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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 199 records · Page 11Linked to original sources
PubMed1993

Variability of coronary blood flow reserve assessed by Doppler catheter after successful thrombolysis in patients with acute myocardial infarction.

To establish whether abnormal function of small coronary vessels might limit the advantages of thrombolytic treatment, coronary flow reserve in the infarct-related artery was measured in nine patients with acute myocardial infarction early after successful coronary thrombolysis by using a Doppler catheter and intracoronary adenosine infusion. In each patient coronary flow reserve was calculated as the ratio between coronary blood flow velocity during the highest tolerated intracoronary dose of adenosine (0.5 mg/min in five patients and 1 mg/min in four patients) and baseline velocity. Coronary flow reserve ranged from 1 to 3 (mean 2 +/- 0.7). No correlation (r = 0.20; p = 0.58) was found between coronary flow reserve and the severity of residual coronary stenosis, which ranged between 23% and 76% (mean 47% +/- 17%). No correlation (r = 0.33; p = 0.39) was found between either coronary flow reserve and the interval between pain onset and administration of the thrombolytic treatment, which ranged between 2.2 and 6 hours (mean 4.2 +/- 1.4 hours). Thus, in patients with acute myocardial infarction, coronary flow reserve early after successful thrombolysis is strikingly variable and may be extremely low despite widely patent epicardial coronary arteries. This restriction of coronary blood flow, probably caused by abnormal function of small coronary vessels, might limit the potential benefit from successful coronary thrombolysis.

Adenosine↗
PubMed1993

Response of human coronary arteries to acetylcholine after injury by coronary angioplasty.

OBJECTIVES: The aim of this study was to investigate the effect of intracoronary administration of acetylcholine on large epicardial vessels 8 days after successful coronary angioplasty. BACKGROUND: Intracoronary infusion of acetylcholine causes vessel dilation in patients without angiographic evidence of coronary atherosclerosis, whereas it causes constriction of stenotic coronary branches. These findings were interpreted as evidence of endothelial dysfunction in patients with coronary atherosclerosis. METHODS: Eight patients who underwent successful single-vessel coronary angioplasty of the proximal left anterior descending artery were studied. Eight days after coronary angioplasty at the time of follow-up coronary angiography, intracoronary acetylcholine was infused (1 ml/min for 2 min) at concentrations ranging from 10(-7) to 10(-4) mol/liter. The diameter of the angioplasty and distal segments of the left anterior descending artery and that of the proximal and distal segments of the circumflex artery (control artery) were measured using computerized edge detection angiography. RESULTS: All patients showed a dose-dependent constriction in response to acetylcholine and experienced chest pain and ST segment changes. Intracoronary nitroglycerin (300 micrograms) relieved the effects of acetylcholine. The maximal tolerated dose of acetylcholine (10(-6) mol/liter in three patients, 10(-5) mol/liter in three patients and 10(-4) mol/liter in two patients) induced a mild constriction of the angioplasty segment from 1.84 +/- 0.11 mm to 1.52 +/- 0.13 mm (p < 0.02) similar to that of the proximal segment of the control artery (from 2.42 +/- 0.23 to 2.07 +/- 0.19 mm, p < 0.02). However, the degree of constriction of the vascular segments distal to the angioplasty site (from 1.24 +/- 0.09 to 0.62 +/- 0.13 mm, p < 0.01) was significantly greater (p < 0.05) than that observed in the distal segments of the control artery (from 1.23 +/- 0.03 to 0.71 +/- 0.01 mm, p < 0.01) and resulted in transient total occlusion in two patients. CONCLUSIONS: Eight days after coronary angioplasty, coronary segments distal to the dilated site but not at the dilated site are hyperreactive to acetylcholine. The response of epicardial coronary arteries to acetylcholine is influenced not only by the dose of acetylcholine and the endothelial function (as currently believed) but also by the location of the coronary segment considered, confirming the presence of a profound alteration of distal coronary vessels.

Acetylcholine↗
PubMed1993

Aspirin, but not heparin, suppresses the transient increase in thromboxane biosynthesis associated with cardiac catheterization or coronary angioplasty.

OBJECTIVES: We sought to study the dose dependence of in vivo suppression by aspirin of enhanced thromboxane biosynthesis in the setting of coronary angioplasty and to evaluate the effects of heparin and aspirin during cardiac catheterization. BACKGROUND: Percutaneous transluminal coronary angioplasty induces a controlled injury of the intima of the diseased arterial segment, with rapid deposition of platelets at the site of dilation. Thus, it provides a clinical model of intracoronary platelet activation. METHODS: The urinary excretion of a major enzymatic metabolite of thromboxane A2, 11-dehydro-thromboxane B2, was measured in 57 patients with stable coronary artery disease undergoing cardiac catheterization (n = 28) or elective single-vessel percutaneous transluminal coronary angioplasty (n = 29). Three consecutive urine collections were obtained from all patients before during and after either procedure. Patients undergoing catheterization were treated with the following regimens: a) no aspirin for > or = 10 days and no heparin (n = 12); b) no aspirin for > or = 10 days but heparin, 10,000 IU, at the time of catheterization (n = 5); c) aspirin, 300 mg/day, for at least 5 days (n = 11). Patients undergoing coronary angioplasty were randomly assigned to short-term treatment with aspirin given as a) 75 mg/day for > or = 5 days before angioplasty (n = 11); b) 300 mg/day for > or = 3 days before angioplasty (n = 9); or c) 300 mg/day for > or = 3 days before angioplasty followed by 1,000 mg during angioplasty (n = 9). RESULTS: In patients undergoing catheterization, urinary 11-dehydro-thromboxane B2 excretion (pg/mg creatinine) increased from 563 +/- 481 (mean +/- SD) to 1,684 +/- 1,332 in the absence and from 620 +/- 191 to 1,588 +/- 597 in the presence of heparin. No increase was observed in the group receiving aspirin (from 240 +/- 141 to 215 +/- 115). In patients undergoing coronary angioplasty treated with aspirin, 75 mg/day, urinary 11-dehydro-thromboxane B2 averaged 180 +/- 112, 223 +/- 178 and 294 +/- 260, respectively, before, during and after the procedure. At 300 mg/day, the corresponding values were 185 +/- 48, 217 +/- 70 and 197 +/- 93. In patients also receiving aspirin, 1,000 mg, during angioplasty, 11-dehydro-thromboxane B2 averaged 151 +/- 66, 138 +/- 43 and 133 +/- 77, respectively. CONCLUSIONS: Enhanced thromboxane biosynthesis associated with cardiac catheterization or coronary angioplasty can be largely suppressed by low dose aspirin. This finding is consistent with the view that this alteration reflects platelet activation.

Aged↗
PubMed1993

Vasodilator reserve in collateral-dependent myocardium as measured by positron emission tomography.

Myocardial blood flow can be accurately quantitated in patients using positron emission tomography and oxygen-15 labelled water. The purpose of this study was to determine the vasodilator reserve in myocardium completely perfused by intramyocardial collateral blood flow. We hypothesized that altered relative flow reserve in such regions would correlate with the degree of ischaemia observed in these patients during exercise. The technique involves the inhalation of the positron emitting tracer C15O2 which is converted to freely diffusible H2(15)O by the lung. With rapid dynamic scanning, arterial and regional myocardial tissue concentrations can be obtained and time activity curves generated. With a two-compartment kinetic model, myocardial blood flow can be accurately quantitated over a wide range of blood flows. Five patients with stable exertional angina and normal ventricular function studies and who had an occluded major epicardial artery which completely opacified via intramyocardial collateral blood flow were studied. Myocardial blood flow (MBF) was measured both at rest and following an infusion of intravenous dipyridamole (0.56 mg.kg-1) and the results were compared with measurements obtained from a group of eight normal volunteers. During resting conditions, MBF in the control group was 0.86 +/- 0.10 ml.g-1.min-1 and in the patient group was 0.99 +/- 0.10 ml.g-1.min-1 in normally perfused myocardium (ns) and 0.86 +/- 0.14 ml.g-1.min-1 in collateral-dependent myocardium (ns). Following dipyridamole, MBF increased to 3.58 +/- 0.89 ml.g-1.min-1 in the control group and to 2.97 +/- 0.94 ml.g-1.min-1 in the normal regions of the patients (ns).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Comparison of coronary angiographic findings in acute and chronic first presentation of ischemic heart disease.

BACKGROUND: It is generally assumed that the clinical manifestations of ischemic heart disease occur randomly on the same underlying pathological process. Therefore, coronary angiographic findings should be similar whether the first presentation of ischemic heart disease is acute myocardial infarction or uncomplicated chronic stable angina. METHODS AND RESULTS: We studied 102 patients (men < or = 60 years old, women < or = 65 years old) presenting with either acute myocardial infarction as first manifestation of coronary artery disease with a concomitant coronary angiogram (55 patients; mean age, 50.2 years) or stable angina for at least 2 years with no history, ECG, or left ventriculographic evidence of any acute event and with an angiogram performed at least 2 years after initial symptoms (47 patients; mean age at symptom onset, 51.7 years). These angiograms were evaluated blindly for severity (number of vessels diseased, stenoses > or = 50%, occlusions), extent of disease (with an index derived by assigning a score of 0-3 per segment, depending on the proportion of lumen length irregularity and dividing the sum by the number of visualized segments), and pattern (discrete: three or fewer loci of disease never involving more than 50% of the length of any segment or diffuse: anything exceeding this). Patients with unheralded myocardial infarction had fewer vessels diseased, fewer stenoses and occlusion, and a lower extent index than those with uncomplicated stable angina (mean +/- SD of 1.3 +/- 0.8 versus 2.1 +/- 0.8, p < 0.001; 2.1 +/- 1.8 versus 3.9 +/- 1.8, p < 0.001; 0.6 +/- 0.6 versus 1.0 +/- 0.9, p < 0.02; and 0.6 +/- 0.5 versus 1.2 +/- 0.5, p < 0.001, respectively). A discrete pattern was present in 54.5% of patients with unheralded infarction and in only 8.5% of those with uncomplicated angina (p < 0.001). CONCLUSIONS: These very different angiographic findings suggest that unheralded acute myocardial infarction and uncomplicated chronic stable angina do not occur randomly on a common atherosclerotic background but rather that additional factors, such as a varying propensity to thrombosis, may predispose to one or the other of these two clinical syndromes.

Angina Pectoris↗
PubMed1993

Effect of inhibition of nitric oxide synthesis on epicardial coronary artery caliber and coronary blood flow in humans.

BACKGROUND: NG-Monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthesis, was used to determine the effects of inhibition of nitric oxide synthesis in the human coronary circulation. METHODS AND RESULTS: Twelve patients (mean age, 52 +/- 2 years) with normal epicardial coronary arteries were studied. The surface ECG, systemic blood pressure, and coronary venous oxygen saturation (coronary SvO2), an index of coronary blood flow, were monitored continuously. Coronary artery diameter was measured by quantitative arteriography. L-NMMA was given as intracoronary infusions at 2 mL/min via the diagnostic arteriography catheter. In two patients, low doses (0.01 to 5 mumol/min) of L-NMMA were infused into the nondominant right coronary artery. There was no evidence of ischemia in these patients, who were not included in the final analysis. In 10 patients, higher doses of L-NMMA (4, 10, and 25 mumol/min, each for 5 minutes) were infused into the left coronary artery. In six patients, incremental doses of acetylcholine were infused (1, 10, and 100 nmol/min, each for 3 minutes) before and after the L-NMMA infusion. Finally, in all patients, sodium nitroprusside, a nitric oxide donor, was infused. No patient developed myocardial ischemia. The heart rate and systemic blood pressure remained unchanged throughout the infusions. L-NMMA (25 mumol/min), compared with the control saline infusion, caused a significant reduction in distal (-5.9 +/- 2.1%, P = 0.021) but not proximal left anterior descending coronary artery (LAD) diameter and a fall in coronary SvO2 from 37.5 +/- 2.8% to 34.3 +/- 2.8% (P = 0.019). Sodium nitroprusside dilated the proximal (17.8 +/- 6.9%, P = 0.033) and distal (24.5 +/- 6.5%, P = 0.006) LAD and increased the coronary SvO2 to 61.6 +/- 5.0% (P = 0.0002). Acetylcholine caused significant dilatation of the distal (13.8 +/- 5.4%, P = 0.049) but not proximal LAD and a significant increase in coronary SvO2 from 36.5 +/- 3.5% to 59.2 +/- 2.8% (P < 0.0001). After L-NMMA, acetylcholine-induced dilatation of the distal LAD was abolished, but the rise in coronary SvO2 was unchanged. CONCLUSIONS: Inhibition of nitric oxide synthesis in the human coronary circulation caused a decrease in basal distal LAD diameter and basal coronary blood flow assessed by coronary SvO2, indicating that there is a small basal release of nitric oxide in the distal epicardial coronary arteries and resistive vessels. Distal epicardial coronary artery dilatation in response to acetylcholine is nitric oxide dependent, but coronary resistive vessel dilatation is not.

Acetylcholine↗
PubMed1993

Coronary vasomotor effects of serotonin in patients with angina. Relation to coronary stenosis morphology.

BACKGROUND: Previous experimental studies have shown that the effect of serotonin on a coronary stenosis depends on whether that stenosis is compliant or fixed. However, the relation between coronary stenosis morphology and the response to serotonin in patients with angina is not known. METHODS AND RESULTS: Using computerized quantitative coronary angiography, we studied the effects of intracoronary infusion of serotonin on 38 coronary stenoses of different morphologies (concentric, eccentric, complicated) in 11 patients with stable angina and 4 with variant angina. In response to the maximum infused concentration of serotonin, 100% of complicated stenoses and 50% of concentric stenoses constricted by > or = 20% (P < .05). The magnitude of constriction was greater at eccentric stenoses (32.08 +/- 4.1%) than concentric stenoses (15.68 +/- 2.8%, P < .05) and greater in complicated stenoses (57.69 +/- 7.6%, P < .05) than eccentric stenoses. At complicated stenoses, the constriction was greater (0.85 +/- 0.16 mm, P < .05) than at the adjacent reference segments (0.42 +/- 0.12 mm). It was similar to the reference segment for both concentric and eccentric stenoses. The constriction at the stenosis was greater for irregular (complicated) lesions than for smooth (concentric and eccentric) lesions in both patients with stable (51.8 +/- 7.3% versus 22.5 +/- 4.1%, P < .001) and those with variant (77 +/- 17% versus 28.2 +/- 8.1%, P < .05) angina. There was a weak correlation (r = .39) of magnitude of constriction with stenosis length but not with baseline stenosis severity (minimum diameter). CONCLUSIONS: In these patients, the magnitude of the vasoconstrictor response to serotonin at the site of an atheromatous coronary plaque depends on the morphological characteristics of the plaque and is more closely related to irregular contour than stenosis severity or length. This relation suggests that variations in receptor type or density or in the smooth muscle cell response to stimulation may determine the response to locally released serotonin in patients with coronary disease.

Angina Pectoris↗
PubMed1993

[Therapy of microvascular angina].

The treatment of microvascular angina (anginal pain resulting from myocardial ischemia due to dysfunction of small coronary arteries) is empiric and often ineffective at present. The poor knowledge of the pathophysiologic mechanisms responsible for the microvascular dysfunction and the possible heterogeneous nature of the disease limit the possibility of a rational therapeutic approach to these patients. The failure of traditional antiischemic therapy is confirmed by the frequent unresponsiveness of angina and by the reduced exercise tolerance with administration of sublingual nitrates. Despite that, beta-blockers and calcium-antagonists, when given either alone or in combination, are beneficial in the control of symptoms in some patients. Alternative forms of treatment, based on some pathophysiological hypotheses and clinical observations, include xanthine derivatives, ACE-inhibitors, alpha-blocking agents, imipramine and, in women, oestrogens. The actual clinical usefulness of these drugs, however, is questionable at present, as their efficacy should be evaluated with more adequate studies in the future.

Adrenergic alpha-Antagonists↗
PubMed1993

[Mechanisms of coronary microvascular dysfunction].

Abnormal constriction of coronary resistive vessels can induce angina and myocardial ischemia. The possibility that a microvascular vasomotor dysfunction could cause ischemia is in contrast with the well-known traditional notion that a metabolically induced vasodilation could compensate for the effect of an epicardial coronary stenosis. Vasoconstrictor stimuli can plausibly act on vessels situated immediately proximal (prearterioles) to those that can be dilated by ischemia metabolites (arterioles). This functional 2-compartment model of resistive vessels is based on the ability of different substances to cause opposite actions on resistive vessels with different sizes. The possible mechanisms of prearteriolar dysfunction, observed in patients with syndrome X, single vessel disease after a successful PTCA and in a subset of chronic stable patients include: an organic reduction of total vascular section; vascular smooth muscle hyperreactivity to heterogeneous constrictor stimuli; an impaired flow-mediated endothelium-dependent vasodilation (possibly due to a reduced NO and/or EDHF synthesis). The first and third hypothesis can only account for anginal episodes at effort while the second model could explain episodes occurring at rest and without an increase in heart rate. Those mechanisms causing an imbalance between myocardial oxygen supply and demand, induce an increased release of adenosine in order to promote a compensating vasodilation. Adenosine can possibly avoid the occurrence of ischemia but, being a powerful algogenic stimulus, causes pain. It is worth noting that the presence of patchy prearteriolar dysfunction induces areas with excessive release of adenosine. Since total vascular section is extremely large a massive adenosine spill-over can occur with a consequential boosting of algogenic and vasodilatory effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Disease↗
PubMed1992

Von Willebrand factor, plasminogen activator inhibitor-1 and C-reactive protein are markers of thrombolytic efficacy in acute myocardial infarction.

Plasma von Willebrand factor, plasminogen activator inhibitor activity and C-reactive protein were assessed as markers of coronary recanalisation in 30 patients with acute myocardial infarction receiving tissue-type plasminogen activator (t-PA). Blood samples were taken before t-PA (time 0), 4-hourly for 24 h and daily up to 72 h. A continuous electrocardiogram was recorded in the first 24 h. Coronary arteriography was performed 90 min and 24 h after the start of t-PA. Patients with a patent infarct artery (n = 17), compared to those with occluded artery (n = 13), showed a fall in von Willebrand factor from 0 to 24 h (p = 0.001), a greater fall in plasminogen activator inhibitor from 24 to 48 h (p = 0.04) and a fall in C-reactive protein from 48 to 72 h (p = 0.002). The accuracy of these indices compared favourably with time to peak plasma MB creatine kinase and > or = 50% resolution of maximal ST-deviation on the electrocardiogram. Thus, changes in plasma von Willebrand factor, plasminogen activator inhibitor and C-reactive protein during the first 3 days of myocardial infarction are indicative of thrombolytic efficacy. Their concordant behaviour may reflect a common regulatory mechanism.

Adult↗
PubMed1992

The significance of a dipyridamole induced 99mTc-MIBI perfusion abnormality on single photon emission tomography: a quantitative validation with labelled water and positron emission tomography.

To relate technetium-99m 2-methoxy-isobutyl-isonitrile (99mTc-MIBI) uptake to regional myocardial blood flow (rMBF), 99mTc-MIBI single photon emission tomography (SPET) and H2(15)O positron emission tomography (PET) scans were obtained at rest and after dipyridamole infusion in six patients with single vessel coronary artery disease. 99mTc-MIBI and H2(15)O data sets were created for each segment perfused by the stenotic vessel and for a normal reference area, assigning regions on the SPET tomograms to comparable regions on the PET by similar transaxial image reconstructions. All patients demonstrated post-dipyridamole 99mTc-MIBI perfusion defects in the territories supplied by the stenotic arteries. Resting rMBF in these regions was slightly lower than that in the normal areas (0.82 +/- 0.05 vs 0.90 +/- 0.09 ml/g/min, P = NS). A 43% +/- 14% reduction in 99mTc-MIBI activity in the area at risk was coupled with on average a 60% +/- 9% reduction in post-dipyridamole rMBF compared with control regions (0.98 +/- 0.08 vs 2.52 +/- 0.51 ml/g/min, P < 0.001). Thus, SPET assessment of 99mTc-MIBI uptake tends to underestimate the perfusion contrast between areas with normal and areas with low coronary vasodilatory reserve when compared to PET. However, these findings may still not affect the clinical usefulness of 99mTc-MIBI and more extensive studies are required to confirm these results in the clinical environment.

Contrast Media↗
PubMed1992

Preangioplasty complicated coronary stenosis morphology as a predictor of restenosis.

To assess whether complicated preangioplasty coronary stenosis morphology is associated with restenosis, 41 patients (47 stenoses) who underwent repeat angiography 6 to 8 months after percutaneous transluminal coronary angioplasty (PTCA) were studied. Stenosis diameter and morphology were assessed by computerized quantitative coronary angiography before and immediately after PTCA and at follow-up angiography. Before PTCA 18 stenoses were concentric (symmetric narrowings with smooth borders), 12 were eccentric (asymmetric narrowings with smooth borders), and 17 were complicated (asymmetric with rough borders and overhanging edges). Restenosis occurred in 18 lesions: two (11%) concentric, four (33%) eccentric, and 12 (70%) complicated (p less than 0.05), whereas 29 lesions remained unchanged. Stenosis diameter before and immediately after PTCA was not significantly different in the 18 patients with and the 23 patients without restenosis. Follow-up angiograms showed that 11 (61%) stenoses in the group with restenosis and 18 (63%) in the group without restenosis had morphology similar to that before PTCA. Restenosis occurred in seven (30%) patients who initially had chronic stable angina and in 11 (61%) who were first seen with unstable angina (p less than 0.05). In patients with stable angina 1 of 13 concentric stenoses, two of eight eccentric stenoses, and four of five complicated lesions restenosed. In patients with unstable angina one of five concentric, two of four eccentric, and 8 of 12 complicated lesions had restenosis. Stenoses that were complicated before PTCA tended to adopt an irregular morphology if they recurred, whereas concentric stenoses rarely occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

A combination of electrocardiographic methods represents a further step toward the noninvasive identification of patients with syndrome X.

Identification of patients with angina but normal coronary arteriograms (syndrome X) using noninvasive means would be desirable. The ability of four established exercise electrocardiographic methods to identify angina patients with and without coronary artery disease was compared with that of a method based on a combination of the above (combined method). A treadmill score, a multivariate method, the ST segment recovery loop, the ST/heart rate adjustment, and the combined method were applied to 112 patients who had typical exertional angina and positive exercise tests (greater than 1 mm ST segment depression); 90 had documented coronary artery disease and 22 had syndrome X. The combined method and the treadmill score had a significantly higher diagnostic accuracy (both 81%, as 91 of the 112 patients were correctly identified by both methods) than the multivariate (66%) and ST segment recovery loop (64%) methods (p less than 0.05). The ST/heart rate adjustment had a lower sensitivity for syndrome X than any other method (1 of 22). Thus methods that involve the assessment of both ST and non ST segment variables have greater accuracy in separating syndrome X and coronary artery disease patients than methods relying more heavily on ST segment changes.

Adrenergic beta-Antagonists↗