Showing papers by "Nilesh J. Samani published in 1999"
TL;DR: A myocardial perfusion reserve index derived from first-pass MRI studies can distinguish between normal subjects and patients with coronary artery disease and provides useful functional information on coronary lesions, particularly where the physiologic significance cannot be predicted accurately from the angiogram.
210 citations
TL;DR: It is concluded that the GPIa 807T allele is not a risk factor for MI in the population either alone or in combination with other major cardiovascular risk factors.
Abstract: The platelet collagen receptor, GPIa/IIa, is an important mediator of platelet adhesion to fibrillar collagens at sites of vascular injury. Recently, a dimorphism at nucleotide 807 of the GPIa cDNA (TTC/TTT in codon 224) was shown to be associated with variation in GPIa/IIa receptor density on the platelet surface. We conducted a case-control study to determine if the 807T allele, linked with increased GPIa/IIa density, contributed to risk of myocardial infarction (MI). DNA from 546 acute MI cases and 507 controls, all aged <75 years, was genotyped for the C807T dimorphism using the TaqManTM system of allelic discrimination. The allelic odds ratio (OR) for MI in the complete cohort was 0.88 (95% CI 0.74-1.05, P = 0.17), indicating that the 807T allele was not associated with an increased risk of MI. There was also no increased risk of MI associated with the homozygous 807TT (P = 0.22) or heterozygous 807CT (P = 0.24) genotypes or for carriers of the 807T allele in any cohort subgroup analysed. We conclude that the GPIa 807T allele is not a risk factor for MI in our population either alone or in combination with other major cardiovascular risk factors.
65 citations
TL;DR: It is concluded that nonlinear mRNA processing can generate tissue-specific transcripts in transcripts of a rat gene (SA) with a normal exon-intron organization.
Abstract: The production of different transcripts (transcript heterogeneity) is a feature of many genes that may result in phenotypic variation. Several mechanisms, that occur at both the DNA and RNA level have been shown to contribute to this transcript heterogeneity in mammals, all of which involve either the rearrangement of sequences within a genome or the use of alternative signals in linear, contiguous DNA or RNA. Here we describe tissue-specific repetition of selective exons in transcripts of a rat gene (SA) with a normal exon–intron organization. We conclude that nonlinear mRNA processing can generate tissue-specific transcripts.
62 citations
TL;DR: The PT20210A allele is not a risk factor for MI and it is suggested that discrepancies in studies relating the PT202 10A allele to MI may be due to difficulties in estimating its low allelic frequency in the general population and thus random differences in the observed frequencies in the control populations studied.
Abstract: The relationship between the prothrombin (PT) 20210A allele and arterial disease is controversial. We conducted a case-control study to assess its contribution to risk of myocardial infarction (MI). Five hundred and thirty-nine acute MI patients and 498 control subjects aged
39 citations
Proceedings Article•
01 Jan 1999TL;DR: In this article, the authors elucidated the mechanism and clinical signiJcance of precordial ST depression in patients with an inferior myocardial infarction using first-pass, contrast-enhanced,myocardial perfusion magnetic resonance imaging (MRI).
Abstract: We elucidated the mechanism and clinical signiJcance of precordial ST depression in patients with an inferior myocardial infarction using first-pass, contrast-enhanced, myocardial perfusion magnetic resonance imaging (MRI). Forty-seven patients with acute inferior myocardial infarction underwent first-pass contrast-enhanced MR studies within 2-6 days postinfarction. Patients were followed-up for a minimum of I year after infarct (range, 12-32 months). Total perfusion deficit scores derived . qualitatively from MRIs were compared in patients with (group I, n = 30) and without (group 2, n = 17) ST depression precordially. Perfusion remote from the infarct zone was also compared. The combined end points of adverse clinical events and/or the need forfurther intervention were assessed for each group. Total perfusion deficit scores were sign@cantly higher in group I than group 2 (medians 9.7 versus 4.5, p 15 versus 0-5 (7/7 versus 1/7, p < 0.01). MRI shows thatprecordial ST depression in inferior myocardial infarction is a marker for a larger global perfusion abnormaliry with posterolateral basal extension and an increase in adverse clinical end points. Furthermore, the magnitude of the perfusion deficit
2 citations
TL;DR: MRI shows that precordial ST depression in inferior myocardial infarction is a marker for a larger global perfusion abnormality with posterolateral basal extension and an increase in adverse clinical end points, highlighting the potential of MRI perfusion studies as a research and clinical tool in myocardia infarct.
Abstract: We elucidated the mechanism and clinical signiJcance of precordial ST depression in patients with an inferior myocardial infarction using first-pass, contrast-enhanced, myocardial perfusion magnetic resonance imaging (MRI). Forty-seven patients with acute inferior myocardial infarction underwent first-pass contrast-enhanced MR studies within 2-6 days postinfarction. Patients were followed-up for a minimum of I year after infarct (range, 12-32 months). Total perfusion deficit scores derived . qualitatively from MRIs were compared in patients with (group I, n = 30) and without (group 2, n = 17) ST depression precordially. Perfusion remote from the infarct zone was also compared. The combined end points of adverse clinical events and/or the need forfurther intervention were assessed for each group. Total perfusion deficit scores were sign@cantly higher in group I than group 2 (medians 9.7 versus 4.5, p 15 versus 0-5 (7/7 versus 1/7, p < 0.01). MRI shows thatprecordial ST depression in inferior myocardial infarction is a marker for a larger global perfusion abnormaliry with posterolateral basal extension and an increase in adverse clinical end points. Furthermore, the magnitude of the perfusion deficit
1 citations