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Biomedical subjects

F Crea

Publications and source records attributed to F Crea.

At least 181 records · Page 10Linked to original sources
PubMed1988

Adenosine-induced chest pain in patients with silent and painful myocardial ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia.

Adenosine is formed from adenosine triphosphate within the ischaemic cells from where it is released into the coronary circulation. Adenosine exhibits several cardiovascular effects which tend to protect the ischaemic myocardium. Based on the observation that in healthy volunteers the intravenous infusion of adenosine produces angina-like chest pain, it has been recently proposed that another cardioprotective action of this substance could be provocation of angina. If this is the case adenosine should not produce chest pain in patients with silent ischaemia. To test this hypothesis we infused this substance intravenously at increasing doses of 50, 100, 150, 200, 250 and 300 micrograms kg-1 min-1 in eight patients with silent ischaemia (group A). All of them developed ST depression (1.8 +/- 0.2 mm) during exercise testing and seven also during adenosine infusion (1.1 +/- 0.8 mm). However, none of the patients had chest pain during exercise while seven had chest pain during adenosine. We then infused adenosine in eight other patients (Group B) who had painful ischaemia and an exercise tolerance similar to that of Group A patients (time to 1 mm ST depression 8.6 +/- 2.7 min and 8.4 +/- 3 min, respectively, P = NS). Adenosine induced chest pain in all Group B patients. The time to pain onset during adenosine was similar in the two groups (9.3 +/- 2.3 min in Group B and 12.4 +/- 4.9 min in Group A).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Laser recanalisation of coronary arteries by metal-capped optical fibres: early clinical experience in patients with stable angina pectoris.

The delivery of laser energy to the coronary circulation by bare optical fibres may cause perforation of the vessel. Experimental studies have shown that this complication can be avoided if the optical fibre is fitted with a metal cap to prevent the potentially dangerous forward projection of the laser beam. This study was performed to assess the feasibility and short term effects of percutaneous coronary laser recanalisation with these modified fibres. Recanalisation of a severe stenosis of the left anterior descending artery was attempted in six patients who were referred for coronary artery bypass grafting. Although the percutaneous technique was used, the laser procedure was performed during coronary bypass surgery before the start of cardiopulmonary bypass to minimise the effects of potential complications. A 1.5 mm diameter metal-capped fibre coupled to an argon laser was advanced percutaneously over a guide wire positioned across the stenosis. In the first patient the delivery of 152 J resulted in the gradual passage of the fibre through a 3 cm long stenosis. Repeat angiography showed a reduction in the severity of the stenosis. In the second patient the delivery of 112 J failed to allow fibre advancement; a further 80 J pulse caused perforation which was repaired. In the remaining four patients the delivery of laser energy in the attempt to traverse the stenosis was limited to less than 90 J. In two of the four patients the severity of stenosis was reduced. No further complications were seen. Percutaneous coronary laser recanalisation with metal-capped optical fibres is feasible but improvements of currently available technology are needed to increase the primary success rate.

Aged↗
PubMed1988

Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia.

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.

Angina Pectoris↗
PubMed1987

Relative roles of preload increase and coronary constriction in ergonovine-induced myocardial ischemia in stable angina pectoris.

To assess the relative role of increased ventricular preload and critical coronary lesions in ergonovine-induced myocardial ischemia, 9 normal subjects (group A), 7 patients with stable angina (group B) and 5 with variant angina (group C) were studied. In all patients, the 12-lead electrocardiogram, blood pressure and left ventricular (LV) volume (technetium-99m blood pool) were continuously recorded before and during administration of incremental doses of ergonovine given at 5-minute intervals. In all subjects, an initial LV dilatation developed; in group B and C patients, this was followed by a decrease in stroke volume and ejection fraction with subsequent onset of electrocardiographic changes and angina. The interval between these events was significantly shorter in group C and in 3 group B patients; in these patients, signs of ischemia appeared with smaller ergonovine doses and at minimal preload increase, coronary constriction being the likely mechanism of ischemia. In the remaining 4 group B patients, the onset of stroke volume, ejection fraction, electrocardiographic changes and angina was significantly delayed, occurring after administration of larger ergonovine doses when LV volume was already considerably increased. This finding suggests that the loading effect of ergonovine on LV volume, rather than on coronary constriction, could be the prevailing mechanism of ergonovine-induced ischemia in these patients.

Angina Pectoris↗
PubMed1987

Usefulness of Holter monitoring to improve the sensitivity of exercise testing in determining the degree of myocardial revascularization after coronary artery bypass grafting for stable angina pectoris.

To assess whether Holter monitoring improves the sensitivity of exercise testing in identifying incomplete myocardial revascularization, both tests were performed in 45 patients from 3 to 5 months after elective coronary artery bypass grafting (CABG) for stable angina pectoris. Coronary angiography revealed incomplete revascularization in 26 patients. Six of these 26 had 52 episodes of ST-segment depression during Holter monitoring and myocardial ischemia during exercise testing. Their exercise capacity was significantly lower than that of 10 other patients in whom the results of exercise testing only were positive (heart rate at 0.1 mV ST-segment depression 112 +/- 9 vs 123 +/- 15 beats/min, p less than 0.001). In the other 10 patients with incomplete myocardial revascularization the results of both investigations were negative. The graft patency rate was lower in patients with a positive response to exercise testing than in those with a negative response (52% vs 71%, p less than 0.005). Myocardial revascularization was angiographically complete in 19 patients. In 18 of these 19 patients the findings of both investigations were negative; in 1 patient Holter monitoring revealed episodes of ST-segment elevation suggestive of variant angina. Thus, after CABG for stable angina pectoris the results of Holter monitoring do not improve the sensitivity of exercise testing in identifying patients with angiographically incomplete myocardial revascularization because findings are positive only in patients with low exercise capacity. Both tests fail to show evidence of myocardial ischemia in most patients with angiographically complete myocardial revascularization.

Aged↗
PubMed1987

Limitations of dipyridamole-echocardiography in effort angina pectoris.

The sensitivity of dipyridamole--2-dimensional (2-D) echocardiography was assessed for detection and localization of ischemia in 21 patients with severe chronic stable angina pectoris, a clearly positive exercise stress test response and multivessel coronary atherosclerosis. Regional wall motion during dipyridamole infusion (0.6 mg/kg intravenously over 4 minutes) was compared with control and recovery by 2 blinded observers in consensus. Transient regional wall motion abnormalities were observed in 11 patients. Angina and ST-segment changes occurred in 9 of these 11 patients with positive responses, but in none of those who showed no transient abnormality of regional wall motion. Localization of regional wall motion abnormalities correlated well with angiographic severity of coronary lesions. Endocardial area contraction, evaluated by a computerized system, was reduced significantly after dipyridamole administration in patients with a positive response (from 51 +/- 10% to 35 +/- 11%, p less than 0.001), whereas it did not change significantly in the others (from 43 +/- 6% to 42 +/- 8%). In the 11 patients with a positive response, coronary reserve assessed by exercise testing (modified Bruce protocol) was more impaired than in those with a negative response (time to 1 mm of ST depression 177 +/- 148 seconds and 472 +/- 179 seconds, respectively, p less than 0.01). In patients with severe angina and multivessel coronary artery disease, dipyridamole--2-D echocardiography appears to identify the vessel in which flow reserve is most limited. Although this information may be valuable, indications for the test are restricted to patients with severely limited exercise capacity.

Adult↗
PubMed1986

Transient myocardial ischemia during daily life in patients with syndrome X.

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.

Adult↗
PubMed1986

Transluminal laser irradiation of coronary arteries in live dogs: an angiographic and morphologic study of acute effects.

In vivo coronary transluminal laser irradiation, using energies known to vaporize atherosclerotic plaques and thrombi, was performed in normal coronary arteries of 5 anesthetized mongrel dogs. A 200-mu core silica optical fiber with a radiopaque tip was advanced through a catheter to either the left anterior descending or circumflex coronary arteries. Coronary artery perforation occurred during manipulation of the fiber in 1 dog. In 4 dogs, argon laser radiation was delivered at 1-second intervals. A total of 45 different sites were irradiated in 8 coronary arteries. In 5 of these arteries 1 W was used and in the 3 other arteries 2 W were used. Coronary angiography showed perforation of 5 of these 8 arteries. Two arteries were perforated using 1 W and 3 using 2 W. Within 30 minutes, 3 dogs with perforation died of cardiac tamponade. In all 4 dogs postmortem examination showed perivascular blood extravasation around all 8 lased coronary arteries. Transluminal lasing of normal dog coronary arteries using delivery systems and energies similar to those known to vaporize atherosclerotic plaques and thrombi resulted in arterial perforation, frequently followed by cardiac tamponade.

Angiography↗
PubMed1986

Variability of results during repeat exercise stress testing in patients with stable angina pectoris: role of dynamic coronary flow reserve.

In some patients with stable angina, the variability of results during repeated exercise tests is higher than in others with similar symptoms. The aim of the study was to assess whether this difference can be explained by a different susceptibility of the coronary arteries to vasoconstrictor stimuli. Ten patients (group A) with stable angina, who developed myocardial ischemia (angina and ST segment depression greater than 0.1 mV) following ergonovine-induced coronary constriction, and 10 other patients (group B) with stable angina, but a negative ergonovine test result, were subjected to two treadmill exercise tests. The variability of heart rate and heart rate-blood pressure product at 0.1 mV ST segment depression was significantly higher in group A than in group B (12 +/- 4 vs 4 +/- 4 bpm, respectively, p less than 0.001 and 3366 +/- 1900 vs 930 +/- 960 bpm X mm Hg, respectively, p less than 0.005), such as the variability of heart rate-blood pressure product at the onset of angina (3887 +/- 2400 vs 1428 +/- 1800 bpm X mm Hg, respectively, p less than 0.04). The remaining exercise parameters were always more variable in group A than in group B, but these differences did not achieve statistical significance. Thus patients with stable angina who develop myocardial ischemia in response to ergonovine have a larger variability of results during repeat exercise testing. Such findings could be explained by an enhanced susceptibility to the coronary constrictor effects of exercise resulting in dynamic changes in coronary flow reserve.

Aged↗
PubMed1986

Differential transmyocardial platelet behavior in response to pacing and ergonovine-induced myocardial ischemia.

In 17 anginal patients with critical narrowing of the left anterior descending artery, we studied the effects of acute ischemia, either induced by atrial pacing or by ergonovine, on transmyocardial platelet behavior. Six other patients with atypical chest pain and normal coronary arteries served as controls. Simultaneous arterial and great cardiac vein samples were drawn during control and ischemia to measure the levels of platelet factor four (PF4) and beta-thromboglobulin (BTG). During pacing-induced ischemia the great cardiac vein-arterial differences of PF4 and BTG decreased significantly, indicating a reduced platelet aggregability; no significant changes were observed in the control patients. By contrast, when ischemia resulted from ergonovine-induced spasm of the left anterior descending artery (five patients), the great cardiac vein-arterial differences increased, indicating enhanced platelet aggregability. Again no differences were observed in the patients with a negative ergonovine test. The results of our study suggest that the transcardiac platelet behavior may vary during different ischemic conditions. When ischemia is due to increased myocardial demands and flow is normal or increased, myocardial metabolites released from the ischemic area may oppose platelet aggregation. By contrast, spasm and the stagnant flow resulting from it may enhance platelet aggregation.

Adult↗
PubMed1986

Provocation of coronary spasm by dopamine in patients with active variant angina pectoris.

The effects of dopamine on arteries are different depending on the dose, route of administration, and receptor population. Its administration can cause vasodilation by stimulation of dopaminergic receptors, vasoconstriction by stimulation of alpha-adrenergic and serotonergic receptors, and even spasm of cerebral arteries when given intracisternally in dogs. The ability of dopamine to provoke coronary spasm was assessed in 18 patients with active vasospastic angina in whom this amine was infused at rates of 5, 10, and 15 micrograms/kg/min for periods of 5 min each. The 12-lead electrocardiogram and blood pressure (cuff) were monitored throughout the whole test. In nine patients dopamine caused angina and ischemic electrocardiographic changes suggestive of coronary spasm: ST segment elevation in six patients and ST segment depression in the absence of important coronary stenoses in the remaining three. Infusion of dopamine was repeated during coronary angiography in three patients with positive test results: this provoked occlusive coronary spasm with ST segment elevation in two patients and nonocclusive spasm with ST segment depression in the remainder. In conclusion, infusion of dopamine provokes coronary spasm in a sizeable proportion of patients with active vasospastic angina. Its administration may be detrimental in patients susceptible to coronary spasm, such as those with acute myocardial infarction.

Adult↗
PubMed1986

Local coronary supersensitivity to diverse vasoconstrictive stimuli in patients with variant angina.

It has been shown in different groups of patients with variant angina that coronary spasm can be reproduced by physiologic maneuvers and pharmacologic agents. It is not known, however, to what extent different stimuli can induce spasm in the same patient. To investigate whether coronary arterial spasm results from specific abnormal agonist-receptor interactions or from a local nonspecific coronary supersensitivity to different stimuli, 28 patients with vasospastic angina were submitted to a series of diverse vasoconstrictive stimuli known to provoke coronary spasm. Ergonovine, hyperventilation, handgrip, cold pressor, and exercise-tests, were carried out in all 28 patients. In the last 15 patients histamine was also administered. Spasm was provoked by ergonovine in 96% of patients, by hyperventilation in 54%, by histamine in 47%, by exercise in 46%, and by the cold pressor and handgrip tests in 11% and 7%, respectively. No significant differences were found in the responses to provocative tests of patients with normal coronary arteries or nonsignificant stenoses and those with significant lesions. In the same individual, spasm was induced by at least two vasoconstrictive stimuli, although with a different mechanism of action, in 82% of patients and spasm was induced by three or more stimuli in 39%. Tests were repeated in at least 23 patients and short-term reproducibility paralleled sensitivity. These results suggest that in patients with variant angina, a local nonspecific supersensitivity rather than an abnormal specific agonist-receptor interaction plays a major role in the genesis of coronary arterial spasm.

Adult↗
PubMed1985

The healing process in normal canine arteries and in atherosclerotic monkey arteries after transluminal laser irradiation.

To evaluate the healing response of both normal and atherosclerotic arteries to laser radiation, 7 mongrel dogs and 4 hypercholesterolemic atherosclerotic monkeys underwent catheterization with a right Judkins catheter-optical fiber system designed to maximize arterial wall injury. Argon laser radiation was then delivered to the abdominal aorta and iliofemoral arteries. In the 11 animals, a total of 917 sites were irradiated in 33 arteries. Angiography did not reveal dissection or aneurysm formation; occlusive thrombosis was found in 2 arteries. Perforation of the arterial wall was a frequent complication. In animals killed between 1 hour and 4 days, light and electron microscopy of lased sites showed craters filled with a coagulum of blood and cellular debris with only a few adherent platelets. Healing occurred with a minimal inflammatory response and involved both fibroblasts and smooth muscle cells. Reendothelialization was seen in all animals killed between 7 and 14 days after lasing and was complete by 30 to 60 days. Within this period, no accelerated atherosclerosis was seen at lased sites in the hypercholesterolemic monkeys. It is concluded that transluminal lasing of normal arteries in dogs and in atherosclerotic arteries of monkeys is followed by healing and reendothelialization within a few weeks.

Angiography↗
PubMed1985

Different susceptibility to myocardial ischemia provoked by hyperventilation and cold pressor test in exertional and variant angina pectoris.

Coronary constriction at the site of atherosclerotic stenoses has been suggested to play an important role in modulating the frequency of symptoms in patients with exertional angina. To investigate whether stimuli triggering coronary constriction have similar effects in patients with exertional and variant angina, responses to hyperventilation (HV) and cold pressor test (CPT) were evaluated. Twenty patients with chronic exertional angina, positive exercise test results and coronary heart disease were compared with 14 patients with variant angina and ST-segment elevation during an ergonovine test. In patients with exertional angina, the CPT produced diagnostic ST-segment depression in 6 of 20 patients (30%) at levels of rate-pressure product much lower than those during the exercise test; all patients had low effort tolerance and severe coronary artery disease. HV produced diagnostic ST-segment depression in only 1 of 20 patients (5%) (p less than 0.05 compared to that with CPT). Conversely, in patients with variant angina, HV produced ST-segment elevation in 11 of 14 patients (78%) and CPT produced elevation in only 2 of 14 (14%) (p less than 0.01). Thus, coronary constriction can provoke myocardial ischemia not only in patients with variant angina but also in some patients with exertional angina. Furthermore, the 2 groups of patients have a different susceptibility to stimuli known to produce coronary constriction.

Adult↗