasty in humans.

To determine whether percutaneous transluminal coronary angioplasty (PTCA) would lead to neutrophil activation with subsequent discharge of proteolytic enzymes, like elastase, and oxygen free radicals, like superoxide anion, blood samples were taken from the coronary sinus and aorta in 14 patients with stable angina and one-vessel disease who underwent PTCA. Neutrophils were separated by means of the Ficoll-Hypaque system and were stimulated to detect release of elastase and generation of superoxide anion. Plasma levels of elastase were also measured by an immunoenzymatic method. PTCA was successful in all patients. Plasma elastase levels increased significantly at the end of the procedure compared with pre-PTCA values both in the coronary sinus (from 129.2 +/- 16.6 to 286.6 +/- 39.7 micrograms/l, p less than 0.005) and in the aorta (from 117.4 +/- 13.6 to 258.1 +/- 41.3 micrograms/l, p less than 0.005). On the other hand, superoxide anion released in the supernatants after neutrophil stimulation by phorbol-myristate-acetate decreased after PTCA in the coronary sinus (before PTCA, 60.1 +/- 7.1; after PTCA, 40.7 +/- 6.8 nmol 1 x 10(7) granulocytes/ml/15 min, p less than 0.05), whereas a mild but not significant decrease was observed in the aorta (from 58.3 +/- 10.9 to 55.3 +/- 8.6 nmol 1 x 10(7) granulocytes/ml/15 min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Evaluation of the effects of vasodilator therapy in primary pulmonary hypertension. Experience in 7 cases].

Primary pulmonary hypertension is an uncommon but serious disease that often results in debilitating symptoms and early death. One approach to treatment has been to attempt a reduction of pulmonary artery pressure and vascular resistance by using vasodilator drugs with conflicting results in several studies. The aim of this study is to review the ten-years (1978-1988) experience of vasodilator therapy for primary pulmonary hypertension at our institute. In this period 7 patients, 5 women and 2 men, mean age 38.4 years (range 15-66) met clinical and hemodynamic criteria for primary pulmonary hypertension. At diagnosis 3/7 patients were in NYHA class III and 2/7 in class II. Diagnosis was confirmed by open lung biopsy in one case. Mean pulmonary artery pressure was 66 +/- 17 mmHg, mean value of pulmonary vascular resistances was 22.5 +/- 11 U.W. and of cardiac index 1.8 +/- 0.58 l/min/m2. Twelve different vasodilator drugs were tested during right heart catheterization in a non randomized manner. Various vasodilators were usually tested in the same patient (2 or more drugs in 6 patients). Only one patient did not tolerate acute therapy because of development of a persistent systemic hypotension. Hemodynamic responses to nitrates showed a general reduction in pulmonary artery pressure and pulmonary vascular resistances with marginal changes in cardiac index. Calcium channel-blocking agents elicited different responses in similar patients with favorable, little, no or adverse effects in pulmonary hemodynamics and sometimes a significant decrease in systemic vascular resistances. Also hydralazine showed favorable hemodynamic results in few cases but exacerbated pulmonary hypertension in others.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Acute haemodynamic effects of diltiazem in patients with recent Q-wave myocardial infarction.

The effects of diltiazem on left ventricular systolic and diastolic function were studied in 14 patients with a recent (12-20 days) Q-wave myocardial infarction. Left ventriculography with simultaneous recording of high-fidelity left ventricular pressure was performed in control conditions, and after i.v. administration of diltiazem (0.2 mg kg-1 as a bolus followed by constant infusion of 0.005 mg kg-1 min-1 lasting 8-10 min). After the administration of the drug, left ventricular systolic pressure decreased by 12.7% and mean circumferential wall stress by 14% (both P less than 0.01); the heart rate did not change; the ejection fraction increased by 9.6% (P less than 0.05) and maximum dP/dt/P by 11% (P less than 0.01). Quantitative segmental wall motion analysis showed that the beneficial effects of diltiazem on global left ventricular systolic function were associated with an increase in contraction in hypokinetic regions, where they were supplied by normal or diseased coronary vessels (both P less than 0.01). Left ventricular end-diastolic pressure decreased by 23.6% (P less than 0.05) and minimal diastolic pressure by 38% (P less than 0.05). Passive diastolic properties of the left ventricular chamber remained unaltered but isovolumic relaxation markedly improved: the T constant decreased 26% (P less than 0.01). Thus, in patients with a recent Q-wave myocardial infarction, the i.v. administration of diltiazem unloads the left ventricular chamber without showing depressant effects on myocardial contractility.

Adult↗

[Relationship between morphology of restenosis and clinical aspects in patients who had undergone coronary angioplasty].

Although restenosis after percutaneous transluminal coronary angioplasty (PTCA) may have morphologic characteristics which are not similar to the original stenosis, it is unknown if a different morphology is also associated with a different clinical presentation. Eleven consecutive patients with angina and single vessel disease had a recurrence of symptoms and restenosis within 6 months of successful PTCA. Seven patients (group I) complained of spontaneous angina before PTCA and had a positive hyperventilation test, while 4 patients complained of exercise-induced angina and had a negative hyperventilation test (group II). In group I restenosis was associated with the same clinical presentation as before PTCA and the hyperventilation test was positive in 6 patients. The angiographic morphology of restenosis was changed in 4 patients. In group II restenosis occurred with the same clinical presentation as before PTCA, the hyperventilation test was negative in 3 patients while the angiographic morphology of restenosis was unchanged in only 1 patient. Although morphology of restenosis is different from the original stenosis, clinical presentation associated with restenosis is generally the same as before PTCA. The response to vasoactive stimuli is independent from the morphology of the lesion.

Angina Pectoris↗

Spontaneous remission of variant angina documented by Holter monitoring and ergonovine testing in patients treated with calcium antagonists.

Twenty-four patients with Prinzmetal's variant angina showing a favorable initial response to calcium antagonist treatment were studied to assess the evolution of the disease and the frequency and time course of spontaneous remission. At 3, 6 and 12 months from the acute phase, patients underwent in-hospital control studies, with 48-hour Holter monitoring and ergonovine testing carried out during treatment and after its interruption. During calcium antagonist therapy complete protection from spontaneous attacks was documented in 22 of 24 patients at 3 months, in 19 of 21 at 6 months and in all 21 at 12 months; ergonovine test results were negative in 16 of 23 patients at 3 months, in 16 of 20 at 6 months and in all 20 studied at 12 months. After stopping treatment spontaneous attacks did not reappear in 7 of 24 patients (29%), 14 of 21 (66%) and 16 of 21 (76%) at 3, 6 and 12 months respectively, while the ergonovine test response remained negative in 6 of 21 (28%), 7 of 18 (39%) and 13 of 20 (65%) of the patients controlled at 3, 6 and 12 months. Thus, complete remission of angina documented by both Holter recording and ergonovine testing occurred in 5 of 24 patients (21%) at 3 months, in 7 of 21 (33%) at 6 months and in 12 of 21 (57%) at 12 months. Patients with remission of angina had a shorter duration of symptoms and more often showed normal or not critically diseased coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Coronary vasoconstrictor response to cold pressor test in variant angina: lack of relation to intracoronary thromboxane concentrations.

To test the hypothesis that intracoronary concentrations of thromboxane (Tx)A2 could influence the response to cold pressor test (CPT) in variant angina, great cardiac vein blood flow (by thermodilution) and the concentration of TxB2 (the stable metabolite of TxA2) in the great cardiac vein and aorta were measured under control conditions and during CPT in 14 patients with angina at rest associated with transient ST-segment elevation in the anterior leads. In seven patients pretreated with aspirin (intravenous administration of 3.6 mg/kg lysine salt of acetylsalicylic acid, corresponding to 2 mg/kg aspirin), TxB2 baseline concentrations were lower in both the great cardiac vein (47 +/- 19 vs 176 +/- 88 pg/ml; p less than 0.005) and the aorta (45 +/- 16 vs 109 +/- 56 pg/ml, p less than 0.02) than in seven patients who were not taking cyclooxygenase inhibitors. In the two groups, great cardiac vein flow and anterior region coronary resistance were similar under control conditions. During CPT anterior region coronary resistance increased in patients pretreated with aspirin (from 1.97 +/- 0.99 to 2.22 +/- 1.11 mm Hg/ml/min; p less than 0.02) and in patients without aspirin pretreatment (from 1.94 +/- 0.43 to 2.06 +/- 0.34 mm Hg/ml/min; p less than 0.05), and the difference between the two groups was not statistically significant. Therefore the vasoconstrictor response of coronary vessels to CPT in variant angina is not influenced by the intracoronary TxB2 concentrations and is not modified by aspirin pretreatment.

Adult↗

Coronary haemodynamic effects of short-term intravenous administration of gallopamil in patients with stable exertional angina.

The effects of short term intravenous administration of gallopamil on coronary haemodynamic variables were studied in 10 patients with stable exertional angina and angiographically confirmed coronary artery disease that affected the proximal portion of the left anterior descending artery. Blood flow in the great cardiac vein was measured by a thermodilution technique, both at rest and during ischaemia induced by atrial pacing, before and after intravenous administration of gallopamil (0.02 mg/kg as a bolus dose given over three minutes, followed by an infusion of 0.0005 mg/kg/min). Gallopamil significantly prolonged the mean (SD) duration of pacing that was tolerated (11 (2.6) vs 14.8 (2.4] min, significantly increased the mean (SD) peak heart rate attained during pacing (142 (15) vs 158 (11) beats/min), and reduced mean (SD) arterial pressure (133 (17) vs 116 (17) mm Hg). There were no changes in mean (SD) blood flow in the great cardiac vein (134.1 (57) vs 112.9 (38) ml/min, mean (SD) anterior regional coronary resistance (1.18 (0.6) vs 1.15 (0.5) mm Hg/ml/min), and mean (SD) anterior regional myocardial oxygen consumption (16.6 (6) vs 13.7 (4) ml/min). These data confirm that gallopamil is an effective antianginal agent and suggest that a reduction of myocardial oxygen demand is the predominant mechanism by which the drug exerts its beneficial effects.

Angina Pectoris↗

Myocarditis and cardiomyopathy: diagnosis by endomyocardial biopsy.

UNLABELLED: To investigate the incidence of myocarditis, 30 patients, with unexplained congestive heart failure, underwent endomyocardial biopsy. For each case three to five samples were examined on light and electron microscopy. Inflammatory infiltrates and injury to adjacent myocytes consistent with myocarditis were detected in 3 of the 30 cases (10%). Changes attributable to cardiomyopathy were found in the remaining 27 cases. Two of the three patients with biopsy-proven myocarditis were treated with prednisone and azathioprine. Their control biopsies six months later showed interstitial fibrosis and absence of inflammatory infiltrates. They clinically improved but hemodynamic and angiocardiographic patterns failed to show the expected improvement. The third patient affected by myocarditis died two weeks later. IN CONCLUSION: in our series of patients with unexplained congestive heart failure, the incidence of biopsy-proven myocarditis resulted low (10%). The results of the immunosuppressive treatment in two patients with myocarditis were unconclusive. Therefore the effectiveness of such therapy should be confirmed in a larger number of patients.

Biopsy↗

Clinical and angiographic findings in angina at rest.

The purpose of this study was to delineate the clinical, ECG, and angiographic features of a large series of consecutive patients with angina at rest. Transient ST segment elevation during pain was observed in 219 patients (group I), while 220 patients showed ST segment depression during pain (group II). Group II patients were found to have higher incidence of hypertension (p less than 0.001), prior myocardial infarction (p less than 0.0005), history of exertional angina (p less than 0.0005), and a progressive aggravation of symptoms before hospitalization (p less than 0.0005), while group I patients had a prevalence of recent onset angina (p less than 0.05) and more frequently developed severe ventricular arrhythmias during pain (p less than 0.0005). Furthermore, a larger number of patients showing ST segment depression during chest pain had multivessel disease (p less than 0.0005), left main involvement (p less than 0.005), and lower values of left ventricular ejection fraction (p less than 0.001) than patients with ST segment elevation during pain. Survival curves of medically treated patients showed a significantly better long-term prognosis in patients of group I (p less than 0.01). The direction of the ST segment shift during anginal attacks at rest may therefore allow a classification of patients included into the broad spectrum of unstable angina. This distinction should be taken into consideration in studies aimed at evaluating long-term prognosis or the results of medical and surgical therapy.

Adult↗

Effects of diltiazem on regional coronary hemodynamics during atrial pacing in patients with stable exertional angina: implications for mechanism of action.

To investigate the mechanism of the antianginal action of diltiazem in stress-induced myocardial ischemia, we studied 12 patients with stable exertional angina and disease of the proximal left anterior descending artery by measuring great cardiac vein flow (GVCF) and calculating anterior regional coronary resistance (ARCR) during myocardial ischemia induced by atrial pacing before and after intravenous administration of diltiazem (0.25 mg/kg in a bolus dose followed by continuous infusion of 0.005 mg/kg/min). Diltiazem increased the pacing time to angina from 6.9 +/- 3.5 to 10.7 +/- 4 min (p less than .001). At peak pacing heart rate was increased after diltiazem (from 128 +/- 17 to 145 +/- 17 beats/min, p less than .005), while mean arterial pressure was decreased (from 131 +/- 19 to 113 +/- 17 mm Hg, p less than .025), leaving the double product unaltered. At peak pacing no changes were observed in GCVF (from 115 +/- 46 to 119 +/- 46 ml/min, p = NS), ARCR (from 1.3 +/- 0.4 to 1.1 +/- 0.4 mm Hg/ml/min), or myocardial oxygen consumption of the anterior region (from 14.5 +/- 4.2 to 13.4 +/- 4.7 ml/min). Reduction of myocardial oxygen demand plays a major role in the antianginal action of diltiazem in patients with stress-induced myocardial ischemia.

Adult↗

Ventricular tachycardia in post-myocardial infarction patients. Preoperative and intraoperative mapping.

Ventricular tachycardia has become a relatively common complication of myocardial infarction and often is an important therapeutic problem, as it is recurrent and life-threatening. Here we report a group of 36 patients with ventricular tachycardia occurring 13 days to 30 years after a myocardial infarction. All patients were resistant to medical treatment and 34 of the 36 patients had had at least one cardiac arrest. All were candidates for surgery for their arrhythmia. The study protocol included prolonged ECG monitoring, a preoperative electrophysiological study with catheter mapping and intraoperative epicardial and endocardial mapping. A total of 52 different tachycardias were mapped in 36 patients. The procedure was facilitated by an automatic mapping device, that allowed the acquisition of 35 simultaneous signals, so that even pleomorphic ventricular tachycardias could be mapped. The information obtained from both preoperative and intraoperative maps guided surgery and restricted the extent of the surgical damage.

Adult↗

Clinical application of monitoring techniques: coronary sinus blood flow monitoring.

Measurement of coronary sinus blood flow by continuous thermodilution is a well established technique for the clinical study of myocardial perfusion. More recently, advances in catheter technology enabled regional left ventricular flow measurements. In particular, measurement of flow from the great cardiac vein appears to accurately reflect the perfusion of the left anterior descending coronary artery. This regional approach allowing the correlation with coronary arterial anatomy, has contributed to an improved understanding of the mechanisms by which functional factors interact with organic narrowing in the genesis of myocardial ischemia at rest, during provocative tests and during exercise. In addition, it has provided useful information in the evaluation of antianginal drugs through the discrimination between the effects on coronary resistance and myocardial oxygen consumption.

Angina Pectoris↗

Effects of cold stimulation on coronary haemodynamics during exercise in patients with coronary artery disease.

To assess if cold-induced vasoconstriction may persist during exercise and contribute to the development of myocardial ischaemia, we studied 11 patients with exertional angina and angiographically proven coronary artery disease, in all cases involving the proximal portion of the left anterior descending artery. Great cardiac vein flow (GCVF) was measured by the thermodilution technique and the coronary resistance of the abnormally perfused anterior region (ARCR) was calculated as the quotient of mean arterial pressure and GCVF. All patients performed a supine bicycle exercise test (ET1) until angina occurred. After recovery, they underwent a cold pressor test (CPT) and then performed a second exercise test (ET2) while cold stimulation was continued. During ET1, ARCR decreased (from 1.53 +/- 0.43 to 1.04 +/- 0.35 mmHg ml-1 min-1, P less than 0.001) as a result of the metabolic vasodilation, while it rose, although non significantly, during CPT despite the increase in double product (P less than 0.001), reflecting the augmented myocardial oxygen consumption. However, such abnormal response to CPT did not persist during ET2, because ARCR decreased to a value non significantly different from that achieved at peak ET1. In five patients, who showed a reduced exercise tolerance during ET2, ARCR dropped by 22% during ET2 compared with 34% decrease during ET1. However, such a difference was unlikely to account for the reduction in exercise tolerance, because the double product at peak ET2 was never lower than the corresponding value at peak ET1. Our data show that the inappropriate vasoconstriction induced by CPT in an abnormally perfused myocardial region does not persist during exercise, when metabolic vasodilation occurs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Exercise-induced coronary artery spasm. A regional coronary blood flow study.

Regional myocardial blood flow during exercise was determined using the thermodilution technique in 2 patients suffering from both spontaneous and exertional chest pain. In both cases we observed that effort-related anginal attacks were due to coronary spasm with sudden reduction of regional left ventricular blood flow. In 1 patient the exercise-induced ST-segment elevation in the anterior leads was accompanied by a reduction of flow in the great cardiac vein. In the second patient the exercise-induced ST-segment depression in the lateral leads was accompanied by a reduction of coronary flow in the area supplied by the circumflex artery. In 1 patient, nifedipine was effective in prolonging exercise tolerance by preventing the occurrence of coronary spasm and by increasing blood supply to the ischemic region during exercise.

Angina Pectoris↗

[Myocardial ischemia during exertion. Correlations between blood levels of thromboxane B2 and changes in coronary flow and resistance].

Platelet activation, with the subsequent generation of Thromboxane (Tx) A2, has been implied as a possible cause of resting as well as exercise induced myocardial ischemia. To verify the latter hypothesis, we measured the exercise release of TxB2, the stable metabolite of TxA2, in 9 patients with exertional angina and left anterior descending coronary artery disease. Three of the patients also suffered from angina at rest, due to coronary vasospasm. The great cardiac vein flow, venous efflux from the myocardial territory supplied by the left anterior descending, was determined by the thermodilution technique in the basal conditions, at peak exercise when angina and/or significant ST changes occurred, and 20 min after exercise. Simultaneous blood samples were drawn from the great cardiac vein and a peripheral artery for TxB2 measurements. Regional coronary resistances were calculated as the ratio of mean arterial pressure and coronary flow. At peak exercise the great cardiac vein flow increased and regional coronary resistances decreased in all patients, except in one who showed exercise induced coronary spasm. An increase in TxB2 release was found in 3 patients, a decrease in 3, while the remaining 3 patients did not show significant changes. After exercise the great cardiac vein flow and regional coronary resistances returned to control values in all, whereas both great cardiac vein and arterial TxB2 levels were increased in 6 patients. Our data show that no apparent relation exists between exercise-induced changes in coronary resistances and generation of TxB2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗