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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 145 records · Page 8Linked to original sources
PubMed1996

Preinfarction angina as a predictor of more rapid coronary thrombolysis in patients with acute myocardial infarction.

BACKGROUND: When a myocardial infarction is preceded by angina, the infarct tends to be smaller than when there is no preinfarction angina. Prompt recanalization of the occluded infarct-related artery is crucial in limiting the size of the infarct. We prospectively studied the relation among preinfarction unstable angina, the speed of coronary reperfusion, and the size of the infarct in patients with acute myocardial infarction receiving thrombolytic therapy. METHODS: We compared 14 patients who had unstable angina during the week before myocardial infarction with 9 patients who had no preinfarction angina. Coronary arteriograms were obtained at base line and 15, 35, 55, and 90 minutes and 24 hours after the start of thrombolytic therapy. The size of the infarct was estimated on the basis of creatine kinase and creatine kinase MB levels, which were measured every 4 hours during the first 24 hours. RESULTS: Complete reperfusion (a flow of grade 3 according to the Thrombolysis in Myocardial Infarction classification) was achieved at 35 minutes in 64 percent of the patients with preinfarction angina but in none of those without preinfarction angina (P = 0.006); at 55 minutes in 86 percent and 38 percent, respectively (P = 0.05); and at 90 minutes in 86 percent and 50 percent, respectively (P = 0.14). The mean (+/- SD) time to reperfusion was 27 +/- 16 minutes in the group with preinfarction angina and 48 +/- 17 minutes in the group without preinfarction angina (P = 0.04); the peak creatine kinase levels were 1118 +/- 783 and 2395 +/- 1615 U per liter, respectively (P = 0.03); the peak creatine kinase MB levels were 102 +/- 67 and 251 +/- 186 U per liter, respectively (P = 0.009); and the 24-hour integrated creatine kinase MB levels were 1716 +/- 1171 and 4267 +/- 3252 U.liter-1 x 24 hours, respectively (P = 0.009). The time to reperfusion was positively correlated with the indexes of infarct size (r > or = 0.53, P < or = 0.02). CONCLUSIONS: In patients with acute myocardial infarction preceded by unstable angina, as compared with those without preinfarction angina, thrombolytic therapy resulted in more rapid reperfusion and smaller infarcts. Earlier myocardial reperfusion may thus account for the smaller infarct size in patients with preinfarction angina.

Adult↗
PubMed1996

Different Effects of Lipopolysaccharide on Plasminogen Activator Inhibitor-1 Production in Aortic Media in Vivo and in Culture.

Background: Lipopolysaccharide (endotoxin) has been shown to increase the expression of plasminogen activator inhibitor type-1 (PAI-1) in the vessel wall. Endotoxin is known to increase PAI-1 production in endothelial cells, but its action on smooth muscle cells (SMCs) is presently not clear. In this study we determined the effect of endotoxin on PAI-1 and tissue plasminogen activator (t-PA) production by aortic SMCs in vivo in two animal species, and in culture. Methods: The aortas of Sprague Dawley rats and of New Zealand White rabbits were rapidly excised after parenteral administration of endotoxin. Total RNA was extracted from the aortic media, and PAI-1 and t-PA mRNA levels were quantified after Northern blotting. In addition, cultured rat aortic SMCs were treated with endotoxin. PAI activity in the conditioned medium was determined with a spectrophotometric assay, and total RNA was extracted from the cells and analyzed. Results: A rapid and strong induction in the aortic medi a of PAI-1 mRNA was observed by endotoxin in both rat (50 mg/kg) and rabbit (1 mg/kg). t-PA mRNA was barely detectable and was not increased by endotoxin. Studies in cultured SMCs showed low expression of PAI-1 mRNA under serum-free conditions and little PAI activity in the cell-conditioned medium. Endotoxin did not increase the levels of PAI-1 mRNA nor PAI activity under serum-free conditions. The effect of endotoxin (10 mg/ml) in the presence of 10% (v/v) newborn calf serum on PAI-1 mRNA was negligible; PAI activity, however, increased by 50.3 +/- 7.3% compared with controls. mRNA levels of t-PA and low-density lipoprotein/receptor-related protein/alpha2-macroglobulin receptor also increased after endotoxin administration. PAI activity was identified as PAI-1 by immunoblotting. Fibrin zymography showed that t-PA was present only in complex with PAI-1. Conclusions: A strong increase in PAI-1 gene expression by endotoxin was observed in aortic SMCs in vivo but not in culture. Th is suggests that the effect of endotoxin on SMCs is indirect. The fibrinolytic/proteolytic potential of the SMCs in the vessel wall is likely to have important implications for the migration of cells during vessel wall remodeling, such as neointima formation, during tumor cell metastasis, and for the fate of intramural thrombi.

Journal Article↗
PubMed1996

Use of the radial artery for myocardial revascularization.

BACKGROUND: The radial artery was first used as a coronary graft by Carpentier and associates in 1973 but, due to the disappointing results, it was abandoned. In 1992 its revival coincided with the widespread use of calcium-channel blockers in cardiovascular surgery, in the belief they could prevent spasm. METHODS: From January 1993 to October 1995 we operated on 109 patients for myocardial revascularization employing the radial artery with two different surgical techniques: in 95 patients (group 1) it was "pretreated" by opening its fascia after a gentle hydrostatic dilation and then anastomosed to the aorta; in 14 patients (group 2) it was branched to another conduit. We had two operative deaths (1.82%). RESULTS: At a mean interval of 532.42 days 105 patients are still alive, 2 (1.86%) having died of abdominal tumors. Fifty-six patients (52.33%) underwent angiography at a mean interval of 334.42 days: the patency of the radial artery was 88.88% in group 1 and 62.50% in group 2. Indications and contraindications are discussed. CONCLUSIONS: The radial artery is an easily manageable conduit whose early patency is very promising, although a longer follow-up is mandatory.

Adult↗
PubMed1996

Altered resistive vessel function after coronary angioplasty is not due to reduced production of nitric oxide.

BACKGROUND: The coronary vasodilator reserve with dipyridamole may be impaired immediately after successful angioplasty due to reduced endothelial production or release of nitric oxide. As the vasodilator response to exogenous nitrates is enhanced by endothelium removal or inhibition of nitric oxide synthesis, an increased vasodilator response to nitrovasodilators, such as nitroprusside, should occur. METHODS: The coronary vasodilator reserve (maximal/basel coronary blood flow) with intravenous dipyridamole (0.56 mg/min for 4 min) was measured by Doppler catheterization before and after angioplasty in 10 patients with single-vessel coronary disease. At peak dipyridamole effect, incremental doses of nitroprusside (4-50 micrograms/min) were given intracoronary until systolic blood pressure fell by > or = 5 mmHg. RESULTS: Before angioplasty, the coronary blood flow increased from 19.7 +/- 6.1 (mean +/- s.d.) at basal to 30.1 +/- 11.9 ml/min at the peak dipyridamole effect (P < 0.01), giving a coronary vasodilator reserve of 1.62 +/- 0.39 (range 1.20 - 1.96). After angioplasty, the coronary blood flow increased from 32.4 +/- 13.2 at basal to 53.4 +/- 23.3 ml/min at the peak dipyridamole effect (P < 0.01), giving a coronary vasodilator reserve of 1.77 +/- 0.64 (range 1.7-2.42). Sodium nitroprusside had no additional effect on coronary flow (49.5 +/- 20.4 and 52.2 +/- 18.0 ml/min) before and after a fall in systolic blood pressure, respectively. CONCLUSIONS: The vasodilator response to dipyridamole was markedly impaired immediately after successful angioplasty, and was not augmented by intracoronary nitroprusside. Thus, a reduced production or release of nitric oxide in the coronary circulation does not seem to be responsible for the impaired vasodilator response after angioplasty.

Adult↗
PubMed1996

Clinical markers of thrombolytic success.

Although a number of markers of successful coronary thrombolysis have been proposed, only a few of these have the two necessary features of a clinically useful marker: (1) widespread early availability and (2) good predictive value. The reduction in ST-segment elevation on the standard 12 lead electrocardiogram 1-4 h after initiation of thrombolysis may be the simplest and most useful clinical 'tool' to gauge the effectiveness of thrombolytic therapy. The predictive value of this single marker might be further improved by combining it with assessment of the rate of increase of serum myoglobin and of troponin T, provided these determinations were rapidly available.

Biomarkers↗
PubMed1996

Expanding concepts in ischaemic heart disease: implications for clinical practice and research.

In the late Eighties, a series of observations from several institutions around the world has dramatically revolutionized the traditional notion that the occurrence of myocardial infarction was related most of the time to the development of critical flow-limiting coronary stenosis. All these studies showed that the infarct-related artery had only minimal or mild stenosis in about two thirds of the cases. Therefore, contrary to our previous beliefs, in clinical practice the detection of coronary stenosis has a lesser role in the prognostic assessment of patients with ischaemic heart disease, unless associated with extensive ischemia or with phases of instability. In fact, the major determinants of prognosis are represented by age, left ventricular function, effort tolerance and especially by the clinical stability or instability of angina. According to the Bayesian an theorem, in low risk patients any diagnostic test has a very low predictive accuracy, unless very high specificity criteria are used. The value of diagnostic tests in the assessment of patients' prognosis should be evaluated in intermediate risk groups. The emphasis of clinical research has, therefore, shifted from the detection of flow-limiting stenosis to the study of the multiple and varied dynamic causes of stable and unstable ischaemia, where the possibilities of making new, seminal observations are greater.

Aged↗
PubMed1996

[Magnetic resonance in the assessment of myocardial viability after infarction: comparison with dobutamine echocardiography and thallium scintigraphy].

UNLABELLED: Revascularization and prognosis after acute myocardial infarction (AMI) depend on the assessment of myocardial viability. Thus, after AMI, the myocardium may still be viable, though with contractile dysfunction. This study was aimed at comparing three tomographic methods, that is, dobutamine echocardiography (DE), thallium scintigraphy after i.v. nitrate bolus (SPET) and MRI at rest, in the assessment of viable tissue. The viability standard was post-revascularization functional recovery, as assessed with echocardiography at rest. Twenty-four patients with previous AMI (3-6 months earlier) were examined: 384 segments in all; 106 segments were a-dyskinetic and they make up our study group. At first follow-up (30-45 days), 38 segments exhibited functional recovery and were considered viable; sensitivity and specificity rates follow: 68% and 75% for DE, 75% and 55% for SPET, and 95% and 34% for MRI, respectively. IN CONCLUSION: 1) this is the first study comparing three different tomographic methods with the same myocardial segmentation for viability assessment; 2) MRI exhibited very high sensitivity, which means no false negatives; 3) SPET and MRI exhibited low specificity, due to their intrinsic limitations, but also to the inadequacy of functional recovery as a viability parameter, as indicated by PET; 4) the authors expect better results from MRI with low-dose dobutamine and first-pass ultrafast MRI with Gd-DTPA for the assessment of myocardial perfusion.

Aged↗
PubMed1995

Circadian variation of ischemic threshold in syndrome X.

To evaluate whether the ischemic threshold has a circadian rhythm in patients with syndrome X, we analyzed 90 episodes of ST depression detected on 24-hour Holter recordings of 12 such patients. Ischemic threshold was considered as heart rate (HR) at 1 mm ST depression. To correct for differences in basal HR among patients, however, the ischemic threshold was also calculated as a normalized index of HR at 1 mm ST depression: [(HR at 1 mm ST-24-hour modal HR)/24-hour modal HR]-100. Mean hourly values of both absolute and normalized HRs at 1 mm ST depression were obtained by grouping and averaging respective values of all episodes detected in every hour of the day in all patients. Chronobiologic analysis was performed by single cosinor method. A significant circadian rhythm was found for HR (mesor 76 beats/min, amplitude 10 beats/min, acrophase at 2:16 P.M., p < 0.001), number of episodes of ST depression (mesor 3.75, amplitude 2.9, acrophase at 2:45 P.M., p < 0.001) and cumulative time of ischemia, with a high correlation of distributions. Episodes of ST depression showed a double peak initially in the morning, and again in the afternoon. Both raw and normalized values of HR at 1 mm ST depression also had a significant circadian variation in ischemic threshold, which was lower in the night and early morning hours, progressively increased until the first afternoon hours, and subsequently decreased in the evening.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Cytomegalovirus replication is not a cause of instability in unstable angina.

BACKGROUND: Unstable angina is most frequently caused by coronary thrombosis, with or without plaque fissure, but the mechanisms underlying these events are still speculative. Since cytomegalovirus (CMV) antigens and DNA encoding CMV major immediate-early (MIE) gene have been detected in atherosclerotic arterial walls, the active replication of CMV may be responsible for plaque instability. Therefore the expression of CMV MIE gene mRNA, an early marker of viral replication, was assessed in coronary atherectomy specimens from patients with stable or unstable angina. METHODS AND RESULTS: Twenty patients with unstable angina (12 men and 8 women; mean age, 62 years; range, 44 to 89 years) and 20 patients with stable angina (16 men and 4 women; mean age, 62 years; range, 43 to 81 years) who underwent successful directional coronary atherectomy were enrolled in the study. The efficiency of mRNA extraction, transcription, and amplification from each coronary atherectomy specimen was assessed by performance of reverse transcription and thermal cycling amplification of a 548-bp human beta-actin cDNA segment. After Southern blotting and hybridization with a specific probe, all specimens but one showed a positive hybridization signal. The negative sample was excluded from the study. Reverse transcription and thermal cycling amplification of a 145-bp CMV cDNA segment of the MIE gene were then carried out. After Southern blotting and hybridization with a specific probe, none of the specimens showed a positive hybridization signal. Plasmid pACYC 184 containing the Xba I-inserted MIE gene cDNA was used as a positive control: as few as 10 molecules of the plasmid per reaction were detectable after amplification. CONCLUSIONS: Our results do not support the hypothesis that, in patients with unstable angina, replication of CMV in coronary atherosclerotic plaques is a major cause of plaque instability. These findings suggest that the research for the causes of unstable angina should be directed toward processes other than CMV replication.

Angina Pectoris↗