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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 271 records · Page 15Linked to original sources
PubMed1990

Comparison of low-dose aspirin and coronary vasodilators in acute unstable angina.

Episodic platelet activation has been shown to occur in unstable angina, and aspirin should have an important therapeutic role in the management of these patients. The response to aspirin alone or to aspirin in combination with vasodilators such as heparin and beta-blockers has been assessed in 41 patients with unstable angina. Therapy was added sequentially in the event of recurrence of transient myocardial ischemia. Patients were randomly assigned to two groups. Group 1 (21 patients) received an intravenous infusion of isosorbide dinitrate and oral diltiazem, and group 2 (20 patients) received intravenous aspirin (60 mg the first day and 20 mg on successive days). This dose of aspirin reduced serum thromboxane B2 from 160 +/- 88 ng/ml (mean +/- SD) to undetectable values (less than 6 ng/ml, p less than 0.01). If episodes of ischemic ST segment shift continued, the therapy of group 1 was added to that of group 2 or vice versa; if further ST segment changes were documented, intravenous heparin and oral beta-blockers were added; if episodes of myocardial ischemia persisted, urgent coronary arteriography and myocardial revascularization were performed. Nine patients in group 1 and six in group 2 (p = 0.8) had no further episodes of myocardial ischemia on their initial therapy; 12 additional patients had no further episodes when taking combined therapy of aspirin and vasodilators. Thus, the administration of aspirin alone was not superior to coronary dilators; 30% of all patients continued to have episodes of myocardial ischemia or had a myocardial infarction develop when heparin and beta-blockers were added. Myocardial infarction occurred in one patient on vasodilator therapy alone, in two on combined therapy, and in two on full therapy. These results suggest that in some patients, the stimulus to coronary thrombosis and vasoconstriction occasionally becomes so strong that it cannot be inhibited by certain antagonist drugs. The unstable tendency to continuation of ischemia or evolution to myocardial infarction is not related to the severity of the persisting stenosis. Those patients not promptly responding to combined therapy immediately from admission should have early coronary angiography and aggressive treatment.

Angina Pectoris↗
PubMed1989

Comparative effects of theophylline and isosorbide dinitrate on exercise capacity in stable angina pectoris, and their mechanisms of action.

While the role of nitrates in the prevention and treatment of myocardial ischemia is well established, the use of theophylline, proposed almost a century ago, is still controversial. Also controversial is its mechanism of action, initially thought to be coronary dilation. In this randomized, single-blind study, the acute effects on exercise capacity of sublingual isosorbide dinitrate (10 mg) and of intravenous theophylline ethylenediamine (7 mg/kg) were assessed in 10 patients with chronic stable angina and positive exercise test. After the administration of theophylline, the time to onset of angina, the heart rate-blood pressure product at 1-mm ST-segment depression and the exercise duration were similar to that after isosorbide dinitrate administration (9.8 +/- 2.3 vs 9.3 +/- 1.7 minutes, 207 +/- 41 vs 207 +/- 48 beats/min.mm Hg.10(-2) and 10.8 +/- 2 vs 10.4 +/- 2 minutes, respectively). Both drugs significantly (p less than 0.001) improved all these parameters compared to the baseline exercise test. The effect of the 2 drugs on the diameters of angiographically normal segments of large epicardial coronary arteries was then assessed using computerized quantitative angiography in 10 other patients with stable angina. Whereas theophylline failed to increase the coronary diameters compared to that in the baseline angiogram (2.9 +/- 0.6 vs 2.9 +/- 0.6 mm, respectively), the subsequent administration of isosorbide dinitrate resulted in an increase up to 3.2 +/- 0.7 mm (p less than 0.02). Thus, in patients with stable angina, theophylline delays the onset of angina, increases the ischemic threshold and prolongs the exercise duration to the same degree as isosorbide dinitrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus.

To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of diltiazem alone or with isosorbide dinitrate or with atenolol both acutely and chronically for stable angina pectoris.

To establish the contribution of combination therapy in stable angina, the short- and long-term effects of diltiazem (120 mg and 360 mg/day, respectively), and the additive effects of sublingual isosorbide dinitrate, 10 mg, and atenolol, 100 mg, were studied in 11 patients with chronic stable angina using an open-label sequential design. All patients underwent exercise testing without therapy, and with each drug and their combinations. Exercise time and heart rate-blood pressure product were measured at 1-mm ST-segment depression, or at peak exercise if the test result was negative. Exercise time increased from a control value of 8.0 +/- 2.3 minutes (mean +/- standard deviation) to 11.4 +/- 2.4 minutes (p less than 0.0001) after the administration of isosorbide dinitrate, to 11.3 +/- 1.8 minutes (p less than 0.001) after short-term diltiazem and to 12.4 +/- 1.5 minutes (p less than 0.001) after long-term diltiazem. The rate-pressure product increased from a control value of 19,070 +/- 3,564 to 24,431 +/- 4,795 beats/min X mm Hg (p less than 0.0001) after isosorbide dinitrate, to 22,287 +/- 4,753 beats/min X mm Hg (p less than 0.01) after short-term diltiazem and to 21,812 +/- 3,976 beats/min X mm Hg (p less than 0.007) after long-term diltiazem. The addition of atenolol to long-term diltiazem significantly reduced the rate-pressure product compared with long-term diltiazem alone (21,812 +/- 3,976 vs 13,926 +/- 2,880 beats/min X mm Hg, (p less than 0.002), although there was no further significant increase in exercise time (12.4 +/- 1.5 vs 13.3 +/- 1.6 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Lack of evidence for alpha-adrenergic receptor-mediated mechanisms in the genesis of ischemia in syndrome X.

Patients with syndrome X (typical angina pectoris, positive exercise tests [greater than or equal to 1 mm of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) have a reduced coronary flow reserve due to inappropriate dilatation of small resistive vessels. To assess whether alpha-adrenergic mechanisms play a role in the genesis of ST-ischemic changes in syndrome X, 12 patients with this syndrome (2 men and 10 women, mean age 50 +/- 6 years) underwent exercise testing and 24-hour ambulatory electrocardiographic monitoring. They were done off treatment and after alpha blockade with prazosin and clonidine on 2 separate weeks. Despite treatment, all exercise tests remained positive and patients were stopped because of progressive angina pain. Compared to the off-treatment tests, exercise duration and heart rate-blood pressure product at 1 mm of ST-segment depression did not change significantly after prazosin (617 +/- 203 vs 663 +/- 203 seconds and 23,857 +/- 6,125 vs 22,098 +/- 4,816 beats/min X mm Hg, respectively) and clonidine (684 +/- 148 vs 649 +/- 80 seconds and 25,514 +/- 2,386 vs 24,567 +/- 2,001 beats/min X mm Hg, respectively). Ambulatory monitoring showed similar results regarding number of episodes of ST-segment depression greater than or equal to 0.1 mV during control and after prazosin (39 vs 38) or clonidine (26 vs 23) treatment. None of the 8 patients who also underwent provocative testing with phenylephrine had ischemic electrocardiographic changes; only 2 experienced chest pain during the test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X.

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Influence of endothelin on human coronary arteries and localization of its binding sites.

Endothelin, a 21 amino acid peptide synthesized by cultured porcine aortic endothelial cells, has recently been identified and shown to produce a potent and prolonged constriction of mammalian blood vessels in vitro. Using tissue obtained from explanted hearts at the time of cardiac transplantation, the response of isolated human epicardial coronary arteries to endothelin was studied. The presence of endothelin binding sites was demonstrated in these vessels using an autoradiographic technique. Endothelin produced a dose-dependent increase of tension in the isolated coronary vessels with a maximal tension achieved equal to 135% of that induced by 90 mM of potassium. The maximal response was slow to develop and had a prolonged duration of 15 to 20 minutes. Nicardipine (4 microM) failed to affect the contraction induced by low doses of endothelin, but decreased the tension obtained at high doses. However, adenosine, substance P and glyceryl trinitrate were all effective in reversing the contraction induced by endothelin, while indomethacin and acetylcholine were ineffective. These features differ from those of other endogenous constrictor agents and make endothelin a potential candidate for long-term modulation of vascular tone.

Autoradiography↗
PubMed1989

Effect of theophylline on exercise-induced myocardial ischaemia.

In a single-blind, placebo-controlled, randomised trial in 20 patients with stable angina pectoris, intravenous theophylline ethylenediamine (aminophylline), 7 mg/kg, increased the time to onset of angina by 46%, the heart-rate/blood-pressure product (an index of myocardial oxygen consumption) at 1 mm ST segment depression by 22%, and exercise duration by 24%. In a subsequent double-blind placebo-controlled trial in 8 patients a single oral dose of theophylline (375 mg) increased the time to onset of angina by 56%, the heart-rate/blood-pressure product at 1 mm ST segment depression by 22%, and the exercise duration by 35%. Infusion of theophylline ethylenediamine during angiography (10 patients) did not affect the diameter of epicardial coronary arteries. The beneficial effects of theophylline may be due to redistribution of coronary blood flow from non-ischaemic to ischaemic myocardium.

Administration, Oral↗
PubMed1989

Ischemic threshold varies in response to different types of exercise in patients with chronic stable angina.

The effects of different types of exercise on ischemic threshold were studied in 33 patients with chronic stable angina, documented coronary artery disease, and reproducible positive exercise test results. On average, ST segment depression developed at a significantly higher heart rate and rate-pressure product when the standard modified Bruce protocol was preceded by a warm-up period (113 +/- 13 vs 119 +/- 15 beats/min and 18,813 +/- 3682 vs 20,357 +/- 4227 beats/min X mm Hg, respectively; p less than 0.05 and less than 0.01). No significant changes were observed when the exercise was started abruptly. Analysis of results in individual patients showed that changes in rate-pressure product at 1 mm ST segment depression greater than or equal to 2000 beats/min X mm Hg developed with different types of exercise in 11 patients (group I), whereas in 22 patients little or no change occurred (group II). All patients also underwent exercise testing before and after 0.5 mg of sublingual nitroglycerin; improvement induced by nitroglycerin was significantly greater in group I than in group II (22 +/- 8 vs 8 +/- 9 beats/min and 4896 +/- 1998 vs 1064 +/- 2145 beats/min X mm Hg; p less than 0.01). Furthermore, isometric handgrip exercise carried out during angiography resulted in significant reduction of luminal diameter at the site of the stenosis of group I (1.22 +/- 0.39 vs 0.99 +/- 0.35 mm; p less than 0.01) but not in group II (1.12 +/- 0.22 vs 1.16 +/- 0.3 mm, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

The natural history of left ventricular thrombus in myocardial infarction: a rationale in support of masterly inactivity.

One hundred five unselected and consecutive patients were prospectively studies after acute transmural myocardial infarction to assess the incidence of mural thrombus formation and to relate the presence of thrombus to patient outcome in terms of systemic embolic events, functional class and survival. In 87 patients, optimal quality two-dimensional echocardiographic studies were obtained and were repeated at daily intervals to detect mural thrombus formation. The site of infarction was anterior in 53 patients and inferior in 34. On admission, all patients received subcutaneous heparin and antiplatelet agents (aspirin, dipyridamole); none received full anticoagulant therapy. Left ventricular mural thrombus was visualized between 2 and 11 days (median 6) after the clinical onset of infarction in 21 (40%) of the 53 patients with anterior infarction. No patients with inferior infarction had echocardiographic evidence of thrombus formation. During follow-up of 22 to 51 months (mean 39), none of the 21 patients with mural thrombus had clinical evidence of systemic embolism. One patient with inferior and one with anterior infarction had a cerebral embolus 7 days and 9 months, respectively, after the acute event, but neither of these patients had echocardiographic evidence of left ventricular thrombus at any stage. Echocardiography performed at 1 and 2 years of follow-up showed persistent evidence of thrombus in only 8 (31%) and 5 (24%) of the 21 patients, respectively. On admission, the functional class of patients with anterior myocardial infarction and thrombus was similar to that of patients without ventricular thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticoagulants↗
PubMed1989

Coronary vasomotor tone: a heterogeneous entity.

Changes in coronary vasomotor tone are undoubtedly involved in the pathogenesis of many ischaemic coronary syndromes. The term coronary artery 'spasm' should be limited to the situations characterized by focal coronary constriction sufficient to cause transient total or sub-total coronary occlusion. Mild coronary artery constriction is also observed in many other situations, without even causing coronary artery occlusion. We present suggestive evidence that the mechanisms underlying coronary artery 'spasm' and 'physiological' coronary artery constriction are different.

Angina Pectoris, Variant↗
PubMed1989

Whole heart distribution of myocardial perfusion, metabolism and myocardial viability by positron emission tomography.

The three dimensional evaluation of regional myocardial perfusion and metabolism of the whole left ventricular wall is now possible using the new generation of Positron Emission Tomography scanners (PET). We have used whole heart PET to study the metabolic consequences of transient myocardial ischaemia distal to critical coronary obstructions and to assess the viability of non contractile myocardium. At present whole heart PET should be considered a sophisticated technique for clinical research but its remarkable potential and further possible technical advances suggest its diagnostic application could be considered in the future, if justified on a cost benefit basis.

Blood Glucose↗
PubMed1989

Endothelin-1 is a potent constrictor in conductive and resistive coronary arteries.

The action of endothelin-1 (ET-1) in canine and porcine coronary artery ring preparations and perfused canine and porcine myocardium was examined in vitro to determine the site of action of ET-1 in the coronary vasculature. ET-1 had a vasoconstrictor effect that was more potent in smaller diameter ring preparations. The EC50s for both canine and porcine ring preparations decreased with a decrease in vessel diameter and the EC50 of ET-1 in the perfused myocardium was three to four times lower than in the smallest ring preparation. The results suggest that ET-1 may cause cardiac ischemia by constriction of resistive vessels rather than by epicardial coronary artery spasm.

Animals↗
PubMed1989

Endothelin-1 is a potent long-lasting vasoconstrictor in dog peripheral vasculature in vivo.

Endothelin-1 (ET-1), a 21 amino acid peptide, has recently been identified and shown to produce a potent and prolonged constriction of mammalian blood vessels in vitro. We have studied the effect of local infusion of this peptide on resistance vessels in the hindlimb of the anesthetized greyhound dog. Incremental doses of ET-1 (3-200 pmol/min) were infused into the left femoral artery. Doses above 10 pmol/min produced a slowly progressive reduction in hindlimb blood flow in a dose dependent fashion, maximally reducing flow by 79.5% +/- 3.2 from 152.3 +/- 29.1 ml/min to 27.8 +/- 5.8 ml/min (+/- SEM, p less than 0.015), with a concomitant rise in vascular resistance. In the control vessel (right femoral artery) there were no statistically significant changes in blood flow observed. Onset time of the response to ET-1 was 3 min, whereas spontaneous recovery of the flow occurred at 30 min following cessation of the infusion. We demonstrated transient reversal of constriction in this arterial model during coinfusion with endothelin-1 (100 pmol/min) of dihydropyridine calcium channel blocking agent nicardipine (0.5-20 nmol/min), substance P (0.5-50 fmol/min), adenosine (10-10,000 pmol/min), and isosorbide dinitrate (0.001-0.1 mg/min).

Animals↗
PubMed1989

Endothelin is a potent long-lasting vasoconstrictor in men.

Endothelin, a 21-amino acid peptide synthesized by cultured porcine aortic endothelial cells, has recently been identified and shown to produce a potent and prolonged constriction of mammalian blood vessels in vitro. We have studied the effect of local infusion of this peptide on resistance and capacitance vessels of normal volunteers. Infusion of endothelin (5 pmol/min) reduced forearm blood flow by 39 +/- 7% from control observations. The maximum response was seen after approximately 55 min of infusion. After stopping the infusion, return of flow to basal values took approximately 120 min. This contrasts with the short onset and duration of action observed when angiotensin II was infused. During coinfusion studies, reversal by nicardipine (0.3-10 micrograms/min) occurred at similar concentrations in both endothelin-induced and angiotensin-induced flow reduction. This observation suggests that nicardipine nonspecifically antagonizes the flow-reducing effects of endothelin. A pattern of slow onset of constriction was found on local infusion of endothelin (5 pmol/min) into dorsal hand veins. During coinfusion of nicardipine (1.5 microgram/min), no reversal of endothelin-induced (5 pmol/min) constriction of dorsal hand veins occurred. The pharmacological profile of this peptide in the peripheral circulation of humans suggests that it may be involved in long-term regulation of vascular tone.

Adult↗