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PubMed1983

Distribution of abnormal Q waves on body surface in relation to left ventricular wall motion abnormalities in myocardial infarction.

This study was undertaken to determine the possible one-to-one relationship between each site of asynergy of the left ventricle and the body surface area to which ensuing abnormal electrical phenomena are reflected. In 140 post-myocardial infarction (MI) patients, distribution of abnormal Q waves on the body surface was correlated with the abnormal segments of LV wall motion identified by left ventriculography (LVG). Unipolar lead electrocardiograms (ECGs) were recorded from 87 lead points over the precordium and the back with Wilson's central terminal as the reference point. Data acquisition and mapping was accomplished through a mapping system HPM 5100 microcomputer. In all cases, coronary arteriography (CAG) and LVG were performed at least 2 months after the acute episode of MI. The LVG findings were evaluated separately in seven wall segments in accordance with the American Heart Association (AHA) reporting system. Sensitivity, specificity, diagnostic accuracy, positive predictive value, and negative predictive value of the abnormal Q wave in each lead point were obtained in cases with abnormal wall motion in segments 2, 3, and 6, respectively, and in infero-posterior segments 4 or 5. Statistical analysis was performed by comparing two groups of patients with or without asynergy of each wall segment concerned. Results of the study revealed some abnormal Q areas of high diagnostic accuracy that correlated highly with the site of abnormal contractility.

Journal Article↗
PubMed1997

Abnormalities of the heart and great arteries in first trimester chromosomally abnormal fetuses.

Pathological examination of the heart and great arteries was performed in 112 chromosomally abnormal fetuses after surgical termination of pregnancy at 11-16 weeks of gestation. The chromosomal abnormalities were diagnosed by chorion villus sampling which was carried out because screening of the pregnancies by a combination of maternal age and fetal nuchal translucency thickness at 10-14 weeks of gestation identified them as being at increased risk. The group consisted of 60 fetuses with trisomy 21, 29 with trisomy 18, 17 with trisomy 13 and 6 with Ullrich-Turner syndrome. The most common cardiac lesion seen in trisomy 21 fetuses was an atrioventricular or ventricular septal defect. Trisomy 18 was associated with ventricular septal defects and/or polyvalvular abnormalities. In trisomy 13, there were atrioventricular or ventricular septal defects, valvular abnormalities, and either narrowing of the isthmus or truncus arteriosus. Ullrich-Turner syndrome was associated with severe narrowing of the whole aortic arch. In all four groups of chromosomally abnormal fetuses, the aortic isthmus was significantly narrower than in normal fetuses and the degree of narrowing was significantly greater in fetuses with high nuchal translucency thickness. It is postulated that narrowing of the aortic isthmus may be the basis of increased nuchal translucency thickness in all four chromosomal abnormalities.

Abnormalities, Multiple↗
PubMed2006

Additional chromosomal abnormalities in patients with a previously detected abnormal karyotype, mental retardation, and dysmorphic features.

The detection of chromosomal abnormalities in patients with mental retardation (MR) and dysmorphic features increases with improvements of molecular cytogenetic methods. We report on six patients referred for detailed characterization of chromosomal abnormalities (four translocations, one inversion, one deletion) detected by conventional cytogenetics, in whom metaphase CGH revealed imbalances not involved in the initially detected rearrangements. The detected abnormalities were validated by real-time PCR. Parents were investigated by CGH in four cases. The genomic screening revealed interstitial deletions of 2q33.2-q34, 3p21, 4q12-q13.1, 6q25, 13q22.2-q31.1, and 14q12. The estimated minimum sizes of the deletions ranged from 2.65 to 9.27 Mb. The CGH assay did not reveal imbalances that colocalized with the breakpoints of the inversion or the translocations. The deletion of 6q included ESR1, in which polymorphisms are associated with variation of adult height. FOXG1B, known to be involved in cortical development, was located in the 14q deletion. The results illustrate that whole-genome molecular cytogenetic analysis of phenotypically affected patients with abnormal conventional karyotypes may detect inapparent molecular cytogenetic abnormalities in patients with microscopic chromosomal abnormalities and that these data provide additional information of clinical importance.

Adolescent↗
PubMed1994

Chromosomal abnormalities in fetuses with absent end-diastolic velocity in umbilical artery: analysis of risk factors for an abnormal karyotype.

OBJECTIVE: Our purpose was to evaluate the incidence and patterns of chromosomal abnormalities in fetuses with absent end-diastolic velocity in umbilical artery and to analyze maternal and fetal factors associated with abnormal karyotype. STUDY DESIGN: One hundred ninety-two fetuses of known karyotype with absent end-diastolic velocity in the umbilical artery at a gestational age > 20 weeks were considered. The following potential risk factors were analyzed in a multiple logistic regression model: maternal age, gravidity, parity, gestational age at diagnosis, presence of gestational hypertension and preeclampsia, presence of fetal malformations, different biometric measurements, head/abdominal circumference ratio, amniotic fluid volume, and several Doppler index values calculated from uterine arteries, fetal heart, and fetal peripheral arteries and veins. RESULTS: Sixteen cases had an abnormal karyotype. In two cases a triploidy was present, whereas the remaining 14 cases had autosomal aberrations. The risk factors statistically significantly and independently associated with the presence of an abnormal karyotype were maternal age > 35 years, gestational age at diagnosis < 27 weeks, presence of multiple malformations, and absence of gestational hypertension and preeclampsia. All the fetuses with an abnormal karyotype but one were correctly identified by at least one risk factor. CONCLUSIONS: An abnormal karyotype is present in 8.3% of fetuses with absent end-diastolic velocity in umbilical artery and is associated with maternal and fetal risk factors. The knowledge of these factors may be useful in the management of such fetuses.

Abnormalities, Multiple↗
PubMed1983

Hereditary inner-ear abnormalities in animals. Relationships with human abnormalities.

A classification scheme for inner-ear abnormalities is defined, based on animals with hereditary inner-ear defects. Three major groups are (1) morphogenetic abnormalities, involving gross structural deformities of the labyrinth; (2) neuroepithelial abnormalities, in which there appears to be a primary organ of Corti defect and Reissner's membrane remains in its normal position; and (3) cochleosaccular abnormalities, showing collapse of Reissner's membranes and restriction of vestibular abnormalities to the saccule. Recent experimental findings in hearing-impaired animal mutants are taken into account. The relevance of the classification of scheme to conditions in humans is discussed. It is suggested that the Mondini and Michel deformities in humans are best considered together in the morphogenetic group. Some cases of inner-ear abnormality in humans might be considered as belonging to the neuroepithelial group.

Animals↗
PubMed2006

A prospective evaluation of uterine abnormalities by saline infusion sonohysterography in 1,009 women with infertility or abnormal uterine bleeding.

OBJECTIVE: To evaluate the role of saline infusion sonohysterography (SIS) in the investigation of uterine abnormalities and malformations in patients referred for infertility work-up compared with women with abnormal uterine bleeding (AUB). DESIGN: Prospective cohort study. SETTING: Academically oriented private practice. PATIENT(S): One thousand nine consecutive women examined by SIS for infertility work-up (n = 600, infertility group) or AUB investigation (n = 409, AUB group). INTERVENTION(S): SIS. MAIN OUTCOME MEASURE(S): Intracavitary abnormalities and uterine anomalies. RESULT(S): Among the women in the infertility group, 16.2% (n = 97) were found to have intracavitary abnormalities, including polyps (13.0%), submucous fibroids (2.8%), and adhesions (0.3%). Significantly, more patients in the AUB group (39.6%, n = 162) revealed intracavitary abnormalities, including polyps (29.8%), submucous fibroids (9.0%), and adhesions (0.7%). In contrast, significantly more uterine anomalies were found in the infertility group (20%, n = 120) compared with the AUB group (9.5%, n = 39). Arcuate uterus was the most common finding (15% vs. 6.4% of patients, respectively). CONCLUSION(S): An SIS procedure for infertility work-up revealed a substantial percentage of infertile patients with intracavitary abnormalities and uterine anomalies. Because the technique is safe, well tolerated, and feasible in an outpatient setting, SIS should be considered routinely in the early stage of infertility and AUB investigation.

Administration, Intravaginal↗
PubMed1985

Carpal tunnel syndrome: associated abnormalities in ulnar nerve function and the effect of carpal tunnel release on these abnormalities.

Twenty of 59 hands (34%) of patients with carpal tunnel syndrome had abnormalities in sensibility testing of both median and ulnar nerves by either two-point discrimination, Semmes-Weinstein monofilament testing, or both. Before surgery, 53% of patients complained of paresthesias and/or numbness in ulnar nerve distribution. Eighty percent of the hands had abnormal Semmes-Weinstein monofilament testing of the ulnar nerve. Thirty-five percent had abnormal two-point discrimination. Forty-one percent had abnormal electromyographic testing of the ulnar nerve. All hands had median nerve decompression alone. Guyon's canal was not released. After surgery, 89% of patients had improvement in paresthesias and/or numbness of the ulnar nerve. Ninety-four percent had improvement in Semmes-Weinstein monofilament testing. Eighty-six percent had improvement in two-point discrimination. Patients with a residual abnormality in ulnar nerve sensibility also had continued abnormality in median nerve sensibility. A significant percentage of patients with carpal tunnel syndrome also have signs and symptoms of ulnar nerve compression. Most improved with carpal tunnel release alone.

Carpal Tunnel Syndrome↗
PubMed2006

Prognostic and biological implications of genetic abnormalities in multiple myeloma undergoing autologous stem cell transplantation: t(4;14) is the most relevant adverse prognostic factor, whereas RB deletion as a unique abnormality is not associated with adverse prognosis.

Fluorescence in situ hybridization (FISH) has become a powerful technique for prognostic assessment in multiple myeloma (MM). However, the existence of associations between cytogenetic abnormalities compels us to re-assess the value of each abnormality. A total of 260 patients with MM at the time of diagnosis, enrolled in the GEM-2000 Spanish transplant protocol, have been analyzed by FISH in order to ascertain the independent influence on myeloma prognosis of IGH translocations, as well as RB and P53 deletions. Survival analyses showed that patients with t(4;14), RB or P53 deletions had a significantly shorter survival than patients without these abnormalities. However, patients with RB deletions without other abnormalities in FISH analysis, displayed a similar outcome to those patients without genetic changes by FISH (46 vs 54 months, P=0.3). In the multivariate analysis the presence of t(4;14), RB deletion associated with other abnormalities, age >60 years, high proportion of S-phase cells and advanced stage of the disease according to the International Staging System retained their independent prognostic influence. In summary, RB deletion as a sole abnormality does not lead to a shortening in the survival of MM patients, whereas t(4;14) confers the worst prognosis in MM patients treated with high-dose chemotherapy.

Adult↗
PubMed2003

Abnormal response to sodium channel blockers in patients with Brugada syndrome: augmented localised wall motion abnormalities in the right ventricular outflow tract region detected by electron beam computed tomography.

OBJECTIVE: To investigate the relation between the wall motion abnormalities and sodium channel abnormalities in cases of the Brugada syndrome. DESIGN: Consecutive prospective case-control study in a single hospital. SETTING: Tertiary referral centre. PATIENTS: 13 consecutive patients with Brugada syndrome and 13 age and sex matched control subjects. INTERVENTIONS: Each subject underwent electron beam computed tomography (EBT) and a 12 lead ECG before and after disopyramide injection. MAIN OUTCOME MEASURES: QRS width and the magnitude of ST segment elevation in the 12 lead ECG; wall motion by EBT. RESULTS: After disopyramide, EBT revealed deterioration of focal wall motion abnormalities in the right ventricular outflow tract region in eight of the 13 patients (62%). Prolongation of the QRS width after disopyramide injection in lead V2, which usually reflects the electrical activity in right ventricular outflow tract region, was greater in these eight patients (p < 0.01) than in the other five patients, in whom wall motion did not change after disopyramide. The degree of augmentation of ST segment elevation did not differ significantly between the two groups CONCLUSIONS: The deterioration of wall motion abnormalities in the right ventricular outflow tract region after disopyramide suggests the presence of functional abnormalities of the sodium channel. Some patients with Brugada syndrome may have arrhythmogenic substrates with abnormal responses to sodium channel blockers.

Adult↗
PubMed1978

Abnormal plasminogen. A hereditary molecular abnormality found in a patient with recurrent thrombosis.

A patient who suffered a recurring thrombosis over the last 15 yr has been investigated. The only abnormality found in this patient was a significantly depressed level of plasminogen activity in plasma. In spite of the depressed plasminogen activity, the patient was found to have a normal level of plasminogen antigen concentration. It was calculated that the activity per milligram of plasminogen of the patient was approximately one-half the values of normal subjects. The same discrepancy between biological activity and antigen concentration was found in the other members of the kindred. A niece was found to have practically no plasminogen activity but possessed a normal concentration of plasminogen antigen. Both her parents were found to have approximately half the normal plasminogen activity and normal antigen levels. These studies suggested that the molecular abnormality was inherited as an autosomal characteristic, and the family members who had half the normal levels of activity with normal plasminogen antigen were heterozygotes whereas the one with practically no plasminogen activity was homozygote. Subsequent studies showed that the pattern of gel electrofocusing of purified plasminogen of the heterozygotes consisted of 10 normal bands and 10 additional abnormal bands, each of which had a slightly higher isoelectric point than each corresponding normal component. This indicates that plasminogen of the heterozygote is a mixture of normal and abnormal molecules in an approximately equal amount, which was substantiated by active site titration of purified plasminogen preparations obtained from the propositus and a normal individual. The gel electrofocusing pattern of the homozygote consisted of abnormal bands only. The defect is a hereditary abnormality of plasminogen.

Adult↗
PubMed2004

Association of an abnormal exercise heart rate recovery with pulmonary function abnormalities.

BACKGROUND: Heart rate recovery (HRR) after exercise correlates with decreased vagal tone and mortality. Patients with COPD may have altered autonomic tone. We sought to determine the association of HRR with spirometry measures of pulmonary function. METHODS: We analyzed 627 patients (mean [+/- SD] age, 58 +/- 12 years; 65% men; mean FEV(1), 2.6 +/- 0.9 L, 80 +/- 20% predicted; patients receiving inhaled beta(2) agonist therapy, 10%; patients receiving inhaled anticholinergic therapy, 3%; patients receiving inhaled steroids, 5%; patients receiving oral prednisone, 4%) who had undergone maximal exercise testing and had undergone pulmonary function tests < 1 year apart. Patients with heart failure, pacemakers, and atrial fibrillation were excluded. Abnormal HRR was defined as a fall in heart rate during the first minute after exercise of <or= 12 beats/min (<or= 18 beats/min with stress echocardiography). Patients were divided into quartiles based on FEV(1) percent predicted. RESULTS: An abnormal HRR was seen in 229 patients (36%). The mean FEV(1) values broken into quartiles 1 to 4 were 54 +/- 11% predicted, 74 +/- 3% predicted, 87 +/- 4% predicted, and 106 +/- 10% predicted. In smokers and nonsmokers, a worsening FEV(1) percent predicted was associated with an abnormal HRR. In a multivariable model accounting for confounding factors including medications and functional capacity, the predictors of an abnormal HRR included FEV(1) percent predicted (adjusted odds ratio for 1 SD decrease, 1.32; 95% confidence interval, 1.07 to 1.65; p = 0.0004), impaired functional capacity, male gender, and age. CONCLUSIONS: Abnormalities found on spirometry are associated with abnormal HRR, which may reflect an altered autonomic tone associated with pulmonary dysfunction, either obstructive or restrictive in nature.

Autonomic Nervous System↗
PubMed1995

Poor prognosis in multiple myeloma is associated only with partial or complete deletions of chromosome 13 or abnormalities involving 11q and not with other karyotype abnormalities.

Chromosomal abnormalities have major biologic and prognostic implications in leukemias. Cytogenetic information in typically hypoproliferative multiple myeloma (MM) is limited because of difficulties in obtaining analyzable metaphases. In this study, karyotypes and other known prognostic factors were analyzed in 155 newly diagnosed MM patients, entered on an intensive treatment program with two autotransplants. Complete remission (CR), event-free (EFS) and overall survival (OS) were analyzed using standard statistical methods. Abnormal cytogenetics were found in 39% of patients and were associated with a significantly lower CR rate (27% v 48%; P = .008). EFS and OS were inferior in patients with either partial or complete deletion of chromosome 13 or 11q abnormalities ("unfavorable" karyotype) when compared with the remaining patients (P < .001) who, as a group, had a similar prognosis irrespective of cytogenetic findings, ie, inevaluable, normal, or abnormal but without an "unfavorable" karyotype. The patients with abnormalities of both chromosomes 11 and 13 had a dismal prognosis with median EFS and OS of only 11 and 12 months, respectively. Significant associations were noted between an "unfavorable" karyotype and IgA isotype, elevated levels of beta-2 microglobulin (B2M, > or = 3 mg/L) and age > 60 years. On multivariate regression analysis, the absence of an "unfavorable" karyotype was the most significant variable associated with prolonged EFS and OS (P = .0001 and .0002, respectively). Other independent favorable variables were age less than 60 years, C-reactive protein (CRP) < or = 0.4 mg/dL and bone marrow plasmacytosis < or = 50% before treatment. On a multivariate analysis without cytogenetics, these same three standard parameters were identified as the only favorable variables. Patients not having all three standard favorable variables had a significantly lower CR rate (P = .03), EFS (P = .0001), and OS (P = .002) if an unfavorable karyotype was detected. We conclude that, in this program of uniformly treated MM patients, a poor prognosis was associated predominantly with abnormalities of chromosomes 11 and 13.

Chromosome Aberrations↗
PubMed2005

Ocular and systemic manifestations of PHACES (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects and coarctation of the Aorta, Eye abnormalities, and Sternal abnormalities or ventral developmental defects) syndrome.

INTRODUCTION: PHACES syndrome (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects and coarctation of the aorta, Eye abnormalities, and Sternal abnormalities or ventral developmental defects) is a rare neurocutaneous syndrome with only 2 case reports published in the ophthalmic literature. This study was conducted to identify ocular and systemic manifestations of PHACES syndrome. METHODS: A retrospective chart review was performed on 8 children with a diagnosis of PHACES syndrome. Information recorded included age at first visit, length of follow-up, gender, race, vision, need for glasses, strabismus, amblyopia, ptosis, proptosis, anterior and posterior segment abnormalities, need for treatment of the hemangioma, type of treatment of the hemangioma, and systemic manifestations. RESULTS: Periocular and ocular findings in patients with PHACES syndrome included hemangioma involving ocular structures (n = 6), strabismus (n = 4), amblyopia (n = 5), proptosis (n = 2), ptosis (n = 5), anterior polar cataract (n = 1), optic atrophy from optic neuropathy (n = 1), heterochromia (n = 1), and refractive error requiring glasses (n = 2). All patients were treated with steroids for the hemangioma. Systemic manifestations of PHACES syndrome included posterior fossa malformation (n = 4), hemangioma (n = 8), arterial anomalies (n = 3), cardiac abnormalities (n = 3), and sternal or ventral deformities (n = 3). CONCLUSION: Children with PHACES syndrome may have significant ocular and systemic abnormalities and are at increased risk for strabismus and amblyopia. They often require steroid therapy of the hemangioma to prevent and/or treat ocular complications. These patients require careful monitoring by a pediatric ophthalmologist in addition to other subspecialists.

Abnormalities, Multiple↗
PubMed1991

Morphological abnormalities, neonatal mortality, and reproductive abnormalities in mice transgenic for diphtheria toxin genes that are driven by the promoter for adipocyte lipid binding protein.

Transgenic mice were used in an experiment that was designed to serve as a model of a possible approach to reducing the amount of carcass fat in meat animals. The objective was to reduce the number of adipocytes in transgenic mice thereby restricting the capacity to accumulate lipid. Our approach employed the technique of genetic ablation. The promoter for the adipocyte lipid binding protein gene was used in an attempt to direct expression of diphtheria toxin genes specifically to adipocytes. Three diphtheria toxin genes were used; they encode, respectively, an extremely cytotoxic wild type toxin, a less toxic attenuated toxin, and a nonfunctional toxin. While it was not possible to accurately assess effects of the transgenes on lipid accumulation, several informative observations were noted. A large percentage of transgenic founder mice that harbor either wild type or attenuated toxin genes are morphologically abnormal, die as neonates, or exhibit reproductive abnormalities including sterility or failure to transmit the transgene to offspring. In contrast, mice that harbor the nonfunctional toxin gene or are nontransgenic rarely have these same abnormalities. These results suggest that the transgenic mice are expressing the transgenes in cells other than adipocytes and that the aberrant production of functional toxin is responsible for the congenital abnormalities. The production of morphological and reproductive abnormalities in transgenic animals should be useful for investigating normal developmental processes.

Animals↗
PubMed1995

Abnormal platelet von Willebrand factor (vWF) as a marker of abnormal function in megakaryocytic dysplasia.

The myelodysplastic syndromes (MDS) are neoplastic disorders of the hemopoietic system; multilineage involvement is also evidenced by specific cellular dysfunctions. The von Willebrand factor (vWF), synthesized and processed in the megakaryocytes (MK), is stored in the alpha granules of the platelets. The platelet vWF multimeric pattern was studied in 18 patients with MDS, and in 4 with pernicious anemia (PA), to investigate whether the processing of vWF is abnormal in the megakaryocytic dysplasia. An abnormal multimeric pattern was observed in 10/18 MDS and 4/4 PA patients. The abnormality of this specific protein is the discrete expression of the basic disorder, and is reversible when hemopoiesis is normalized. Although the data do not allow any conclusion, abnormal synthesis is the likely explantation of the abnormality.

Anemia, Pernicious↗
PubMed1985

Abnormal transverse tubule system and abnormal amount of receptors for Ca2+ channel inhibitors of the dihydropyridine family in skeletal muscle from mice with embryonic muscular dysgenesis.

We have found two important sets of abnormalities in skeletal muscle from mice with embryonic muscular dysgenesis. These abnormalities involve the internal structural organization of the muscle fiber and its content of voltage-dependent Ca2+ channels. The first abnormality concerns the ultrastructural aspects of the membranous couplings between sarcoplasmic reticulum and the transverse tubules, known as triads. The triads are less numerous, are disorganized, and lack spaced densities (feet). The second abnormality is a significant decrease in specific binding sites for the dihydropyridine derivatives, (known as Ca2+ channel inhibitors) in striated skeletal muscle, but not in cardiac muscle. Both sets of abnormalities are potentially directly linked to the uncoupling of excitation and contraction.

Animals↗
PubMed1995

Abnormalities in intramyocardial arteries detected in cardiac transplant biopsy specimens and lack of correlation with abnormal intracoronary ultrasound or endothelial dysfunction in large epicardial coronary arteries.

OBJECTIVES: We sought to determine whether abnormalities in small intramyocardial vessels could be detected on routine cardiac transplant biopsy specimens and whether these features correlate with intimal thickening by intracoronary ultrasound and endothelial dysfunction in large epicardial vessels. BACKGROUND: Variability in clinical presentation of allograft vasculopathy suggests differential involvement of large and small vessels. Intracoronary ultrasound and endothelial function studies detect large-vessel abnormalities but may not reflect changes in small intramyocardial arteries. The latter could be detected in routine cardiac biopsy specimens by histologic and immunohistochemical studies. METHODS: Thirty-nine cardiac transplant recipients underwent intracoronary ultrasound and acetylcholine studies 5 to 7 days after endomyocardial biopsy. Biopsy tissue was evaluated for coronary artery endothelial plumping and intimal thickening and increased immunostaining for fibronectin, tumor necrosis factor-alpha and receptor for hyaluronan-mediated motility. Large-vessel disease was assessed by calculating an average intimal index from intracoronary ultrasound of the left anterior descending coronary artery. Endothelial function was determined by quantitative coronary analysis after acetylcholine challenge. RESULTS: Coronary arteries were found in the biopsy tissue of 30 (76%) of the 39 patients who formed the study group. Fourteen of 30 patients had abnormal histologic findings. Immunohistochemical analysis for fibronectin, possible in 20 of 30 patients, was positive in 14 (70%) of 20 and correlated with abnormal histologic findings (p = 0.01). Immunostaining was positive for tumor necrosis factor-alpha and receptor for hyaluronan-mediated motility in 12 (40%) and 13 (43%) of 30 patients, respectively. All patients had intimal thickening by intracoronary ultrasound, but intimal index did not correlate significantly with small-artery disease by histologic or immunohistochemical analysis. Large-vessel endothelial dysfunction in 13 patients (43%) did not correlate with either abnormal ultrasound findings or small-vessel disease. CONCLUSIONS: Intramyocardial arteries are readily observed in biopsy specimens from cardiac transplant recipients and provide useful information about allograft vasculopathy. Lack of correlation between intramyocardial and epicardial vessel disease suggests discordant progression of allograft vasculopathy.

Adult↗