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Biomedical subjects

F Crea

Publications and source records attributed to F Crea.

At least 163 records · Page 9Linked to original sources
PubMed1991

Daily monitored cardiovascular effects of carbamazepine in chronic crack cocaine users.

During a 20-day, double-blind, placebo-controlled, fixed-dose outpatient trial of carbamazepine (either 200 mg or 400 mg) for potential anticocaine treatment effects in volunteers who were unmotivated for treatment and who lacked any external coercion for cocaine abstinence, we monitored cardiovascular effects in 30 subjects on a daily basis. All individual cardiovascular measures obtained were within clinically normal limits. Corrected QT interval under carbamazepine was shorter than under placebo condition, although both were in the normal range. Systolic pressure was elevated by 2.1 mm Hg. No differences in pulse rate were found. With carbamazepine and concurrent ad lib cocaine use, heart rate was significantly, although not clinically, elevated (mean increase = 2.3 beats/minute). The analysis of these approximately 600 observations indicates that carbamazepine in cocaine users, alone and in combination with ad lib street crack use, causes no clinically significant cardiovascular effects.

Carbamazepine↗
PubMed1991

[Morphofunctional changes in the left ventricle of the elderly person and the vulnerability to myocardial necrosis].

In the Western world the percentage of subjects over the age of 60 years is rapidly increasing. Therefore, elderly individuals represent a progressively increasing proportion of patients with ischemic heart disease (IHD), which is the most prevalent disease in this age range. In the elderly both the clinical presentation and the outcome of IHD have some peculiar features which may have important therapeutic implications. The prevalence of both coronary atherosclerosis and uncomplicated angina pectoris increases up to the sixth decade when it reaches a plateau. Conversely, the prevalence of myocardial infarction increases progressively at increasing ages without reaching any plateau at all. These findings indicate that the higher prevalence of myocardial infarction in the elderly is not caused by a worsening of the atherosclerotic background, but rather by a greater prevalence and/or severity of the functional factors such as local smooth muscle hyperreactivity, local thrombotic stimuli and alterations of the systemic thrombosis-thrombolysis equilibrium which are more directly responsible for the irreversible occlusion of a coronary artery branch. Therefore, the prevention of IHD in the elderly should focus mainly on the ischemic stimuli leading to coronary thrombosis rather than on the atherosclerotic background. Another important feature of IHD in the elderly is the high short and medium-term mortality of acute myocardial infarction. This excess of mortality is caused mainly by a much higher incidence of cardiac rupture, which does not appear to be related to the severity of coronary atherosclerosis nor to the infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Effects of theophylline, atenolol and their combination on myocardial ischemia in stable angina pectoris.

The effects of theophylline (400 mg twice a day), atenolol (50 mg twice a day) and their combination on myocardial ischemia were studied in 9 patients with stable angina pectoris in a randomized, single-blind, triple crossover trial. Placebo was administered to the patients during the run-in and the run-off periods. A treadmill exercise test and 24-hour ambulatory electrocardiographic monitoring were obtained at the end of each treatment period. Compared with placebo, theophylline significantly improved the time to onset of myocardial ischemia (1 mm of ST-segment depression) from 7.8 +/- 3.7 to 9.5 +/- 3.7 minutes (p less than 0.03) and the exercise duration from 9 +/- 3.4 to 10.1 +/- 3.5 minutes (p less than 0.04). During atenolol and during combination treatment, the time to the onset of ischemia and the exercise duration were similar (10.8 +/- 4.2 and 11.2 +/- 3.2 minutes, 11.2 +/- 3.6 and 11.5 +/- 3.2 minutes, respectively) and longer than during theophylline administration (p less than 0.05). Ambulatory electrocardiographic monitoring showed that, during theophylline administration, the heart rate was higher than during placebo throughout the 24 hours (p less than 0.05). During atenolol and during combination treatment the heart rate was similar and in both cases lower than during placebo (p less than 0.05). Compared with placebo, theophylline decreased the total ischemic time from 97 +/- 110 to 70 +/- 103 minutes (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Myocardial ischemia caused by distal coronary-artery constriction in stable angina pectoris.

BACKGROUND: In patients with stable coronary artery disease, the ischemic threshold for the production of effort-related angina is often quite variable. Although this feature is commonly attributed to changes in the caliber of coronary arteries at the site of stenosis, it could also be caused by the constriction of distal vessels, collateral vessels, or both. METHODS: In order to test this hypothesis, we studied 11 patients with stable angina, total occlusion of a single coronary artery that was supplied by collateral vessels, normal ventricular function, no evidence of coronary-artery spasm, and no other coronary stenoses. These conditions precluded the modulation of coronary flow by vasomotion at the site of the coronary stenosis. RESULTS: The ischemic threshold--assessed by multiplying the heart rate by the systolic blood pressure at a 1-mm depression of the ST segment during exercise testing--increased by 19 percent after the administration of nitroglycerin (P less than 0.05) and decreased by 18 percent after the administration of ergonovine (P less than 0.01). Ambulatory electrocardiographic monitoring of the patients when not receiving treatment detected 73 ischemic episodes that, in keeping with the history, showed variations of 25 to 52 beats per minute in the heart rate at a 1-mm depression of the ST segment; 12 episodes of sinus tachycardia exceeded the lowest ischemic heart rate by a mean (+/- SD) of 22 +/- 13 beats per minute without ST-segment depression. Furthermore, 21 ischemic episodes occurred at a heart rate more than 25 beats per minute below that at a 1-mm depression of the ST segment during exercise testing. Delayed and reduced filling of collateral and collateralized vessels associated with depression of the ST segment similar to that observed during ambulatory monitoring was detected on angiographic evaluation after the intracoronary administration of ergonovine in three patients. CONCLUSIONS: We propose that the constriction of distal coronary arteries, collateral vessels, or both may cause myocardial ischemia in patients with chronic stable angina.

Adult↗
PubMed1990

Similar time course of ST depression during and after exercise in patients with coronary artery disease and syndrome X.

To assess whether the time course of ST segment depression differs in patients with coronary artery disease and patients with angina and normal coronary arteries, the exercise tests of 54 patients with documented coronary artery disease and 25 patients with syndrome X (angina, positive exercise test, no evidence of coronary artery spasm, and normal coronary arteries) were compared. All tests were performed with therapy withheld, using the modified Bruce protocol. In each test, time, heart rate and blood pressure were measured at the onset and at 1 mm of ST segment depression, and at peak exercise. Recovery (return of the ST segment to baseline +/- 0.2 mm) time was also assessed. Peak ST segment depression was similar in coronary artery disease and syndrome X patients (1.5 +/- 0.3 versus 1.6 +/- 0.4 mm). In 42 coronary artery disease patients, ST segment depression developed early (less than or equal to 6 minutes) during exercise; this was associated with a short recovery (less than or equal to 3 minutes) in 17 (40%) and with a long recovery (greater than 3 minutes) in 25 (60%) patients. In 17 patients with syndrome X, ST segment depression developed early; it was associated with a short recovery in six (35%) and with a long recovery in 11 (65%) patients. Late (greater than 6 minutes) onset of ST segment depression was observed in 12 coronary artery disease patients; of these, eight (67%) had a short recovery and 4 (33%) had a long recovery. Late onset of ST segment depression occurred in eight patients with syndrome X; six (75%) had a short recovery and two (25%) had a long recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Very early prediction of restenosis after successful coronary angioplasty: anatomic and functional assessment.

To investigate the time course of restenosis, serial treadmill exercise testing was performed in the absence of medical therapy by 31 patients with single vessel coronary disease who underwent successful angioplasty. Exercise tests were performed before angioplasty and at 3 days and 1, 3 and 6 months after angioplasty; if the test was positive, it was repeated after administration of 10 mg of intravenous verapamil. At arteriography 6 months after coronary angioplasty, 17 patients (group 1) showed no restenosis but 14 patients (group 2) did. Before angioplasty all 31 patients had a positive exercise test with ST segment depression greater than or equal to 1 mm. At 3 days after angioplasty, three patients in group 1 had a positive exercise test compared with 11 patients in group 2 (p = 0.08). At 1, 3 and 6 months, 1 patient in group 1 had a positive exercise test compared with 14 patients in group 2 (p less than 0.01). The heart rate-blood pressure product (beats/min.mm Hg) calculated at 1 mm ST segment depression, or at peak exercise if the test was negative, was used as an index of the ischemic threshold. In group 1 (no restenosis) the ischemic threshold increased progressively from 14,840 +/- 1,075 (mean value +/- SEM) before angioplasty to 21,210 +/- 1,049 at 3 days and to 25,140 +/- 1,177 (p less than 0.001) at 6 months. In group 2 (restenosis) the ischemic threshold increased from 16,270 +/- 828 before angioplasty to 20,400 +/- 984 (p less than 0.0004) at 3 days but decreased to 16,090 +/- 1,298 (p less than 0.006) at 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Assessment of colour flow imaging in the grading of valvular regurgitation.

To assess the accuracy of colour flow imaging in the grading of valvular regurgitation, we studied 100 consecutive patients with angiographic mitral regurgitation (55), aortic regurgitation (35) or both (10). The etiology of valve regurgitation was rheumatic in 42 and non-rheumatic in 58 patients. For comparison, 28 subjects with no structural cardiac disease were studied. Mitral valve regurgitation was assessed with colour flow imaging by measuring the maximal regurgitant jet area and the maximal jet area normalized to left atrial area; aortic valve regurgitation was assessed from jet area and jet width normalized to ventricular outflow tract width. The best correlation between colour flow imaging and angiography was obtained with normalized measurements for both mitral (r = 0.82, P less than 0.0001) and aortic regurgitation (r = 0.94, P less than 0.0001). A proportion of patients and controls without angiographic regurgitation showed evidence of mild mitral (31% and 32%) and aortic (14% and 11%) regurgitation on colour flow imaging. There was a large overlap in the normalized colour flow measurements between angiographically mild and moderate mitral regurgitation (43%); the overlap was greater when regurgitation was rheumatic in origin (45%) rather than non-rheumatic (10%) (P less than 0.001). There was also overlap in the normalized colour flow findings in patients with angiographic aortic regurgitation, which was greater in rheumatic vs non-rheumatic disease. Knowledge of the etiology significantly improved the separation of all angiographic grades of aortic regurgitation using colour flow measurements (P = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Role of adenosine in pathogenesis of anginal pain.

The intravenous infusion of adenosine provokes anginalike chest pain. To establish its origin, an intracoronary infusion of increasing adenosine concentrations was given in 22 patients with stable angina pectoris. During adenosine infusion, 20 patients had chest pain without electrocardiographic signs of ischemia. They all reported that the chest pain was similar to their usual anginal pain. In 10 of the 22 patients adenosine was also infused into the right atrium, but it never produced symptoms at the doses that had provoked chest pain during intracoronary infusion. In seven other patients, the intracoronary adenosine infusion was repeated after intravenous administration of aminophylline, an antagonist of adenosine P1-receptors. Aminophylline decreased the severity of adenosine-induced chest pain (assessed with a visual analog scale) from 42 +/- 22 to 23 +/- 17 mm (p less than 0.002). In the remaining five of the 22 patients, monitoring of blood oxygen saturation in the coronary sinus during intracoronary adenosine administration showed that maximum coronary vasodilation was achieved at doses lower than those responsible for chest pain. A single-blind, placebo-controlled, randomized trial of the effect of aminophylline on exercise-induced chest pain was also performed in 20 other patients with stable angina. Aminophylline, compared with placebo, decreased the severity of chest pain at peak exercise from 67 +/- 21 to 51 +/- 23 mm (p less than 0.02), despite the achievement of a similar degree of ST-segment depression. Finally, the effect of intravenous adenosine was compared in 10 patients with predominantly painful myocardial ischemia and in 10 patients with predominantly silent ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
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

Type 1 fiber abnormalities in skeletal muscle of patients with hypertrophic and dilated cardiomyopathy: evidence of subclinical myogenic myopathy.

Abnormalities of skeletal muscle have been described in patients with dilated and hypertrophic cardiomyopathy. Eleven patients with dilated and eight with hypertrophic cardiomyopathy without overt symptomatic skeletal myopathy underwent extensive neuromuscular studies. Quantitative electromyography showed abnormal reduction of motor unit potential duration, indicative of myogenic myopathy, in four patients (36%) with dilated and in three (37%) with hypertrophic cardiomyopathy. Values were 21% to 40% (mean 28%) lower than those in age-matched normal control subjects. The presence of normal nerve conduction velocities and of normal motor unit fiber density in all patients indicated lack of neurogenic abnormalities. Skeletal muscle biopsy was performed in five patients with dilated and in four with hypertrophic cardiomyopathy. In all nine patients light and electron microscopy showed central hyporeactive cores, selective atrophy and mitochondrial abnormalities of type 1 fibers but not of type 2 fibers. The degree of impairment of left ventricular function in patients with electromyographic abnormalities was similar to that of those without (percent fractional shortening at two-dimensional echocardiography 21 +/- 9 versus 25 +/- 10, ejection fraction at angiography 39 +/- 13% versus 42 +/- 13% and left ventricular end-diastolic pressure 21 +/- 6 versus 21 +/- 8 mm Hg) as well as symptom duration (9 +/- 4 versus 12 +/- 8 months). Thus, subclinical electromyographic alterations indicative of myogenic myopathy are frequent in patients with dilated and hypertrophic cardiomyopathy and are unrelated to the degree of impairment of left ventricular function. The concomitant histologic alterations, characterized by selective type 1 atrophy, are similar to those observed in congenital and idiopathic myopathies, but different from those described in secondary heart failure.

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

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

Intravascular delivery of laser energy with metal-capped optical fibers: the potential hazard of distal embolism.

To assess the risk of embolism resulting from plaque fragmentation during laser angioplasty with metal-capped optical fibers, laser energy of 4, 8, and 12 W for 10 or 20 seconds was delivered through these fibers to 60 coronary endarterectomy segments fitted in a silicone tube filled with saline solution. Twenty specimens manipulated in the same way but without delivering laser energy were used as controls. The effluent was filtered through in-line filters of 225, 70, and 25 microns. Treatment with laser energy resulted in weight loss and shortening of the specimens compared to control specimens (23 +/- 4 mg versus 5.4 +/- 0.8 mg; p less than 0.001 and 0.2 +/- 0.02 mm versus 2.5 +/- 0.5 mm; p less than 0.001). However, this also produced significant debris formation for all combinations of power and time (up to 275 +/- 38 micrograms versus 155 +/- 21 micrograms in controls). Results of scanning electron microscopy showed the presence of fragments up to 300 microns in diameter. Another potential hazard of laser angioplasty with metal-capped optical fibers in thromboembolism. This was studied by delivering laser energy through metal-capped fibers during perfusion with aliquots of blood at 5 or 40 ml/min. At each flow rate nine aliquots were treated with either 4, 8, or 12 W for 3, 6, or 9 seconds and a tenth was used as a control aliquot. The effluent was filtered with five filters between 225 microns and 25 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
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↗