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Biomedical subjects

D Ferrini

Publications and source records attributed to D Ferrini.

36 records · Page 2Linked to original sources
PubMed1988

[Angina of effort with a variable threshold: a unique entity due to different mechanisms?].

Variable threshold during exertion is a common feature in patients with chronic exertional angina. Changes in coronary vasomotor tone, when occurring at sites of critical narrowings, are a plausible explanation for variability of symptoms in these patients. However, the evidence supporting this hypothesis is still uncertain. Accordingly, we performed four computer assisted, multistage bicycle ergometer tests, without drugs, in 30 patients with chronic exertional angina, exercise induced ST depression, and a history of variable anginal threshold during exertion. Significant coronary artery disease was documented in each case by coronary arteriography. Patients were tested at the same time of day within a two week period. Comparison was made between each single test and the average of the remaining three. Time to 0.1 mV ST depression showed significant (+/- 20%) changes in 27 (90%) patients. Variability was shown in two out of four tests in 25 patients (83%), in three tests in 10 (33%), and in four tests in 2 (7%). Rate pressure product at 0.1 mV ST depression was concurrently changed (+/- 20%) in 20 patients (67%). Variability in two, three and four tests was observed in 7 (22%), 2 (7%) and 2 (7%) patients, respectively. Changes in time to 0.1 mV ST depression paralleled those in rate-pressure product at the onset of ischemia in 6 patients (22%) (dynamic ischemic threshold). Rate pressure product at 0.1 mV ST depression was unchanged despite variations in time to 0.1 mV ST depression in 10 patients (37%) (fixed ischemic threshold). The remaining 11 patients (41%) showed variable exercise tolerance associated with fixed (13 tests) and dynamic (13 tests) ischemic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Myocardial ischemia during intravenous prostacyclin administration: hemodynamic findings and precautionary measures.

This study reports coronary and systemic hemodynamics, and metabolic responses to atrial pacing, prostacyclin (PGI2), and iloprost, its stable analogue, in 16 patients with severe coronary obstruction as well as predominant narrowing in the left anterior descending artery. PGI2 caused ischemia in six patients with low anginal threshold during pacing. In three of them ischemia was also precipitated by iloprost. Drugs were infused at therapeutic doses and were discontinued when pain occurred. Angina disappeared promptly (less than or equal to 3 minutes) and spontaneously after the infusion of PGI2, whereas after the analogue it was long lasting (greater than or equal to 5 minutes) and was relieved by 125 mg intravenous aminophylline, an antagonist of dipyridamole-induced coronary dilation. Ischemia was associated with a drug-induced decrease in arterial blood pressure and reflex tachycardia, and occurred despite increased great cardiac vein (GCV) blood flow and decreased resistance, which is consistent with either a failure of regional flow to increase proportionally to the metabolic demand or a subendocardial-subepicardial steal. However, the following findings favor the latter hypothesis: heart rate and rate-pressure product at the onset of pain were lower with drugs than with pacing, and GCV blood flow, measured at a comparable heart rate, was less with pacing than with drugs. In conclusion, PGI2 and analogues may induce ischemia in patients with advanced coronary artery disease. The mechanism appears to be related to a dipyridamole-like maldistribution of flow. Counteraction of ischemia can be achieved by aminophylline.

Cardiovascular Agents↗
PubMed1986

Effects of iloprost, a stable prostacyclin analog, on exercise capacity and platelet aggregation in stable angina pectoris.

The effects of iloprost, a chemically stable compound with prostacyclin mimetic activity, on exercise capacity and platelet aggregation were assessed in 24 patients with effort angina and proved critical (at least 70% diameter narrowing) coronary artery disease. Upright bicycle ergometer testing (25-W increments every 2 minutes) was performed during drug and placebo infusions using a crossover, randomized, single-blind protocol. Samples for measurements of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma were obtained in all patients before and during the study. Compared with placebo, intravenous iloprost consistently (p less than 0.001) prolonged exercise duration and time to onset of significant (0.1 mV) ST depression. Angina and ST depression occurred at a greater heart rate and rate-pressure product. Benefits were remarkable in some patients (67%) and not in others. Iloprost administration resulted in reduced platelet aggregation at peak exercise in all patients, whether they had consistent or little response to the drug. Thus, iloprost administration may improve exercise capacity in patients with stable exertional angina pectoris. Improvements are independent of changes in the major determinants of myocardial oxygen demand and associated with markedly reduced platelet aggregation, which may account for increased myocardial perfusion in patients with high sensitivity to coronary constriction.

Angina Pectoris↗
PubMed1986

[Opposing effects of propranolol and diltiazem on the angina threshold during an exercise test in patients with syndrome X].

Patients with angina pectoris, exercise induced myocardial ischemia, normal coronary arteries and no evidence of epicardial spasm, i.e. patients with syndrome x, have been suggested to haven inadequate increase in coronary blood flow during tachycardia, possibly due to a functional disorder of small coronary vessels. To evaluate the best medical management of this syndrome we studied 13 patients who showed the above set of findings. Patients were given propranolol (160 mg daily), diltiazem (360 mg daily) and placebo for 2 weeks, using a randomized single blind protocol. Upright bicycle ergometer testing was performed at the end of each period of treatment. Compared to placebo, diltiazem significantly (p less than 0.001) prolonged exercise duration (x +/- SD: 365 +/- 86 vs 303 +/- 89 sec) and time to onset of angina (358 +/- 88 vs 276 +/- 90 sec). Angina appeared in 7 patients with diltiazem vs 13 patients with placebo and occurred at a higher rate pressure product (26.3 +/- 3.5 vs 24.1 +/- 2.8 X 10(-3); p less than 0.02). Conversely, following propranolol exercise duration and time to onset of angina were unchanged and angina appeared in all patients at a lower rate pressure product (18.3 +/- 2.9 vs 24.4 +/- 3.6 X 10(-3); p less than 0.001). The most likely explanations for these findings are: propranolol counteracts beta 2-adrenergic receptors, thus further reducing coronary reserve. This may lower the anginal threshold; Diltiazem reduces smooth muscle tone in small coronary vessels. This may result in increased coronary reserve and exercise duration.

Adult↗
PubMed1985

Myocardial ischemia induced by prostacyclin and iloprost.

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."

Adult↗
PubMed1985

[The relation between myocardial oxygen consumption and ischemia during exertion in patients with angina pectoris: effect of propranolol].

Patients with coronary artery disease exhibit a reduced coronary vasodilator reserve in response to exercise testing. Drugs which block coronary beta adrenergic receptors could exacerbate this abnormality leaving the vasoconstrictor alpha tone unopposed and/or counteracting the beta 2-mediated vasodilation elicited by the increase in myocardial oxygen demand. To test this hypothesis we administered propranolol 40 mg qid and placebo, using a cross over randomized single blind protocol, to 14 patients each with effort angina and critical coronary stenosis (greater than or equal to 75%). We performed computer-assisted multistage bicycle ergometer testings (25 W increments at 2 min intervals) after 2 weeks open label placebo (control) and at 2 week intervals following daily administration of propranolol and placebo. Compared to placebo, propranolol reduced significantly (p less than 0.001) peak heart rate (x +/- SD: 114 +/- 6 vs 150 +/- 11 beats/min) and rate pressure product (20.1 +/- 2.1 vs 28.0 +/- 3.9 X 10(-3)) and increased exercise duration (462 +/- 91 vs 355 +/- 85 sec). Conversely 0.1 mV ST segment depression was observed at lower heart rate (106 +/- 9 vs 127 +/- 8 beats/min, p less than 0.001) and rate pressure product (16.9 +/- 3.6 vs 22.4 +/- 2.4 X 10(-3), p less than 0.001). No significant differences were found between placebo and control. Moreover, we assessed the regression lines of the relationship between ST segment depression (ST) and heart rate (HR) during exercise. These have been shown to be shifted to the right after surgical revascularization and are an indirect measure of coronary reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Myocardial ischemia induced by the cold pressor test in patients with exertion angina. Case contribution].

The aim of the present study was to assess the incidence of myocardial ischemia during cold pressor test in patients with stable exertional angina pectoris. Thirty-seven patients with proven coronary artery disease were submitted to cold pressor and exercise stress testing; computer assisted electrocardiographic recordings were obtained throughout the examinations. Cold stimulation provoked electrocardiographic signs of subendocardial ischemia only in 3 patients. They had suffered of a previous myocardial infarction and showed low exercise tolerance and severe coronary lesions (one with triple vessel and 2 with left main disease). Interestingly, only one of these patients gave an history of angina during cold exposure. Thus these data indicate that chest pain and electrocardiographic signs of ischemia are an uncommon event during cold pressor stimulation which occurs more likely in patients with fairly severe coronary narrowings. More sensitive markers of ischemia and/or different modalities of cold application are required for studies concerning the relationship between cold exposure and angina pectoris.

Angina Pectoris↗
PubMed1985

[Changes in angina threshold induced by administration of ergonovine maleate during pacing in patients with chronic exertional angina].

It is widely accepted that the occurrence of chest pain and/or ST segment elevation during ergonovine testing is a hallmark of abnormal coronary constriction. However, the negativity of this test cannot be considered as an incontrovertible proof of the absence of coronary sensitivity to vasoconstriction. Indeed, it could only indicate that the resulting effect is inadequate to critically reduce coronary blood flow. To test this hypothesis we studied 12 patients with proven coronary artery disease and negative ergonovine test who had complained of chronic exertional angina pectoris and referred variable threshold for the occurrence of pain. They were submitted to atrial pacing (starting from 90 bpm, with 10 bpm increments every 2 min) before (control) and after ergonovine administration (total dose = 0.675 mg). Time, heart rate and rate pressure product were evaluated at the onset of angina and significant ischemia (0.1 mV ST segment depression). After ergonovine, angina was achieved earlier (405 +/- 173 vs 526 +/- 180 sec, p less than 0.005) than during control and at a lower heart rate (116 +/- 15 vs 131 +/- 15 bpm, p less than 0.001) and rate pressure product (15.8 +/- 2.0 vs 18.8 +/- 2.3 X 10(3) U, p less than 0.001). Changes in anginal threshold were widely variable among cases being that the time to onset of pain was dramatically reduced in certain patients but unchanged in one. Similar results were obtained when substituting the ischemic to the anginal threshold. Thus, negativity to ergonovine testing does not imply the absence of coronary constriction which may be revealed when increasing myocardial oxygen demand by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1981

[Markers of necrosis and anoxia in the post-infarct heart failure: determination of infarct size (author's transl)].

28 patients with acute myocardial infarct (AMI), 10 of whom presenting left ventricular failure, have been studied. By serial determinations of alpha-hydroxybutyrate dehydrogenase (HBDH) and creatine kinase (CK), the releasing times (RT) and the total releases (TR) of the two enzymes have been calculated, according to the Shell's method modified by Norris. The RT of HBDH have resulted more prolonged in the decompensated patients (48.1 +/- 16.0 vs 37.3 +/- 9.1 h; t = 2.297; p less 0.05). Highly significant correlations have been demonstrated between the total releases of the two enzymes; r = 0.816, p less than 0.01 (with failure); r = 0.766, p less than 0.001 (without failure). For neither enzyme, instead, significant differences have been shown between the TR of the two patient groups. The following conclusions can be drawn. 1) infarct size probably is not the only factor able to induce heart failure during AMI; 2) infarct size can be equally calculated from both HBDH or CK values, though some considerations may make preferable the choice of CK; 3) the more prolonged release of HBDH during heart failure suggests the hypothesis that lactate accumulation is an important factor influencing the appearance of this compliance.

Adult↗
PubMed1981

[Relationships between the initial area of necrosis and prognosis of acute myocardial infarct].

85 patients with acute myocardial infarction (AMI) have been studied retrospectively. 25 of them died within the 40th day after admission. Serum CK release during AMI can be described by the logistic equation: (formula: see text). We have evaluated for each patient both the final infarct size (calculated at the time of maximal enzyme activity: Tmax) and the initial one (calculated at the inflection time of the curve: Tflex). The total enzyme release in 1 ml of blood has been considered as an indirect index of infarct size. Our results show a good correlation between the initial and the final infarct size. We have considered as limits between survivors and non-survivors the following values: 2.2 IU/ml and 0.6 IU/ml for total CK release at Tmax and at Tflex respectively. The percentage of mortality in those groups is very similar (69% and 75%). However only 38% of non-survivors shows higher values than both 2.2 IU/ml and 0.6 IU/ml. The calculation of infarct size at Tflex allows an early identification of the high risk patients.

Clinical Enzyme Tests↗
PubMed1980

[The protective effects of glucose in ischaemia, anoxia and reoxygenation (author's transl)].

In the present study we used a model of underperfusion or anoxia followed by reperfusion to assess the role of glycolysis by substituting pyruvate or mannitol for glucose as substrate. Hearts were removed from male Sprague-Dawley rats (250-400 g) and perfused by the technique of Langendorff. The perfusate was Krebs-Henseleit bicarbonate buffer gassed with 95% O2, 5% CO2 or with 95% N2, 5% CO2 mixture and containing substrates as can be seen in the figures. The mild ischemia was obtained by reducing the perfusion pressure by 70%, from 60-70 cm H2O to 10-20 cm H2O. The coronary flow was rapidly reduced to 0.8 +/- 0.03 ml/min within the first 5 minutes. After mild ischemia anaerobic glycolysis was accelerated because lactate production in ischemic hearts perfused with glucose (36.2 +/- 15.3 microM/g/min-1) was higher than in the ischemic hearts perfused with mannitol (6.8 +/- 1.9 microM/g/min-1). During mild ischemia or anoxia there was little difference in the rate of release of creatin-kinase for all the substrates tested, but major differences become apparent on reperfusion. In that period the highest values of CK release were found in mannitol perfused hearts, the lowest in glucose perfused hearts. These results suggest that the rate of glycolytic flux during mild ischemia or anoxia may prevent enzyme release. The beneficial effect of glucose has been observed also during reperfusion. In fact enzyme release was higher in hearts reperfused with glucose than with pyruvate. When pyruvate is the only exogenous substrate available for isolated oxigenated hearts, tissue levels of citric acid cycle intermediates are high and oxidation of these substrates can account for 100% of the oxygen consumption. Therefore we suppose that oxidation of noncarbohydrate substrates such as pyruvate in reperfusion is complicated by the high mitochondrial damage. As a consequence anaerobic glycolytic pathway may play a special role in the maintenance of the membrane integrity also in the early phases of reperfusion.

Animals↗
PubMedDate not supplied

Side effects of prostacyclin in patients with angina pectoris and coronary artery disease.

Although the exposure of human subjects to prostacyclin (PGI2) infusion has been broad, no systematic approaches have been made in order to investigate the dose-related side effects in patients with angina pectoris and coronary artery disease (CAD). We studied 25 patients with typical chest pain and overt CAD. All patients underwent a cycloergometer stress testing (25 W increments at 2-min intervals). PGI2 was infused in scalar doses up to 10 ng/kg/min. During the infusion 25 patients (100%) had facial flushing, 7 (28%) moderate headache and one (4%) had nausea. In addition, 4 patients experienced the typical chest pain and had significant (greater than or equal to 0.1 mV) ST segment depression at 8.10 ng/kg/min infusion rates. These patients had lower tolerance to exercise (6.7 +/- 1.7 vs. 8.8 +/- 1.9 min; p less than 0.05) and coronary artery lesions more severe than those observed in patients without drug-induced angina pectoris. Our data therefore indicate that PGI2 at therapeutic doses may induce myocardial ischemia in patients with angina pectoris, low tolerance to exercise and severe CAD. In patients with mild to moderate degree of CAD, PGI2 was found to be well tolerated. These findings suggest that patients with angina pectoris and low tolerance to exercise should be excluded from clinical studies directed at elucidating the effectiveness of PGI2 in cardiovascular disorders.

Angina Pectoris↗