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Biomedical subjects

E Bramucci

Publications and source records attributed to E Bramucci.

At least 55 records · Page 3Linked to original sources

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↗

Silent ischaemia in post-myocardial infarction patients submitted to physical training.

Recently, more attention has been focused on the detection and treatment of silent myocardial ischaemia. Electrocardiographic signs of exercise-induced asymptomatic myocardial ischaemia are very common findings among survivors of acute myocardial infarction. From data of our population we found that silent exercise-induced ischaemia is present in 15-20% of all patients, and that about half of the patients with exercise-induced ST-segment depression were free of symptoms. Ergometric data at the ischaemic threshold are similar between asymptomatic and symptomatic patients while the presence of symptoms is more frequent in patients who were also symptomatic before the myocardial infarction. During the training period, the majority of the 'silent' patients remained asymptomatic, 23% developed effort angina, and 9% developed angina at rest. Training monitoring may be helpful in identifying the variability of symptoms. Physical training, in particular an intermittent programme, increased the work-load at which the ECG ischaemic signs appeared. Among the possible mechanisms responsible for exercise-induced silent ischaemia, a different pain tolerance and control of analgesia may be ascribed to explain the absence of pain, perhaps also determined by different endogenous beta-endorphin levels.

Coronary Circulation↗

[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↗

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↗

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↗

Hemodynamic evaluation during exercise test after acute and chronic ibopamine treatment in patients with congestive heart failure.

The hemodynamic effects of ibopamine (SB-7505), the orally active 3,4-diisobutyryl ester of N-methyldopamine, were studied in 12 patients with congestive heart failure (CHF) after acute dosing, after 20 days of maintenance therapy and after 20 days of drug discontinuation. Acute ibopamine administration increased at rest cardiac index (CI p less than 0.05) and stroke work index (SWI p less than 0.05), and reduced pulmonary capillary wedge pressure (PCWP), mean pulmonary arterial pressure (PAP), total systemic (SVR p less than 0.05) and pulmonary vascular resistance (PVR). These beneficial hemodynamic effects were maintained during supine bicycle exercise: CI and SWI increased more markedly (p less than 0.05) and PCWP increased at a lower extent (p less than 0.05) after ibopamine than on control conditions. PVR exhibited a more pronounced decrease (p less than 0.02), while SVR showed superimposable reductions before and after ibopamine. After chronic therapy with the drug, hemodynamics and left ventricular function again improved during exercise, while withdrawal of ibopamine resulted in hemodynamic deterioration. Heart rate and systemic arterial pressure did not change significantly after the drug. This study demonstrates that ibopamine is able to improve cardiac performance during exercise in CHF patients after both acute and chronic administration.

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↗

[Effects of medical and surgical therapy on the long-term survival of patients with variant angina].

To determine the effects on survival of the medical and surgical treatment of variant angina, we compared the prognosis of 75 surgically treated subjects with that of 75 medically treated patients, selected from a series of 340 consecutive patients observed between January 1969 and December 1982. The patients were selected on the basis of a developed computer program to match each medically treated patient with one surgically treated patient so that each pair was similar according to the following clinical and angiographic variables: sex, age, previous myocardial infarction, severe ventricular arrhythmias during pain, site of ST elevation (anterior or inferior), coronary artery disease (single or multivessel), left ventricular function (normal or abnormal). Patients who were considered unoperable because of poor ventricular function or distal vessel disease were not included in this study. Mantel-Haenszel log-rank analysis demonstrated a significantly better prognosis in surgically treated patients, particularly in those with multivessel disease as well as in those with ST elevation in anterior leads. However survival in 63 medical patients who were treated with calcium-antagonists was not significantly different from that of their surgical matched patients. During the follow-up period, anginal symptoms were more frequently found in medically treated patients (p less than 0.05). We conclude that in patients with variant angina surgical treatment does not improve survival as compared to medical treatment with calcium blocking drugs. Coronary artery bypass surgery can be carried out at low risk and is particularly indicated in those patients with angina refractory to medical treatment.

Angina Pectoris, Variant↗

Mental arithmetic stress testing in patients with coronary artery disease.

A mental arithmetic stress test was performed by 122 consecutive patients undergoing diagnostic coronary arteriography. Twenty-two patients showed significant ST segment abnormalities during the test (group 1). Of these patients, 20 performed a bicycle exercise test, which was positive in all of them. Seventy patients had a negative mental stress but a positive exercise test (group 2), whereas in 30 patients both tests were negative (group 3). There were no patients with a positive mental stress test and a negative exercise test. Mental stress induced a significant increase in heart rate and systolic blood pressure in the three groups of patients. Group 1 patients, however, achieved higher values of double product during mental stress and had a shorter exercise duration than group 2 and group 3 patients. The extent of coronary artery disease (CAD) was similar in groups 1 and 2, while group 3 patients had a significantly lower prevalence of two or more vessel disease. To investigate the pathogenetic mechanism of mental stress-induced myocardial ischemia, great cardiac vein flow was measured by means of the thermodilution technique in four patients with isolated left anterior descending artery disease, who showed ST segment depression in anterior leads in response to mental stress. In three patients without vasospastic angina the calculated coronary resistance decreased during mental stress, as a result of a normal vasodilatory response to the increased myocardial oxygen consumption induced by the test. By contrast, in one patient with variant angina, coronary resistance increased suggesting coronary vasoconstriction. Our findings demonstrate that mental arithmetic stress testing may induce significant ST segment abnormalities in patients with CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Effects of the cold pressor test and mental stress on coronary flow and resistance in patients with angina pectoris].

We compared the effects of cold pressor test and mental stress on coronary hemodynamics in 16 patients with coronary artery disease. The patients were divided into 2 groups according to the clinical characteristics of chest pain. Group I included 5 patients complaining of angina at rest associated with transient ST-segment changes, while Group II comprised 11 patients with stable exertional angina. In all patients coronary arteriography disclosed a proximal left anterior descending artery disease. Thermodilution measurements of the great cardiac vein flow, the venous efflux from the territory supplied by the left anterior descending artery, were obtained during cold pressor test and, after return to control conditions, during a mental arithmetic stress, consisting of serial subtractions of a two-figure number from a four-figure number. Coronary resistance of the anterior region was calculated as the quotient of mean arterial pressure and the great cardiac vein flow. In both groups of patients heart rate, mean arterial pressure and the great cardiac vein flow increased significantly during cold pressor test as well as during mental stress. During cold pressor test, coronary resistance of the anterior region increased in all patients of Group I (p less than 0.05), but did not change significantly in Group II patients. During mental test, coronary resistance of the anterior region increased in 3 patients and decreased in 2 patients of Group I (p:NS), while a significant decrease in coronary resistance of the anterior region was found in all patients of Group II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Variable threshold exertional angina in patients with transient vasospastic myocardial ischemia. Repeat exercise test results and therapeutic implications.

Thirty-five of 70 patients with vasospastic angina at rest complained of chest pain during exercise or during usual daily activity. In 22, the angina threshold was described as variable during exercise: that is, the amount of exertion that induced angina was not always the same. In 12 patients with variable threshold exertional angina, 3 exercise tests performed in the morning on different days yielded different results, because chest pain and ischemic electrocardiographic changes occurred at different work loads with a wide range in heart rate-systolic pressure product. Two patients, in whom great cardiac vein flow was measured during exercise before and after taking nifedipine, tolerated heavier work loads after receiving the drug, with a more marked increase in flow during exercise. It is concluded that variable threshold exertional angina can be objectively demonstrated by repeat exercise tests in patients with vasospastic angina. Variability of the angina threshold may be due to a functional mechanism that causes myocardial ischemia in addition to the increased myocardial metabolic requirements provoked by exercise. Because in such patients fluctuations in coronary arterial tone play an important role in determining the response to exercise, calcium antagonistic drugs, which lower coronary tone and prevent the occurrence of coronary spasm, are effective in increasing exercise capacity.

Adult↗

Effects of nifedipine on coronary hemodynamic findings during exercise in patients with stable exertional angina.

To investigate the mechanism by which nifedipine improves exercise tolerance in patients with coronary artery disease, we studied 14 patients with stable exertional angina and left anterior descending artery disease by measuring great cardiac vein flow (GCVF) and calculating anterior regional coronary resistance (ARCR) during exercise before and after sublingual administration of 20 mg of nifedipine. After nifedipine seven patients (group I) had no increase in exercise capacity and showed a similar magnitude of ST segment depression at peak exercise, while another seven patients (group II) had prolonged exercise duration (p less than .001) with less ST segment depression at peak exercise (p less than .01). Such effects were achieved despite a significant increase in double product, an indirect index of myocardial oxygen consumption. In group I patients no significant change was induced by nifedipine in GCVF or in ARCR either at rest or at peak exercise. In contrast, in group II patients nifedipine significantly increased GCVF at rest (p less than .05) and at peak exercise (p less than .001). Moreover, resting ARCR was decreased (p less than .01) and remained significantly lower at peak exercise (p less than .01) compared with the prenifedipine values. These data show that nifedipine may increase GCVF and decrease ARCR at rest and at peak exercise in patients with left anterior descending artery disease. Such increase in myocardial oxygen supply seems the most likely mechanism by which nifedipine may improve exercise capacity in patients with stable exertional angina.

Adult↗